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For the Herd’s Sake, Vaccinate!

2011-12-30T14:50:00.000-08:00

By STEVEN L. WEINREB

West Hartford, Conn.

I HAVE chronic lymphocytic leukemia. Three months ago, I underwent an allogeneic stem-cell transplant, in which my wise, 52-year-old white blood cells were replaced by bewildered, low-functioning cells from an anonymous European donor. For the next seven months or so, until those cells mature, I have a newborn’s immunity; I am prey to illnesses like chickenpox, the measles and the flu.

These diseases are rarely fatal, unless you’re a newborn or someone with a suppressed immune system like me. My newborn buddies and I do have some protection, however: the rest of you.

Young babies, the immuno-compromised and people who get chemotherapy are not able to process most vaccinations. Live vaccines in particular, like those for measles and chickenpox, can make us sick. But if 75 percent to 95 percent of the population around us is vaccinated for a particular disease, the rest are protected through what is called herd immunity. In other words, your measles vaccine protects me against the measles.

It’s the reasoning of Clarence, the angel from “It’s a Wonderful Life”: If you are vaccinated, you won’t pass a disease on to someone else, who won’t pass it on to six more people, and on and on. To quote Clarence, “Strange, isn’t it? Each man’s life touches so many other lives.”

Unfortunately, vaccination rates for many diseases in Europe and in areas of the United States are falling. This is partly due to Andrew Wakefield, a British doctor who published a paper, now discredited, in 1998 in The Lancet tying childhood vaccines to autism. Celebrities like Jim Carrey have also taken a strong antivaccine view. As a result of these unwarranted fears, childhood diseases are returning. The rate of whooping cough cases has spiked over the past 20 years. In 1990, the incidence was 2 per 100,000 people; in 2000 it was 3; by last year, it had risen to nearly 10.

Measles cases are also increasing. For each year between 2001 and 2008, the median number of cases in the United States was 56. In the first six months of this year alone, there were more than 150 reported cases — the most since 1996. A vast majority of those who were sickened had not been vaccinated or had uncertain vaccination histories. Before the vaccine was introduced in 1963, 400 to 500 Americans died of measles every year.

During last year’s flu season there were 55,403 reported cases of influenza A and B; 116 children died of the disease. And now flu season is back.

The truth is, we should not get vaccinated for ourselves alone; we should do it for one another. Having cancer has taught me the value of living in a community. We assist the infirm, pay our taxes and donate to charity, and getting vaccinated — for the flu, for adult whooping cough, for pneumonia — is just another important societal responsibility. After all, we’re in the same herd.

Steven L. Weinreb, an internist who is certified in oncology and hematology, is on medical leave from his job at a private practice.

A Drug That Wakes the Near Dead

2011-12-24T09:05:00.001-08:00

The moment she saw him, Judy Cox knew her son was dead. It was an October morning in 2008, and she had just stepped out the door to run an errand when she found him lying faceup in the driveway, ghost white, covered in purple splotches. He wasn’t breathing, and when she couldn’t revive him, she ran screaming into the house where her husband, Wayne, was still asleep. “Chris is dead,” she cried. “Call 911!”

Wayne jumped out of bed and raced down to the driveway, where he knelt over his son’s limp frame and tried frantically to elicit a breath or a heartbeat. As he pumped Chris’s chest and scooped out the vomit that had collected in his mouth, Judy ran to the kitchen and steadied herself long enough to call for an ambulance.

Chris was 26. He had not been well. An A.T.V. accident the previous August left him with debilitating back pain that physical therapy did nothing to alleviate. His doctor had recently prescribed Oxycontin. His parents learned later that he had taken too much.

By the time the ambulance arrived, Chris’s heart had been still for at least 15 minutes. It took the paramedics another 15 to get it pumping again; even then, doctors had little hope he would survive. Brain cells begin dying off just five minutes after blood stops delivering oxygen. After 30 minutes, there is likely to be more dead tissue than living.

Nonetheless, the emergency-room staff members at the local hospital did their best. They hooked Chris up to a tangle of tubes and machines and injected him with drugs to stabilize his heart rate. Wayne and Judy watched helplessly from the hallway. After four hours, a doctor finally summoned them to a secluded corridor.

Chris was in a coma, the doctor said, and in all likelihood had suffered severe, irreversible brain damage. He was breathing only with the help of a ventilator and would probably have a series of heart attacks in the night.

“First they asked us to let them pull the plug,” Judy recalled one recent afternoon, as we sat in the living room of the Coxes’ house in a Memphis suburb. “Then they tried getting us to sign a do-not-resuscitate order.” Without one, the doctor explained, hospital staff would be forced to revive Chris each time he started slipping away, which could mean cracking his ribs and shocking him with electricity. Even if they managed to keep his body alive, what was left of his brain would surely die in the days ahead.

Wayne and Judy refused to sign. “This is not some dog we’re talking about putting down,” Wayne shouted. “This is our son.” Chris still lived with his parents. He was a good kid, a joker, but bashful, especially around girls. He liked playing basketball and fishing in the pond near his house. He was planning to take over the family repo business when Wayne retired in a few years. Before the A.T.V. accident, he’d never given them much trouble at all. He deserved every chance the hospital could give him.

The heart attacks never came. Four days later, Chris woke up.

It was not the awakening of Hollywood movies in which the patient comes to, just as he was, speaking full sentences and completely mobile. Three years later, Chris still cannot talk. Although he breathes on his own, his lungs battle a steady barrage of infections; a feeding tube provides all his sustenance, and his muscles have contracted into short, twisted knots. He can move only the slightest bit — his fingers and eyelids twitch, but his arms and legs remain mostly immobile — and his neck is not quite strong enough to hold up his head, which leans against a crescent-shaped support around his wheelchair headrest.

Still, Wayne and Judy say that his cognition is improving. On good days, they say, he can respond to basic commands — blink his eyes for yes, wiggle his finger for no, give a thumbs up when asked. Doctors agree that Chris has progressed beyond a vegetative state, to a hazy realm known as minimal consciousness. What that means — what it says about his experience of the world around him or his prospects for further recovery — is something they are still trying to figure out.

Convinced that the son they know and love is still “in there,” Chris’s parents have spent the past three years searching for a way to bring him back out. So far, their best hope has come from an unlikely source: Ambien. A growing body of case reports suggests that the popular sleep aid can have a profound — and paradoxical — effect on patients like Chris. Rather than put them to sleep, both Ambien and its generic twin, zolpidem, appear to awaken at least some of them. The early reports were so pronounced that until recently, doctors had a hard time believing them. Only now, more than a decade after the initial discovery, are they taking a closer look.

The first report of a zolpidem awakening came from South Africa, in 1999. A patient named Louis Viljoen, who, three years before, was declared vegetative after he was hit by a truck, had taken to clawing at his mattress during the night. Thinking he was suffering from insomnia, his family doctor suggested zolpidem to help him sleep. But 20 minutes after his mother ground the tablet up and fed it to him through a straw, Viljoen began to stir. His eyes, which normally wandered the room, vacant and unfocused, flickered with the light of consciousness. And then he began to talk (his first words were “Hello, Mummy”), and move (he could control his limbs and facial muscles). A few hours later he became unresponsive. But the next day, and for many days after that, zolpidem revived him, a few hours at a time.

Here was a case worthy of Hollywood: three years was well past the point at which doctors would expect any sort of spontaneous recovery. Viljoen awoke with the ability to speak in complete sentences. Not only did he recognize his mother, but he also recognized the voices of people who had spoken to him only when he was apparently vegetative. He remembered nothing of the mysterious realm he kept receding back into. When doctors asked him what it was like to slip away, he said he felt no changes at all. But he could recall conversations from the previous day’s awakening, along with bits and pieces of his former life: his favorite rugby team, specific matches he attended, players that he rooted for and against. As time passed, his cognition improved. He could laugh at jokes, and his awakenings stretched from a few hours to entire days. Eventually, he no longer needed zolpidem.

In the years that followed, a steady trickle of similar reports emerged — some from doctors who tried zolpidem after hearing about the Viljoen case, others from those who discovered its benefits accidentally, as Viljoen’s doctor had. The drug did not work for everyone, and even when it did, its effects typically wore off after an hour or two. But for a lucky few, those effects were profound. People who seemed vegetative for years were waking up.

There are roughly 200,000 patients in the United States trapped in the borderlands between consciousness and oblivion. Until recently, most doctors believed that recovering from this condition was not possible. Vegetative states were considered permanent after three months if the injury was caused by oxygen deprivation, or one year if it was caused by blunt trauma. And since minimally conscious patients did not fare much better than those who were vegetative, most doctors did not bother to draw the distinction.

But in the past decade, a series of developments have coalesced into a far more complicated picture than previously imagined. In 2003, an Arkansas man named Terry Wallis emerged, after 19 years, from a minimally conscious state. Neuroimaging suggested that his brain had essentially reconfigured itself — surviving neurons bypassed dead ones and forged new connections to one another. In a 2007 Nature paper, Nicholas Schiff, a neurologist from Weill Cornell Medical College, and his colleagues showed that deep brain stimulation — surgically implanting a “brain pacemaker” that sends electrical impulses to specific regions of the brain — can help some severely injured patients recover the ability to speak and eat, years after the injury. And just this month, Adrian Owen, a British neuroscientist, reported in the journal The Lancet that the brains of some patients who seemed vegetative responded to basic commands: their bodies didn’t move, but distinct patterns of neuronal firing were detected on EEG scans when these patients were told to make a fist (which triggered one region of the premotor cortex) or wiggle their toes (which triggered another).

This year, scientists at Moss Rehabilitation Research Institute and at the University of Pennsylvania, both in the Philadelphia area, began the first large-scale clinical study of zolpidem as a treatment for disorders of consciousness. (Amantadine, a drug used to treat Parkinson’s disease, and the anti-anxiety medication Ativan also show promise in increasing awareness in minimally conscious patients.) So far, the evidence suggests that less than 10 percent of brain-injured patients will experience the drug’s paradoxical effects, and that among those, only a few will respond as profoundly as Viljoen did. For families like the Coxes, such odds provide a tortured kind of hope. For doctors, they bring questions. Why does a sleeping pill induce awareness in some patients but not others? And what can these bizarre awakenings tell us about the brain’s ability to heal?

Two weeks after Chris first emerged from the coma, he began tracking objects with his eyes. At one month, he could follow simple commands. “His friends would come in the room, and there’d be two or three on each side of the bed,” Judy recalled. “And eventually, when they’d say, ‘Look at Jim,’ or ‘Look at Bob,’ he’d fix his eyes on the right guy.” Wayne and Judy asked for a follow-up M.R.I., but their neurologist said it would be pointless. Chris’s behaviors were entirely reflexive, he said; they were produced by his brainstem, which regulates basic functions like breathing and body temperature, not by his cortex, the region responsible for higher-order thinking. That Chris’s friends and family saw him following commands was proof of their denial, not of Chris’s recovery.

“Every couple days, the doc would stop in the doorway and shout Chris’s name to see if Chris responded,” Judy said. “But he wouldn’t come in the room and look at Chris up close. So one day, I practically grabbed his arm and dragged him into the room, over to Chris’s bed.” She told Chris to blink his eyes. He did. Then she made the doctor walk across the room and told Chris to keep his eyes on the doctor. He did. Finally, with the doctor standing across the room, eyes fixed on Chris, she asked Chris to give her a thumbs up. When he wiggled his thumb, just the tiniest bit, the doctor’s jaw dropped. Chris was not in a vegetative state after all. He was minimally conscious.

Still, there was little that the community hospital could do for him. It had neither the resources nor the expertise to tease out a prognosis or chart a course of therapy. The same was true of local nursing homes, which is where many patients like Chris end up.

So Wayne and Judy took over their son’s care, bringing him first to a premier brain-injury center in Atlanta (where Chris had a device implanted in his spine, which releases drugs to help with spasticity) and then to a clinic in Destin, Fla. (where he tried an experimental treatment known as hyperbaric oxygen therapy). They had just made their way back home to Tennessee when a friend told them about the Ambien paradox and the clinical trial in Philadelphia.

One hallmark of the minimally conscious state is a rapid fluctuation between levels of awareness. Spend 10 or 20 minutes with Chris Cox, and you might conclude that there is nothing going on upstairs. But spend a full hour, and at some point you’ll see his puppy-dog eyes come into focus. They will appear to search for one of his parents, or to settle quizzically on the new person in the room. Ask him to say something, and he’ll smack his lips frantically before leaning forward and tapping his feet in apparent frustration. You’ll swear that he is there with you and that only his physical infirmities (he cannot quite swallow or control his jaw) prevent him from describing the netherworld from which he has just emerged.

And then, a few minutes later, he’ll slip away again.

This fluidity makes diagnosis a challenge. “If a patient follows every command you give them, you know that,” says Dr. John Whyte, director of the Moss Institute and lead investigator on the zolpidem trial. “If a patient has never, ever followed a command, you know that too. But if you tell a patient to wiggle their finger, and they do it occasionally — which is the case for most of these folks — how do you figure out if that ‘occasionally’ means something or not?”

Whyte has spent his entire career trying to answer this question. His first job after his residency was at a facility with a large number of vegetative patients. While working there, he was struck by the amount of contention over diagnoses. For all their experience with this population, clinicians could not seem to agree on whether any given patient was actually conscious. Family members also argued, with one another and with staff, over the meaning of every wince, twitch and eye flutter.

It turned out that a lot of people — staff members included — were drawing their conclusions from pure coincidence. Whyte told me about one mother who insisted that her son would point down toward his feeding tube to indicate that fluid was leaking onto his stomach, causing irritation. “He did it while I was there,” Whyte says. “And she lifted his shirt and said: ‘See, doctor, there’s the liquid. He’s communicating with us.’ And I said: ‘How often do you look under there when he isn’t pointing like this? Never? Not even once?’ ” It was possible that the pointing corresponded to the leak, Whyte explained. But it was also possible that the leaking was constant and the pointing was random. There were countless other examples. “Behaviors would be exceptions if they happened at the wrong time, and evidence if they happened at the right time,” Whyte says.

To help eliminate this bias, Whyte developed what he calls the single-subject assessment, in which doctors design a set of tests specific to each patient’s idiosyncrasies to determine whether the patient is vegetative or minimally conscious. It is painstaking work, but the information it yields is significant. “Patients who achieve minimal consciousness early tend to have a better prognosis,” Whyte says. “And you can at least try to build a communication system with them, because you have a foundation to work from.”

With a reliable assessment method in place, he began searching for ways to build on that foundation. Then the curious Ambien awakenings caught his attention.

It’s not entirely surprising that Ambien would arouse instead of sedate. The pill has long been linked to reports of bizarre sleepwalking behavior (not to mention sleepeating, sleeptalking, even sleepdriving). Some scientists call this phenomenon “paradoxical excitation.” So far, none of the accepted determinants of prognosis — age, overall health, the nature of the initial injury or the extent of brain damage as determined by an M.R.I. — have proved useful in predicting which brain-injured patients will experience it and which won’t. To begin answering that question, Whyte says, you need to study both responders and nonresponders in an unmedicated state.

One morning this past March, I met Chris, Wayne and Judy at the University of Pennsylvania’s main hospital, where they had been flown in from Tennessee, at the study’s expense, so that Chris could be tested in an unmedicated state. From the corner of a small hospital room, we watched as Whyte’s research assistant, Andras Szeles, attached dozens of tiny electrodes to Chris’s face and scalp, then fitted him with a large headset. The electrodes would measure Chris’s brain activity as Szeles administered a series of cognitive tests.

For one test, Szeles placed a rubber glove on Chris’s right hand. A voice coming through the headset told Chris to either “squeeze glove” or “squeeze bare,” several times over. Chris did not seem to be responding at all, but Szeles explained that the electrodes would measure what the naked eye could not. “We’re not so interested in whether or not Chris can squeeze,” he said. “We just want to know if he’s trying to squeeze.” Different neurons fire when you move your left hand versus your right hand. They also fire if you imagine moving it, prepare to move it or start to move it but stop, all of which the electrodes would detect.

“The term ‘consciousness’ can be a real can of worms,” Szeles said. “There are degrees of awareness, and it’s not always clear what the threshold should be. What we’re really looking for here is evidence of comprehension and will.” If Chris understood the words “squeeze” and “glove,” knew that this very specific thing was being asked of him, and possessed, at the most basic level, the will to respond, a distinct pattern of brain waves would show up in the results.

After Whyte and his team have tested 80 patients, they will compare the results of zolpidem responders to those of nonresponders and look for clues that might help explain the difference — maybe a specific brain region that lights up unexpectedly, or a pattern of neuronal firing common to one group but not the other. Any such discovery could light a path not only through the labyrinths of Chris’s fractured mind but to a better understanding of consciousness itself.

Wayne and Judy have a more immediate question: they want to know their son’s long-term prognosis. Has he reached the pinnacle of his cognitive recovery? Or is it a launching pad from which greater heights might be reached?

“Once a patient progresses to minimal consciousness, we can’t predict what’s going to happen,” says Dr. Joseph J. Fins, chief of medical ethics at Weill Cornell Medical College and author of a coming book, “Rights Come to Mind: Brain Injury, Ethics and the Struggle for Consciousness.” Some patients have recovered full consciousness, but many more remain stuck in limbo. The only way to know the outcome is to give the patient time.

But offering time is a complex proposition. “Early on, when families have the option to pull the plug, it’s almost impossible to tell what the long-term prognosis will be,” says Dr. Soojin Park, a neurointensivist at the University of Pennsylvania Hospital, and an investigator on the zolpidem trial. “And then later, when we have the certainty — that this is as good as it’s going to get — that option is gone. Because by then, the patient is breathing on their own. There’s no more plug to pull.” At that point, families who want to end a loved one’s suffering must either have the feeding tube removed, or agree to let the next bacterial infection win out, unhindered by antibiotics. Many families find choosing these deaths much more difficult than turning off a ventilator. It’s an instinct reinforced by religious edicts that forbid the withholding of basic sustenance but allow, for example, unplugging artificial respirators.

It is not uncommon for doctors to assume the worst and advise family members to withdraw care early. They do so in part because they see their duty as helping loved ones face reality. But Fins argues that this is a cop-out. “It’s glossing over all the unknowns for the sake of a quicker, cleaner solution,” he says. “It’s wrong to be so uniformly fatalistic so early on, especially with all the data emerging about the prospects for later-stage recovery.”

According to several studies, about 40 percent of patients who have been declared vegetative are actually minimally conscious. Other studies have shown that a surprising number of vegetative and minimally conscious patients made huge strides toward recovery much later than conventional wisdom would predict.

Park says that more doctors are trying drug therapy on vegetative and minimally conscious patients, but for the most part, they are groping in the dark. “We still don’t understand which drugs should work on which patients, or at what dosage, or at what point in their recovery,” she says. “And that makes it tough for families to know when they should fight and when they should give up.”

There is also the matter of cost. Treating and monitoring patients like Chris — designing and performing single-subject assessments that can discern random twitches from deliberate behavior, managing the host of medical complications that can stymie brain recovery and continually evaluating progress — is significantly more expensive than placing them in nursing homes, where they receive basic care but have no access to brain-injury specialists. Proponents argue that the measures will save money in the long run — if the patient is able to go home, for instance. Still, it’s unclear whether even the most aggressive care will make much difference for many patients. “The payers need a better sense of what the likely outcome is for any given patient,” says Tom Smith, program director at Moss, “so that they can say with confidence which patients are likely to benefit from treatment, and how significant that benefit is likely to be. And I hate to sound this way, but then it’s basically: ‘Am I going to invest this amount of money to get this outcome? Is that worth it?’ And that is a tough, tough question to answer.”

When Chris first returned from the hospital, the Coxes’ house was flooded with well-wishers. A former teacher brought a quilt that Chris and his classmates made in grade school. Old girlfriends, acquaintances and childhood pals visited regularly. His high-school friends even held a fund-raiser to help pay for some of his therapy. But as time wore on, and it became clear that he would neither die nor fully recover, the guests dwindled. Besides Chris’s sister, Amber, who visits often, Wayne and Judy are now mostly on their own.

The couple surrendered their bedroom, which is on the ground floor of their split-level house, to Chris. They take turns sleeping there, on a small cot in the corner of the room, surrounded by medical equipment: a hospital bed with a queen-size air mattress that helps prevent bed sores, a special chair called a “sit-stand,” which can be cranked into an upright position and is supposed to help ease muscle contractions. A mechanical lift. A breathing machine.

Judy is especially keen to show me Chris’s latest gadget, a device called an Eyegaze, that looks a bit like an iPad, and which Chris is learning to use to communicate. She mounts it to a handlebar on Chris’s wheelchair. At first, Chris’s eyes move rapidly across several rows of icons — words with pictures, partial sentences like “I want” or “I like,” and cartoon images of friends and family members with their names in bold. Tracking his eyes, the computer reads: “Green. Brit. I want.” And then, “Brit–Brit–Brit–Brit–Brit.” Brit is his cousin. It’s unclear if he’s asking for her, or if his eyes are just not cooperating.

Judy puts the computer away. He still needs practice, she says. When they first tried it, in February, during outpatient rehab, the therapist asked Chris what color went with Valentine’s Day, and he was able to look at the “red” icon. But so far, “I want a drink,” is the only full sentence he has managed.

Each day begins with the same routine: Judy helps Chris up, forcing him to sit on the edge of the bed, without neck or back support, for several minutes. The goal is to strengthen his neck muscles so that one day he can hold his own head up. A nurse helps her bathe him and then lift him into his chair, so that he can be wheeled into the living room or taken outside. Three times a week, a van delivers mother and son to a rehab center, where a therapist works to stretch and stimulate Chris’s contracted muscles. And almost as often, either Wayne or Judy spends several hours on the phone, battling Chris’s insurance company, which they say has covered private nursing and weekly therapy but denied an extended stay at a brain-injury rehab center. The couple arrange their schedules so that their son is never without at least one parent.

The Coxes have surrounded themselves with a new group of friends — other parents with children like Chris. The families in this informal group share strategies and trade information on emerging research and experimental treatments. They also talk of weariness and isolation. “At the end of the day, you feel like you’re a thousand years old,” Judy says. “And you have no idea how you’re going to get up and do it all over again tomorrow.” Both Wayne and Judy admit to being frustrated by the slow pace of Chris’s progress. But he’s come this far; they can’t help hoping that he might come further still. “I know that some people, even people who loved Chris, think maybe he should have just died,” Wayne says. “But he didn’t die. He lived. And as long as he’s still breathing, we have to do the absolute best we can for him.”

The reports on zolpidem are still mixed. Viljoen and a few others have improved steadily over time; some of them are now fully conscious on their own, without medication. (Viljoen is confined to a wheelchair and has cognitive disabilities but has improved over the years.) But such improvement is rare. According to Whyte, most responders fall into one of two categories: those who can take zolpidem daily, with no appreciable loss of efficacy, and those for whom the “awakenings” wane with continued use. The latter type, he says, may be the most common.

With no way of knowing which type of responder Chris might be, the Coxes play it safe. They give Chris Ativan every day; it has a similar though less profound effect on his behavior. But zolpidem they hoard like pixie dust, giving it only on special occasions, when friends and family can be there.

They gave him some when I visited, so I could see how it works.

A few minutes after receiving the zolpidem, Chris opened his eyes and smiled. Judy sat on the bed, facing him. “Hey, buddy!” she said. “Can I have a kiss?” She leaned in, cheekward, but he turned his head up in what looked like a deliberate slight. “Chris!” she admonished, playfully. He smiled and grunted. He was teasing her. Just as she pulled away, he thrust forward and grazed her cheek with puckered lips. Confident that he was there with us, Judy took out a marker and some paper and wrote one command after another, each of which Chris followed: Stick out your tongue, give me five, give me a thumbs up. And then, “Show us your Elvis grin.” Chris curled his upper lip into a sneer. When Judy ran out of commands, Chris began smacking his lips and moving his tongue. “Talk to us, buddy,” Wayne said. “Say, ‘Mom,’ ” Judy said. After several moments, Chris managed a loud, slow “Maaaa.”

Led by the child who simply knew

2011-12-12T16:15:00.001-08:00

The twin boys were identical in every way but one. Wyatt was a girl to the core, and now lives as one, with the help of a brave, loving family and a path-breaking doctor’s care.
Jonas and Wyatt Maines were born identical twins, but from the start each had a distinct personality.

‘Wyatt
needs hair
accessories, clothes, shoes . . . likes to wear bikinis, high heels,
mini-skirts.’

Jonas was all boy. He loved Spiderman, action figures, pirates, and swords.

Wyatt favored pink tutus and beads. At 4, he insisted on a Barbie birthday cake and had a thing for mermaids. On Halloween, Jonas was Buzz Lightyear. Wyatt wanted to be a princess; his mother compromised on a prince costume.

Once, when Wyatt appeared in a sequin shirt and his mother’s heels, his father said: “You don’t want to wear that.’’

“Yes, I do,’’ Wyatt replied.

“Dad, you might as well face it,’’ Wayne recalls Jonas saying. “You have a son and a daughter.’’

That early declaration marked, as much as any one moment could, the beginning of a journey that few have taken, one the Maineses themselves couldn’t have imagined until it was theirs. The process of remaking a family of identical twin boys into a family with one boy and one girl has been heartbreaking and harrowing and, in the end, inspiring - a lesson in the courage of a child, a child who led them, and in the transformational power of love.

Wayne and Kelly Maines have struggled to know whether they are doing the right things for their children, especially for Wyatt, who now goes by the name Nicole. Was he merely expressing a softer side of his personality, or was he really what he kept saying: a girl in a boy’s body? Was he exhibiting early signs that he might be gay?Was it even possible, at such a young age, to determine what exactly was going on?

Until recently, there was little help for children in such situations.But now a groundbreaking clinic at Children’s Hospital in Boston - one of the few of its kind in the world - helps families deal with the issues, both emotional and medical, that arise from having a transgender child - one who doesn’t identify with the gender he or she was born into.

The Children’s Hospital Gender Management Services Clinic can, using hormone therapies, halt puberty in transgender children, blocking the development of secondary sexual characteristics - a beard, say, or breasts - that can make the eventual transition to the other gender more difficult, painful, and costly.

Founded in 2007 by endocrinologist Norman Spack and urologist David Diamond, the clinic - known as GeMS and modeled on a Dutch program - is the first pediatric academic program in the Western Hemisphere that evaluates and treats pubescent transgenders. A handful of other pediatric centers in the United States are developing similar programs, some started by former staffers at GeMS.

It was in that clinic, under Spack’s care, that Nicole and her family finally began to have hope for her future.

The Maineses decided to tell their story, they say, in order to help fight the deep stigma against transgender youth, and to ease the path for other such children who, without help, often suffer from depression, anxiety, and isolation.

“We told our kids you can’t create change if you don’t get involved,’’ says Wayne, 53, sitting in the living room of their comfortable home in a southern Maine community they do not want identified.

They have good reason for caution. Their journey has included a lawsuit to protect their daughter’s rights, and a battle against bullying and insensitivity that led them to move to a new place and new schools.

It has been a hard road, but nothing that compares with the physical transformation of Wyatt into Nicole.

“I have always known I was a girl,’’ says Nicole, now 14. “I think what I’m aiming for is to undergo surgery to get a physical female body that matches up to my image of myself.’’

Early confusion

When Wyatt and Jonas were born, their father was thrilled. Wayne looked forward to the day when he could hunt deer with his boys in the Maine woods. The family lived in Orono, near the University of Maine campus, where Wayne is the director of safety and environmental management.

They had no preparation for what would come next.

When Wyatt was 4, he asked his mother: “When do I get to be a girl?’’ He told his father that he hated his penis and asked when he could be rid of it. Both father and son cried. When first grade started, Wyatt carried a pink backpack and a Kim Possible lunchbox.

His parents had no idea what was going on. They had barely heard the term “transgender.’’ Baffled, they tried to deflect Wyatt’s girlish impulses by buying him action figures like his brother’s and steering him toward Cub Scouts, soccer, and baseball.

When the boys were 5, Kelly and Wayne threw a “get-to-know-me’’ party for classmates and parents. Wyatt appeared beaming at the top of the stairs in a princess gown, a gift from his grandmother.

Kelly whisked him off and made him put on pants. Though she and Wayne were accustomed to his girly antics, they were afraid of what others might think.

To this day, she feels guilty about it. “I know she was totally confused and felt like she had done something wrong,’’ says Kelly, 50, who works in law enforcement.

“Even when we did all the boy events to see if she would ‘conform,’ she would just put her shirt on her head as hair, strap on some heels and join in,’’ Kelly says. “It wasn’t really a matter of encouraging her to be a boy or a girl. That came about naturally.’’

Kelly and Wayne didn’t look at it as a choice their child was making.

“She really is a girl,’’ Kelly says, “a girl born with a birth defect. That’s how she looks at it.’’

Fear of the unknown

After Wyatt began to openly object to being a boy, his mother started doing research on transgender children. There was little out there; it seemed they would have to find their way largely on their own.

During those early years, while Kelly was doing her research, Wayne was hoping that this was no big deal, that this was a stage Wyatt just had to go through.

“I felt it had nothing to do with how they would grow up,’’ he says.

But as they grew older, his concern grew. “I feared the unknown,’’ he says.

Even the family Christmas card became a challenge. They would write about Jonas’s affinity for sports and Wyatt’s “flair for the dramatic.’’

Their elderly pediatrician, nearing retirement, did not want to discuss the matter with them. Finally, Kelly picked another pediatrician out of the phone book. “I told her how it was, and it turned out that she understood and was very supportive.’’

When the twins were in the first grade, their parents found a therapist for Wyatt, who was starting to act out. In the third grade, before the GeMS Clinic was even open, Kelly heard about Dr. Spack and made an appointment with him.

“He told us everything,’’ Wayne says, recalling that first meeting. “I didn’t understand it all, but I saw the weight lift off Kelly’s shoulders and a smile in Nicole’s eyes. That was it for me. There were tons of challenges for us after that, but I knew my daughter was going to be OK, medically.’’

Elementary school changes

In elementary school, Wyatt told classmates that he was a “girl-boy.’’ In the fourth grade, he grew his hair longer and started talking about a name change. That same year, he drew a self-portrait as a girl, and in a class essay, wrote: “Wyatt needs hair accessories, clothes, shoes . . . likes to wear bikinis, high heels, mini-skirts.’’

Emma Peterson of Orono, a close friend from the elementary years at the Asa Adams School, recalls playing dolls with Nicole’s giant dollhouse, and the two of them putting on makeup. “Before Nikki started growing her hair out, she looked exactly like Jonas,’’ Emma says.

In fourth grade, Wyatt started using “Nicole’’ as a name, and many classmates were calling him “Nikki.’’ The next year, the family went to court and had the name legally changed to Nicole.

To Kelly, it seemed the next logical step. Family discussions merely centered around what the name would be. In the end, Nicole chose it. “I believed in Nicole,’’ her mother says. “She always knew who she was.’’

Wayne was nervous. Could he call his son Nicole? As usual, he relied on his wife’s instincts. “I have to tell you, Kelly’s the leader in our family,’’ he says. “Both she and Nicole are extremely strong-willed, and I went with the flow.’’

At first, though, he couldn’t bring himself to use the new name. An Air Force veteran and former Republican, he realizes now he was grieving the loss of a son. “But once you get past that, I realize I never had a son,’’ he says.

Legal battles

When fifth grade started, Wyatt was gone. Nicole showed up for school, sometimes wearing a dress and sporting shoulder-length hair. She began using the girls’ bathroom. Nikki’s friends didn’t have a problem with the transformation; there were playdates and sleepovers.

“They said, ‘It was about time!’ ’’ Nicole says. She was elected vice president of her class and excelled academically.

But one day a boy called her a “faggot,’’ objected to her using the girls’ bathroom, and reported the matter to his grandfather, who is his legal guardian. The grandfather complained to the Orono School Committee, with the Christian Civic League of Maine backing him. The superintendent of schools then decided Nicole should use a staff bathroom.

“It was like a switch had been turned on, saying it is now OK to question Nicole’s choice to be transgender and it was OK to pursue behavior that was not OK before,’’ Wayne says. “Every day she was reminded that she was different, and the other kids picked up on it.’’

According to a 2009 study by the Gay, Lesbian and Straight Education Network, 90 percent of transgender youth report being verbally harassed and more than half physically harassed. Two-thirds of them said they felt unsafe in school.

To protect her from bullying at school, Nicole was assigned an adult to watch her at all times between classes, following her to the cafeteria, to the bathroom. She found it intrusive and stressful. It made her feel like even more of an outsider.

“Separate but equal does not work,’’ she says.

It was a burden that Jonas shouldered as well. The same boy who in fifth grade objected to her using the girls bathroom made the mistake of saying to Jonas in sixth grade that “freaking gay people’’ shouldn’t be allowed in the school. Jonas jumped on him and a scuffle ensued.

“He’s taken on a lot,’’ Wayne says. “Middle school boys and sexuality, you know . . . boys can get picked on.’’

Nicole and her parents filed a complaint with the Maine Humans Right Commission over her right to use the girls bathroom. The commission found that she had been discriminated against and, along with the Maines family, filed a lawsuit against the Orono School District. The suit is pending in Penobscot County Superior Court, and the Maines family is represented by lawyers from the Gay & Lesbian Advocates & Defenders (GLAD) in Boston and by Jodi Nofsinger, who serves on the Maine ACLU board.

“What Nicole and Jonas both went through in school was unconscionable,’’ says Jennifer Levi, one of the GLAD lawyers on the case. “Their one huge stroke of luck was having Kelly and Wayne as parents.’’

A huge relief

Since that first visit to Spack when Nicole was 9, her parents discussed putting her into the GeMS Clinic when the right time came. They were glad there was time to adjust to the idea. “Baby steps,’’ Kelly calls their path toward treatment.

“I wasn’t always on board,’’ Wayne says. “Kelly and I were not on the same page. My question was, what is this doctor doing? It scared me. I was grieving. I was losing my son.’’

But the more he watched his child struggle, the better he felt about going to Spack. And once he got there, he says, it was a huge relief. “Not only does he know what he’s doing, he’s extremely comforting. He’s got to deal with a ton of dads who are just freaking out, and he made me feel good.’’

Spack’s experience runs deep; before the clinic was established, he had long worked with transgender youth, as well as with adults. “The most striking thing about these kids was the fact that they were just normal young people who had this incredibly unusual and problematic situation,’’ says Spack, 68.

He believes it is crucial to intervene with such children before adolescent changes begin in earnest.

“Most of us look pretty similar until we hit puberty,’’ he says. “I bet I could go to any fourth or fifth-grade class, cut the hair of the boys, put earrings on various kids, change their clothing, and we could send all those kids off to the opposite-gender bathrooms and nobody would say boo.’’

He adds: “We can do wonders if we can get them early.’’

Second-guessing

Not everyone agrees that they should, of course, and Spack has heard the arguments: Man should not interfere with what God has wrought. Early adolescents are too young for such huge decisions, much less life-altering treatment.

Though GeMS treatment is now considered the standard of care by mainstream medical groups, some have their doubts. Dr. Kenneth Zucker, a psychologist and head of the gender-identity service at the Center for Addiction and Mental Health in Toronto, says he worries about putting youngsters on puberty blockers, drugs that suppress the release of testosterone in boys and estrogen in girls.

“One controversy is, how low does one go in starting blockers?’’ Zucker says. “Should you start at 11? At 10? What if someone starts their period at 9?’’ Nicole started on the blockers at age 11.

He also questions the role the parents have played; have they simply followed the child’s lead? “Say a 5-year-old says repeatedly that he wants to be a girl,’’ Zucker says. “The parents deduce this must mean the child is transgender, so they socially transition him to living in the other gender.’’

Spack and others, however, say the issue is a medical one and that early intervention makes sense. “We’re talking about a population that has the highest rate of suicide attempts in the world, and it’s strongly linked to nontreatment, especially if they are rejected within their family for being who they think they are,’’ says Spack, who adds that nearly a quarter of his patients admitted to “serious self-harm’’ before coming to him.

As for the criticisms about “playing God,’’ Spack quotes from the Old Testament: “Leviticus says, ‘If thy neighbor is bleeding by the side of the road, you shall not stand idly by the blood of thy neighbor.’ It’s a mandate. I think these kids have been bleeding.’’

The next step

The clinic, which includes geneticists, social workers, psychiatrists, psychologists, and nurses, has so far treated 95 patients for disorders that range from babies born with ambiguous genitalia to cases where normal sexual development does not occur.

About a third of the patients have undergone puberty suppression.

Each patient must have been in therapy with someone familiar with transgender issues and who writes a letter recommending the treatment. The child’s family also must undergo extensive psychological testing before and during treatment. And the patient must be in the early stage of puberty, before bodily changes are noticeable.

Nicole and Jonas are the first set of identical twins the program has seen, and they have provided critical comparative data, Spack says.

The effects of the blockers - an injection given monthly to prevent the gonads from releasing the unwanted hormones - are reversible; patients can stop taking them and go through puberty as their biological sex. This is critical, Spack says, because a “very significant number of children who exhibit cross-gender behavior’’ before puberty “do not end up being transgender.’’

Since the 1970s, the blockers have been used for the rare condition of precocious puberty, when children as young as 3 can hit puberty. They are kept on the blockers until they are of appropriate age. “The drugs have a great track record; we already know that these kids do fine,’’ says Spack. “There are no ill consequences.’’

It is the next big step - taking sex hormones of the opposite gender - that creates permanent changes, such as breasts and broadened hips, that cannot be hormonally reversed.

“In puberty,’’’ Spack says, “when your body starts making a statement, you either have to accept it or reject it.’’

There is no definitive answer to the question of what causes gender identity disorder, though studies suggest a genetic contribution. “It’s still a very open question,’’ Zucker says. And how could it affect just one of two identical twins? “There can be genetic changes during fetal development that maybe hit one twin but not the other.’’

Changed atmosphere

After the family’s lawsuit against the Orono schools was publicized, the atmosphere in town changed. When they went to the movies, people pointed and whispered. There were fewer party invitations, fewer sleepovers.

In the sixth grade, the twins joined the school’s Outing Club. All year they attended meetings to prepare for the crowning event: a whitewater rafting trip. Wayne went to several meetings, too, so he could serve as a chaperone.

Wayne thought he had a good relationship with the club leader. But then the man informed him that Nicole would not be allowed to sleep in the tent with the girls - the same girls who had slept over her house several times. She and her father could have a separate tent.

A difficult family conversation followed. Jonas and Wayne went on the trip. Nicole stayed home.

After that episode, Kelly and Wayne decided a new start would be good for the family. The summer after the sixth grade, they moved to a larger, more diverse community in southern Maine, and the twins enrolled in public school. Wayne still works at UMaine and stays in Orono during the week, spending weekends with his family.

For two years, in seventh and eighth grade, Nicole went “stealth,’’ as she calls it: passing as a girl. She did not tell anyone that she was biologically male. Though she made friends at school, she never brought them to the house. After that hard last year in Orono, the family was afraid to come out.

This fall the twins entered high school, transferring to a smaller, private school known for open-mindedness. Before they arrived, the school changed its bathrooms to unisex. And before classes started, the family met with members of the school’s Gay Straight Alliance - “so she’d have older kids watching her back,’’ says Wayne. After the meeting, the group changed its name to include transgender; it is now the Gay Straight Transgender Alliance.

“It made me a lot more comfortable,’’ Nicole says. “I thought, this is OK. I can do this.’’

She recently started telling some of her new friends her story. One girl replied: “Does this mean you’re going to start wearing boys’ clothes to school?’’

“No,’’ replied Nicole. “I’m male to female.’’

The girl’s reaction? “She was like, ‘Ohhhhhhhhhhhhhhh.’ ’’

Concerns about safety

The male hormone suppressors have done their job, and the next step is to add female hormones so that Nicole will undergo puberty as a girl and develop as a woman, with breasts and curvy hips. She is due to see Spack in January, and a date may then be set for adding estrogen, which she will take every day for the rest of her life. Though she will have a higher risk of breast cancer than if she were a male, she will have a lower risk of prostate cancer, Spack says. The treatment will leave her infertile.

But before the estrogen is administered, the GeMS clinic will reevaluate Nicole to make sure that she still identifies as a female and wants to continue.

“In my experience, the patients just blossom physically and mentally when they get the hormones of the gender they affirm,’’ Spack says. “It’s quite amazing. I feel good about Nicole and who she is and where she’s going.’’

An endocrinologist in Maine now administers the blockers Nicole needs, but Spack still sees her in Boston every four to six months. The Maines family has grown close to him and others in the clinic. “I love going to see him,’’ says Wayne, who has thanked Spack for “saving my daughter’s life.’’ The Maines family declined to talk about the cost of the treatment but said insurance has covered much of it.

But as well as things are going, the Maines family still worries about Nicole’s safety. Last year Wayne and Nicole attended Transgender Day of Remembrance in Maine, which honors those who have been killed in hate crimes.

Wayne spoke to the crowd, telling them that as much as Nicole is loved at home, her family cannot always protect her.

“I remind her that she needs to always be aware of her surroundings, to stay close to friends and her brother if she feels uncomfortable, and to call me anytime she feels threatened,’’ he said.

Lobbying the Legislature

Last winter, Maine state representative Kenneth Fredette, a Republican from Penobscot County, sponsored a bill that would have repealed protections for transgender people in public restrooms, instead allowing schools and businesses to adopt their own policies. The bill was a response to the Maines’ 2009 lawsuit against the Orono School District.

Last spring Wayne and Nicole roamed the halls of the State House, button-holing legislators and testifying against the bill. “I’d be in more danger if I went into the boys bathroom,’’ Nicole told the lawmakers, who ultimately rejected the bill.

“She knows how to work a room,’’ her father says proudly. “She even convinced a cosponsor to vote the other way.’’

In October, the family was honored for its activism in helping defeat the transgender bathroom bill. The Maineses received the Roger Baldwin Award, named for a founder of the American Civil Liberties Union, from the Maine chapter of the ACLU.

Surrounded by Kelly and the kids, Wayne told the audience that he and his wife have had top-notch guides as they confronted the unknown.

“As a conventional dad, hunter, and former Republican, it took me longer to understand that I never had two sons,’’ he told them. “My children taught me who Nicole is and who she needed to be.’’

Typical teens

In some respects, Jonas has had as tough a time as Nicole. For one thing, there’s the personality difference: Nicole is the dominant twin, talkative and tough, while Jonas is cautious and reserved.

“If this had been Jonas, I would have had to home school him,’’ his mother says.

The twins have always been close. During an interview, Nicole sits next to her brother on the couch and occasionally lays her head on his shoulder. At one point, when Jonas goes silent as the twins talk of their lives, she whispers words of encouragement into his ear.

But the next minute, like typical teenage siblings, they’re teasing and tussling. Jonas displays a faint scar on his arm where Nicole jabbed him with a pencil. Both have black belts in tae kwon do, which they started at age 5.

They often hang out in Jonas’s spacious basement room, where they watch TV and play video games.

“I love having a sister,’’ says Jonas, who acknowledges being protective of her. “We have a very strong relationship.’’

Nicole calls Jonas her closest friend.

“I would say my brother got lucky with me. Because we grew up with only boy neighbors, I developed a liking to shoot-’em-up and military video games,’’ she says. “I could have come out a lot girlier.’’

At 14, Jonas is handsome, Nicole pretty. Jonas is midway through puberty. His shoulders have broadened, his voice has deepened, and there’s a shadow on his upper lip. He’s 5 feet 6 and weighs 115 pounds, with a size 11 shoe.

Nicole is petite: 5 feet 1, 100 pounds. She’s got long, dark hair and she wears girls’ size 14-16. Her closet contains nice shirts and jeans, party dresses, glittery shoes, and a pair of footy pajamas.

“The thought of being a boy makes me cringe,’’ she says. “I just couldn’t do it.’’

Excited, worried about surgery

Nicole’s final step on her journey to womanhood would be gender reassignment surgery. Doctors generally won’t perform it until the age of consent, which is 18. No hospitals in New England perform such surgery, says Spack. The nearest that do are in Montreal and Philadelphia.

Nicole says she’s excited about the idea of surgery, though a bit worried about the results - “and maybe the pain, too.’’

While she’s interested in boys, she has expressed fear that “nobody is ever going to love me.’’

She has gone on weekend retreats sponsored by the Trans Youth Equality Foundation and to summer camp for transgender children, where she developed her first crush on a boy.

Over the years, the family has become close to several adult transsexuals, and Nicole has seen that some have found happy marriages. “She says she does feel better about it,’’ Kelly says, “but still wonders if she ever met a boy who falls for her, and then found out that she was trans, if he would still like her, or say awful things as he skedaddled out the door.’’

Nicole knows there is a long road ahead, but she feels she’s on the right path.

“Obviously my life is not going to be as easy as being gender-conforming, but there are perks like being able to get out there and do things that will benefit the [transgender] community,’’ she says. “I think everything’s going to turn out pretty well for me.’’

For now, at least, life feels more normal to the Maines family.

Wayne recently spoke at GLAD’s Spirit of Justice dinner in Boston and was introduced by Nicole. She kept her composure in her brief remarks and thanked GLAD for giving them a rare chance to “safely speak out.’’

Wayne choked up when thanking the group for its support. He recounted young Wyatt asking him, sadly, “Daddy, why can’t boys wear dresses?’’ Wayne hated to tell his son that society wouldn’t accept that.

But today, when Nicole asks her father what he thinks of a certain dress she’s wearing, his typical response, he told the audience, is: “That dress is too short. Go change your clothes.’’

In conversation later, Wayne tells another story of how things have changed, for good and forever. He and the twins were getting out of the car recently, and he grabbed their hands to walk with them.

Jonas, being a teenage boy, shook his father off, while Nicole was happy to walk hand-in-hand, swinging arms.

“She’ll do that the rest of her life,’’ Wayne says with a wide grin. “It was an epiphany for me.’’

Phys Ed: Why Doesn’t Exercise Lead to Weight Loss?

2011-12-01T06:40:00.000-08:00

For some time, researchers have been finding that people who exercise don’t necessarily lose weight. A study published online in September in The British Journal of Sports Medicine was the latest to report apparently disappointing slimming results. In the study, 58 obese people completed 12 weeks of supervised aerobic training without changing their diets. The group lost an average of a little more than seven pounds, and many lost barely half that.

How can that be? Exercise, it seems, should make you thin. Activity burns calories. No one doubts that.
Phys Ed

“Walking, even at a very easy pace, you’ll probably burn three or four calories a minute,” beyond what you would use quietly sitting in a chair, said Dan Carey, Ph.D., an assistant professor of exercise physiology at the University of St. Thomas in Minnesota, who studies exercise and metabolism.

But few people, an overwhelming body of research shows, achieve significant weight loss with exercise alone, not without changing their eating habits. A new study from scientists at the University of Colorado School of Medicine in Denver offers some reasons why. For the study, the researchers recruited several groups of people. Some were lean endurance athletes; some sedentary and lean; some sedentary and obese. Each of the subjects agreed to spend, over the course of the experiment, several 24-hour periods in a special laboratory room (a walk-in calorimeter) that measures the number of calories a person burns. Using various calculations, the researchers could also tell whether the calories expended were in the form of fat or carbohydrates, the body’s two main fuel sources. Burning more fat than carbohydrates is obviously desirable for weight loss, since the fat being burned comes primarily from body fat stores, and we all, even the leanest among us, have plenty of those.

The Denver researchers were especially interested in how the athletes’ bodies would apportion and use calories. It has been well documented that regular endurance training increases the ability of the body to use fat as a fuel during exercise. They wondered, though, if the athletes — or any of the other subjects — would burn extra fat calories after exercising, a phenomenon that some exercisers (and even more diet and fitness books) call “afterburn.”

“Many people believe that you rev up” your metabolism after an exercise session “so that you burn additional body fat throughout the day,” said Edward Melanson, Ph.D., an associate professor in the division of endocrinology at the School of Medicine and the lead author of the study. If afterburn were found to exist, it would suggest that even if you replaced the calories you used during an exercise session, you should lose weight, without gaining weight — the proverbial free lunch.

Each of Melanson’s subjects spent 24 quiet hours in the calorimeter, followed later by another 24 hours that included an hourlong bout of stationary bicycling. The cycling was deliberately performed at a relatively easy intensity (about 55 percent of each person’s predetermined aerobic capacity). It is well known physiologically that, while high-intensity exercise demands mostly carbohydrate calories (since carbohydrates can quickly reach the bloodstream and, from there, laboring muscles), low-intensity exercise prompts the body to burn at least some stored fat. All of the subjects ate three meals a day.

To their surprise, the researchers found that none of the groups, including the athletes, experienced “afterburn.” They did not use additional body fat on the day when they exercised. In fact, most of the subjects burned slightly less fat over the 24-hour study period when they exercised than when they did not.

“The message of our work is really simple,” although not agreeable to hear, Melanson said. “It all comes down to energy balance,” or, as you might have guessed, calories in and calories out. People “are only burning 200 or 300 calories” in a typical 30-minute exercise session, Melanson points out. “You replace that with one bottle of Gatorade.”
Related

This does not mean that exercise has no impact on body weight, or that you can’t calibrate your workouts to maximize the amount of body fat that you burn, if that’s your goal.

“If you work out at an easy intensity, you will burn a higher percentage of fat calories” than if you work out a higher intensity, Carey says, so you should draw down some of the padding you’ve accumulated on the hips or elsewhere — if you don’t replace all of the calories afterward. To help those hoping to reduce their body fat, he published formulas in The Journal of Strength and Conditioning Research last month that detailed the heart rates at which a person could maximize fat burning. “Heart rates of between 105 and 134” beats per minute, Carey said, represent the fat-burning zone. “It’s probably best to work out near the top of that zone,” he says, “so that you burn more calories over all” than at the extremely leisurely lower end.

Perhaps just as important, bear in mind that exercise has benefits beyond weight reduction. In the study of obese people who took up exercise, most became notably healthier, increasing their aerobic capacity, decreasing their blood pressure and resting heart rates, and, the authors write, achieving “an acute exercise-induced increase in positive mood,” leading the authors to conclude that, “significant and meaningful health benefits can be achieved even in the presence of lower than expected exercise-induced weight loss.”

Finally and thankfully, exercise seems to aid, physiologically, in the battle to keep off body fat once it has been, through resolute calorie reduction, chiseled away. In other work by Melanson’s group, published in September, laboratory rats that had been overfed and then slimmed through calorie reduction were able to “defend” their lower weight more effectively if they ran on a treadmill and ate at will than if they had no access to a treadmill. The exercise seemed to reset certain metabolic pathways within the rats, Melanson says, that blunted their body’s drive to replace the lost fat. Similar mechanisms, he adds, probably operate within the bodies of humans, providing scientific justification for signing up for that Thanksgiving Day 5K.

Cash receipts can be harmful

2011-11-30T07:44:00.000-08:00

I guess I’m supposed to get excited about all the holiday shopping going on and the deals you can get on days like Black Friday. But to me it just means it takes longer to get the same things done. The lines, the crowds... and the discounts don’t thrill me. I’d rather be somewhere else.

But if you do go shopping, there’s something you should know about your health.

I’m talking about the little slip of paper you tuck into your pocket or purse every time you buy anything. From gas to all those Christmas presents you’re getting for all your friends and family this week.

That receipt is most likely covered with bisphenol A (BPA) – the cancer-causing, estrogen-mimicking chemical.

Paper receipts are coated with BPA to get the ink from the receipt printer to develop on the paper. Problem is, BPA doesn't stay on the receipt, making it easy to be absorbed by anyone handling the paper.

What’s worse is that a new study found that BPA transfers readily from receipts to skin and can penetrate the skin to such a depth that it cannot be washed off.1

BPA is dangerous, even in small amounts. Studies show that it may cause cancers, diabetes, heart disease, obesity, and more.
Nearly every modern register uses this kind of paper. And every one of those receipts, according to new research, contains from 250 to 1,000 times more BPA than a plastic water bottle or soda can lining. Several states, and Canada and Europe, have banned using BPA in some of those kinds of products.
Two other new studies looked at how much of the BPA from each receipt gets from your skin into your bloodstream.
One looked at 15 different types of paper products. including thermal receipts, flyers, magazines, tickets, mailing envelopes, newspapers, food contact papers, food cartons, airplane boarding passes, luggage tags, printing papers, business cards, napkins, paper towels, and toilet paper, collected from several cities around the world.
Thermal papers accounted for 98% of the BPA you are exposed to.
The second study says that you absorb as much as 60% of the BPA you get on your skin.2
Fortunately, there are some good ways to avoid taking in BPA while you’re doing your seasonal shopping.
First, the easiest way to avoid getting BPA on your hands is to decline getting a receipt. If you don't need a receipt, leave it and ask the cashier not to print it if possible. For many small purchases and unless you're purchasing something you may want to take back, you probably don’t need one anyway.
Second, shop at stores that don’t have thermal printers that use BPA.
The Environmental Working Group’s research shows that some of the stores that use BPA-containing receipts in at least some outlets include McDonald's, CVS, KFC, Whole Foods, Wal-Mart, Safeway and the U.S. Postal Service.
Receipts from some major chains including Target, Starbucks and Bank of America ATMs issued receipts that were BPA-free or contained only trace amounts.3
Third, handle your receipts as little as possible, and make sure you wash your hands the right way when you get home. Washing your hands is one of the quickest, safest, easiest and most overlooked things you can do to protect your health on many levels. Unfortunately, few of us do it properly. Keep these three things in mind:

You don’t need a special soap. Expensive antibacterial soap is a waste of money and can contain toxic chemicals. Same goes for hand sanitizers.

Ordinary, plain, unscented soap is the best. It kills just as many microbes and bacteria as antibacterial soap. A U.S. FDA advisory committee found that use of antibacterial soaps provides no benefits over plain soap and water.4

Your choice of hot or cold water makes no difference. For comfort, I like warm water.

The length of time washing your hands is important. Twenty seconds is the optimum length – that’s about the time it takes to sing the “Happy Birthday” song – twice.

Make sure you rinse the soap off your hands with running water and dry them well – preferably on a disposable paper towel.

To Your Good Health,
Al Sears, MD

Adjuvants May Hold Key To Unlocking Cancer Immunotherapy Revolution

2011-09-20T16:28:00.000-07:00

Adjuvants May Hold Key To Unlocking Cancer Immunotherapy Revolution

The FDA approval of sipuleucel-T (Provenge), a patient-specific immunotherapy for androgen independent prostate cancer developed by Dendreon Corporation (DNDN), and ipilimumab (Yervoy), the first immune check point molecule for melanoma by Bristol-Myers Squibb (BMY), has renewed interest in the concept of immunotherapy as an approach to cancer treatment. Often overlooked, however, adjuvants can be an essential part of an effective vaccine and could help advance the field even further.

Adjuvants are substances that can:

Accelerate the generation of robust, longer lasting immune responses
Generate antibodies with increased avidity and neutralization capacity
Enhance immune responses in individuals with weakened immune systems
Reduce the amount of antigen and number of doses needed, reducing the cost of vaccination programs
Activate the cellular arm of the adaptive response, specifically T helper type 1 and cytotoxic T cell responses

For next generation cancer vaccines that require T cell immunity or a broader range of antibody response, adjuvants are playing an essential and central role. For example, GlaxoSmithKline’s (GSK) melanoma antigen epitope-3 (MAGE-A3) antigen-specific cancer immunotherapeutic (ASCI) uses the company’s AS15 adjuvant system [1], which incorporates three different adjuvants (QS-21, MPL, and CpG) and is currently in pivotal Phase III trials for both non-small cell lung cancer (NSCLC) and melanoma with data expected in 2012.

History

During the last 80 years many adjuvants have been used in experimental settings, but due to various shortcomings of most of them only three have made it into regular clinical usage [2] – largely for infectious diseases. Of the three adjuvants, only two have been used in vaccines licensed by the U.S. Food and Drug Administration.

Alum (1930s)

For infectious disease vaccines, the most commonly used adjuvants are aluminum salt based (aluminum phosphate and aluminum hydroxide, alum), which are safe and effective for antibody induction. Alum is a component of many licensed human vaccines, including diphtheria-pertussis-tetanus (DPT), diphtheria-tetanus (DT), DT combined with Hepatitis B virus (HBV), Haemophilus influenza B or inactivated polio virus (IPV), hepatitis A (HAV), Streptococcus pneumonia, meningococcal, and human papilloma virus (HPV).

MF59 (1997)

MF59 is a potent vaccine adjuvant that has been licensed for more than 13 years for use in an influenza vaccine focused on elderly subjects (Fluad) by Novartis (NVS) [3]. It consists of an oil-in-water nano-emulsion composed of shark oil (squalene). It is licensed in Europe for use in influenza vaccines, but not in the U.S.

MPL (2009)

MPL (monophosphoryl lipid A) is a derivative of bacterial endotoxin and a potent immunostimulant. MPL was the second FDA licensed adjuvant molecule and is used in Cervarix by GlaxoSmithKline (GSK), which is a prophylactic vaccine against HPV types 16 and 18. GlaxoSmithKline obtained MPL through the $300 million acquisition of Corixa Corporation in 2005. MPL is also the first and only toll-like receptor (TLR) ligand approved in a human vaccine. TLRs are a class of proteins that play a key role in the innate immune system [4].

Few adjuvants approved

Adjuvants do not receive FDA approval as stand-alone products, but rather as part of a registered vaccine adjuvant–antigen combination [5]. The fact that safety regulations are often much more stringent with vaccines, as they are prophylactic and the main targets are often pediatric patients, partly explains why there are so few adjuvants approved to date [6].

Several recent developments have favorably altered the landscape for adjuvant development. First, GSK’s Cervarix vaccine received approval in 2009 and contained the first adjuvant (MPL) licensed by the FDA since the approval of Alum back in the 1930s. The second development has been FDA approval of sipuleucel-T (Provenge) by Dendreon and ipilimumab (Yervoy) by Bristol-Myers Squibb, which has renewed interest in the concept of immunotherapy as an approach to cancer treatment. In the cancer setting, adjuvants are being tested as part of a therapeutic vaccine as opposed to being use as a prophylactic vaccine, which may result in a shorter duration of exposure and reduced safety concerns. Third, if an influenza pandemic were to occur, such as the 2009-10 H1N1 pandemic, the potential vaccine supply would fall several billion doses short of the amount needed to provide protection to the global population [7]. The antigen-sparing effect of adjuvants could allow for expansion of vaccine supply to meet the necessary global demands during a pandemic, as evidenced by supporting grants from the Biomedical Advanced Research and Development Authority (BARDA), part of the U.S. Department of Health and Human Services.

Investigational adjuvants

Several companies are developing promising new candidates that may finally adjunct or displace aluminum substances as a popular adjuvant:

Agenus (AGEN)

Agenus Inc. (AGEN) is developing QS-21, a saponin extracted from the bark of the Quillaja saponaria tree, also known as the soap bark tree or Soapbark, an evergreen tree native to warm temperate central Chile. (Author's note: Agenus is a client of MD Becker Partners.) Quillaia raw material has been used for decades as an ingredient to create the foaming in beverages such as root beer, low-alcohol beers and foaming carbonated beverages. It has also been widely used as an adjuvant in veterinary vaccines.

QS-21 has extensive clinical experience with thousands of patients receiving vaccines containing QS-21 adjuvant. Agenus has licensed QS-21 to various Big Pharma partners and today there are 15 vaccine candidates using QS-21 in clinical development for infectious diseases, oncology, and central nervous system disorders, including the following Phase III programs by GlaxoSmithKline that could address large markets:

MAGE-A3 ASCI vaccine candidate, which is being studied in the largest-ever trial in the adjuvant treatment of NSCLC and also in Phase III trials for melanoma, with data expected in 2012.
Mosquirix (RTS,S), the world’s most advanced malaria vaccine candidate, with Phase III data expected by the end of 2011

Agenus is entitled to receive milestone payments and royalties from corporate partners that have licensed QS-21.

Antigen Express, Inc., a wholly-owned subsidiary of Generex Biotechnology Corporation (GNBT)

Antigen Express is advancing its proprietary Ii-Key hybrid technology. (Author's note: Antigen Express is a client of MD Becker Partners.) Ii-Key modification entails attaching a four-amino acid peptide (LRMK) to virtually any antigen and results in increased stimulation of CD4+ helper T cells and a more robust specific response to the antigen. Using this technology platform, Antigen Express is building a deep pipeline of therapeutics aimed at a variety of major diseases, including cancer, infectious diseases and autoimmune-based syndromes.

The company’s lead product candidate using Ii-Key modification is AE37, a peptide vaccine derived from a fragment of the HER-2/neu protein, which is expressed in a variety of tumors including 75-80% of breast cancers as well as a high percentage of prostate, ovarian and other cancers [8].

A controlled, randomized, and single-blinded Phase II clinical study of AE37 in HER-2 expressing breast cancer patients is currently underway to establish clinical efficacy. The study endpoint is a reduction in cancer relapse after two years compared to the current standard of care treatment. There are currently over 200 patients enrolled in the study with either node positive or high-risk node-negative breast cancer.

Celldex Therapeutics (CLDX) and 3M Company (MMM)

3M Drug Delivery Systems has a portfolio of patent protected TLR agonists that have shown promise as vaccine adjuvants. The lead candidate, resiquimod (TLR7/8 agonist) has shown promising results in a number of animal models and has an extensive toxicology and clinical data package to support further development as a vaccine adjuvant.

Celldex Therapeutics entered into a non-exclusive clinical research collaboration with 3M Drug Delivery Systems to access resiquimod for clinical study with the company’s Antigen Presenting Cell (APC) Targeting Technology in exchange for an undisclosed licensing fee, milestones and royalties. Celldex is developing CDX-1401, a fusion protein consisting of a fully human monoclonal antibody with specificity for the dendritic cell receptor DEC-205 linked to the NY-ESO-1 tumor antigen, which is currently in a Phase I/II trial in combination with immune stimulating agents (resiquimod and/or poly-ICLC) for advanced cancers of the bladder, breast, ovary, non-small cell lung cancer, myeloma, sarcoma or melanoma.

Colby Pharmaceutical Company (private) and Juvaris BioTherapeutics

In September 2011, Juvaris BioTherapeutics, Inc. entered into an exclusive license agreement with Colby Pharmaceutical Company for the worldwide development and commercialization of Juvaris’ Cationic Lipid-DNA Complex (CLDC) technology and related JVRS-100 product candidate. Gene array studies with JVRS-100 show up-regulation of multiple immune response pathways compared to competing technologies. When combined with a vaccine antigen, JVRS-100 stimulates the adaptive immune response including specific antibodies and T-cell responses.

Idera Pharmaceuticals (IDRA)

Idera is developing numerous compounds that act as agonists for TLRs 3, 7, 8, or 9, which the company believes have the potential to be used as adjuvants in vaccines. In preclinical animal models, Idera’s TLR agonists have shown adjuvant activity when combined with various types of antigens.

In December 2007, Idera entered into an exclusive, worldwide licensing and collaboration agreement with Merck KGaA for the research, development and commercialization of Idera’s TLR9 agonists, including IMO-2055, for the treatment of cancer, excluding vaccines. Merck KGaA refers to IMO-2055 as EMD 1201081.

Merck KGaA expects to complete an ongoing Phase 2 clinical trial of IMO-2055 in combination with cetuximab (Erbitux) in second-line cetuximab-naïve patients with recurrent or metastatic squamous cell carcinoma of the head and neck (SCCHN). However, based on increased incidence of neutropenia and electrolyte imbalances reported in its Phase 1 trial of IMO-2055 in combination with cisplatin/5-FU and cetuximab in patients with first-line SCCHN and subsequent re-evaluation of its clinical development program, in July 2011 Merck KGaA informed Idera that it will not conduct further clinical development of IMO-2055.

Immune Design Corporation (private)

Founded by the co-founder of Corixa Corporation, Immune Design Corporation is developing its proprietary adjuvant known as glucopyranosyl lipid A (GLA). GLA is a novel, clinical-stage, human TLR-4 agonist, representing the next generation of MPL. According to the company, GLA is unique because it is a pure synthetic small molecule, straightforward to manufacture with excellent stability, rationally designed to optimally activate human TLR-4 receptors, induces Th1 CD4 helper cells and elicits broad humoral immunity and active in multiple formulations and compatible with most antigens. GLA was also shown to be safe and well-tolerated in humans subjects in a Phase I clinical study in combination with the influenza virus vaccine Fluzone by Sanofi Pasteur, the vaccines division of sanofi-aventis Group (SNY). Immune Design Corporation is developing its own proprietary pipeline of vaccine candidates formulated with the GLA adjuvant for evaluation in further human clinical trials.

Vical Inc. (VICL)

Vical is developing Vaxfectin, a novel proprietary cationic lipid-based formulation that has been shown to effectively enhance plasmid DNA-based (as well as protein- and peptide-based) vaccines. It is a commixture of a cationic lipid (GAP-DMORIE) and a neutral phospholipid (DPyPE) which, when combined in an aqueous vehicle, self-assemble to form liposomes. In mechanism of action studies, Vaxfectin has been shown to increase a number of cytokines and chemokines, while toll-like receptor signaling was contributory.

Vical is developing several products that utilize Vaxfectin as an adjuvant. These include CyMVectin, the company’s prophylactic vaccine against cytomegalovirus (CMV) infection, and its pandemic influenza vaccines.

Conclusion

Beyond their established role in infectious diseases, adjuvants will also likely become important in cancer immunotherapy where they will be critical for targeting weakly immunogenic tumor antigens in order to overcome various tolerance mechanisms and facilitate induction of cytotoxic T lymphocytes. Several promising new adjuvants are currently being developed that offer superior properties and a set of desired characteristics, with clinical data expected in the near future.

The topic of adjuvants in cancer immunotherapy will covered in an upcoming panel session at the second annual Cancer Immunotherapy: A Long-Awaited Reality conference being held in New York City on October 6, 2011.

References

[1] Recent clinical experience with vaccines using MPL- and QS-21-containing adjuvant systems. Garçon N, Van Mechelen M. Expert Rev Vaccines. 2011 Apr;10(4):471-86. Review.

[2] The ABC of clinical and experimental adjuvants–a brief overview. Brunner R, Jensen-Jarolim E, Pali-Schöll I. Immunol Lett. 2010 Jan 18;128(1):29-35. Epub 2009 Nov 4.

[3] MF59 adjuvant: the best insurance against influenza strain diversity. O’Hagan DT, Rappuoli R, De Gregorio E, Tsai T, Del Giudice G. Expert Rev Vaccines. 2011 Apr;10(4):447-62.

[4] Impaired TLR3/IFN-beta signaling in monocyte-derived dendritic cells from patients with acute-on-chronic hepatitis B liver failure: relevance to the severity of liver damage. Li N, Li Q, Qian Z, Zhang Y, Chen M, Shi G. Biochem Biophys Res Commun. 2009 Dec 18;390(3):630-5. Epub 2009 Oct 13.

[5] Adjuvants for malaria vaccines. Coler RN, Carter D, Friede M, Reed SG. Parasite Immunol. 2009 Sep;31(9):520-8. Review.

[6] Delivery Technologies for Biopharmaceuticals: Peptides, Proteins, Nucleic Acids and Vaccines edited by Lene Jorgensen and Hanne Mørck Nielsen

[7] Global pandemic influenza action plan to increase vaccine supply by the World Health Organization at http://www.who.int/vaccines-documents/DocsPDF06/863.pdf

[8] AE37: a novel T-cell-eliciting vaccine for breast cancer. Sears AK, Perez SA, Clifton GT, Benavides LC, Gates JD, Clive KS, Holmes JP, Shumway NM, Van Echo DC, Carmichael MG, Ponniah S, Baxevanis CN, Mittendorf EA, Papamichail M, Peoples GE.

U.S. Scrambling to Ease Shortage of Vital Medicine

2011-08-20T02:48:00.000-07:00

By GARDINER HARRIS

WASHINGTON — Federal officials and lawmakers, along with the drug industry and doctors’ groups, are rushing to find remedies for critical shortages of drugs to treat a number of life-threatening illnesses, including bacterial infection and several forms of cancer.

The proposed solutions, which include a national stockpile of cancer medicines and a nonprofit company that will import drugs and eventually make them, are still in the early or planning stages. But the sense of alarm is widespread.

“These shortages are just killing us,” said Dr. Michael Link, president of the American Society of Clinical Oncology, the nation’s largest alliance of cancer doctors. “These drugs save lives, and it’s unconscionable that medicines that cost a couple of bucks a vial are unavailable.”

So far this year, at least 180 drugs that are crucial for treating childhood leukemia, breast and colon cancer, infections and other diseases have been declared in short supply — a record number.

Prices for some have risen as much as twentyfold, and clinical trials for some experimental cures have been delayed because the studies must also offer older medicines that cannot be reliably provided.

On Wednesday, Dianne Nomikos, 65, went to M. D. Anderson Cancer Center in Houston for a 9 a.m. appointment to receive Doxil, a vital medicine for her ovarian cancer. She was told to go home and wait until new supplies arrived.

“My life is in jeopardy,” she said through tears in a telephone interview. “Without the drug, who knows what’s going to happen to me?”

The Obama administration is considering creating a government stockpile of crucial cancer medicines. The Centers for Disease Control and Prevention already stockpile antibiotics, antidotes and other drugs needed in the event of a terrorist attack or earthquake.

Under one plan, the government would store the dry ingredients for cancer drugs and, in the face of a shortage, distribute them to hospitals, where pharmacists could mix them into injectable compounds.

Dr. Richard Schilsky, a professor of medicine at the University of Chicago, said the number of cancers diagnosed in a year was easy to predict. “So we ought to be able to make a pretty good estimate of the grams required to treat every patient in the country in any given year,” he said.

Legislation proposed in both the House and the Senate would give the Food and Drug Administration the power to demand that drug makers give early warnings of possible supply disruptions. Senator Amy Klobuchar, Democrat of Minnesota, said the idea behind the bipartisan bill came after she found that the agency had prevented 38 shortages last year after getting early alerts of problems at drug makers.

“I can’t say the drug companies are excited” about the proposed legislation, she said in an interview. “But we need to give the F.D.A. more time.”

A group of leading oncologists has started a not-for-profit drug company that it hopes will soon be able to import supplies of some of the missing medicines. The company will eventually manufacture the drugs itself, according to Dr. George Tidmarsh, a pediatric oncologist and biotechnology entrepreneur who will lead it.

“We have a meeting with the F.D.A. next week,” Dr. Tidmarsh said. “This unfolding tragedy must stop, and right now.”

More than half the recent shortages have resulted because government or company inspectors found problems like microbial contamination that can be lethal on injection. Others have occurred because of capacity problems at drug plants or lack of interest because of low profits, according to the F.D.A.

Doxil, the cancer drug Ms. Nomikos needs, is made by Johnson & Johnson. Monica Neufang, a company spokeswoman, said, “Our third-party manufacturer has had some manufacturing issues related to capacity.”

Heather Bresch, president of the generic drug giant Mylan, says the shortages grow out of a sweeping consolidation of the generic drug industry into a few behemoths that compete only on price and have foreign plants that are rarely inspected.

“The race to the bottom has led to an increase of products coming from plants in China and India that may have uncertain supply and may have never been inspected,” Ms. Bresch said. “If the F.D.A. was required to inspect foreign drug plants at the same rate it does domestic ones, we might not have so many of these shortages.”

Ms. Bresch has helped to broker an agreement that would require the industry to pay $299 million a year for increased inspections of foreign drug plants, a deal that must be approved by Congress and one she says will prevent some shortages.

Top government officials have held a blizzard of meetings in recent weeks to tackle the shortage issue, and more are expected over the next month — including a public advisory meeting at the F.D.A. and hearings in Congress.

“Drug shortages represent a pressing public health issue, and we are actively working to understand the causes, the full scope of the problem in the U.S. and internationally, and possible solutions,” said Dr. Howard K. Koh, an assistant secretary for health.

A crucial problem is disconnection between the free market and required government regulation. Prices for many older medicines are low until the drugs are in short supply; then prices soar. But these higher prices do little to encourage more supply, because it can be difficult and expensive to overcome the technical and regulatory hurdles. And if supplies return to normal, prices plunge.

Executives at Premier, a hospital buying cooperative, said that in April and May its members received hundreds of offers from obscure drug wholesalers to sell drugs in short supply at vastly inflated prices. Of the 636 offers that included a price, 45 percent were at least 10 times the normal rate and 27 percent were at least 20 times normal.

Such sales offers are legal as long as suppliers prove that they bought the drugs appropriately. Some wholesalers buy certain drugs in large quantities because they are betting there will be a shortage. The excessive buying can help make their predictions come true. “We never like to see a situation where people can profit off of a national crisis and engage in price gouging,” Mike Alkire, Premier’s chief operating officer, said in an interview.

Joyce Burke, 47, of Mooresville, N.C., has breast cancer and is worried that she might not be able to get Taxol, which is in short supply. A drug that might have been substituted for Taxol has a side effect that leads some patients to lose their fingernails.

“I was not looking forward to losing my fingernails,” she said.

On Thursday, she received her first dose of Taxol, and her doctor said he had secured enough of the drug to give her a second dose in a little more than a week. She will need four doses to complete the treatment.

“And I asked, ‘What happens if you can’t find the rest?’ ” Ms. Burke said. “It’s not nearly as effective if you switch drugs midway through.”

Is eating too many smoked and cured foods bad for me?

2011-01-06T10:28:00.000-08:00

Dr Thomas Stuttaford
A 55-year-old reader from Chiswick has written to ask if eating cured foods, especially smoked cured foods, is dangerous. He fears that they may represent an appreciable medical hazard. He especially enjoys eating traditionally wood-smoked bacon, ham, chicken breast and kippers. He always prefers wood smoked products to unsmoked cured meats, but wonders if this is a wise decision.
Our reader shares a similar palate to my own. However, unlike him I am able to enjoy smoked goose breast or Yarmouth bloaters without worrying about the possibility that the cancer-forming (carcinogenic) chemicals found in cured meats or fish represent a significant danger to the ordinary diner.

For rather than being concerned about the curing process, which is well controlled by manufacturers, I am grateful that the salt and sodium nitrite used in the process deal a death blow to any Clostridium botulinum present. This is the bacterium that can cause botulism, a form of food poisoning that can have devastating, even occasionally fatal, results. The curing process also stops the meat going bad.

Most cured meats contain nitrosamines. These are formed when amines — breakdown constituents of proteins — are mixed with the sodium nitrite that, with salt (sodium chloride), is used to cure and preserve meat. The combination of small quantities of salt and sodium nitrite is such an effective mixture in preventing food poisoning and preserving the meat that no comparable alternative has been found.

Although there is evidence that nitrosamines are carcinogenic, it is doubtful if, in the small amounts the average person takes, it increases appreciably the risk of developing cancer after exposure to cured ham, bacon, other meats and fish. Choosing smoked meats and fish as an occasional hors d’oeuvre, or even having them as a main course from time to time, is unlikely to be significant. Research suggests that most people derive far more nitrates from vegetables, including such old faithfuls as spinach and cabbages, than from cured meats. It is estimated that only 1 per cent of someone’s nitrite concentration in the gut has been derived from cured meats and 90 per cent from vegetables. Nitrates are reduced to nitrites by organisms in the intestinal tract. Even so, it wouldn’t be considered a good idea to dine exclusively on cured and smoked foods.

Anxious lovers of smoked foods may also worry about the effect of benzopyrenes — potentially potent carcinogens — produced by smoking food. In smoked foods the levels of these may exceed 50 micrograms per kilogram. The relevant factor in considering possible problems caused either by the curing with salt and sodium nitrite or by the benzopyrenes from smoking is the amount of exposure to them. People who have a mixed diet can occasionally relish smoked foods without fearing that a few mouthfuls of smoked eel need to be followed by an immediate call to their local solicitor to update their will.

Those people who are obsessed with possible carcinogens in their food may also worry about the standard rasher or two of bacon in what hotels call the traditional English breakfast. They should perhaps choose to send back any burnt toast. Burnt toast, too, has a theoretical carcinogenic potential. Likewise, so has any unsaturated fat cooked at a high temperature. Research on cooking bacon has shown that the microwave is safer than the frying pan. The level of the nitrosopyrrolidines, a toxic substance produced by heating nitrosamines, is virtually undetectable when the bacon is cooked at a low temperature very slowly.

The crispier the bacon the higher the content of nitrosopyrrolidines. A medium well-done rasher cooked at 210F (99C) has ten times the quantity of nitrosopyrrolidines asmin slowly heated bacon. Cooked at 400F quickly, it has 17 times the amount and in crisped (virtually burnt) bacon there are 19 times as much nitrosopyrrolidines.

The good news is that the evidence that crispy bacon has ever harmed anyone is lacking. In fact there are more carcinogens in very hot fat. Another piece of reassuring news is that vitamin C in breakfast fruit juices may help to counteract nitrosamines.

A Different Kind of Eyeglasses

2010-10-29T03:10:00.000-07:00

By MICHAEL TOTTY

For many people past the age of 40, focusing on close objects—restaurant menus, for instance—just gets harder and harder.

Most people with this condition, called presbyopia, eventually give in and get reading glasses, bifocals or glasses with progressive lenses.

But what if there were another alternative that didn't require people to carry an extra set of glasses or have only part of their field of vision in focus at any one time?

Zoom Focus Eyewear LLC, of Van Nuys, Calif., has just such an option, and with it won this year's Silver Innovation Award. The solution: eyeglasses, called TruFocals, that the wearer can manually adjust to give clear, undistorted vision whether reading a book, working on a computer or looking into the distance.

The judges praised the potential large-scale benefit of TruFocals. Richard S. Lang, one of the judges and a physician at the Cleveland Clinic, called the technology a paradigm shift in the way it addresses a problem "that has been handled the same way for many years."
Mimicking the Eye

For more than 100 years, researchers have tried to come up with adjustable eyeglasses; a Baltimore inventor filed a patent on the idea in 1866. But a workable product that's easy to adjust, thin, lightweight and accurate proved elusive.

For the Wall Street Journal's 10th annual Tech Innovation Awards, Taiwan's Industrial Technology Research Institute received the Gold award for its technology to make paper-thin computer screens with a twist. The company beat out nearly 600 entries for its top ranking, along with Silver-award-winner Zoom Focus and Bronze-winner Counsyl of Silicon Valley.

Stephen Kurtin, a California inventor who previously devised one of the first word-processing programs, turned to the problem in the early 1990s. His solution, TruFocal eyeglasses, mimic the way that the lens of the human eye stretches and contracts to adjust focus.

Each TruFocal lens is actually a set of two lenses: an outer lens, and an inner lens made of a flat glass plate attached to a flexible membrane that contains a clear, silicone-based liquid. A manual slider on the bridge of the eyeglasses adjusts the focus by changing the shape of the membrane. The outer lens can be custom made to correct other vision problems besides presbyopia, including nearsightedness and astigmatism.

Once the TruFocal lenses are adjusted, the entire field of vision is in focus, unlike bifocals and progressive lenses, which keep only a limited area in sharp focus. So a user can adjust the glasses to focus only on the book he's reading, then look up and readjust them to focus solely on the TV across the room.
One Shape, Several Colors

There were some false starts along the way. Mr. Kurtin considered using liquid-crystal electronics to adjust the focus, but the batteries proved problematic. The first model weighed seven pounds. But after nearly 20 years of refinements, the first TruFocal glasses were introduced in 2009.

There's a downside for the fashion conscious: The glasses come in one shape—round—and have been compared to the spectacles worn by Harry Potter. (They are sold in several colors, though.) The circular lenses are necessary to the workings of the technology; with any other shape, the flexible membrane couldn't keep a spherical shape when compressed.

TruFocals aren't the only glasses with adjustable lenses. But other products are mainly designed for users in the developing world, where optometrists aren't widely available; they are meant to be adjusted once by the user to correct the focus at a given distance and then set that way. The Zoom Focus product is aimed at wearers who want to make constant adjustments in their vision.

Next month, TruFocals will be rebranded as Superfocus glasses. The company will also change its name, to Superfocus LLC.

Targeting tumors without the pain of radiation

2010-10-28T08:00:00.000-07:00

Israeli scientists have developed an innovative new nano-particle treatment for cancerous tumors that could replace traditional radiation therapy.

Traditional radiation treatment has a range of damaging side effects, but Prof. Israel Gannot believes he can provide an alternative.

Scientists from Israel are developing a new way to destroy cancerous tumors that will have fewer side effects than traditional radiation therapy, and cause minimal damage to surrounding tissue.

The innovative method developed by a professor at Tel Aviv University uses heat to kill the tumor cells, while leaving the surrounding healthy tissue intact.

Today, radiation therapy is one of the most important weapons against cancerous tumors, but the therapy can have a significant impact on the health of a patient as it harms healthy tissue as well as malignant cells.

Patients often experience anything from nausea to hair loss, fatigue, skin irritation, and a lowered white blood cell count.

Prof. Israel Gannot, whose method is soon to be published in the journal Nanomedicine, uses a special mixture of nano-particles - already approved by the Food and Drug Administration (FDA) - and antibodies to locate individual tumors and bind directly to them.

A targeted rise in temperature

The specialized cocktail is administered safely and simply, through topical local injection or injection into the blood stream.

"Once the nano-particles bind to the tumor, we excite them with an external magnetic field, and they begin to heat very specifically and locally," Gannot explains. The magnetic field is manipulated to create a targeted rise in temperature, and it is this directed heat elevation that kills the tumors, he says.

Once the treatment is completed, the nano-particles are washed out of the body naturally without leaving a trace, minimizing side effects.

So far, the treatment has been proven effective against epithelial cancers, which can develop in almost any area of the body, such as the breast or lung. By using a special feedback process, also developed in his laboratory, the process can be optimized for individual treatment.

Gannot claims the method is effective against almost any type of tumor, as long as its specific markers and its antibodies can be identified.

Recuperation at home

Aside from being minimally invasive, Gannot says that the treatment is also fast and efficient. The entire treatment lasts only six hours, and can be administered during an out-patient procedure, enabling patients to recuperate in the comfort of their own homes.

It's early days yet, however. Gannot is currently applying his technique to cell lines and to ex vivo tissues and tissue-like substitutes in his lab, and plans to start in vivo experiments by next year.

If long-term clinical trials are successful, however, Gannot believes the technique could become a mainstay of patient care.

In Israel, Growing Tobacco to Save Lives

2010-10-20T10:00:00.000-07:00

By John Bernard

In a greenhouse in northern Israel, a company is growing tobacco plants yielding a surprising product that is vastly different from cigarettes. These plants produce genetically-engineered human collagen, a protein vital for tissue repair that is used by surgeons to fill bone voids in cancer patients, fix heart valves and heal severe wounds.

The genetic engineering technology that allows the tobacco plants to generate the collagen was developed by CollPlant based in Rehovot in central Israel. This novel use of the tobacco plant answers a major unmet medical need.

A scientific achievement with commercial potential

“Collagen is used in about a thousand important medical products, but until now manufacturers have had to derive it from pigs, cows or human corpses,” says CollPlant CEO Yehiel Tal, noting that the US Food and Drug Administration (FDA) and other international health regulatory agencies have expressed serious safety concerns with respect to the use of both animal and human corpse tissues.

CollPlant’s plant-derived collagen poses no safety risks and can be considered a green technology, eliminating the industrial waste and ecological damage associated with the raising of livestock. In addition, the company is providing tobacco farmers with a healthier and more lucrative use for their crops.

“The leaves of a single tobacco plant can yield about 100 grams of tobacco (for cigarettes) or about a gram of genetically-engineered human collagen,” says Prof. Oded Shoseyov, CollPlant’s co-founder and the inventor of the technology. “And from a single gram of collagen it is possible to produce, for example, about three injections of highly-valuable wound healing gel for patients suffering from diabetic ulcers.”

In developing CollPlant’s innovative technology, Shoseyov had to overcome a formidable scientific challenge. “Most proteins in the body are the result of a single gene but there are five different genes responsible for the production of collagen.”

Shoseyov’s success in transferring all five genes into a transgenic plant that could produce collagen was acknowledged earlier this year when he was awarded the prestigious Hebrew University Kaye Innovation Award for “scientific excellence with commercial potential.”

Good news from the FDA

CollPlant is well on the way to leveraging the commercial potential of Shoseyov’s invention. The company has begun to market collagen as a raw material to Japanese manufacturers and in August received good news from the FDA about its first product.
“The FDA informed us that they have agreed to classify our Vergenix wound dressing as a medical device, rather than as a drug or biologic product,” says Tal. “This is a breakthrough because the medical device regulatory review process is much simpler and quicker than that used for products defined as drugs or biologics.”

Vergenix is just the first of several regenerative tissue products in the CollPlant pipeline that target the multi-billion dollar wound management market. These products include gel formulations for deep-tunneled wounds associated with diabetic ulcers, as well as wound dressings for acute and chronic wounds.

Other CollPlant products will attempt to meet the growing demand for collagen-based orthopedic products. In the US alone, each year there are about 800,000 ligament and tendon repair procedures, 400,000 shoulder operations and more than 500,000 bone graft procedures, all of which require collagen.

CollPlant has received strong support from leading investors since its inception. Investment funds headed by two prominent healthcare industrialists, former Teva Pharmaceuticals CEO Eli Hurvitz and Perrigo founder Mory Arkin, were among the founding investors. Earlier this year the company began to trade publicly on the Tel Aviv Stock Exchange.

Invasive shrub increases risk of human disease

2010-10-12T12:20:00.000-07:00

There are many ways of fighting disease, but Brian Allan from Washington University has suggested a most unusual one – a spot of weeding. Allan’s research shows that getting rid of a plant called the Amur honeysuckle might be one of the best ways of controlling an emerging human disease called ehrlichiosis. The plant, however, doesn’t cause the disease. The connection between the two is far more complicated than that.

The Amur honeysuckle is an Asian plant that’s naturally alien to American shores. But, like many species that are brought to new habitats, it has become an invader. It forms thick growths that deprive native plants of light, causing local diversity to plummet in the face of an expanding blanket of honeysuckle. This story has been repeated all over the world with different species cast as invasive villains, and different communities cast as suffering victims. But the true consequences of these invasions often go unnoticed.

The honeysuckle doesn’t just crowd out local plants; Allan has found that it also attracts white-tailed deer. Where the deer go, so do their parasites, and these include the lone star tick, the animal that spreads ehrlichiosis. Through their blood-sucking bites, the ticks spread five species of bacteria that infect and kill white blood cells. This weakens the immune systems of their hosts and causing the flu-like symptoms that accompany a bout of ehrlichiosis.

More honeysuckle means more deer, which means more ticks, which means more bacteria, which means more potentially infected humans. This invasive shrub might help to explain why cases of ehrlichiosis have gone up by around 6 times in the early part of the 21st century. In 1999, the Centers for Disease Control and Prevention recorded just 100 or so cases of ehrlichiosis in the United States. By 2006, that number had risen to just under 600.

Allan discovered this remarkable chain of events by carrying out a series of field surveys in the Missouri woodlands. He found that compared to honeysuckle-free areas, invaded zones had 18 times as much plant matter and around five times as many deer (which presumably are drawn to areas with more shelter and potential food). As a result, they also had 10 times as many ticks that were infected by ehrlichiosis-causing bacteria. Clearly, the risk of catching the disease is higher in areas that contain honeysuckle.

To test his hypothesis, Allan removed the honeysuckle from selected patches of woodland. The result: far fewer signs of deer and far fewer infected ticks. Allan also found that the presence of honeysuckle didn’t affect the odds of a tick being infected with the problematic bacteria, or their odds of survival. This suggests that the removal of the honeysuckle was indeed lowering the numbers of ticks by driving away the deer, rather than simply creating conditions that are more hostile towards ticks.

This is a good example of an invasive species increasing the burden of human disease and it’s unlikely to be the only one. Other studies have found that in the northeastern United States, the honeysuckle and the Japanese barberry (another invasive shrub) might increase the risk of Lyme disease, another tick-borne bacterial disease.

To Allan, these domino effects mean that removing invasive species isn’t just an environmental cause – it’s a public health issue too. Honeysuckle might repress local plants but through a convoluted chain of events, it could end up repressing the immune systems of local people. That should provide even more incentive to deal with these invaders. As Allan himself writes,

“Our finding that removal of the invader mitigates disease risk, coupled with the benefits of invasive plant removal to wildlife communities, suggests a potential “win-win” scenario for biodiversity conservation and human health.”

High-speed filter uses electrified nanostructures to purify water at low cost

2010-09-07T05:33:00.000-07:00

August 31, 2010 By Louis Bergeron High-speed filter uses electrified nanostructures to purify water at low cost

This scanning electron microscope image shows the silver nanowires in which the cotton is dipped during the process of constructing a filter. The large fibers are cotton. Credit: Courtesy of Yi Cui, Stanford University

(PhysOrg.com) -- By dipping plain cotton cloth in a high-tech broth full of silver nanowires and carbon nanotubes, Stanford researchers have developed a new high-speed, low-cost filter that could easily be implemented to purify water in the developing world.

Instead of physically trapping bacteria as most existing filters do, the new filter lets them flow on through with the water. But by the time the pathogens have passed through, they have also passed on, because the device kills them with an electrical field that runs through the highly conductive "nano-coated" cotton.

In lab tests, over 98 percent of Escherichia coli bacteria that were exposed to 20 volts of electricity in the filter for several seconds were killed. Multiple layers of fabric were used to make the filter 2.5 inches thick.

"This really provides a new water treatment method to kill pathogens," said Yi Cui, an associate professor of materials science and engineering. "It can easily be used in remote areas where people don't have access to chemical treatments such as chlorine."

Cholera, typhoid and hepatitis are among the waterborne diseases that are a continuing problem in the developing world. Cui said the new filter could be used in water purification systems from cities to small villages.

Faster filtering by letting bacteria through

Filters that physically trap bacteria must have pore spaces small enough to keep the pathogens from slipping through, but that restricts the filters' flow rate.

Since the new filter doesn't trap bacteria, it can have much larger pores, allowing water to speed through at a more rapid rate.

"Our filter is about 80,000 times faster than filters that trap bacteria," Cui said. He is the senior author of a paper describing the research that will be published in an upcoming issue of Nano Letters. The paper is available online now.

The larger pore spaces in Cui's filter also keep it from getting clogged, which is a problem with filters that physically pull bacteria out of the water.

Cui's research group teamed with that of Sarah Heilshorn, an assistant professor of materials science and engineering, whose group brought its bioengineering expertise to bear on designing the filters.

Silver has long been known to have chemical properties that kill bacteria. "In the days before pasteurization and refrigeration, people would sometimes drop silver dollars into milk bottles to combat bacteria, or even swallow it," Heilshorn said.

Cui's group knew from previous projects that carbon nanotubes were good electrical conductors, so the researchers reasoned the two materials in concert would be effective against bacteria. "This approach really takes silver out of the folk remedy realm and into a high-tech setting, where it is much more effective," Heilshorn said.

Using the commonplace keeps costs down

But the scientists also wanted to design the filters to be as inexpensive as possible. The amount of silver used for the nanowires was so small the cost was negligible, Cui said. Still, they needed a foundation material that was "cheap, widely available and chemically and mechanically robust." So they went with ordinary woven cotton fabric.

"We got it at Wal-mart," Cui said.

To turn their discount store cotton into a filter, they dipped it into a solution of carbon nanotubes, let it dry, then dipped it into the silver nanowire solution. They also tried mixing both nanomaterials together and doing a single dunk, which also worked. They let the cotton soak for at least a few minutes, sometimes up to 20, but that was all it took.

The big advantage of the nanomaterials is that their small size makes it easier for them to stick to the cotton, Cui said. The nanowires range from 40 to 100 billionths of a meter in diameter and up to 10 millionths of a meter in length. The nanotubes were only a few millionths of a meter long and as narrow as a single billionth of a meter. Because the nanomaterials stick so well, the nanotubes create a smooth, continuous surface on the cotton fibers. The longer nanowires generally have one end attached with the nanotubes and the other end branching off, poking into the void space between cotton fibers.

"With a continuous structure along the length, you can move the electrons very efficiently and really make the filter very conducting," he said. "That means the filter requires less voltage."

Minimal electricity required

The electrical current that helps do the killing is only a few milliamperes strong - barely enough to cause a tingling sensation in a person and easily supplied by a small solar panel or a couple 12-volt car batteries. The electrical current can also be generated from a stationary bicycle or by a hand-cranked device.

The low electricity requirement of the new filter is another advantage over those that physically filter bacteria, which use electric pumps to force water through their tiny pores. Those pumps take a lot of electricity to operate, Cui said.

In some of the lab tests of the nano-filter, the electricity needed to run current through the filter was only a fifth of what a filtration pump would have needed to filter a comparable amount of water.

The pores in the nano-filter are large enough that no pumping is needed - the force of gravity is enough to send the water speeding through.

Although the new filter is designed to let bacteria pass through, an added advantage of using the silver nanowire is that if any bacteria were to linger, the silver would likely kill it. This avoids biofouling, in which bacteria form a film on a filter. Biofouling is a common problem in filters that use small pores to filter out bacteria.

Cui said the electricity passing through the conducting filter may also be altering the pH of the water near the filter surface, which could add to its lethality toward the bacteria.

Cui said the next steps in the research are to try the filter on different types of bacteria and to run tests using several successive filters.

"With one filter, we can kill 98 percent of the bacteria," Cui said. "For drinking water, you don't want any live bacteria in the water, so we will have to use multiple filter stages."

Cui's research group has gained attention recently for using nanomaterials to build batteries from paper and cloth.

More information: Research paper on Nano Letters website - http://pubs.acs.or … 21/nl101944e

Provided by Stanford University

Reusable Grocery Bags Can Make You Sick

2010-07-01T02:50:00.000-07:00

Once again the cure is as bad as the illness. It seems as if going green can really cause someone to turn green. Those reusable grocery bags can make you sick.

Remember the good old days, when you went to the grocery store and brought food home in brown paper bags. Those bags were great, they had so many uses once you brought them home, everything from "trick or treating," to trash bags. Heck, they even inspired a popular comedian "The Unknown Comic"

Throughout my school years every text book I had was named Walbaums, because they were protected by brown paper bags from my mom's favorite Supermarket.

But those bags used paper and the environmentalists wanted to save the rain forests so they switched to those thin plastic bags. The plastic could still be used for Halloween, and are perfect for your wet bathing suits when coming home from the beach. But plastic uses petroleum and take centuries to decompose so the environmentalists didn't like them either. To be honest neither do I, they aren't really strong enough to hold the groceries without tearing.

Enter the reusable grocery bags, they are good for groceries and Halloween, but you can't use them for book covers. It doesn't kill trees and will slow the build-up of plastic in the land fills. The only real problem with them is they are great incubators of E.coli, and salmonella

Tests on shoppers' bags revealed half contained traces of E.coli, a lethal toxin which killed 26 people in Scotland in 1996 in one of the worlds worst food poisoning outbreaks.

Scientists also found many were contaminated with salmonella.

Researchers blame the fact that consumers do not realise reusable bags need to be washed regularly at high temperatures to kill off bugs deposited by raw meat packaging.

They warned the levels of bacteria they found were high enough to cause a wide range of serious health problems and even death.

Think of it this way, the environmentalists may save the rain forests, and clean up land fills, with the unintended consequence of killing children, as kids are particularly vulnerable to the effects of organisms such as E.coli.

The tests were carried out by experts at the University of Arizona, who stopped a total of 84 shoppers in Tucson, Los Angeles and San Francisco to check the state of their bags.

The popularity of reusable eco-friendly shopping bags has soared in Britain, as in the US, as the growth in the recycling culture means fewer consumers rely on disposable plastic bags.

Many of the new bags are made from jute or woven polypropylene.

But while they are better for the environment, the new research suggests they could be harmful to health if not cleaned regularly.

Oh and the hotter the climate, the worse the contamination so imagine what will happen if Al Gore is telling the truth (about climate change, not that massage in the hotel)

Professor Charles Gerba, who led the study said: "Our findings suggest a serious threat to public health, especially from bacteria such as E.coli, which were detected in half of the bags sampled.

"Consumers are alarmingly unaware of these risks and the critical need to sanitise their bags on a weekly basis."

A poll revealed 97 per cent of shoppers who used eco-friendly bags never washed or bleached them.

Here's an idea, throw out the reusable bags and the plastic and lets go back to the best option of all, paper bags. Think of all the trees and plastic we won't be using for book covers.

Two Drugs Appear to Surpass Landmark Novartis Leukemia Treatment

2010-06-05T16:51:00.000-07:00

By PETER LOFTUS

CHICAGO—Novartis AG's Gleevec is one of the closest things to a miracle drug to come out of the battle against cancer in recent years. But new research suggests two newer drugs are even more effective for the form of leukemia whose treatment Gleevec has transformed.

In separate studies published Saturday, Bristol-Myers Squibb Co.'s Sprycel and Novartis's Tasigna each were superior to Gleevec in treating people with newly diagnosed chronic myeloid leukemia. The two newer drugs are currently approved to treat patients whose disease persisted after trying Gleevec.

The new studies could help widen the patient populations for both Sprycel and Tasigna if doctors begin choosing them over Gleevec for newly diagnosed patients.

Switzerland-based Novartis has already applied for regulatory approval to market Tasigna as a first-line treatment, and New York-based Bristol said it is in the process of doing so for Sprycel. Some doctors may not wait for formal regulatory approval to try the newer drugs as first-line treatments.

But some doctors might still stick with Gleevec until Tasigna and Sprycel can demonstrate a long-term survival advantage over Gleevec. Also, Gleevec could be viewed as a more cost-effective option when the drug loses patent protection and cheaper generic versions become available in coming years.

"We don't know yet about long-term survival," said Sonali Smith, oncologist at the University of Chicago Medical Center. "We probably won't have that data for quite some time."

Gleevec was introduced in 2001 and quickly became the standard of care for people newly diagnosed with CML, a cancer of the blood, based on its ability to induce remission and significantly improve survival versus older drugs, with relatively low toxic effects.

Studies have shown at least 80% of Gleevec users were still alive eight to 10 years after beginning therapy, much higher than the historical survival rate of less than 20% for CML patients before Gleevec. Gleevec had world-wide sales of $3.9 billion last year.

But not all patients improve on Gleevec, and newer drugs were initially aimed at helping these patients. Sprycel was introduced in 2006 and had 2009 sales of $421 million. Tasigna, which came out in 2007, had 2009 sales of $212 million.

Both Sprycel and Tasigna are more potent in going after a certain molecular target than Gleevec, so researchers studied whether they would work better than Gleevec in the first-line setting. Results were released at the annual scientific meeting of the American Society of Clinical Oncology and published simultaneously by the New England Journal of Medicine on Saturday.

In the Bristol-funded Sprycel study of 519 newly diagnosed CML patients, some 77% of Sprycel users had "complete cytogenetic" responses after 12 months of follow-up, versus 66% in the Gleevec users. This is one measure of remission, when the disease is virtually undetectable in bone marrow.

In a separate, 846-patient study supported by Novartis, some 80% of Tasigna users had complete cytogenetic responses, versus 65% of Gleevec users.

Both studies, while not designed identically, also looked at another measure of remission, known as major molecular response. This was achieved in about 44% of Tasigna users after 12 months, versus 22% for Gleevec. In comparison, the corresponding rates in the Bristol study were 46% for Sprycel and 28% for Gleevec.

Novartis also released data showing Tasigna continued to be superior to Gleevec after 18 months of follow-up.

Hagop Kantarjian, an oncologist at University of Texas M.D. Anderson Cancer Center in Houston who served as an investigator in both trials, said Sprycel and Tasigna were superior to Gleevec at inducing remissions, but some doctors may want to wait for three- to five-year follow-up data before substituting these drugs for Gleevec.

There were various side-effects associated with each drug in the studies, such as skin problems and headaches for Tasigna and accumulation of fluid in the chest for Sprycel. But Charles Sawyers, a cancer specialist at the Memorial Sloan-Kettering Cancer Center in New York, wrote in an editorial in the NEJM that all three drugs have "outstanding safety profiles."

Dr. Sawyers raised the question of whether the new data would render Gleevec "forever enshrined in the history of oncology but no longer useful." But he said Gleevec may get new life when it goes generic: "With rising pressure to balance cost and efficacy, patients and payers may be forced to select the cheapest among three excellent treatment options."

Novartis has patent protection for Gleevec in the U.S. until 2015.

Dr. Kantarjian said Sprycel and Tasigna would have to show significant improvement in survival to justify their prices versus generic Gleevec in first-line CML.

Pfizer Inc. is developing a similar CML drug, bosutinib, that would compete against the others if it reaches the market.

This is wonderful!

2010-05-28T03:32:00.000-07:00

8-month-old deaf toddler Jonathan reacts to the activation of his cochlear implant.

Snakebites About to Get a Lot More Deadly

2010-05-11T20:26:00.000-07:00

The cure for North American coral snake bite is about to disappear. Why an unprofitable anti-venom may end up costing lives.
By Glenn Derene

As venomous snakes go, the coral snake is a clumsy biter. Unlike pit vipers such as rattlesnakes and cottonmouths, which have gruesomely efficient fangs that articulate forward during a strike and inject venom like hypodermic needles, the brightly colored coral snake has small, rear-facing fangs that guide venom into a wound. This process doesn't always work well--experts estimate that 25 percent of coral snake envenomations are dry bites--which is perhaps why the coral is so unaggressive. The snake is found throughout Florida, as well as in parts of Alabama, South Carolina, Louisiana, Texas and Arizona, but there are generally only about 100 or so bites each year.

What the coral lacks in belligerence, it makes up for in neurotoxicity. Unlike bites from pit vipers, which cause immense pain and swelling at the wound site, coral snake victims usually report little pain after being bitten. But the effects begin to show within hours, with symptoms such as tingling sensations in the extremities, dysarthria (slurred speech) and ptosis (droopy eyelids). Then a victim's lungs shut down. "The venom acts as a neuromuscular blockade to the lungs," University of Florida professor of medicine Craig Kitchens says. "Without antivenom, you need artificial respiration or you die."

Unfortunately, after Oct. 31 of this year, there may be no commercially available antivenom (antivenin) left. That's the expiration date on existing vials of Micrurus fulvius, the only antivenom approved by the Food and Drug Administration for coral snake bites. Produced by Wyeth, now owned by Pfizer, the antivenom was approved for sale in 1967, in a time of less stringent regulation.

Wyeth kept up production of coral snake antivenom for almost 40 years. But given the rarity of coral snake bites, it was hardly a profit center, and the company shut down the factory that made the antivenom in 2003. Wyeth worked with the FDA to produce a five-year supply of the medicine to provide a stopgap while other options were pursued. After that period, the FDA extended the expiration date on existing stock from 2008 to 2009, and then again from 2009 to 2010. But as of press time, no new manufacturer has stepped forward.

Antivenom shortages are a surprisingly common occurrence. The entire state of Arizona ran out of antivenom for scorpion stings after Marilyn Bloom, an envenomation specialist at Arizona State University, retired in 1999. Bloom had been single-handedly making all the scorpion antivenom for state hospitals. Recently, Merck & Co, the only FDA-licensed producer of black widow antivenom, has cut back distribution because of a production shortage of the drug. In a 2007 report, the World Health Organization listed worldwide envenomations as a "neglected public health issue."

New scorpion and black widow antivenoms are currently in the pipeline, thanks to efforts by several poison-control associations to speed foreign drugs into the market through FDA research programs. There is also a coral snake antivenom produced by Mexican drug manufacturer Instituto Bioclon that researchers believe could be even more effective and safe than the outgoing Wyeth product. But that drug, Coralmyn, is not currently licensed for sale by the FDA. The tests required for licensing would cost millions of dollars, and for such a rare treatment (there are 15 times as many scorpion stings per year as coral snake bites), it could take decades for Bioclon to make its money back.

Envenomation experts express exasperation and disbelief at the situation. "It's ridiculous that we're losing a technology that we already have," says Joe Pittman, a snakebite treatment specialist at the Florida Poison Information Center in Tampa. "It's even more ludicrous that we have a product that's available, and we have to jump through so many hoops to get it approved." In July 2009, an FDA advisory board determined that Coralmyn qualified for an accelerated approval process, but there is still no one with the estimated $3 million to $5 million to pay for the required studies.

"Nobody in this situation is being a bad actor," says Eric Lavonas of the Rocky Mountain Poison and Drug Center. "We just don't have a system set up to deal with it." With no adequate replacement for coral snake antivenom, hospitals are likely to appeal to local zoos, many of which maintain small stocks for their staff. But zoos are under no obligation to provide the medicine.

If and when shortages do occur, many hospitals will have no other option but to intubate coral snake bite victims on ventilators for weeks until the effects of the toxin wear off--potentially costing hundreds of thousands of dollars per bite. "It's probably going to end up costing us far more not to deal with this than to deal with it," Lavonas says, "both in human suffering, and in dollars and cents."

Parkinson's patient's cycling ability stuns doctors

2010-04-06T16:41:00.001-07:00

BY GINA KOLATA
NEW YORK TIMES
Monday, Apr. 05 2010
Dr. Bastiaan R. Bloem of the Radboud University Nijmegen Medical Center in the
Netherlands thought he had seen it all in his years of caring for patients with
Parkinson's disease. But the 58-year-old man who came to see him recently was a
total surprise.

The man had had Parkinson's disease for 10 years, and it had progressed until
he was severely affected. Parkinson's, a neurological disorder in which some of
the brain cells that control movement die, had made him unable to walk. He
trembled and could walk only a few steps before falling. He froze in place, his
feet feeling as if they were bolted to the floor.

But the man told Bloem something amazing: He said he was a regular exerciser —
a cyclist, in fact — something that should not be possible for patients at his
stage of the disease, Bloem thought.

"He said, 'Just yesterday I rode my bicycle for 10 kilometers' — six miles,"
Bloem said. "He said he rides his bicycle for miles and miles every day.

"I said, 'This cannot be,'" Bloem, a professor of neurology and medical
director of the hospital's Parkinson's Center, recalled in a telephone
interview. "This man has end-stage Parkinson's disease. He is unable to walk."

But the man was eager to demonstrate, so Bloem took him outside where a nurse's
bike was parked.

"We helped him mount the bike, gave him a little push, and he was gone," Bloem
said. He rode, even making a U-turn, and was in perfect control, all his
Parkinson's symptoms gone.

Yet the moment the man got off the bike, his symptoms returned. He froze
immediately, unable to take a step.

Bloem made a video and photos of the man trying to walk and then riding his
bike. The photos appear in the April 1 issue of The New England Journal of
Medicine.

After seeing that man, Bloem asked 20 other severely affected patients about
riding a bike. It turned out that all could do it, though it is not clear why.

Bloem and other Parkinson's specialists were amazed. People with Parkinson's
disease can often dance, run, walk smoothly and do complex movements for a few
minutes if they are given appropriate signals — emotional or visual cues. There
are famous examples, such as a group of Parkinson's patients who were caught in
a fire and managed to run down steps and escape, only to freeze in place when
they got outside.

But this effect, known as the kinesia paradox, does not last long. Riding for
miles and miles is very different from walking for a few minutes. And until
now, Bloem said, it was not known that patients with Parkinson's could ride
bikes.

He said bicycling offers patients an opportunity to be symptom-free while they
are riding, to look and feel normal, and to get some real cardiovascular
exercise.

Bloem said he hoped that perhaps regular exercise might slow the progress of
Parkinson's disease. It does in rats, he said.

A finch's decoded genome might help us with speech

2010-04-02T13:23:00.000-07:00

By Kim McGuire
ST. LOUIS POST-DISPATCH
03/31/2010

When we hear a song for the first time, it often seems like it goes in one ear and out the other, sometimes only few catchy words from a chorus leaving much of an impression.
bullet Hear the sounds of the zebra finch

But when the Australian zebra finch hears its father sing for the first time, those simple melodies activate large, complex gene networks in the bird’s brain, according to new research by an international team of scientists that includes researchers from Washington University and the University of Illinois at Urbana-Champaign.

The findings, published today in the journal Nature, reveal how the team successfully decoded the genome of the zebra finch, only the second bird to have its genetic code completely mapped.

The project provides new insights that will help scientists understand how humans learn language and may someday provide insights into diseases like autism that can inhibit speech, team members say.

"Now we can look deep into the genome, not just at the genes involved in vocal learning, but that the complex ways in which they are regulated," said Richard K. Wilson, the research’s senior author and director of Washington University’s Genome Center. "This information provides clues to how vocal learning occurs at the most basic molecular level in birds and people."

Past research has shown that hundreds of genes light up in the finch’s brain as the bird learns a new song.

The new research show that significantly more genes — about 800 total — are activated by the act of singing.

The team selected the zebra finch for study because songbirds are among few animals that learn how to sing — just like humans. As young birds, the finch "babbles" but eventually learns how to imitate its father.

In contrast, a chicken, the other bird to have its genome sequenced, instinctively knows how cluck. It is not a form of communication learned from other birds.

"There is a functional development parallel between the way a bird learns to sing and a human learns to speak," said David Clayton, a neuroscience professor at the University of Illinois and leader of the group that proposed the genome sequencing project. "The avian brain is quite different in a superficial detail from the mammalian brain or the human brain, but some striking parallels have emerged."

Wes Warren, lead author and genetics professor at Washington University, explained that the zebra finch proved to be the model study organism because they learn to sing in a predictable way over a relatively short span of time and many of their genes are conserved in humans.

Now, scientists can conduct future studies to identify a core set of genes in the finch’s brain and see if any of these are disrupted in people with speech disorders caused stuttering, or stroke and by diseases like autism and Parkinson’s, Warren said.

"It’s just amazing to know that when the finch hears a song, there’s always a gene that corresponds in the brain," he said. "Clearly, that’s going to be even more complex in humans."

Warren said as more animals have their genes sequenced, scientists will be able to draw more comparisons that might yield insight into human development.

Next up for some of the Washington University scientists who participated in the finch project is the sequencing of the parrot genome, which is slated for completion sometime later this year.

Sex-Crazed Bugs Unleashed in Israel

2010-03-28T15:03:00.001-07:00

One of the great challenges of modern agriculture is how to use technology to mass produce crops while sparing consumers from the harmful chemicals and byproducts of the agricultural process. Though meant to kill harmful insects, pesticides carry a very serious risk to the environment.

While studies have shown that mankind is developing cancer and other diseases at a higher rate due to exposure to pesticides, the crop-killing vermin are only becoming more immune to its effects. At the Hebrew University of Jerusalem, researchers have discovered a way to safely eliminate insects without the need for harmful chemicals.

Professor Boaz Yuval at the university’s Robert H. Smith Faculty of Food, Agriculture and the Environment believes that sex is the key.

If you can sterilize male insects before they copulate with females, these females will be unable to lay eggs. The problem, however, is that males who are sterilized also lose their sex drive, leaving the females to mate with male insects who are not sterilized.

Researchers at the Hebrew University of Jerusalem have created a special, high protein, bacteria-enhanced “breakfast of champions” to sterilize males. By greatly increasing their sex drive and sexual performance, females spend all of their time with these Casanova sex-crazed males and never are able to lay eggs of their own.

While original applications of this research will be for plant and animal pests, many are looking to see how this work can be applied to stop the spread of organisms carrying human diseases.

Eye Spy Israeli Nanotechnology

2010-03-28T14:53:00.000-07:00

The Wall Street Journal’s MarketWatch website reports that Nano Retina, based in Herzliya, has developed a system of retinal implants to help people suffering from macular degeneration, complications of diabetes, and other diseases that affect vision.

Without getting all technical, the Bio-Retina would be implanted into the eye and actually glued over one’s natural but damaged retina. As light enters the eye, the Bio-Retina converts it into tiny electrical impulses and sends them off to the brain, essentially functioning just as a normal, healthy retina would. Best part? The procedure takes about half an hour. Heck, that’s faster than most dentist visits.

Unsurprisingly, Nano Retina’s innovative chief executive Ra’anan Gefen comes from a background of technology development in Israel’s military. Nano Retina isn’t a one-man show, though. The company is a joint venture of Rainbow Medical, also of Herzliya, and Zyvex Labs of Texas. (And, to be fair, we should mention that U.S.-based Second Sight Medical Products is also working on its own solution.)

Will bionic eyes become standard fare? Will macular degeneration become a thing of the past? Will the carrot industry survive? Only time will tell.

The Truth About Urine

2010-03-11T16:14:00.000-08:00

The Truth About Urine
What do urine color and odor changes mean? How often should you 'go'? Find out.
By Stephanie Watson
WebMD FeatureReviewed by Louise Chang, MD
March 11, 2010

Urine isn't something most people talk about. We barely give it more than a passing glance as it swirls out of sight down the toilet bowl. Yet changes in the urine – its color, odor, and consistency – can provide important clues about the status of your body. Your urine can reveal what you've been eating, how much you've been drinking, and what diseases you have.

"Urine and urinalysis have, for hundreds of years, been one of the ways physicians have looked at health," says Tomas Griebling, MD, MPH, vice chair of the urology department at the University of Kansas.

"From a historical view, urinalysis was one of the original windows into what's happening in the body," Griebling says. That's because many of the substances circulating in your body, including bacteria, yeast, excess protein and sugar, eventually make their way into the urine.

Urine is an important part of the body's disposal process. Its job is to remove the extra water and water-soluble wastes the kidneys filter out of the blood. "The urine is there primarily to get rid of toxins or things that would otherwise build up in the body that would be bad for the body," says Anthony Smith, MD, professor and chief of urology at the University of New Mexico.

When you notice that your urine has changed color, or there's a strange odor wafting up from the toilet, the cause might be something as harmless as what you had for dinner (which could have included beets or asparagus). It also might be a sign of a more serious condition, such as an infection or cancer.

Before you flush, here are a few urine changes to look out for, and what they might be saying about your health.

Color Changes
Urine gets its yellow color from a pigment called urochrome. That color normally varies from pale yellow to deep amber, depending on the concentration of the urine. Darker urine is usually a sign that you're not drinking enough fluid. "Your body needs a certain amount of fluid to function, so the body will hold on to fluid and the urine will become very strong and concentrated. When that happens, it will turn a darker color," Griebling says.

The opposite is also true. If your urine is very pale, it means that you're either drinking a lot of fluid, or you're taking a diuretic -- a drug that forces the body to get rid of excess water.

Urine can turn a rainbow of colors, and an unusual hue isn't necessarily cause for alarm. Certain medications can turn the urine fluorescent green or blue, carrots can tint it orange, vitamins can give it a yellow hue, and an inherited disease called porphyria can shade it the color of port wine.

Seeing red is typically a sign that there is blood in the urine, but before you panic, know that a little blood can produce a dramatic color change. "What I always tell patients is it takes one drop of blood to turn a toilet bowl red," Smith says.

That said, just a little blood in the urine can be a sign of something serious, like an infection or cancer, and it warrants a visit to your doctor or urologist. If you're seeing blood and your urine is also cloudy, there's a good chance you've picked up an infection, Smith says.

Odor Changes
Urine normally doesn't have a very strong smell. If you get a whiff of something particularly pungent, you could have an infection or urinary stones, which can create an ammonia-like odor. Diabetics might notice that their urine smells sweet, because of excess sugar. In the past, doctors would actually taste urine for this sweetness to diagnose diabetes.

Some foods can also change urine odor. Asparagus is among the most notorious. What people are smelling when they eat asparagus is the breakdown of a sulfur compound called methyl mercaptan (the same compound found in garlic and skunk secretions). If you catch a whiff of something after eating a plate of asparagus, it means that you've inherited the gene for the enzyme that breaks down mercaptan. Not everyone has this enzyme and, therefore, not everyone can smell it.

How Often Do You Need to Go?
How often you need to go can be as important an indicator of your health as the color or smell of your urine. Most people take bathroom breaks about six to eight times a day, but you might go more or less depending on how much fluid you drink. If you're constantly feeling the urge to go and it's not because you're not drinking extra fluid, causes can include:

Overactive bladder -- involuntary contractions of the bladder muscle
Urinary tract infection
Interstitial cystitis -- a condition that causes the bladder wall to become inflamed and irritated
Benign prostate enlargement -- growth of the prostate that causes it to squeeze the urethra and block the normal flow of urine out of the body
Neurological diseases, including stroke and Parkinson's disease
Diabetes
The opposite problem -- not going to the bathroom enough -- can occur when there is a blockage or infection. Or, it can be the result of bad bathroom habits. Some people -- especially teachers, surgeons, and anyone else who doesn't have time for regular bathroom breaks throughout the day -- tend to hold it in.
Delaying urination can be problematic, says Smith, who compares the bladder to a Slinky: It stretches and then contracts repeatedly, but eventually it can stretch too much to bounce back. "The bladder can develop a chronic overdistension…a chronic emptying problem," he says.

Developing Healthy Bathroom Habits
Take good care of your bladder, and it will thank you by helping you urinate regularly. To avoid having to make too many bathroom visits, stay hydrated, but not overhydrated. Drink whenever you're thirsty, but don't feel as though you have to adhere to the eight-glasses-a-day recommendation (unless you have kidney or bladder stones, in which case you'll need to increase your fluid intake).

If you're getting up during the night to use the bathroom, stop drinking three to four hours before bedtime. Limit caffeine, which can irritate the lining of the bladder. Also watch your intake of alcohol, which can have similar effects.

Finally, don't hold it in. As soon as you feel the urge to go, excuse yourself from whatever you're doing and find a bathroom.

Anti-melanoma drug seems to be miracle cure

2010-03-06T04:53:00.000-08:00

Sunday, Feb. 28 2010
For the melanoma patients who signed on to try a drug known as PLX4032, the
clinical trial was a last resort. Their bodies were riddled with tumors,
leaving them almost certainly just months to live.

But a few weeks after taking their first dose, nearly all of them began to
recover.

Lee Reyes, 30, of Fresno, Calif., who had begun using a feeding tube because of
a growth pressing against his throat, bit into a cinnamon roll.

Nothing, he told his mother, had ever tasted as good.

Rita Quigley, who had been grateful just to find herself breathing each morning
since learning she had the virulent skin cancer, went shopping for new clothes
with her daughters at a mall in Huntsville, Ala.

Randy Williams, 46, who drove 600 miles from his home in Jonesboro, Ark., to
the M.D. Anderson Cancer Center in Houston, the nearest place he could get the
experimental drug, rolled out of bed. "Something's working," he thought,
"because nothing's hurting."

It was a sweet moment, in autumn 2008, for Dr. Keith Flaherty, the University
of Pennsylvania oncologist leading the drug's first clinical trial. A new kind
of cancer therapy, it was tailored to a particular genetic mutation that was
driving the disease, and after six years of disappointments, his faith in the
promise of such a "targeted" approach finally seemed borne out. His
collaborators at five other major cancer centers, melanoma clinicians who had
tested dozens of potential therapies for their patients with no success, were
equally elated.

In a kind of "pinch me" exercise, the six doctors sent each other "before and
after" CT scans of their patients.

One was of Mark Bunting, 52, an airline pilot in Sandy, Utah. His initial scan
in early October showed the cancer in his bones, an incursion considered
virtually impossible to reverse. After two months on the drug, it had all but
disappeared.

"Holy Cow!" Flaherty typed in reply to the slide from Dr. Toni Ribas at the
University of California-Los Angeles, that Dec. 17.

"Are you sure it is the same patient??" added Dr. Jeffrey A. Sosman at the
Vanderbilt-Ingram Cancer Center in Nashville.

From New York, Dr. Paul B. Chapman of Memorial Sloan-Kettering Cancer Center,
perhaps the most determined skeptic of the group, acknowledged, "This looks
impressive."

NEW DRUGS

The trial of PLX4032 offers a glimpse at how doctors, patients and drug
developers navigate a medical frontier at a time when more drugs tailored to
the genetic profile of a cancer are being widely tested on humans for the first
time.

Throughout the fall, the only two patients on the trial whose tumors continued
to grow were the ones who did not have the particular gene mutation for which
the drug had been designed. They were removed from the trial. By late December,
tumors in the 11 patients who did have the mutation had shrunk. Those involved
in the trial held their collective breath waiting to see how long the
remissions would last.

It was a far cry from where they had been a year earlier, when a previous
incarnation of the drug had no effect. Urged on by Flaherty and Chapman, the
companies that owned it had spent months devising a new formulation that could
be absorbed at higher doses.

But the new drug, still in the earliest phase of testing, had to pass several
more hurdles before federal regulators would determine whether it was safe and
effective enough for widespread use.

In December, as the doctors added more patients to the Phase 1 trial, looking
for the highest dose they could give without intolerable side effects, they
scrambled to prepare slides with graphs and statistics to convince the Food and
Drug Administration that the drug should be tested in a larger Phase 2 trial.
The agency required a summary of any and all side effects — there had been only
a few — and any deaths of patients on the study; thankfully, there had been
none since the drug was reformulated. In a matter of days they needed to submit
their findings for a prestigious meeting of clinical oncologists in June.

The side effects struck at the 1,120-milligram dose.

Many patients had been taking the reformulated drug for five months with no
signs of relapsing. The doctors had hoped that by pushing up the dose they
could shut down the cancer more effectively. Some patients were taking as many
as 28 pills a day.

SIDE EFFECTS

Kerri Adams, in Oklahoma City, woke up one morning covered in a rash.
Frightened that she would be dropped from the trial, she tried to ignore it.
But at work, her boss was horrified and insisted that she call the doctor.
Another woman's hand swelled up, and she could not make a fist. A Philadelphia
patient had horrible nausea and diarrhea, and Bunting's joints grew so stiff
that he had to hand jars to his wife to remove the lids, even when they had
already been opened.

Maybe the drug, designed to turn off only the defective B-RAF protein, was, at
high doses, also affecting its role in healthy cells. Or perhaps it was
interfering with other proteins the body needed to function properly.

On their next conference call, the doctors agreed that they had to dial back
the dose.

As the side effects began to subside, many of the patients began to believe
they had beaten their cancer.

One evening, Bunting performed what had become his pill-taking ritual as his
wife puttered around the kitchen.

He liked the water to be room temperature, so he heated it in the microwave and
added cold from the tap. He burped, and some powder from the pills came out of
his mouth just as she turned to look.

They both laughed.

ONE STEP FORWARD ...

When Christopher Nelson strolled into the University of Pennsylvania for a
scheduled day of blood work and monitoring in mid-March, he was greeted as if
he had risen from the dead.

Gazing out the window of the clinic room, he spied a hot dog stand.

"Dirty water dogs," he exclaimed.

"Can you get me one?" he asked his wife's sister. "Actually, two?"

"Chris is feeling better," the nurse told Flaherty casually when she saw him.

"What do you mean?" he pressed.

"Well, he's off pain meds," she said.

Flaherty was not scheduled to see Nelson until three weeks later. But between
appointments that day, the doctor found time to visit his patient. In Nelson's
room, Flaherty broke into a wide smile, a tension he had not realized he was
holding seeping out of him.

He had never seen a melanoma patient who had been that sick improve that much.
He was not sure he had ever seen a melanoma patient that sick who improved at
all.

Sharlene Nelson hugged him. In the weeks that followed, Christopher Nelson
gained 17 pounds. One morning a friend drove him to Atlantic City, where for a
$35 buy-in, they played his favorite game, Texas hold 'em, all day. The drug
had made him sensitive to the sun, and he burned his skin cleaning the pool one
afternoon, even with strong sunblock. Sharlene Nelson bought an umbrella, and
he spent much of the spring sitting underneath it.

"Today's a nice day," he said over the phone to a friend one day in early May.
"There's a cloud, and the sun is behind it."

NOT TOTAL SUCCESS

In mid-May, right before he was to fly to Orlando, Fla., to present the trial's
data, Flaherty received a message on his BlackBerry as he was walking on
campus.

The first patient to respond in the trial, Elmer Bucksbaum, had been admitted
to the hospital. The cancer had spread to his brain.

Flaherty stopped walking.

The drug, Flaherty knew, was powerless in the brain. But had the drug held off
the cancer elsewhere in Bucksbaum's body? Or would other patients, too, begin
to relapse?

Bucksbaum died a few days later.

Flaherty called his family and offered his condolences. It had been not quite
eight months.

Protecting Yourself Against Swine Flu in 15 Seconds

2010-02-12T12:53:00.000-08:00

Hand sanitizers have become a $200-million-a-year industry in the U.S., and the industry continues to grow. While the fear of contracting swine flu has been a significant engine behind the growth of the industry, most people don’t realize that according to the Center for Disease Control, there is no hand sanitizer proven to kill the swine flu virus.

Until now that is.

Professor Elka Touitou, a world renowned expert in the field of drug delivery, on the Faculty of Medicine at the Hebrew University of Jerusalem, has created an antiviral hand sanitizer, which, according to an FDA certified laboratory in the U.S., is highly effective against the H1N1 virus. The innovative product, known as EtoClean (TM), deactivates the swine flu virus in just 15 seconds.

Additionally, EtoClean has also been found to inactivate other viruses that are not effected by regular alcohol-based sanitizers such as hepatitis and norovirus (a common cause of gastroenteritis).

For more information on EtoClean and the company that produces it, click here.
http://www.yissum.co.il/upload/Forbes.pdf

Pathologist warns herbal remedies can be lethal

2010-02-10T05:55:00.000-08:00

A forensic pathologist has sounded a worldwide alert about the dangers of herbal medicines, saying "these substances may cause serious illnesses."
What Professor Roger Byard of the University of Adelaide writes in the Journal of Forensic Sciences is in reference to the false assumptions many people have about herbal medicines.
“There’s a false perception that herbal remedies are safer than manufactured medicines, when in fact many contain potentially lethal concentrations of arsenic, mercury and lead,” Professor Byard says.
“These substances may cause serious illnesses, exacerbate pre-existing health problems or result in death, particularly if taken in excess or injected rather than ingested.”
Professor Byard declares there can also be fatal consequences when some herbal medicines interact with prescription drugs. “As access to such products is largely unrestricted and many people do not tell their doctor they are taking herbal medicines for fear of ridicule, their contribution to death may not be fully appreciated during a standard autopsy.”
After examining 251 Asian herbal products that were found in stores in the United States, analysts found a significant level of harmful ingredients that included arsenic in 36 of them, mercury in 35 and lead in 24 of the products.
“Herbal medicines are frequently mixed with standard drugs, presumably to make them more effective. This can also have devastating results,” Professor Byard adds.
Not only can herbal medicines have a deleterious effect on individuals, the interaction of herbal medicines and traditional therapies can have very serious consequences, as Professor Byard explains. He tells his readers how St. Johns Wort can reduce the effects of warfarin and can also cause intermenstrual bleeding in those women who take oral contraceptive medications. Other herbal remedies such as gingko and garlic can increase the risk of bleeding. Borage Oil and Evening Primrose Oil can lower the threshold at which epileptic seizures can occur.
Around 30 percent of people in the United States use herbal medicines as do a high number of people in Canada and the United Kingdom. This is why Professor Byard underlines the significance of a worldwide warning on the use of herbal medicines.
Despite warnings such as these, articles, books and websites continue to proliferate and are devoted to recommending herbal medicines. The emphasis is on the curative value of these remedies, while few mention the problems taking them.
What's interesting is that not only are people able to buy herbal products, often without knowing the potential risks of some of them, plenty of places on the web give instruction on how to make Chinese herbal remedies, some of which, as noted in Byard's research, can cause harm.
The website gives information on how to make herbal medicines with an organized presentation, but without any apparent warnings for readers to review. Instead the warnings are directed towards the user making sure that he or she uses the right remedy for the right medical condition.
There are risks involved when taking herbs for medical purposes, doctors warn. This new research underlines what many doctors have noted for years: when in doubt check with your doctor.

Unrolled, Unbridled and Unabashed

2010-02-06T11:00:00.000-08:00

Exhibition Review | 'Rubbers: The Life, History & Struggle of the Condom'
Unrolled, Unbridled and Unabashed
By EDWARD ROTHSTEIN

In the 18th century Casanova referred to them as “English frock coats” and made prodigious use of the “little preventive bag invented by the English to save the fair sex from anxiety.” In 1709 the English literary journal The Tatler alluded to their supposed invention by an eponymous doctor of “eminent Quality”; the success of his “Engine” eventually “made it an Immodesty to name his Name.”

But there was never a Dr. Condom as far as we can tell, and no one really knows who first created condoms (or named them), since bladders, animal membranes, sheaths and salve-coated cloths have been used for similar purposes since the beginning of recorded history.

Spend some time at the fascinating new exhibition at the Museum of Sex, “Rubbers: The Life, History & Struggle of the Condom,” and their origins hardly matter: their history is what is extraordinary. These commonplace objects — widely used and rarely spoken of, often seen but infrequently displayed — are icons of far more than the phallus.

The museum’s curator, Sarah Forbes, has gathered condom boxes and vending machines, horrific photos of disease and collections of birth-control devices, American military videos and a dress made out of dyed condoms, television commercials and artworks, creating a modest exhibition that elevates the status of the condom. And, not incidentally, the show explicitly encourages its use — particularly, as one major section reminds us, to prevent the spread of H.I.V. and AIDS.

It is no wonder that the company that makes Trojan condoms became a sponsor of the exhibition, though the extent of its presence here is limited, including a display of contemporary equipment used in making condoms (metallic phallic molds that are dipped into liquid latex, for example) and a video of laboratory tests showing their resiliency. (Condoms are attached to valves and inflated, becoming enormous balloons well before they finally burst.)

The evolution of the condom is too briefly told, but it includes Charles Goodyear’s discovery of a treatment for rubber that retained its flexibility; a photograph of a well-preserved reusable rubber sheath from mid-20th-century London is here. In Germany, we learn, condoms are colloquially referred to as Fromms because that was the name of the Jewish manufacturer who, before the Nazis came to power, sold 50 million condoms a year. (His condoms were also, interestingly, packaged with slips of paper that could be discreetly handed to a pharmacist, ordering another supply.) But Julius Fromm had to flee to London and lost the factory.

It is partly because condoms graphically suggest the sex act that they have so often been known through their covers: a collection of boxes and containers here range from antique exoticism (picturing desert camels) to whimsical contemporaneity (portraits of candidates from the last presidential election). A New York pharmacy case has wooden doors that would have decorously concealed the contents until the customer was prepared to survey the various Sheik condoms for sale. Condoms have also accumulated nicknames that are covers of sorts, hiding their identity while provocatively suggesting it. (A wall displays a roster of aliases, including, most mildly, “copper hat,” “love sock,” “frogskin,” “night cap.”)

Condoms have encouraged sophomoric humor (a historical etching of Casanova shows him blowing into a condom and inflating it for the amused delectation of his lady admirers) and avant-gardish flirtatiousness (as in Randy Polumbo’s artworks on display, which include a ribbed dirigible and a solar-powered flying machine that inflates and deflates attached condoms).

And they have a dark side, which casts its shadow over such play. There are early photographs here of victims of syphilis, including a chilling image of a pox-covered baby nursing at a pox-covered breast.

Like the diseases they prevent, condoms have also proliferated with the march of armies. As the show points out, 18,000 American soldiers a day were on sick leave with venereal diseases during World War I, inspiring the United States government to begin a campaign about the transmission of disease and the distribution of military “pro-kits” to allow cleansing and protection.

The show’s grim accounting of sexually transmitted disease is tempered by an upbeat 2006 news account of a Florida retirement community in which condom use is being encouraged for its residents because of the spread of sexual diseases. The cure and the prevention have become so routine, they scarcely intrude on the pleasures.

But the last half of the exhibition is more preoccupied with controversy: the condom becomes a political instrument in long-running cultural and religious debates. A 1915 edition of Margaret Sanger’s once-controversial book, “What Every Girl Should Know,” is here. (Her birth-control advocacy led to the creation of Planned Parenthood.) So is a 1989 poster of deliberate crudity attacking the pope and the Roman Catholic Church for opposing the use of condoms for birth control and disease prevention.

The onset of H.I.V. and AIDS in the 1980s created another crisis in which advertisements and educational materials invoked death and disease, just as the warnings about sexual diseases did in earlier centuries. One series of commercials shown here, from MTV’s Staying Alive Foundation, depicts passionate sex, ending with the man pulling a gun on his lover: unprotected sex is murder.

But while the earlier response to similar dangers was chastisement (avoid prostitutes; keep a “healthy mind and clean body,” warns a 1941 United States Army film), here the condom offers another possibility: a series of Keith Haring drawings promote both sexual activity and protection, offering satisfaction along with immunity.

This message is literally a promotion of the condom; the condom even becomes a cause. This is one impulse behind the purple couture cocktail dress displayed here, designed by Adriana Bertini: it is constructed from 1,200 hand-dyed condoms. In such a form the condom is not private but public, not hidden but extravagantly and profusely evident. It is associated with pleasure, not prevention, but is meant to provide both. Such is the new image of the condom.

Yet this is just a variation on a theme. The history of condoms is a chronicle of appetite and fear, of desire and darkness. The aspect of condoms that offends some orthodox religious beliefs, after all, is that it treats the possibility of pregnancy as something as unwanted as a disease, something to be prevented for the sake of sexual gratification: the condom is an indulgence, an avoidance.

If the condom appears to be a sign of promiscuous satisfaction, though, it is also, in its essence, a compromise: at the moment of greatest potential pleasure, it interferes. It requires that the rush of desire be interrupted, its course modified, its sensation diminished. At the moment of being consumed by the present, a concern with the future intrudes. The condom is a declaration of sacrifice in the midst of indulgence. It is evidence of civilization and its discontents.

“Rubbers: The Life, History & Struggle of the Condom” is on view at the Museum of Sex, 233 Fifth Avenue, at 27th Street; (212) 689-6337, museumofsex.com.

Medical Clowns

2010-01-14T05:15:00.000-08:00

This report takes a look at the increasingly popluar trade of Medical Clowns in Israel.

Detecting skin cancer at an earlier stage

2009-12-04T11:29:00.000-08:00

Detection of skin cancer is usually done by the eye alone. Now Israeli researchers have developed a new device that can detect cancerous tumors at an earlier stage.

Sunbathers are particularly at risk of developing skin cancer if they don't protect their skin from the sun.

Researchers in Israel are developing a new device that can detect cancerous skin tumors, including melanomas that aren't visible to the naked eye, at an earlier stage of the disease.

The Optical Spectro-Polarimetric Imaging (OSPI) instrument, developed at Ben-Gurion University of the Negev (BGU), reveals new textures of lesions that have never been seen before - including melanoma in patients who were diagnosed with various skin lesions and were awaiting surgery for their removal. The instrument diagnosed 73 types of lesions, some of them cancerous.

More than one million cases of skin cancer are diagnosed in the US every year according to the American Cancer Society. Of the 11,590 deaths due to skin cancer in 2009, some 8,650 will be due to melanoma, the most serious and dangerous type of skin cancer.

Today, dermatologists and plastic surgeons typically diagnose skin tumors with the naked eye and only rarely use a dermatoscope - a magnifying tool that allows tumors to be examined in detail.

Skin cancer and beyond

Cancerous mole detection is usually done by looking for one or more telltale visible symptoms: if the mole is asymmetrical; if it's outline is blurred or irregular; if it has multiple colors; if it is larger than five millimeters in diameter; and if stands up above the skin.

The OSPI biosensor, however, uses safe, infrared wavelengths and LC devices to measure tumor characteristics, including contours and spread, identifying tumors at an earlier stage.

"This is an exciting preliminary development since the initial testing shows that we can now identify microscopic tumors in the biological layers of the skin," explains Prof. Ibrahim Abdulahim, who is head of the BGU Electro-Optical Unit in the Faculty of Engineering Sciences and is leading the research group.

"As we continue to develop the OSPI, we also see an opportunity to use this technology for detecting other types of cancerous growths."

Abdulahim is supervising this research with Ph.D candidate Ofir Aharon and MS.c student Avner Safrani. He is also collaborating with BGU Prof. Lior Rosenberg and Dr. Ofer Arnon from the Department of Plastic Surgery at Soroka University Medical Center.

5+ Foods to Fight the Flu

2009-12-02T06:44:00.000-08:00

Keep your digestive system happy. When the digestive system is healthy it is able to breakdown and access nutrients from the foods you eat, it is better able to get rid of toxicity, and process “bad” bugs such as bacteria & viruses

ChicagoHealers.com Practitioner Dr. Helen Lee offers the following free flu-fighting foods:

Ginger: The volatile oils in ginger warm the body, helping the body to sweat, break a fever and eliminate toxins. Ginger also stimulates mucous release. Ginger is also a metabolic enhancer and the warming also helps with nausea, is a great digestive aid, lung and chest decongesting, and a body cleansing herb. Add fresh ginger to your food or in tea, or eat alone. Ginger tea (especially combined with honey) helps too sooth the throat.

Garlic: Garlic has allicin as an active ingredient giving it antiviral and antibacterial properties. Garlic cleans your liver (which cleans your blood) since your blood cycles through your liver every three minutes. So thereby stimulating the white blood cells and in turn boosting the immune system. An onion garlic syrup can help with mucous release.

Honey: Honey acts as a natural antibiotic with antiseptic properties. There are vitamins such as B-complexes, C, D, E, minerals enzymes and propolis. The propolis in honey boosts the immune system, disables viruses and fights infections. Furthermore, pediatric studies have shown that honey is more effective than cough syrup because it coats the throat better. Locally grown honey is best for seasonal allergies, asthma and respiratory conditions because you are treating with the irritants that are common to your area. Take a tablespoon 4 times per day, taken straight or in tea.

Cayenne: Cayenne pepper has a high vitamin C content making it a natural choice for a cold, as well as vitamin A, B, calcium and potassium. Cayenne also increases the circulation in the body. You may take in capsule form taking 2 – 40,000 heat units (950mg), or liquid 4 drops of the 200,000 heat units. Place a few drops in water and gargle with it every 15-30 minutes to make a sore throat disappear.

“Good” Bacteria: Increase “good” bacteria such as acidophilus and bifidus which can be found yogurt or kefir.

Go Green: Eat dark leafy green vegetables like kale, swiss chard, and spinach provides vitamins B12, folic acid, potassium, vitamins A, C & K which supports a healthy immune system.

Acid and Alkaline: Keep your internal acid/alkaline chemistry balanced by squeezing a half lemon into a cup of hot water to break up congestion, stimulate digestion, and create an alkaline or healing pH chemistry in the body

Reconstructive memory

2009-11-25T10:57:00.000-08:00

The term 'Rashomon effect' is often used by psychologists in situations where observers give different accounts of the same event,and describes the effect of subjective perceptions on recollection. The phenomenon is named after a 1950 film by the great Japanese director Akira Kurosawa. It was with Rashomon that Western cinema-goers discovered both Kurosawa and Japanese film in general - the film won the Golden Lion at the Venice Film Festival in 1951, as well as the Academy Award for Best Foreign Language film the following year.

Rashomon is an adaptation of two short stories by Akutagawa Ryunosuke. Set in the 12th century, the film depicts the trial of a notorious bandit called Tajomaru (played by Kurosawa's frequent collaborator Toshiro Mifune), who is alleged to have raped a woman and killed her samurai husband. In flashbacks, the incident is recalled by four different witnesses - a woodcutter, a priest, the perpetrator and, via a medium, the murder victim. Each of the testimonies is equally plausible, yet all four are in mutual contradiction with each other.

The film is an examinantion of human nature and the nature of reality. It compels the viewer to seek the truth. Each testimony is influenced by the intentions, experiences and self-perceptions of the witness. They all tell their own 'truth', but it is distorted by their past and by their future. Under Kurosawa's masterful direction, the characters start off happy in the knowledge that they know exactly what happened between the samaurai, his wife and the bandit. One by one, each character begins to doubt their own account of the incident. In the end, both the cast and the viewer are left in a state of confusion and bewilderment.
The idea that we do not remember things as they actually happened is usually attributed to Sir Frederick Bartlett (1886-1969), who spent much of his professional career at Cambridge University, where he became head of the psychology department. He describes the process of memory in his classic 1932 book, Remembering: A Study in Experimental and Social Psychology:

Remembering is not a completely independent function, entirely distinct from perceiving, imaging, or even from constructive thinking, but it has intimate relations with them all...One's memory of an event reflects a blend of information contained in specific traces encoded at the time it occurred, plus inferences based on knowledge, expectations, beliefs, and attitudes derived from other sources.

According to Bartlett, memories are organized within the historical and cultural frameworks (which Bartlett called 'schemata') of the individual, and the process of remembering involves the retrieval of information which has been unknowingly altered in order that it is compatible with pre-existing knowledge.

Bartlett's ideas about how memory works came to him during a game of Chinese whispers, in which a short story is relayed through a chain of people, each of whom makes minor retrieval errors, such that the final retelling may be completely different from the original. One of his experiments involved asking subjects to read a Native American folk story called The War of the Ghosts, and then recall it several times, sometimes up to a year later. He chose it because the cultural context in which it is set was unfamiliar to the participants in his experiments.

Bartlett found that upon recall, the subjects altered the narrative of the story to make it fit in with their existing schemata. Participants omitted information they regarded as irrelevant, changed the emphasis to points they considered to be significant, and rationalized the parts that did not make sense, to make the story more comprehensible to themselves. In other words, memory is reconstructive rather that reproductive.

Although Remembering was largely ignored upon its publication, it is today highly influential. Elizabeth Loftus, a professor of psychology and law at the University of California, Irvine, has devoted her career to studying the reconstructive nature of memory in relation to eyewitness testimony.

Loftus is concerned mainly with how the recollections of eyewitnesses can be deliberately manipulated by misinformation. In extreme cases, this can lead to completely false memories of events that did not take place. One of Loftus's more famous studies addresses the use of 'leading' questions in the courtroom. In the study, students were shown film clips of a car accident, and then asked a question about the accident. Those asked "About how fast were the cars going when they smashed into each other?" gave answers which averaged about 39 mph, whereas those asked "About how fast were the cars going when they contacted each other?" gave answers with an average speed of 32 mph.

Loftus's research, like that of Bartlett's, shows that our memories are quite often not as accurate as we would like to think they are. The knowledge that memory is to some extent confabulation has very serious implications for the use in the courtroom of eyewitness testimonies, because if eyewitness testimonies can be unreliable, then the validity of criminal convictions based upon them is open to question.

As well as confabulating the past, the brain also envisages events that have not yet occurred. The process of anticipating oneself attending a future event probably involves drawing on past experiences to generate a 'simulation' of the future event. Daniel Schacter argues that this 'episodic-future' thinking is entirely dependent on reconstructive memory:

...future events are not exact replicas of past events, and a memory system that simply stored rote records would not be well-suited to simulating future events. A system built according to constructive principles may be a better tool for the job: it can draw on the elements and gist of the past, and extract, recombine and reassemble them into imaginary events that never occurred in that exact form. Such a system will occasionally produce memory errors, but it also provides considerable flexibility.

Most of the evidence that reconstructive memory may be essential for envisioning future events comes from amnesic patients who also have difficulties picturing themselves in the future, and now there is also some experimental evidence. For example, recent functional neuroimaging studies show that some of the brain regions that are activated when recalling a personal memory - the posterior cingulate gyrus, parahippocampal gyrus and left occipital lobe - are also active when thinking about a future event.

Amnesia in the movies

2009-11-25T10:44:00.000-08:00

Despite occuring only rarely, amnesia (or memory loss) has featured often in Hollywood films for almost a century. By 1926, at least 10 silent films which used amnesia as a plot device had been made; more recent productions, such as 50 First Dates and Eternal Sunshine of the Spotless Mind, are therefore part of a well established tradition.

In a review published in the British Medical Journal in 2004, clinical neuropsychologist Sallie Baxendale of the Institute of Neurology in London points out that cinematic depictions of amnesia are consistenly inaccurate, and usually "bear no relation whatsoever to any authentic neurological or psychiatric condition".

In her review, Baxendale examines common misconceptions of amnesia found in the cinema, and suggests that knowledge of them can guide clinicians when informing patients and their relatives about diagnoses. She also points out several exceptional films which depict amnesic syndromes accurately.

In the romantic comedy 50 First Dates (2004), Adam Sandler plays veterinarian Henry Roth, who falls for Lucy Whitmore (played by Drew Barrymore) after meeting her in a cafe one morning. The two hit it off, and arrange to meet again. The following day, Roth returns to the café to meet her, but she claims to have no recollection of him. As he leaves, the owner of the café takes him to one side, and explains that Whitmore "lost her short-term memory" after a "terrible car accident". We also learn that she can form new memories during the day, which are then wiped clean during her sleep, so that she wakes up to a "clean slate" every morning.
50 First Dates propagates a number of misconceptions which are common in the films which refer to amnesia. Whitmore's amnesia is the result of a head injury incurred in the car accident; other amnesic characters may lose their memory after being assaulted, or bumping their head in some other way. In reality, memory loss rarely occurs following a head injury; it is most often caused by stroke, brain infection or neurosurgery. The idea that new memories are wiped clean at night is also unrealistic, and unlike any documented amnesic syndrome.

In many cases of cinematic amnesia, head injuries lead to loss of memory of earlier events (retrograde amnesia), but the character usually goes on to lead an otherwise normal life. Real patients who incur brain damage usually suffer from anterograde amnesia - they lose the ability to form new memories, but their memories of events that occured before the amnesia often remain intact. Often they lose memories of many important aspects of their lives - of loved ones and daily routines - and so day-to-day functioning is affected severely.

Amnesic film characters often undergo personality changes or a loss of identity. This confuses amnesia with a poorly-understood condition called dissociative fugue. It also blurs the distinction between the causes of the different amnesic syndromes, as the characters experience psychiatric symptoms, which in reality do not have an organic cause, which are attributed to neurological damage.
Personality changes after a head injury can be seen in the 1987 film Overboard, starring Goldie Hawn and Kurt Russell. Hawn plays a rich and spoilt socialite who loses here memory after bumping her head when falling from her yacht. The character then undergoes a sudden transformation - she becomes warm-hearted and loving and is duped into raising the children of Russel's character as her own. Her memory loss, like that of most other characters, is readly reversible - towards the end of the film, it is cured by another bump on the head. In others, the memories return when they see a familiar object or person. Both of these scenarios are equally implausible.

Memento (2000) is a rare example of a film which depicts amnesia accurately. It is apparently inspired in part by the case of Henry Molaison (H.M.), the famous amnesic who died last December. Guy Pearce plays Leonard, who suffers severe anterograde amnesia after sustaining a head injury in an attack in which his wife is killed. Unlike most amnesic characters, Leonard retains his identity and the memories of events that occurred before the attack, but loses all ability to form new memories. The film's fragmented narrative powerfully depicts how difficult everyday life would be for a severely amnesic patient - Leonard spends much of the film frantically scribbling scraps of information on pieces of paper and, once he has estalished something to be a fact, has it tattooed onto his body.

Another accurate depiction of amnesia is found in the CGI-animated film Finding Nemo (2003). One of the characters, a reef fish called Dory, has a profound memory deficit which, to frustration of her peers, prevents her from learning or retaining any new information, remembering names, or knowing where she is going. As a result, she gets lost when left alone and is often found in a state of confusion. The exact origin of Dory's impairment is not mentioned in the film, but her memory loss accurately reflects the difficulties faced by amnesic patients and those who know them.
Realistic amnesic characters are few and far between in the cinema. Baxendale refers to only one other film, called Se Quien Eres (I Know Who You Are, 2000), containing an accurate depiction of amnesia, in the form of a patient with Korsakoff's Syndrome, the amnesic syndrome condition associated with chronic alcoholism. However, Columbia Pictures announced last month it has acquired the rights to make a film about the life of H.M., based on a book which is to be written by Susanne Corkin, the MIT researcher who worked with him for 4 years.

On a related subject is Rashomon (1950), Akira Kurosawa's masterful examination of the reconstructive nature memory Rashomon depicts a crime as seen from the perspective of four eyewitnesses. As each gives their testimony, the same event is described in four radically different ways. Each of the testimonies contradicts the others, and each of the witnesses initially insists that their version of the event is the right one. Then, as they consider each others' descriptions, something which at first seemed clear becomes utterly confusing, as all the characters and the audience begin to question the accuracy of their own memories.

* Hands-on Tech: Double Amputee Gets Mind-Controlled Arms

2009-11-23T18:42:00.000-08:00

When Christian Kandlbauer lost both of his arms in a work accident in 2005, he thought he’d lost his independence. But thanks to amazing advances in prosthesis technology, he now has two high-tech prosthetic arms that allow him to function in many of the ways he did before his accident – and they’re controlled by his thoughts. The arms, developed in a joint venture between the Otto Bock health care company and the Medical University of Vienna, were fitted in 2007. But before they could go on, Kandlbauer had to undergo a complex procedure to re-wire the nerves in his arm stumps, a procedure that only three surgeons in the world can perform. The nerves that used to control his arms were moved to his chest to allow him to control his new bionic arms via electronic sensors.

Now, Kandlbauer moves his new arms the way he moved his old ones: he activates “muscle” movement with impulses from his brain. The prosthetic arms aren’t quite as articulate as natural arms, but they have seven degrees of movement as opposed to the three degrees of movement offered by conventional prostheses. And four years after losing his arms, Kandlbauer was able to achieve one of his biggest goals: he passed his driving test. He’s now able to drive himself around with the help of a modified vehicle, thanks to his high-tech arms.When Christian Kandlbauer lost both of his arms in a work accident in 2005, he thought he’d lost his independence. But thanks to amazing advances in prosthesis technology, he now has two high-tech prosthetic arms that allow him to function in many of the ways he did before his accident – and they’re controlled by his thoughts. The arms, developed in a joint venture between the Otto Bock health care company and the Medical University of Vienna, were fitted in 2007. But before they could go on, Kandlbauer had to undergo a complex procedure to re-wire the nerves in his arm stumps, a procedure that only three surgeons in the world can perform. The nerves that used to control his arms were moved to his chest to allow him to control his new bionic arms via electronic sensors.

A new antidepressant really turns women on

2009-11-17T04:31:00.000-08:00

To all the men (and women) I've ever heard complain about the female libido, it's time to take the batteries out of your high-tech remote-control sex toys.

Flibanserin appears to be a highly effective libido booster in women who report low sexual desire, three new trials find.

Flibanserin, a drug originally designed to fight depression, turns out to be an ineffective antidepressant but a highly effective libido booster in women who report low sex drives, according to results pooled from three separate clinical trials. (It's long been thought that antidepressants suppress sex drives, so it makes its own strange sense that a poor antidepressant might not have the same suppressing effect.)

"It's essentially a Viagra-like drug for women in that diminished desire or libido is the most common feminine sexual problem, like erectile dysfunction is in men," reports John Thorp Jr., a principal investigator in the studies and the McAllister distinguished professor of obstetrics and gynecology at the University of North Carolina at Chapel Hill School of Medicine.

It's not terribly surprising that flibanserin was not originally designed to boost the female libido, since this is a notoriously complicated task compared to the notoriously uncomplicated approach in men of simply regulating blood flow. More surprising is that these are purported to be the first trials ever to test a female libido therapy in the brain; one would think that all the scoffing women do about men thinking with their "other" heads would indicate women's tendency to do that sort of thinking with the head that sits on their shoulders.

Hypoactive sexual desire disorder, a bulky arrangement of syllables that risks causing the very thing it names, affects anywhere from 9 percent to 26 percent of women in the U.S., studies show. But that doesn't mean you should throw away those high-tech sex toys and run to your local pharmacy; flibanserin is still an investigational drug, available only to those women who've agreed to participate in clinical trials.

The trial results were presented by principal investigator Elaine E. Jolly from the University of Ottawa in Canada on Monday at the Congress of the European Society for Sexual Medicine in Lyon, France.

All three trials were funded by Boehringer Ingelheim Pharmaceuticals, a manufacturer of flibanserin. That means until further studies are done without BIP funding, these results should be viewed with a level of skepticism; developing the first successful female libido booster could be a way for the company that designed such a poor antidepressant to save face.

That brings me to a final point: since women who do not suffer from hypoactive sexual desire disorder might be just the type to enjoy such things as sex toys and libido boosters recreationally (some women take Viagra for fun), one wonders what effect, if any, flibanserin will have on them.

The Best Exercises for Healthy Bones

2009-11-14T16:49:00.000-08:00

By GRETCHEN REYNOLDS
Digital Images/Getty Images

Several weeks ago, The Journal of the American Medical Association published a study that should give pause to anyone who plans to live a long and independent life. The study looked at the incidence of hip fractures among older Americans and the mortality rates associated with them. Although the number of hip fractures has declined in recent decades, the study found that the 12-month mortality rate associated with the injury still hovers at more than 20 percent, meaning that, in the year after fracturing a hip, about one in five people over age 65 will die.
Phys Ed

Meanwhile, another group of articles, published this month as a special section of Medicine & Science in Sports & Exercise, the journal of the American College of Sports Medicine, underscore why that statistic should be relevant even to active people who are years, or decades, away from eligibility for Medicare. The articles detailed a continuing controversy within the field of sports science about exactly how exercise works on bone and why sometimes, apparently, it doesn’t.

“There was a time, not so long ago,” when most researchers assumed “that any and all activity would be beneficial for bone health,” says Dr. Daniel W. Barry, an assistant professor of medicine at the University of Colorado, at Denver, and a researcher who has studied the bones of the elderly and of athletes. Then came a raft of unexpected findings, some showing that competitive swimmers had lower-than-anticipated bone density, others that, as an earlier Phys Ed column pointed out, competitive cyclists sometimes had fragile bones and, finally, some studies suggesting, to the surprise of many researchers, that weight lifting did not necessarily strengthen bones much. In one representative study from a few years ago, researchers found no significant differences in the spine or neck-bone densities of young women who did resistance-style exercise training (not heavy weight lifting) and a similar group who did not.

Researchers readily admit that they don’t fully understand why some exercise is good for bones and some just isn’t. As the articles in this month’s Medicine & Science in Sports & Exercise make clear, scientists actually seem to be becoming less certain about how exercise affects bone. Until fairly recently, many thought that the pounding or impact that you get from running, for instance, deformed the bone slightly. It bowed in response to the forces moving up the leg from the ground, stretching the various bone cells and forcing them to adapt, usually by adding cells, which made the bone denser. This, by the way, is how muscle adapts to exercise. But many scientists now think that that process doesn’t apply to bones. “If you stretch bone cells” in a Petri dish, says Alexander G. Robling, an assistant professor in the department of anatomy and cell biology at Indiana University School of Medicine and the author of an article in Medicine & Science in Sports & Exercise, “you have to stretch them so far to get a response that the bone would break.”

So he and many other researchers now maintain that bone receives the message to strengthen itself in response to exercise by a different means. He says that during certain types of exercise, the bone bends, but this doesn’t stretch cells; it squeezes fluids from one part of the bone matrix to another. The extra fluid inspires the cells bathed with it to respond by adding denser bone.
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Why should it matter what kind of message bones are receiving? Because, Professor Robling and others say, only certain types of exercise adequately bend bones and move the fluid to the necessary bone cells. An emerging scientific consensus seems to be, he says, that “large forces released in a relatively big burst” are probably crucial. The bone, he says, “needs a loud signal, coming fast.” For most of us, weight lifting isn’t explosive enough to stimulate such bone bending. Neither is swimming. Running can be, although for unknown reasons, it doesn’t seem to stimulate bone building in some people. Surprisingly, brisk walking has been found to be effective at increasing bone density in older women, Dr. Barry says. But it must be truly brisk. “The faster the pace,” he says — and presumably the greater the bending within the bones — the lower the risk that a person will fracture a bone.

There seems to be a plateau, however, that has also surprised and confounded some researchers. Too much endurance exercise, it appears, may reduce bone density. In one small study completed by Dr. Barry and his colleagues, competitive cyclists lost bone density over the course of a long training season. Dr. Barry says that it’s possible, but not yet proved, that exercise that is too prolonged or intense may lead to excessive calcium loss through sweat. The body’s endocrine system may interpret this loss of calcium as serious enough to warrant leaching the mineral from bone. Dr. Barry is in the middle of a long-term study to determine whether supplementing with calcium-fortified chews before and after exercise reduces the bone-thinning response in competitive cyclists. He expects results in a year or so.

In the meantime, the current state-of-the-science message about exercise and bone building may be that, silly as it sounds, the best exercise is to simply jump up and down, for as long as the downstairs neighbor will tolerate. “Jumping is great, if your bones are strong enough to begin with,” Dr. Barry says. “You probably don’t need to do a lot either.” (If you have any history of fractures or a family history of osteoporosis, check with a physician before jumping.) In studies in Japan, having mice jump up and land 40 times during a week increased their bone density significantly after 24 weeks, a gain they maintained by hopping up and down only about 20 or 30 times each week after that.

If hopping seems an undignified exercise regimen, bear in mind that it has one additional benefit: It tends to aid in balance, which may be as important as bone strength in keeping fractures at bay. Most of the time, Dr. Barry says, “fragile bones don’t matter, from a clinical standpoint, if you don’t fall down.

The Peril of Palatability

2009-11-09T19:43:00.000-08:00

A former FDA chief sounds the alarm about dangerously delicious food.

The End of Overeating: Taking Control of the Insatiable American Diet, by David A. Kessler, Emmaus, Pa.: Rodale Books, 320 pages, $25.95

According to The Washington Post, David Kessler’s research for The End of Overeating included late-night forays into the trash bins behind Chili’s restaurants across California. From the chain’s garbage he retrieved ingredient boxes with nutritional labels that revealed the secret of dishes such as Southwestern Eggrolls and Boneless Shanghai Wings. It turned out they “were bathed in salt, fat and sugars.”

Kessler could have saved considerable time and trouble by paying a Chili’s employee to write down this information for him. Or by visiting the Chili’s website, which provides numbers for the calories, fat, saturated fat, carbohydrates, protein, fiber, and sodium in the company’s food. Or simply by assuming that food promoted as a mouth-watering yet affordable indulgence probably has a lot of fat, salt, and sugar in it. But as The End of Overeating more than amply demonstrates, Kessler is the sort of crusader who spares no effort to uncover the obvious.

Kessler, a professor at the University of California at San Francisco’s medical school, grabbed headlines as head of the Food and Drug Administration under Bill Clinton by taking on Big Tobacco. In this book he mounts an assault on Big Food, but the results are even feebler than his unsuccessful effort to regulate cigarettes without statutory authority. He combines banal observations, dressed up as scientific insights and revelations of corporate misdeeds, with presumptuous advice that overgeneralizes from his own troubled relationship with food.

Kessler urges readers to eschew pasta, French fries, bacon cheeseburgers, candy, and other “hyperpalatable” foods that he and some people he interviewed for the book have trouble consuming in moderation. Kessler wants us to know he is powerless over chocolate-chip cookies and “those fried dumplings at the San Francisco airport.” Using himself and several similarly voracious acquaintances as models, he argues that “conditioned hypereating” is largely responsible for the “obesity epidemic.” He exhorts its victims to resist the machinations of the food industry, “the manipulator of the consumers’ minds and desires” (in the words of a “high-level food industry executive”).

Kessler fearlessly accuses major restaurant chains of a crime they brag about, relying on unnamed “insiders” to reveal that comestible pushers such as Cinnabon and The Cheesecake Factory deliberately make their food delicious—or, as he breathlessly puts it, “design food specifically to be highly hedonic.” Kessler certainly has the goods on the corporate conspiracy to serve people food they like. “We come up with craveable flavors, and the consumers come back, even days later,” a “research chef at Chili’s” confesses to him. Kessler also reveals that Nabisco lures Oreo eaters through a dastardly combination of sweet white filling and crunchy, bittersweet chocolate wafers, achieving “what’s called dynamic contrast.” Or maybe it’s “what the industry calls ‘dynamic novelty,’ ” as Kessler claims in another Oreo discussion elsewhere in the book. Either way, it’s so good it must be bad.

Not only do these sneaky bastards create irresistible food; they then turn around and tell people about it. “With its ability to create superstimuli, coupled with its marketing prowess, the industry has cracked the code of conditioned hypereating and learned exactly how to manipulate our eating behavior,” Kessler writes. “It has figured out the programming that gets us to pursue the food it wants to sell.”

If Kessler hadn’t been so distracted by that plateful of chocolate-chip cookies, perhaps he would have noticed the contradiction between his description of how the food industry goes to great lengths to give consumers exactly what they want and his claim that it arbitrarily decides what products it wants to sell, then uses marketing magic to create a demand for them. The only way to deal with such logic-defying nefariousness, he suggests, is to regulate advertising and require restaurants to nag their customers with conspicuous calorie counts. He also encourages readers to “feel angry at the marketing and advertising techniques designed to get you to eat more, at the huge portion sizes served at restaurants, and at the layered and loaded food you encounter everywhere.” It’s all about “reframing seemingly well-meaning acts as hostile ones.” Thinking back on all those times my mother offered me a second helping, I now realize how much she hates me.

Kessler’s discussion of the science behind his theory of conditioned hypereating is at least as enlightening as his economic analysis of the food industry. “Palatable foods arouse our appetite,” one expert tells him. “They act as an incentive to eat.” Once he’s made sure we know what palatable means, Kessler tries to explain why some foods have this quality. It turns out that palatable foods affect neurotransmitter levels, stimulate “the pleasure center,” and activate “the body’s reward system.” Since the same could be said of pretty much everything that people enjoy, this observation is not very illuminating. It falls into the same true-but-dull category as Kessler’s discovery that “people get fat because they eat more than people who are lean.”

Kessler’s neurological reductionism gives him an excuse to talk about rat studies and MRI scans, but it does not have much explanatory power. “The food we ate for comfort has left its mark on the brain, creating a void that will need to be filled the next time we are cued,” he writes. “The result is a spiral of wanting.” Since all experiences leave a “mark on the brain,” what does this really tell us about why some people eat a few potato chips and stop, while others finish the bag and look for more in the cupboard?

It’s not clear what percentage of the population reacts to food the way Kessler and his hypereating friends do. The government says two-thirds of Americans are “overweight,” but that does not mean they routinely engage in the out-of-control gorging that Kessler describes. Then again, Kessler says “overeating is not the sole province of the overweight,” since thin people can scarf down big bowls of ice cream or M&Ms but compensate by exercising more. It does not make much sense to claim that people who burn all the calories they consume are overeating—unless, like Kessler, you’re promoting a trademarked treatment for overeating called Food Rehab™.

According to The Washington Post, “Kessler estimates that about 15 percent of the population is not affected” by conditioned hypereating, meaning 85 percent is. That seems inconsistent not only with everyday experience but with Kessler’s own analysis of questionnaire data from the Reno Diet Heart Study. He says “one-third of the study population scored high” on one or more of three factors—“loss of control over eating,” “lack of feeling satisfied by food,” and “preoccupation with food”—that characterize the syndrome he typifies.

Yet the section of the book where Kessler describes his Food Rehab™ method seems to be aimed at a general audience, which is like expecting all drinkers to follow the 12 Steps of Alcoholics Anonymous. “I don’t offer a one-size-fits-all technique,” Kessler claims, adding that “few foods will be totally out of bounds.” Yet he lays down some pretty categorical-sounding imperatives. “Neither sugar nor refined carbohydrates that behave much like sugar in the body, such as white flours and pasta, belong in the diet in significant amounts,” he writes, calling for “a diet based largely on lean protein and whole grains or legumes, supplemented with fruits and nonstarchy vegetables.” For everyone? Just for hypereaters? Maybe both, because by this point Kessler seems to have convinced himself that his impulsive, gluttonous reaction to tasty food is a universal trait.

But what about those of us who reject Kessler’s ethic of rigidly ordered abstemiousness, which replaces hypereating with hypervigilance? Consider celebrity chef and food writer Anthony Bourdain, who supplied a blurb for this book (“disturbing, thought-provoking, and important”) that suggests he hasn’t read it. As anyone who watches No Reservations, Bourdain’s show on the Travel Channel, can attest, his attitude toward food is about as far from Kessler’s as it’s possible to get. While Kessler says we should be wary of delicious dishes, Bourdain conspicuously consumes all manner of fatty, salty, calorie-packed food in large quantities without apology (and nevertheless keeps a trim figure). Bourdain’s fans see a man who relishes life and refuses to sacrifice pleasure on the altar of health. Kessler presumably would see a victim of conditioned hypereating who desperately needs a course of Food Rehab™.

Israeli scientists find stroke drug could help cure cancer

2009-11-06T16:53:00.000-08:00

By Ofri Ilani, Haaretz Correspondent
Tags: cancer, Tel Aviv University

Israeli scientists have identified a substance that can kill cancerous cells without harming healthy ones, paving the way for more effective cancer treatment.
The findings by researchers at Tel Aviv University and Sheba Medical Center, Tel Hashomer, were published in the current issue of the international peer-reviewed journal Breast Cancer Research.
"We actually found the Achilles heel of the cancer cell," said Prof. Malka Cohen-Armon from Tel Aviv University, who headed the research team. "As soon as you can target cancerous cells without killing healthy ones, you can produce medications that would cause a lot less suffering to the patient. We can even give a much more aggressive treatment without worrying about harming healthy tissues."
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The substance identified by the researchers, which delays cell proliferation in healthy and cancerous cells, is a component of a drug developed a decade ago to preserve nerve cells and prevent them from dying after a stroke.
But while the drug causes the rapid death of cancer cells, healthy cells activate a mechanism that overcomes the delay in proliferation within hours, and those cells continue to proliferate exactly like cells not exposed to the substance.
Cohen-Armon said the drug's effectiveness in treating cancer cells was discovered accidentally.
"I'm not even a cancer researcher," she said. "But two years ago an article we published on various functions in the cell got me interested in cancer cells."
She said the scientists involved in the discovery - who include doctoral student Asher Castiel and Professor Shai Izraeli's research group at the Sheba Cancer Research Center - haven't figured out why the drug affects the cells the way it does.
"We don't even fully understand why this is happening, but we see cancerous cells die and healthy cells overcome this obstacle," said Cohen-Armon. "They somehow find a way to proliferate even in the presence of the substance."
She said the drug was tested on several types of cancer, but so far only the breast cancer tests results have been published.
The experiment has been carried out on female mice, which were injected with human cancerous cells. The substance was gradually released over two weeks. The mice that weren't treated with the substance developed malignant tumors - but in those that got the treatment, the substance either prevented or significantly stalled the development of the cancerous cells.
The experiments did not find any changes in the behavior of the mice treated with the substance.
One of the obstacles to applying the discovery to all forms of cancer is that the medicine is registered as a patent of an American pharmaceutical company. Tel Aviv University's technology transfer company, Ramot, has secured a usage patent enabling it to develop the drug to treat only breast cancer.
The future development of the drug depends on the goodwill of the American company, or on another company developing a similar substance.
"We really want to develop this drug, but there are some completely non-scientific obstacles," Cohen-Armon said. "I hope the research doesn't fade away because of that."

Blind patient sees again with eye tooth

2009-09-29T03:03:00.000-07:00

A 60-year-old woman blind for nine years has regained useful vision following a rare operation in Miami in which surgeons removed one of her teeth, drilled a hole in it, inserted a plastic lens into the hole and implanted the tooth-lens combination into her eye.

Experimental HIV Vaccine Raises Hopes

2009-09-24T06:31:00.000-07:00

BANGKOK -- For the first time, an experimental vaccine has prevented infection with the AIDS virus, a watershed event in the deadly epidemic and a surprising result. Recent failures led many scientists to think such a vaccine might never be possible.

The vaccine cut the risk of becoming infected with HIV by more than 31% in the world's largest AIDS vaccine trial of more than 16,000 volunteers in Thailand, researchers announced Thursday in Bangkok.

Even though the benefit is modest, "it's the first evidence that we could have a safe and effective preventive vaccine," Col. Jerome Kim said in a telephone interview. He helped lead the study for the U.S. Army, which sponsored it with the National Institute of Allergy and Infectious Diseases.

The institute's director, Anthony Fauci, warned that this is "not the end of the road," but said he was surprised and very pleased by the outcome.

"It gives me cautious optimism about the possibility of improving this result" and developing a more effective HIV vaccine, Dr. Fauci said in a telephone interview. "This is something that we can do."

Even a marginally helpful vaccine could have a big impact. Every day, 7,500 people world-wide are newly infected with HIV and two million died of AIDS in 2007, the U.N. agency UNAIDS estimates.

"Today marks an historic milestone," said Mitchell Warren, executive director of the AIDS Vaccine Advocacy Coalition, an international group that has worked toward developing a vaccine.
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* Researchers' statement | Study info

"It will take time and resources to fully analyze and understand the data, but there is little doubt that this finding will energize and redirect the AIDS vaccine field," he said in a statement.

The Thailand Ministry of Public Health conducted the study, which used strains of HIV common in Thailand. Whether such a vaccine would work against other strains in the U.S., Africa or elsewhere in the world is unknown, scientists stressed.

The study actually tested a two-vaccine combo in a "prime-boost" approach, where the first one primes the immune system to attack HIV and the second one strengthens the response.

They are ALVAC, from Sanofi Pasteur, the vaccine division of French drug maker Sanofi-Aventis; and AIDSVAX, originally developed by VaxGen Inc. and now held by Global Solutions for Infectious Diseases, a nonprofit founded by some former VaxGen employees.

ALVAC uses canarypox, a bird virus altered so it can't cause human disease, to ferry synthetic versions of three HIV genes into the body. AIDSVAX contains a genetically engineered version of a protein on HIV's surface. The vaccines are not made from whole virus -- dead or alive -- and can't cause HIV.

Neither vaccine in the study prevented HIV infection when tested individually in earlier trials, and dozens of scientists had called the new one futile when it began in 2003.

"I really didn't have high hopes at all that we would see a positive result," Fauci confessed.

The results proved the skeptics wrong.

"The combination is stronger than each of the individual members," said the Army's Col. Kim.

The study tested the combo in HIV-negative Thai men and women ages 18 to 30 at average risk of becoming infected. Half received four "priming" doses of ALVAC and two "boost" doses of AIDSVAX over six months. The others received dummy shots. No one knew who got what until the study ended.

All were given condoms, counseling and treatment for any sexually transmitted infections, and were tested every six months for HIV. Any who became infected were given free treatment with antiviral medicines. Participants were followed for three years after vaccination ended.

According to the results: New infections occurred in 51 of the 8,197 given vaccine and in 74 of the 8,198 who received dummy shots. That worked out to a 31% lower risk of infection for the vaccine group.

The vaccine had no effect on levels of HIV in the blood of those who did become infected. That had been another goal of the study -- seeing whether the vaccine could limit damage to the immune system and help keep infected people from developing full-blown AIDS.

That result is "one of the most important and intriguing findings of this trial," Dr. Fauci said. It suggests that the signs scientists have been using to gauge whether a vaccine was actually giving protection may not be valid.

"It is conceivable that we haven't even identified yet" what really shows immunity, which is both "important and humbling" after decades of vaccine research, Dr. Fauci added.

Details of the $105 million study will be given at a vaccine conference in Paris in October.

This is the third big vaccine trial since 1983, when HIV was identified as the cause of AIDS. In 2007, Merck & Co. stopped a study of its experimental vaccine after seeing it did not prevent HIV infection. Later analysis suggested the vaccine might even raise the risk of infection in certain men. The vaccine itself didn't cause infection. In 2003, AIDSVAX flunked two large trials, the first late-stage tests of any AIDS vaccine at the time.

It is unclear whether vaccine makers will seek to license the two-vaccine combo in Thailand. Before the trial began, the U.S. Food and Drug Administration said other studies would be needed before the vaccine could be considered for U.S. licensing.

Also unclear is whether Thai volunteers who received dummy shots will now be offered the vaccine. Researchers had said they would do so if the vaccine showed clear benefit, defined as reducing the risk of infection by at least 50%.

Those issues, plus how to proceed with future studies, will be discussed among the governments, study sponsors and companies involved in the trial, Kim said. Scientists want to know how long will protection last, whether booster shots will be needed, and whether the vaccine helps prevent infection in gay men and injection drug users, since it was tested mostly in heterosexuals in the Thai trial.

The study was done in Thailand because U.S. Army scientists did pivotal research in that country when the AIDS epidemic emerged there, isolating virus strains and providing genetic information on them to vaccine makers. The Thai government also strongly supported the idea of doing the study.

Cure for radiation sickness found?

2009-07-28T04:09:00.000-07:00

Exclusive: Dramatic discovery by Jewish-American scientists could change world; anti-radiation medication proves effective, safe in tests. Further experiments to be fast tracked, FDA approval possible within 1-2 years
Ronen Bergman

The ground-breaking medication, developed by Professor Andrei Gudkov – Chief Scientific Officer at Cleveland BioLabs - may have far-reaching implications on the balance of power in the world, as states capable of providing their citizens with protection against radiation will enjoy a significant strategic advantage vis-à-vis their rivals.

For Israel, the discovery marks a particularly dramatic development that could deeply affect the main issue on the defense establishment's agenda: Protection against a nuclear attack by Iran or against "dirty bomb" attacks by terror groups.

Gudkov's discovery may also have immense implications for cancer patients by enabling doctors to better protect patients against radiation. Should the new medication enable cancer patients to be treated with more powerful radiation, our ability to fight the disease could greatly improve.

Dramatic test results
The process that led up to the medical innovation dates back to 2003, when Professor Gudkov came up with the idea of using protein produced in bacteria found in the intestine to protect cells from radiation.

Gudkov recounted an experiment he held with two groups of mice.

"We exposed both groups to lethal radioactive radiation," he said. "All the mice in the control group died within a short period of time. A few days later, when I approached the cage with the mice that received the protein, I could see that they're ok, that they're alive. They survived. It's hard to describe the joy all of us felt. We realized that finally, after so many years and so many experiments and frustrations, we made a breakthrough that may save the lives of millions."

Prof. Gudkov published the findings of the protein experiment in Science, the world's leading scientific journal; however, the discovery of the medication was kept secret until now, while Gudkov and his associated waited for the results of two series of critical tests examining the medication's effectiveness and safety.

The first series of tests included experiments on more than 650 monkeys. Each test featured two groups of monkeys exposed to radiation, but only one group was given the medication. The radiation dosage was equal to the highest dosage sustained by humans as result of the Chernobyl mishap.

The experiment's results were dramatic: 70% of the monkeys that did not receive the cure died, while the ones that survived suffered from the various maladies associated with lethal nuclear radiation. However, the group that did receive the anti-radiation shot saw almost all monkeys survive, most of them without any side-effects. The tests showed that injecting the medication between 24 hours before the exposure to 72 hours following the exposure achieves similar results.

Another test on humans, who were given the drug without being exposed to radiation, showed that the medication does not have side-effects and is safe. Prof. Gudkov's company now needs to expand the safety tests, a process expected to be completed by mid-2010 via a shortened test track approved for bio-defense drugs. Should experiments continue at the current rate, the medication is estimated to be approved for use by the FDA within a year or two.

'Stable, safe, and easy to inject'
The company's subcontractor in Europe is already prepared to embark on mass production. Meanwhile, emergency regulations in Israel allow the government to purchase drugs on short notice, even if they are still in the process of being approved. Notably, the medication in question is not a vaccine, but rather, a preventative drug administered via one or several shots.

The medication works by suppressing the "suicide mechanism" of cells hit by radiation, while enabling them to recover from the radiation-induced damages that prompted them to activate the suicide mechanism in the first place.

Prof. Gudkov heads a group of Jewish-American scientists and has cooperated with an Israeli researcher and Israeli investors. A large part of the revolutionary medication's development process was funded by the US Defense and Health departments, which thus far earmarked $40 million to the project. About two weeks ago, the US Defense Department announced that in light of the successful tests, it will continue to fund the project.

The Israeli scientist involved in the research, Dr. Elena Feinstein, made Aliyah to Israel in 1985 and for many years served as a cancer researcher at the Weizmann Institute of Science. Dr. Feinstein met Prof. Gudkov while they worked together in Moscow and was among the founders of the company, serving as its deputy director for some time.

Today, Feinstein works for an Israel company engaged in cancer research and continues to cooperate with Gudkov. Referring to the innovative medication, she says: "Both its effectiveness and safety had been proven. It is stable, safe, and easy to inject."

Both Feinstein and Gudkov stress that the innovative drug does not provide 100% protection against radioactive damage. However, should the discovery announced by the scientists meet all the required tests and permits, it may change the 21st Century.

David Kessler "The End of Overeating."

2009-06-12T05:06:00.000-07:00

David Kessler visits Google's Mountain View, CA headquarters to discuss his book "The End of Overeating." This event took place on May 28, 2009, as part of the Authors@Google series.

Before we can begin to address America's eating epidemic, we need to understand WHY we have such difficulty controlling what we eat. Kessler spent the past seven years meeting with top scientists, physicians, psychologists, and food industry insiders, and conducting his own research to reveal how specific foods produced by giant food corporations and restaurant chains ("Big Food") feed our desire to eat by stimulating the brain with an infinite variety of diabolical combinations of salt, fat and sugar. People of all ages are being set up for a lifetime of food obsession due to the ever-present availability of foods laden with salt, fat and sugar. It is no wonder that millions of Americans are gaining weight and getting sick. The End of Overeating provides a highly readable and indispensable picture of the problems we face and offers solutions for how to fight them and regain control.

David Kessler, MD, served as commissioner of the US Food and Drug Administration. Dr. Kessler, a pediatrician, has been dean of the medical schools at Yale and the UCSF. He is the father of two grown children and lives with his wife in California.

Health Officials Declare Flu Pandemic

2009-06-11T09:55:00.000-07:00

GENEVA -- The World Health Organization declared an H1N1 flu pandemic Thursday -- the first global flu epidemic in 41 years -- as infections in the United States, Europe, Australia, South America and elsewhere climbed to nearly 30,000 cases.
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The long-awaited pandemic announcement is scientific confirmation that a new flu virus has emerged and is quickly circling the globe. WHO will now ask drugmakers to speed up production of an H1N1 flu vaccine. The declaration will also prompt governments to devote more money toward efforts to contain the virus.

WHO chief Dr. Margaret Chan made the announcement Thursday after the U.N. agency held an emergency meeting with flu experts. Dr. Chan said she was moving the world to phase 6 -- the agency's highest alert level -- which means a pandemic, or global epidemic, is under way.

"The world is moving into the early days of its first influenza pandemic in the 21st century," Dr. Chan told reporters. "The (H1N1 flu) virus is now unstoppable."

On Thursday, WHO said 74 countries had reported 28,774 cases of H1N1 flu, including 144 deaths. Chan described the virus as "moderate." According to WHO's pandemic criteria, a global outbreak has begun when a new flu virus begins spreading in two world regions.

The agency has stressed that most cases are mild and require no treatment, but the fear is that a rash of new infections could overwhelm hospitals and health authorities -- especially in poorer countries.

Still, about half of the people who have died from H1N1 flu were previously young and healthy -- people who are not usually susceptible to flu. H1N1 flu is also crowding out regular flu viruses. Both features are typical of pandemic flu viruses.

The last pandemic -- the Hong Kong flu of 1968 -- killed about 1 million people. Ordinary flu kills about 250,000 to 500,000 people each year.

H1N1 flu is also continuing to spread during the start of summer in the northern hemisphere. Normally, flu viruses disappear with warm weather, but H1N1 flu is proving to be resilient.

The decision might have been made much earlier if WHO had more accurate information about H1N1 flu's rising sweep through Europe. Dr. Chan said she called the emergency meeting with flu experts after concerns were raised that some countries like Britain were not accurately reporting their cases.
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After Thursday's meeting, Dr. Chan said the experts agreed there was wider spread of H1N1 flu than what was being reported.

Dr. Chan would not say which country tipped the world into the pandemic, but said all countries and experts were agreed that it was time to declare a global outbreak.

WHO said it was now recommending that flu vaccine makers start making H1N1 flu vaccine. Drug giant GlaxoSmithKline PLC said they could start large-scale production of pandemic vaccine in July but that it would take several months before large quantities would be available.

The pandemic declaration will require all countries, including the dozens that haven't yet reported any cases, to launch pandemic-prevention plans.

Peter Cordingley, a spokesman for the WHO based in Manila, noted that the term pandemic was "a measure of the spread of the virus, not the severity of the virus." The virus's effects are moderate at the moment, he noted. "But it's still going to infect an awful lot of people."

Nearly half the world's confirmed cases, or 13,217, are in the U.S., including 27 deaths, according to the WHO.

In Australia, the number of the new disease, also known as swine flu, has more than tripled in the past week, reaching 1,263 on Thursday, when three new cases were confirmed in the state of Tasmania. It recorded its first case of the disease on May 9.

"Australia catches our eye particularly not because of the number of cases but because of strong evidence of community transmission," particularly in the southern state of Victoria and its capital, Melbourne, said Mr. Cordingley. He said the WHO is also focusing on similar evidence in the U.K., Spain, Japan and Chile.

More than 1,000 Australia's swine flu cases are in Victoria, which has been hit by the cold temperatures and dry conditions that flu viruses thrive in.
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Victorians now account for around 3.6% of total confirmed cases globally, and authorities are struggling to understand exactly why the virus has taken such a hold in the state, Victoria's acting chief health officer, Rosemary Lester, said Thursday.

"Perhaps we may never have a definitive answer on that," Lester told Australian Broadcasting Corp. radio. "We do know that we have had an extensive testing regime so we have uncovered a lot of cases that were there to be uncovered. And because the disease is so mild in the majority of people, that allowed it to spread undetected," she said.

Cases detected so far have been relatively mild, with no deaths from the virus yet recorded in the country. The majority of sufferers in Australia have been aged between five and 18, but the virus continues to strike healthy adults including several professional Rugby League players who competed in an interstate match in Victoria's capital, Melbourne, last week.

Those players were quarantined from their clubs, and earlier this week, authorities canceled a major swim meet due to be held in Melbourne. Victoria is on a higher level of alert than other Australian states.

On the streets of Melbourne there is little evidence of major concern among the city's nearly four million residents. Shops, bars and cafes -- while affected by the economic slowdown -- are still busy, and the city's public transport has shown no signs of reduced patronage.

Schools in the nation are no longer being closed if a student is reported as having the virus, although authorities have requested that school aged children at risk from the virus stay home for seven days.

In contrast, Hong Kong's government on Thursday ordered the closure of all nurseries, kindergartens and primary schools for two weeks after a dozen students at one school tested positive for swine flu.

Australian health authorities have stopped testing every suspected case of the virus -- drawing some condemnation from critics -- and Victoria is now focusing treatment on those most vulnerable to viral infections, such as the very old or very young.

New York City health officials say three more people have died from swine flu, bringing the city's total to 15. One victim was a child under the age of 5, one was a person between 5 to 24 years old, and another was between 30 to 39 years old.

The city health department says a telephone poll of over 1,000 residents found nearly 7% had flu-like symptoms in April and May. That suggests more than half a million New Yorkers were ill.
—Lyndal McFarland in Melbourne, Peter Stein in Hong Kong and the Associated Press contributed to this article.

Swine Flu Is Way Worse Than Expected

2009-06-08T10:46:00.001-07:00

When we began writing about the impending swine flu pandemic, many readers thought we were buying into some kind of government created panic. Our view was exactly the opposite: the government was understating the risks of swine flu, worried that a "panic" would hurt the economy. Mainstream media sources started by being "responsible" and under-reporting the risks in the US, bought into the panic for a week or so, then quietly dropped the story.

The story of swine flu has now effectively dropped out of public discussion. In fact, when it is discussed it usually as a critique of health authorities for needlessly creating a scare.

Once again, however, this is exactly backwards. Swine flu has not turned out to be a non-event. It is not more confined than intially feared. Indeed, the official risk models of swine flu dramatically underestimated how widespread it has become.

As the New York Times reports, two rival supercomputer teams made projections about the swine flu epidemic. One said that swine flu would hit 2,000 people by the end of May. Another said the number would be 25 percent higher: 2,500. (The innumerate editors of the New York Times call these estimate "surprisingly similar," but that's not important for now.)

In fact, the Centers for Disease Control and Prevention estimate that by the end of May there were upwards of 100,000 cases of swine flu in the country. So much for the models that told us the risks weren't so big.

Chagas Disease: A Century Later

2009-06-06T07:49:00.000-07:00

Chagas Disease: A Century Later

By Kara Rogers on Health

In 1909 Brazilian physician Carlos Chagas discovered American trypanosomiasis, better known as Chagas disease. In the 100 years since, there have been two drugs developed that can cure the disease and a lot learned about how it can be prevented. Yet, it affects between 8 and 11 million people in the Americas and Caribbean. So instead of celebrating a centennial marked by successful control or elimination of Chagas, researchers and public health officials are calling for assistance, especially increased government and private funding.

Chagas has fallen unceremoniously into the pile of neglected tropical diseases, a group of human afflictions that thrive in the poorest and most destitute rural and urban regions of the world. The urgency with which health organizations have had to respond to diseases like malaria and AIDS has overshadowed Chagas, which is endemic to Mexico and countries in Central and South America. There are roughly 50,000 new cases of Chagas diagnosed annually in these places, and at the rate that its incidence appears to be increasing, there is concern that in the Americas and Caribbean the disease actually may be as prevalent as or even more so than malaria.

Chagas is a vector-borne disease, and thus it involves a carrier (vector), a parasite, and a mechanism of transmission to humans. The carrier is a bloodsucking insect known as the kissing bug, or barber beetle, because its favorite place to bite an unsuspecting victim is the face. The kissing bug attacks at night and is most commonly found in poorly constructed or dilapidated houses that have cracks in their walls or roofs, which serve as entry points for the bugs. Trypanosomas cruzi.

The parasite that causes Chagas disease is Trypanosomas cruzi, a protozoan that has a flagellum to propel it from place to place. When a kissing bug bites its victim, it deposits the infectious parasite in its feces. The victim scratches the bite and rubs the feces into the wound, thereby facilitating the entry of the parasite into nearby cells. Once inside a cell, the parasite matures and multiplies. The organisms eventually burst out of the cell and into the bloodstream. They then travel to and infect various tissues, though they seem to have an affinity for muscle cells and neuroglia, cells that function to support neurons.

Chagas is a frightening and sometimes unpredictable disease. It is characterized by acute and chronic stages, both of which may be silent, meaning that obvious symptoms do not always manifest. Acute disease in which there are no or only very mild symptoms often goes undiagnosed and therefore untreated. As a result, the parasite remains in the body, setting the stage for chronic disease, which can take one or more decades to develop and is often fatal. Chronic disease often appears in the form of heart abnormalities, which may lead to sudden cardiac death or heart failure, or in the form of gastrointestinal disease, which arises due to the parasitic destruction of nerve cells.

Only two drugs—nifurtimox and benznidazole—are effective for the treatment of Chagas, and they are useful only in the acute stage of disease, when they can cure infection. If treatment is delayed or if infection persists, the chance for ridding the body completely of parasites drops significantly. More importantly, however, Chagas can be prevented in the first place. Improving the construction of houses, spraying insecticides, using bed nets, and improving basic hygiene can stop kissing bugs from getting into houses and transmitting the disease.

Prevention and proper treatment are the most practical ways to break the cycle of infection from insect to human to insect. These approaches also can reduce the likelihood that people migrating from one place to another will carry the parasite with them. But delivering the needed preventative, educational, and therapeutic resources to affected regions requires money and people. Researchers and health workers hope that their efforts this year will draw attention to Chagas. After all, a century has passed. Perhaps it is time to bring this otherwise preventable disease under control.

Are Cancer Drugs Worth The Money?

2009-05-31T20:21:00.000-07:00

Matthew Herper and Robert Langreth 05.30.09, 4:15 PM ET

ORLANDO - At the annual meeting of the American Society for Clinical Oncology, giant banners with pictures of heroic cancer patients proclaim doctors are "Personalizing Cancer Care."

But many companies seem to be maximizing cancer profit instead. Big drug companies are making big money off smaller and smaller improvements in cancer care. Newfangled cancer drugs can cost $50,000 a year, and that doesn’t mean they will add a year to the patient’s life--you might spend $50,000 for a year and extend the patient's life by only weeks.

The numbers would look better if drug companies did a better job of targeting drugs at the patients most likely to benefit. But that targeting has occurred in only a few scattered examples.

The skyrocketing costs for limited benefit are leading some experts to worry about whether the medical system has the right incentives.

"We are wasting a lot of resources treating people with treatments they don't need," says Otis Brawley, chief medical officer at the American Cancer Society. Novartis, Wyeth and Pfizer all sell very expensive cancer pills. "We would like to believe that cost should be no object, but that is not reality," says Leonard Saltz, a colon-cancer expert at Memorial Sloan-Kettering Cancer Center.

The poster child for high-cost cancer drugs is Roche's Avastin. The drug has $4.8 billion in sales and is approved to treat breast, colon, lung and brain cancer. It was first approved in 2004 after research showed it could extend survival in advanced colon-cancer patients by five months.

The hope was that further studies of Avastin in other types of cancer or in earlier stages of the disease would show even greater survival benefits. But they haven’t. In several breast-cancer trials--including a new one being presented at the meeting this weekend--Avastin slowed the progression of disease but did not extend patient survival at all. But doctors still use the drug in treating breast cancer because they figure it helps symptoms, even if patients don’t live longer. Avastin costs up to $55,000 a year.

In another major study presented at the meeting, Avastin failed to prevent colon cancer from recurring after surgery. In the first year of treatment, more patients who got Avastin remained free of detectable cancer. But after a year, the drug was stopped, and by the end of the study, the apparent initial benefit had faded completely.

Historically, the goal of therapy in early-stage cancer has been to increase the cure rate. But results hint that Avastin may not be curing anyone--it may suppress microscopic cancer deposits without killing them by preventing the growth of their blood vessels. The doctor who conducted the trial, Norman Wolmark of Allegheny General Hospital, is talking about testing Avastin for twice as long in order to get an effect, but that may not be enough. To make a difference in early-stage disease, "the patient may need very, very long-term or even permanent treatment with Avastin," says Saltz. "It gets phenomenally expensive."

Roche says the hints of efficacy support Avastin's future prospects. "It is a validation of the fact that Avastin has a role in early-stage disease," says William Burns, head of Roche's pharmaceuticals division. He forecasts Avastin could still reach sales of $8 billion by 2012 or 2013, even without use in earlier stages of cancer. "With Herceptin, we have learned that it is a drug to start with and stay with" at multiple stages of disease, says Burns, referring to the company's targeted breast cancer drug. "We are start[ing] to piece together exactly the same journey for Avastin."

Burns says the company will consider altering its ongoing trials of Avastin in early-stage breast and lung cancer to include longer-term Avastin use.

Roche is also combining other expensive drugs with Avastin. One study at the meeting showed that adding Tarceva, from OSI Pharmaceuticals and Roche, delayed by one month the median time it takes lung tumors to grow. While it is not yet possible to tell whether there is an effect on survival, the results were statistically significant and financially momentous. U.S. sales of Tarceva were $457 million last year. "We estimate we have the potential for at least $500 million in new [U.S.] business from this study," says OSI Chief Executive Colin Goddard.

One problem is that doctors have no idea which patients are likely to benefit from Avastin, so they give it to everyone in hopes that a few will benefit. Another strategy might be to amp up the search for blood-test results that could predict whether a patient will respond to Avastin, says Angela DeMichele, an oncologist at the University of Pennsylvania whose research focuses on breast cancer. There are clues as to how patients most likely to benefit from Avastin might be identified, she says, but these avenues haven't been pursued yet. "We're still treating people in an unselected way," DeMichele says.

"Avastin is probably not a targeted therapy, as far as I am concerned," says MD Anderson Cancer Center breast cancer expert Franciso Esteva.

Drugs like Tarceva and AstraZeneca's Iressa, which is no longer used in the U.S., work best in patients whose tumors have a mutation in the gene for the epidermal growth factor receptor (EGFR), which is involved in cell growth. In another lung cancer study, Tarceva only slightly delayed the median progression in the overall group of patients, but the small subset of patients with EGFR mutations in their tumors had a tenfold lower risk of the tumor progressing when they took Tarceva.

Since Iressa, AstraZeneca has made a point of pairing drugs with diagnostic work. But it didn’t with Zactima. This experimental drug delayed the progression of lung cancer by three weeks to 17 weeks. Although promising--and viewed as one of AstraZeneca’s most important new products--it has not been paired with a test. Doctors hope for a greater benefit if it is used in earlier stages of the disease.

One of the most impressive results was not from a fancy new therapy at all. Alimta, a more traditional chemotherapy pill sold by Eli Lilly, didn't just slow tumor progression but also increased survival for patients with non-small-cell lung cancer by a median 2.8 months, extending survival to 13.4 months.

Sanofi's Breast Cancer Bet

2009-05-31T20:07:00.000-07:00

Sanofi's Breast Cancer Bet
Robert Langreth and Matthew Herper 05.31.09, 1:50 PM ET

ORLANDO, Fla. -- North Carolina resident Terri M. Allen noticed two strange pimple-like bumps on her scalp in June 2007. When she finally got them checked out, her worst fears were confirmed. Her breast cancer that had been removed in 2005 had returned with a vengeance, spreading to her sternum, hipbone and both lungs. Worse, she had a particularly nasty form called triple negative that doesn't respond to several standard treatments.

"I thought I was not going to make it," says Allen, now 54. Then her doctor told her about an experimental drug from Sanofi-Aventis that is looking promising in patients with her form of cancer. She started taking the drug along with chemo in March 2008. Within three months the tumors had virtually disappeared. "This is incredible to me," says Allen, who remains on the Sanofi drug and in remission. "I have no side effects and a completely normal standard of life."

Allen is among the first to benefit from a new class of drugs that aim at a weak spot in certain breast and ovarian cancers: limitations in their inability to repair DNA damage. While not cures, the drugs, called PARP inhibitors, may work well in triple negative breast cancers, about 15% of cases. They also show promise in patients with cancer due to inherited mutations in the BRCA1 and BRCA2 genes.

PARP inhibitors are among the few hot new drugs being highlighted at an otherwise sleepy meeting of the American Society of Clinical Oncology in Orlando. In a trial on 116 triple negative patients, patients who got the Sanofi parp drug lived 3.5 months longer than those who just got standard cell-killing chemotherapy regimens. "It is a big deal," says study leader Joyce O'Shaughnessy of the Baylor Charles A. Sammons Cancer Center. "We don't see survival advantages very often in [advanced] breast cancer." Adds Eric Winer, a breast cancer expert at the Dana-Farber Cancer Institute: "This is one of the most exciting results we have seen in a long time" for these patients. Triple negative cancers aren't responsive to standard hormone therapy or the drug Herceptin.

Sanofi-Aventis Chief Executive Christopher Viehbacher hopes that the drug will reinvigorate his company's cancer franchise. Sanofi sells some of the world's most used chemotherapy drugs, but has never made a name in the newer targeted drugs that are mainstays for Roche, Eli Lilly and Novartis. The PARP drug could help change this. Sanofi got the drug with its $500 million acquisition of BiPar Sciences, a biotech firm with only 18 employees that Sanofi bought earlier this year.

"This is a first-in-class drug, so it puts us back in the game of really innovative medicine," says Viehbacher. "There are other PARP inhibitors out there, but for the moment we've been able to stay in the lead." Parp stands for poly (ADP-ribose) polymerase.

Sanofi's biggest competition is AstraZeneca. It has tested its drug in an even narrower group of patients, women with inherited mutations in the BRCA1 or BRCA2 genes. (About 5% of breast cancer patients, including Allen, have one of these mutations.) Two small studies at the meeting found that the AstraZeneca's drug helped shrink 41% of breast cancer patients with the mutations and also helped ovarian cancer patients, without the need for chemotherapy.

One patient it helped is 70-year-old Los Angeles resident Barbara Shellow. She started on the AstraZeneca PARP inhibitor for her advanced ovarian cancer in July 2007, and her tumors quickly shrank. She has now gone 18 months without a relapse. "The drug has been a miracle for me," she says. Larger trials will be needed to confirm the benefits of both drugs before they can be approved.

If AstraZeneca or Sanofi had tested their drugs on all breast cancer patients, they likely would not have worked, as most breast tumors probably aren't being driven by aberrant DNA repair. "One of the key things is to match the cancer drug to the right patient population," says Alan Ashworth at the Institute of Cancer Research in London, who did an early experiment showing that patients with BRCA mutations might be susceptible to PARP blockers.

Many tumor types besides breast and ovarian may have DNA repair defects. A problem is there is no good test yet to determine which tumors have such defects. Researchers are furiously working to find one, says Ashworth.

"Getting at the molecular defects that are driving cancer is the only way to intelligently apply targeted therapy," says William Audeh, an oncologist at Cedars-Sinai Medical Center in Los Angeles who is testing the AstraZeneca drug. He says researchers need to start treating patients based on what mutations lie hidden inside their tumors, instead of based on what part of the body the tumor is in.

Top 5 Cholesterol Myths

2009-05-26T14:21:00.000-07:00

Even if you think you know everything there is to know about cholesterol, there may be a few more surprises in store. Check out these common myths about high cholesterol; find out who’s most likely to have it, what types of food can cause it, and why—sometimes—cholesterol isn’t a bad word.

By Health.com

Myth 1: Americans have the highest cholesterol in the world

One of the world’s enduring stereotypes is the fat American with cholesterol-clogged arteries who is a Big Mac or two away from a heart attack. As a nation, we could certainly use some slimming down, but when it comes to cholesterol levels we are solidly middle-of-the-road.

According to 2005 World Health Organization statistics, American men rank 83rd in the world in average total cholesterol, and American women rank 81st; in both cases, the average number is 197 mg/dL, just below the Borderline-High Risk category. That is very respectable compared to the top-ranked countries: In Colombia the average cholesterol among men is a dangerous 244, while the women in Israel, Libya, Norway, and Uruguay are locked in a four-way tie at 232.

Myth 2: Eggs are evil

It’s true that eggs have a lot of dietary cholesterol—upwards of 200 mg, which is more than two-thirds of the American Heart Association’s recommended limit of 300 mg a day. But dietary cholesterol isn’t nearly as dangerous as was once thought. Only some of the cholesterol in food ends up as cholesterol in your bloodstream, and if your dietary cholesterol intake rises, your body compensates by producing less cholesterol of its own.

While you don’t want to overdo it, eating an egg or two a few times a week isn’t dangerous. In fact, eggs are an excellent source of protein and contain unsaturated fat, a so-called good fat.

Myth 3: Kids can’t have high cholesterol

Most people think high cholesterol is a problem that’s strictly for the middle-aged. But guess what? Research has shown that atherosclerosis—the narrowing of the arteries that leads to heart attacks—can start as early as age eight. In July 2008, the American Academy of Pediatrics released guidelines on kids and cholesterol that recommended that children who are overweight, have hypertension, or have a family history of heart disease have their cholesterol tested as young as two years of age.

Children with high cholesterol should be on a diet that restricts saturated fat to 7% of calories and no more than 200 mg per day of dietary cholesterol, according to the guidelines. Fiber supplements and more exercise are also recommended.

While the guidelines prompted a bit of an outcry from parents worried that doctors would be pushing cholesterol-lowering drugs for kids, a new study suggests that less than 1% of adolescents aged 12 to 17 would be considered candidates for medication.

Myth 4: Food is heart-healthy if it says “0 mg cholesterol”

The Cholesterol portion of the nutritional label refers to dietary cholesterol, which is only one of the things found in food that can cause your cholesterol to go sky-high. (A bigger contributor to elevated cholesterol? A high-fat diet.) It’s also believed to be the least important. Saturated fat (found in animal foods and dairy products) and trans fats (found in packaged foods) appear to have a far greater impact on low-density lipoprotein (LDL), the so-called bad cholesterol that causes atherosclerosis, than dietary cholesterol.

Myth 5: Cholesterol is always a bad thing

When most people hear “cholesterol” they think “bad.” Like most things in life, the reality is more complex. High cholesterol can be dangerous, but cholesterol itself is essential to various bodily processes, from insulating nerve cells in the brain to providing structure for cell membranes. That’s why your body makes the white, waxy substance (about 75% of the cholesterol in your blood is made by the liver and cells elsewhere in your body).

The role of cholesterol in heart disease is often misunderstood. Cholesterol is carried through the bloodstream by low-density and high-density lipoproteins (LDL and HDL). LDL, known as bad cholesterol, and not the cholesterol it carries per se, is responsible for atherosclerosis.

WU engineers develop ultrasound cell phone

2009-05-24T05:41:00.000-07:00

William D. Richard (left) takes an ultrasound probe of colleague David Zar's carotid artery with a low-power imaging device he designed.
(David Kilper/WUSTL Photo)
By Liz Stoever
ST. LOUIS POST-DISPATCH
05/18/2009

Everyone knows cell phones can pinpoint your location by GPS signals, record photos and video, browse the Internet and keep your schedule. They even can make phone calls.

But now, thanks to engineers at Washington University, cell phones can scan your insides.

Computer engineers David Zar and David Richard have invented a combination ultrasound and high-end smart phone — a super-portable device to scan the body using sound waves.

The new device, adapted from existing portable ultrasounds, will provide a cheaper and more portable alternative to ultrasounds typically limited to hospitals.

In a world where 70 percent of the population does not have access to medical imaging, Zar said, he and his partner expect the device to permanently change the current medical and global computer landscape.

"Twenty-first century medicine is defined by medical imaging," Zar said. "But it's typically not used."
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Although ultrasounds are very practical, they can be difficult to use because the machines are large, old and shared, Zar said. With the cell phone ultrasound, doctors can use it more often.

"This fits in a coat pocket and the whole thing can start up in 10 to 15 seconds," Zar said.

The device also allows patients with diseases such as Duchenne muscular dystrophy to do ultrasounds at home and send information to any centralized unit in the world for a diagnosis.

The device's mobility will also be helpful in developing countries where hospitals are far, but cell phone towers may be more abundant.

Everyone, not just medical professionals, can purchase the ultrasound device from California-based Interson Corp., the manufacturer, in about a month. While ultrasounds are relatively safe, Zar said frequent use can be problematic, and he does not recommend it to pregnant mothers.

Zar and Richard received a $100,000 grant from the Microsoft Corp. in 2008 as part of its larger project to make health care mobile in remote areas. Microsoft External Research has funded approximately $2 million dollars toward projects using cell phones for health care.

About 15 other projects are already under way under the grant program and have produced results including a device that also attaches to a cell phone and can help children with autism communicate more effectively through picture-based communication. Another cell phone compatible device monitors heart rhythms and can diagnose heart problems.

Kristin Tolle, senior research program manager at Microsoft External Research, said the mobile health care project is more prominent than others because it can work anywhere in the world.

"We wanted to encourage ideas," she said. "We are really trying to help underserved communities."

Dr. Antonella Quattromani, a cardiologist on staff with DePaul Health Center, who went on a mission to Ecuador in March, said the device would be very practical on her other mission trips to remote areas.

"The quality of the image is good," she said. "It would be really useful."

The only limitation is the cell phone reception needed to send images in some remote areas, Quattromani said.

By next year, however, everyone in the world should have access to a cell phone tower, Tolle said.

Before the device becomes available to developing countries, Zar said they will need help developing training and distribution for the device.

"This is much bigger than two geeks at Washington University can support," Richard said. "We need layers of people between us and the people on the ground in India."

The Obamacare to Come

2009-05-22T20:59:00.000-07:00

The Obamacare to Come
Dems’ health-care plans do not provide the reform most Americans seek.

By Michael Tanner

Drip by painful drip, the details of the Democratic health-care-reform plan have been leaking out. And from what we can see so far, it looks like bad news for American taxpayers, health-care providers, and, most important, patients.

The plan would not initially create a government-run, single-payer system such as those in Canada and Britain. Private insurance would still exist, at least for a time. But it would be reduced to little more than a public utility, operating much like the electric company, with the government regulating every aspect of its operation.

It would be mandated both that employers offer coverage and that individuals buy it. A government-run plan, similar to Medicare, would be set up to compete with private insurers. The government would undertake comparative-effectiveness and cost-effectiveness research, and use the results to impose practice guidelines on providers. Private insurance would face a host of new regulations, including a requirement to insure all applicants and a prohibition on pricing premiums on the basis of risk. Subsidies would be extended to help middle earners purchase insurance. And the government would subsidize and manage the development of a national system of electronic medical records.
The net result would be an unprecedented level of government control over one-sixth of the U.S. economy, and over some of the most important, personal, and private decisions in Americans’ lives.

Let’s look at some of the most troubling ideas in detail.

An employer mandate. Employers would be required to insure their workers through a “pay or play” mandate. Those who did not provide “meaningful coverage” for their workers would pay a penalty, equal to some percentage of their payroll, into a national fund that would provide insurance to uncovered workers. Such a mandate is, of course, simply a disguised tax on employment. As Princeton University professor Uwe Reinhardt, the dean of health-care economists, points out, “[That] the fiscal flows triggered by mandate would not flow directly through the public budgets does not detract from the measure’s status of a bona fide tax.” Estimates suggest that an employer mandate could cost 1.6 million jobs over the first five years.

An individual mandate. As is the case with an employer mandate, an individual mandate is essentially a disguised tax. It is also the first in a series of dominoes that will lead to greater government control of the health-care system.

To implement an insurance mandate, the government will have to define what sort of insurance fulfills it. As the CBO puts it, “an individual mandate . . . would require people to purchase a specific service that would have to be heavily regulated by the federal government.” At the very least, deductible levels and lifetime caps will have to be specified, and a minimum-benefits package will likely be spelled out. This means the oft-repeated promise that “if you are happy with your current insurance, you can keep it” is untrue. Millions of Americans who are currently satisfied with their coverage will have to give it up and purchase the insurance the government wants them to have, even if the new insurance is more expensive or covers benefits the buyer does not want.

A “public option.” The government would establish a new universal-health-care program, similar to Medicare, that would compete with private insurance. Regardless of how it is structured or administered, such a plan would have an inherent advantage in the marketplace because it would ultimately be subsidized by taxpayers. It could, for instance, keep its premiums artificially low or offer extra benefits, then turn to the U.S. Treasury to cover any shortfalls. Consumers would naturally be attracted to the lower-cost, higher-benefit government program.
A government program would also have an advantage because its tremendous market presence would allow it to impose much lower reimbursement rates on doctors and hospitals. Government plans such as Medicare and Medicaid traditionally reimburse providers at rates considerably below those of private insurance. Providers recoup the lost income by raising prices for those with private insurance. It is estimated that privately insured patients pay $89 billion annually in additional insurance costs because of cost-shifting from government programs. If the new public option would have similar reimbursement policies, it would result in additional cost-shifting of as much as $36.4 billion annually. Such cost-shifting would force insurers to raise their premiums, making them even less competitive with the taxpayer-subsidized public plan. Lewin Associates estimates that as many as 118.5 million Americans, nearly two out of every three people with insurance, would shift to the government program. The result would be a death spiral for private insurance.

Given that many of the most outspoken advocates of the “public option” have, in the past, supported a government-run single-payer system, it is reasonable to suspect they support a public option precisely because it would squeeze out private insurance and eventually lead to such a system. President Obama himself has said that if he were designing a health-care system from scratch, his preference would be a single-payer system “managed like Canada’s.” He has also said that, while his proposal is a less radical approach, “it may be that we end up transitioning to such a system.”
Comparative- and cost-effectiveness research. In an attempt to control health-care costs, the government would undertake research to determine which health-care procedures and technologies are most effective and, more ominously, cost-effective. Of course, there is a great deal of waste in the U.S. health-care system, and if the government’s goal were simply to provide better information there would be little cause for concern. But there is every reason to believe such research would be used to impose restrictions on how medicine is practiced. For example, some reform advocates have said that when an insurance company fails to comply with government practice guidelines, workers should no longer be able to exempt the value of that company’s plans from their taxable income.

There is no doubt that other countries use comparative-effectiveness research as the basis for rationing. For example, in Great Britain, the National Institute on Clinical Effectiveness makes such decisions, including a controversial determination that certain cancer drugs are “too expensive.” The U.K. government effectively puts a price tag on each citizen’s life — about $44,305 (£30,000) per year, to be exact, under NICE’s guidelines. That’s just a baseline, of course, and, as NICE chairman Michael Rawlins points out, the agency has sometimes approved treatments costing as much as $70,887 (£48,000) per year of extended life. But such treatments are approved only if it can be shown they extend life by at least three months and are used for illnesses that affect fewer than 7,000 new patients per year.

The final health-care-reform bill is likely to include a number of other bad ideas: a host of new insurance regulations that will drive up costs and limit consumer choice (under one leaked proposal, Americans would be limited to a choice of four standardized insurance plans); subsidies for middle-class families (a family of four earning as much as $83,000 per year would receive subsidized care under one proposal); and government preemption of private investment and research into health IT. All of this would come at a cost to taxpayers of at least $1.5 trillion over the next ten years.

The American people are right to demand health-care reform. The current system is broken. But taken individually, most of the ideas currently being considered by Congress would make the problems we face even worse. Taken together, they amount to a complete government takeover of the American health-care system. That is not the type of reform most Americans seek.

— Michael Tanner is a senior fellow at the Cato Institute, author of Leviathan on the Right: How Big Government Conservatism Brought down the Republican Revolution, and co-author of Healthy Competition: What's Holding back Health care and How to Free It.

Vitamins Found to Curb Exercise Benefits

2009-05-14T05:41:00.000-07:00

Vitamins Found to Curb Exercise Benefits
By NICHOLAS WADE

If you exercise to improve your metabolism and prevent diabetes, you may want to avoid antioxidants like vitamins C and E.

That is the message of a surprising new look at the body’s reaction to exercise, reported on Monday by researchers in Germany and Boston.

Exercise is known to have many beneficial effects on health, including on the body’s sensitivity to insulin. “Get more exercise” is often among the first recommendations given by doctors to people at risk of diabetes.

But exercise makes the muscle cells metabolize glucose, by combining its carbon atoms with oxygen and extracting the energy that is released. In the process, some highly reactive oxygen molecules escape and make chemical attacks on anything in sight.

These reactive oxygen compounds are known to damage the body’s tissues. The amount of oxidative damage increases with age, and according to one theory of aging it is a major cause of the body’s decline.

The body has its own defense system for combating oxidative damage, but it does not always do enough. So antioxidants, which mop up the reactive oxygen compounds, may seem like a logical solution.

The researchers, led by Dr. Michael Ristow, a nutritionist at the University of Jena in Germany, tested this proposition by having young men exercise, giving half of them moderate doses of vitamins C and E and measuring sensitivity to insulin as well as indicators of the body’s natural defenses to oxidative damage.

The Jena team found that in the group taking the vitamins there was no improvement in insulin sensitivity and almost no activation of the body’s natural defense mechanism against oxidative damage.

The reason, they suggest, is that the reactive oxygen compounds, inevitable byproducts of exercise, are a natural trigger for both of these responses. The vitamins, by efficiently destroying the reactive oxygen, short-circuit the body’s natural response to exercise.

“If you exercise to promote health, you shouldn’t take large amounts of antioxidants,” Dr. Ristow said. A second message of the study, he said, “is that antioxidants in general cause certain effects that inhibit otherwise positive effects of exercise, dieting and other interventions.” The findings appear in this week’s issue of The Proceedings of the National Academy of Sciences.

The effect of vitamins on exercise and glucose metabolism “is really quite significant,” said Dr. C. Ronald Kahn of the Joslin Diabetes Center in Boston, a co-author of the report. “If people are trying to exercise, this is blocking the effects of insulin on the metabolic response.”

The advice does not apply to fruits and vegetables, Dr. Ristow said; even though they are high in antioxidants, the many other substances they contain presumably outweigh any negative effect.

Dr. Kahn said it might be that reactive oxygen is beneficial in small doses, because it touches off the body’s natural defense system, but harmful in higher doses.

Andrew Shao of the Council for Responsible Nutrition, a trade association of dietary supplement makers, said the new study was well designed but was just one bit of evidence in a complex issue. Most available evidence points to the opposite conclusion, that antioxidants benefit health by reducing oxidative stress, he said.

“I wouldn’t change recommendations for anyone based on one study,” he said. “This is one small piece of the puzzle.”

Nation's first face transplant patient reveals her face

2009-05-06T07:00:00.000-07:00

Connie Culp, after an injury to her face, left, and after a face transplant, right. (Cleveland Clinic-HO Photo)

Connie Culp, before her injury in 2004.

Connie Culp, before and after the transplant. No information has been released about the donor or how she died, but her family members were moved when they saw before-and-after pictures of Culp, Dr. Siemionow said.
CLEVELAND -- Five years ago, a shotgun blast left a ghastly hole where the middle of her face had been. Five months ago, she received a new face from a dead woman.

Connie Culp stepped forward Tuesday to show off the results of the nation's first face transplant, and her new look was a far cry from the puckered, noseless sight that made children run away in horror.

Culp's expressions are still a bit wooden, but she can talk, smile, smell and taste her food again. Her speech is at times a little tough to understand. Her face is bloated and squarish, and her skin droops in big folds that doctors plan to pare away as her circulation improves and her nerves grow, animating her new muscles.

But Culp had nothing but praise for those who made her new face possible.

"I guess I'm the one you came to see today," the 46-year-old

Ohio woman said at a news conference at the Cleveland Clinic, where the groundbreaking operation was performed. But "I think it's more important that you focus on the donor family that made it so I could have this person's face."

Up until Tuesday, Culp's identity and how she came to be disfigured were a secret.Connie Culp, center, who underwent the first face transplant surgery in the U.S., is helped to the podium by her head surgeon, Dr. Maria Siemionow, right, as well as Renee Bennett, the nurse manager for the Clinic's transplant program, far left, and Pat Lock, a nurse with the transplant team, third from left, before speaking to the media at a news conference at the Cleveland Clinic in Cleveland, on Tuesday.

Culp's husband, Thomas, shot her in 2004, then turned the gun on himself. He went to prison for seven years. His wife was left clinging to life. The blast shattered her nose, cheeks, the roof of her mouth and an eye. Hundreds of fragments of shotgun pellet and bone splinters were embedded in her face. She needed a tube into her windpipe to breathe. Only her upper eyelids, forehead, lower lip and chin were left.

A plastic surgeon at the Cleveland Clinic, Dr. Risal Djohan, got a look at her injuries two months later. "He told me he didn't think, he wasn't sure, if he could fix me, but he'd try," Culp recalled.

She endured 30 operations to try to fix her face. Doctors took parts of her ribs to make cheekbones and fashioned an upper jaw from one of her leg bones. She had countless skin grafts from her thighs. Still, she was left unable to eat solid food, breathe on her own, or smell.

Then, on Dec. 10, in a 22-hour operation, Dr. Maria Siemionow led a team of doctors who replaced 80 percent of Culp's face with bone, muscles, nerves, skin and blood vessels from another woman who had just died. It was the fourth face transplant in the world, though the others were not as extensive.

"Here I am, five years later. He did what he said -- I got me my nose," Culp said of Djohan, laughing.

In January, she was able to eat pizza, chicken and hamburgers for the first time in years. She loves to have cookies with a cup of coffee, Siemionow said.

Connie Culp, before and after the transplant. No information has been released about the donor or how she died, but her family members were moved when they saw before-and-after pictures of Culp, Dr. Siemionow said.

Connie Culp, before and after the transplant. No information has been released about the donor or how she died, but her family members were moved when they saw before-and-after pictures of Culp, Dr. Siemionow said.

No information has been released about the donor or how she died, but her family members were moved when they saw before-and-after pictures of Culp, Siemionow said.

Culp said she wants to help foster acceptance of those who have suffered burns and other disfiguring injuries.

"When somebody has a disfigurement and don't look as pretty as you do, don't judge them, because you never know what happened to them," she said. "Don't judge people who don't look the same as you do. Because you never know. One day it might be all taken away."

It's a role she has already practiced, said clinic psychiatrist Dr. Kathy Coffman.

Once while shopping, "she heard a little kid say, 'You said there were no real monsters, mommy, and there's one right there,"' Coffman said. Culp stopped and said, "I'm not a monster. I'm a person who was shot," and pulled out her driver's license to show the child what she used to look like, the psychiatrist said.

The transplant team looks at a model of the patient's face during the first face transplant surgery in the U.S. on Connie Culp.

The transplant team looks at a model of the patient's face during the first face transplant surgery in the U.S. on Connie Culp.

Culp, who is from the small town of Unionport, near the Pennsylvania line, told her doctors she just wants to blend back into society. She has a son and a daughter who live near her, and two preschooler grandsons. Before she was shot, she and her husband ran a painting and contracting business, and she did everything from hanging drywall to a little plumbing, Coffman said.

Connie Culp, who underwent the first face transplant surgery in the U.S., said she wants to help foster acceptance of those who have suffered burns and other disfiguring injuries. Culp, who is from the small town of Unionport, near thePennsylvania line, told her doctors she just wants to blend back into society. Culp left the hospital Feb. 5 and has returned for periodic follow-up care. She has suffered only one mild rejection episode that was controlled with a single dose of steroid medicines, her doctors said. She must take immune-suppressing drugs for the rest of her life, but her dosage has been greatly reduced and she needs only a few pills a day.

The clinic expects to absorb the cost of the transplant because it was experimental, doctors said. Siemionow estimated it at $250,000 to $300,000. That is less than the $1 million that other surgeons estimate it costs them to treat other severely disfigured people through dozens of separate operations, she said.

Also at the Cleveland Clinic is Charla Nash of Stamford, Conn., who was attacked by a friend's chimpanzee in February. She lost her hands, nose, lips and eyelids, and will be blind, doctors said. Clinic officials said it is premature to discuss the possibility of a face transplant for her.

In April, doctors at Harvard-affiliated Brigham and Women's Hospital in Boston performed the nation's second face transplant, on a man disfigured in a freak accident. It was the world's seventh such operation. The first, in 2005, was performed in France on Isabelle Dinoire, a woman who had been mauled by her dog.

Swine flu has blindsided the world

2009-05-01T05:57:00.000-07:00

What’s Different (and Dangerous) About Swine Flu?
Kara Rogers - April 29th, 2009

Swine flu has blindsided the world, and the participation of countries in the global effort to control the spread of the virus is now imperative in preventing a pandemic. But why has swine flu put the world on pandemic alert? And what is it about the swine influenza virus that suddenly set it apart from all other influenza viruses?

The first question is relatively simple to answer. The disease is highly infectious and contagious and can be deadly in humans. Furthermore, its outbreak in Mexico City and its subsequent spread to the United States present real opportunity for its spread to other countries worldwide. And, of course, such spread has already happened. With viral containment and isolation now impossible, we are on pandemic alert and must rely on controlling viral spread, rapid reporting of new cases, and warning against travel to and from affected areas to prevent a full-scale catastrophe.Domestic pigs.

However, the second question is much more difficult to answer, because the details of what make swine influenza virus so infectious in humans are largely unknown. The swine virus that is at the root of the current outbreak is called H1N1—the same labeling given to the virus that caused the devastating 1918-19 flu pandemic. But not all H1N1 flu viruses are created equally, and the swine virus appears to be quite different from all other H1N1 viruses.

Different strains of H1N1 are distinguished by any number of genetic variations, including many that affect the hemagglutinin (H) and neuraminidase (N) proteins found on the surface of the virus. In the case of the emergence of new swine H1N1 variants, several factors are at play, a major one of which is that pigs are susceptible to infection by swine, human, and avian influenza viruses. In addition, influenza viruses from different species have readily interchangeable segments of RNA. Thus, a pig simultaneously infected by human and avian viruses provides the perfect opportunity for a genetic swap between the different viruses.

An Influenza Perfect Storm

This scenario is not as far-fetched as it may seem. In fact, it is believed that sometime in the late 1990s, a sort of perfect storm involving swine, human, and avian influenza viruses took place in pigs in the United States. The result was a so-called triple reassortant swine influenza virus—part swine, part human, and part avian. As time passed, reassortant viruses mutated, and the genes affected were not always the ones encoding the H and N proteins of the viral coat. Mutations occurred in genes still largely unheard of in the public sector, genes like PB1 and PB2, which encode enzymes called RNA polymerases that function in viral replication.

Reassortant H1N1 swine virus appears to be more deadly in pigs than classical H1N1 swine virus, which was first isolated from pigs in the 1930s and did not possess genes from the human and avian viruses. The mutations in polymerase genes and in other viral genes are believed to further increase the virulence of swine influenza viruses, causing severe respiratory disease and death in pigs. Perhaps, the sicker the pigs the more likely the virus is to be spread to humans, whether through physical contact with sick animals or through inhaling infectious virus circulating in the air. Reassortant H1N1 swine influenza virus is common in pigs in the United States, and since the initial reassortant viruses emerged, the number of cases of human swine flu in the United States has increased annually.

A triple reassortant swine H1N1 virus appears to be the cause of the ongoing outbreak, and this virus is infectious and deadly in humans, particularly in people between ages 25 and 40. Why it is causing the death of presumably healthy adults remains unclear. However, all adult deaths from swine flu have occurred only in Mexico, despite the growing number of cases in other countries. This raises serious questions about the outbreak there, especially in light of the fact that adults elsewhere who are affected by the virus and who are treated within 30–48 hours of the onset of flu-like symptoms are experiencing full recovery from their illness.

Swine Flu Made Simple

2009-04-29T06:22:00.001-07:00

What It Is and What to Do: A Primer

By JACOB GOLDSTEIN

What is swine flu?

It's a flu that occurs in pigs, and in rare cases is passed from pigs to humans. The strain now circulating is worrisome because it can pass from person to person. Like human flu, the effects of swine flu can range from mild to severe.

Is the disease the same in Mexico and the U.S.?

The virus appears to be the same. It is suspected of causing more than 80 deaths in Mexico, but the symptoms have been mild in the confirmed U.S. cases so far, with most patients recovering without a hospital stay. It remains unclear why. An official at the Centers for Disease Control and Prevention warned Sunday that as cases continue to emerge in the U.S., some may prove fatal.
[What It Is and What to Do: A Primer] European Pressphoto Agency

St. Francis Preparatory School in New York City was cleaned Sunday after eight students were found to have human swine flu.

What are the symptoms?

Symptoms are similar to those of a standard flu: fever, as well as combinations of cough, sore throat, body aches, headaches, chills and fatigue. Some cases have also included reports of vomiting or diarrhea.

What should I do if I feel sick?

People with ordinary flu symptoms don't need to seek emergency care, officials said. Health officials recommend seeking urgent medical help for children when flu symptoms also include difficulty breathing, bluish skin color, fever with rash, and symptoms that begin to improve then return with fever and a worse cough. In adults, serious warning signs include difficulty breathing, pain or pressure in the chest or abdomen, dizziness, confusion and persistent vomiting.

Can the swine flu be treated with drugs?

Two drugs, sold under the brand names Tamiflu and Relenza, may reduce the swine flu's severity and duration. Most U.S. patients have recovered without the drugs. Both of these medications have also been approved to reduce the risk of contracting the seasonal flu. But, unlike a vaccine, they don't provide long-lasting protection. So their preventive use is limited to certain, narrow circumstances. The two drugs, which are included in the federal government's pandemic stockpile, are available only with a doctor's prescription.

Does my flu shot protect against the swine flu?

The CDC says the seasonal flu vaccine is "unlikely to provide protection" against the swine flu. The agency has created a "seed vaccine" tailored to this swine flu. That could be used to manufacture a targeted vaccine if officials decide it's necessary, but that could take months.

Are there ways to reduce the spread of the disease?

Cover your nose and mouth when you cough or sneeze. Wash your hands often. Avoid touching your eyes, nose or mouth. Avoid close contact with infected people. People who have mild symptoms should stay home until 48 hours after the symptoms have passed to avoid spreading the disease, health officials said.

HK experts develop new anti-cancer drug

2009-04-07T05:33:00.000-07:00

HONG KONG, April 7 (Xinhua) -- The Hong Kong Polytechnic University has developed a new drug proven to be able to inhibit the growth of cancer cells, according to a press release Xinhua received Tuesday.

Developed by the university's Department of Applied Biology and Chemical Technology, the new drug works on the mechanism of starving cancer cells through depletion of arginine which is a key nutrient for many cancer cells.

The main constituent of the novel drug is arginase, which is anenzyme that degrades arginine, with urea as an end-product.

In the laboratory settings, the new drug has been proven being able to work in cell culture for breast cancer, cervical cancer, skin cancer, pancreatic cancer, lung cancer, colorectal cancer, and gastric cancer.

According to the university, this anti-cancer therapy only affects cancer cells but not normal cells, causing less side effects than traditional cytotoxic chemotherapy.

The innovation has recently been awarded the Prize of the State of Geneva and a Gold Medal with Jury's Commendation at the 37th International Exhibition of Inventions, New Techniques and Products of Geneva.

Telescope eye implant restores sight lost from macular degeneration

2009-04-03T05:59:00.001-07:00

California-based VisionCare Ophthalmic Technologies has an ocular implant that, once inserted, would help out anyone suffering from macular degeneration (which means the elderly, in most cases). With macular degeneration, you typically lose your vision in the center of your eyesight, so VisionCare's telescope implant, which uses two lenses inside a small glass tube, would restore that central blind spot. The downside of the telescope, however, is that you'd experience a loss in your peripheral vision with that eye.

That's why doctors recommend only implanting one eye. "Instead of using two parts of the same eye, they must switch between two eyes," Eli Peli, a scientist at The Schepens Eye Research Institute, told the Technology Review, "If they see someone coming but can't tell who it is, they need to switch to other eye."

It may sound like a hassle, but it's just a matter of training yourself — and the benefit of being able to see straight ahead again is worth it. The implant is still waiting for FDA approval. If it does get a green light, then doctors can begin surgically implanting the telescope, which is held in place by the tissue of the eye.

Super Brain Yoga

2009-03-31T16:50:00.000-07:00

Superbrain Yoga® is a simple and effective technique to energize and recharge the brain. It is based on the principles of subtle energy and ear acupuncture. This powerful technique is explained in Master Choa Kok Sui's latest book Superbrain Yoga®.

Pilot studies on the effects of Superbrain Yoga® on school children include children with disabilities such as ADHD/ADD, developmental and cognitive delays, Down syndrome and specific learning disabilities. Children studied showed significant increase in academic and behavioral performance, greater class participation and improved social skills. In one study, the result of an electroencephalograph showed increased amplitude in the parieto-occipital region of the brain following the Superbrain Yoga®. This indicates increased brain electrical activity following the exercise. More studies on the effects of Superbrain Yoga® are being conducted.
www.superbrainyoga.org

Stroke indicators

2009-01-29T15:39:00.000-08:00

STROKE: Remember the 1st Three Letters.... S.T.R.

STROKE IDENTIFICATION

It only takes a minute to read this...

A neurologist says that if he can get to a stroke victim within 3 hours he can totally reverse the effects of a stroke... totally . He said the trick was getting a stroke recognized, diagnosed, and then getting the patient medically cared for within 3 hours, which is tough.

RECOGNIZING A STROKE

Thank God for the sense to remember the '3' steps, STR . Read and Learn!

Sometimes symptoms of a stroke are difficult to identify. Unfortunately, the lack of awareness spells disaster. The stroke victim may suffer severe brain damage when people nearby fail to recognize the symptoms of a stroke.

Now doctors say a bystander can recognize a stroke by asking three simple questions:

S * Ask the individual to SMILE.
T * Ask the person to TALK and SPEAK A SIMPLE SENTENCE (Coherently)
(i.e. It is sunny out today)
R * Ask him or her to RAISE BOTH ARMS.

If he or she has trouble with ANY ONE of these tasks , call emergency number immediately and describe the symptoms to the dispatcher.

New Sign of a Stroke -------- Stick out Your Tongue

NOTE: Another 'sign' of a stroke is this: Ask the person to 'stick' out his tongue.. If the tongue is 'crooked', if it goes to one side or the other , that is also an indication of a stroke.

A cardiologist says if everyone who gets this e-mail sends it to 10 people; you can bet that at least one life will be saved.

I have done my part. Have you?

Aubrey de Grey: Why we age and how we can avoid it

2009-01-28T06:27:00.000-08:00

Cambridge researcher Aubrey de Grey argues that aging is merely a disease -- and a curable one at that. Humans age in seven basic ways, he says, all of which can be averted.Aubrey de Grey, British researcher on aging, claims he has drawn a roadmap to defeat biological aging. He provocatively proposes that the first human beings who will live to 1,000 years old…

HEALTH Israeli researcher proves the healing power of the cranberry

2009-01-16T20:26:00.000-08:00

Israeli researcher proves the healing power of the cranberry
By Ilana Teitelbaum April 29, 2008

Cranberries have long been known as a popular folk remedy for the treatment of urinary tract infections, but until recently there was no scientific evidence to back up this claim. Now Professor Itzhak Ofek of Tel Aviv University has discovered that the benefits ascribed to cranberries are not only real - there are several more as well.

"Cranberries started as a folk medicine in the US," Ofek told ISRAEL21c. "Every fourth American in the '60s knew it was good for urinary tract infection." Ofek's goal was to find out the truth behind the myth.

With his research funded by the cranberry juice-producing monolith Ocean Spray, Ofek recently published his findings in the journal Molecular Nutrition & Food Research. There is only one snag: the benefits of cranberries, though prodigious, appear to apply only to women.

"It appears that in certain infections, such as ulcers caused by H. pylori bacteria, a clinical trial showed that the cranberry has beneficial effects for women only," says Ofek. "In urinary tract infections (UTI), the cranberry has been tested only on women and has proven to be beneficial, although UTI is primarily an infectious disease most common in women."

Ofek has been researching the healing properties of the cranberry for more than a decade, and has discovered numerous benefits in the course of his research. He began at the logical starting point: the claim that cranberries prevent urinary tract infections. Ofek explains that while other researchers had investigated this phenomenon in the past, they had been looking for an antibiotic substance in cranberries.

"We thought: perhaps they did the wrong test?" says Ofek. Sure enough, he and his colleagues found the answer when they tested cranberries for an anti-bacterial substance.

He discovered that cranberries contain a heavy molecule, also known as non-dialyzable material or NDM. This molecule, isolated by Ofek and collaborator Professor Nathan Sharon of the Weizmann Institute, seems to coat some bodily surfaces with Teflon-like efficiency, preventing infection-causing agents from taking root. Surprisingly, the NDM has no effect on good bacteria.

More recently in collaboration with other researchers, Ofek discovered that the NDM substance inhibits the flu virus from attaching to cells. This NDM also has a gastrointestinal benefit: it inhibits unhealthy bacteria from attaching to gastric cells, thereby preventing ulcers.

But cranberries don't have to be swallowed to provide benefits. When Ofek explored other properties of the cranberry in collaboration with Professor Ervin Weiss of Hadassah Medical Center, they discovered that the benefits of cranberries extend to the teeth as well; a property of cranberries is that it can reduce the bacteria in the mouth that causes cavities. This find could end up giving current brands of mouthwash a run for their money.

However, Ofek cautions against gargling with cranberry juice. "The cranberry is very tart and acidic, so dentists say it will hurt your teeth. That's why we're isolating the substance that helps, to put in mouthwash."

This substance has been patented by Ramot, TAU's technology transfer company, and is currently the subject of negotiations with companies and investors.

Ramot is also commercializing this active substance in pill form, for people who don't like to drink cranberry juice but want to reap the benefits.

Ofek's work isn't done: he's still investigating the cranberry for further health benefits, and to see if it can also help men. While he acknowledges that other fruits may also contain healing properties that are waiting to be explored, Ofek also says that in comparison to other fruits, "Cranberries are unique." And since his research was publicized, cranberry juice consumption has gone up. "The sales of cranberry juice were tripled since our study," says Ofek.

IBM microscope 100 million times stronger than MRI

2009-01-12T16:20:00.000-08:00

BM Research on Monday announced that it has built a new nanoscale microscope capable of creating images with 100 million times finer resolution than existing MRI technology. The project was made possible through a process called magnetic resonance force microscopy, which, according to IBM, detects "ultra-small magnetic forces. The technique is said to be able to "see" beneath surfaces and be safe for sensitive biological materials.

IBM said that it ran a test using the new system that established for the first time, magnetic resonance imaging on nanometer-scale items. By running it on a tobacco mosaic virus that is 18 nanometers across--18 billionths of a meter--the new system achieved resolution down to four nanometers.
According to IBM Research, this is an image of the most important features of a magnetic resonance force microscope: 'An ultrasensitive silicon cantilever detects the tiny magnetic force between a nanoscale magnetic tip--green--and the hydrogen nuclei present in the virus particles placed at the end of the cantilever--blue, seen in the reflection. Nanoscale magnetic resonance imaging is achieved by manipulating the hydrogen nuclei in the sample with a radiofrequency magnetic field generated by a 'microwire'--red. A sensitivity improvement of 100 million is achieved compared to conventional magnetic resonance imaging.'

Cocaine and other Drug Products of the Past

2008-12-15T20:56:00.000-08:00

Cocaine toothache drops (c. 1885) were popular for children.
Not only would the medicine numb the pain, but it could also put the user in a “better” mood.
Bayer heroin bottle. From 1898 to 1910 heroin was marketed as a non-addictive morphine substitute and cough medicine for children!
Metcalf’s Coca Wine was one of a large number of cocaine-containing wines available on the market.
All claimed medicinal effects, although they were undoubtedly consumed for their “recreational” value as well.
Vin Mariani (c. 1865) was the leading Coca Wine of its time.
Pope Leo XIII purportedly carried a hipflask of Vin Mariani with him, and awarded a Vatican gold medal to its creator, Angelo Mariani.
Coca wine was made by the Maltine Manufacturing Company (New York). The dosage indicated on the back of the bottle reads: “A wine glass full with, or immediately after, meals. Children in proportion.”
Cocaine-containing throat lozenges (c. 1900) were “indispensable for singers, teachers, and orators.” In addition to quieting a sore throat, these lozenges undoubtedly provided the “pick-me-up” to keep these professionals performing at their peak.
Paperweight advertisement for C.F. Boehringer & Soehne (Mannheim, Germany), “largest makers in the world of quinine and cocaine.” This chemical manufacturer was proud of its leading position in the world’s cocaine market.
This bottle of Stickney and Poor’s paregoric (mixture of opium and alcohol) was distributed much like the spices for which the company is better known. Doses for infants, children, and adults are given on the bottle. At 46% alcohol, this product is 92 proof which is pretty potent in itself.
This ad is for Glyco-Heroin manufactured by Martin H. Smith Company (New York). Heroin was widely used not only as an analgesic but also as a remedy for asthma, coughs, and pneumonia. Mixing heroin with glycerin (and often adding sugar or spices) made the bitter-tasting opiate more palatable for oral consumption.
This National Vaporizer Vapor-OL (opium) Treatment no. 6 for asthma may have provided a unique method of essentially “smoking” opium. The volatile liquid was placed in a pan that was heated by a small kerosene lamp (see below). Other substances were also used in these early (c. 1890) vaporizers, but this mixture probably ensured plenty of visitors for the spasmodically affected.

US teen lives 118 days without heart

2008-11-19T14:26:00.000-08:00

By Jim Loney

MIAMI, Nov 19 (Reuters) - An American teen-ager survived for nearly four months without a heart, kept alive by a custom-built artificial blood-pumping device, until she was able to have a heart transplant, doctors in Miami said on Wednesday.

The doctors said they knew of another case in which an adult had been kept alive in Germany for nine months without a heart but said they believed this was the first time a child had survived in this manner for so long.

The patient, D'Zhana Simmons of South Carolina, said the experience of living for so long with a machine pumping her blood was "scary."

"You never knew when it would malfunction," she said, her voice barely above a whisper, at a news conference at the University of Miami/Jackson Memorial Medical Center.

"It was like I was a fake person, like I didn't really exist. I was just here," she said of living without a heart.

Simmons, 14, suffered from dilated cardiomyopathy, a condition in which the patient's heart becomes weakened and enlarged and does not pump blood efficiently.

She had a heart transplant on July 2 at Miami's Holtz Children's Hospital but the new heart failed to function properly and was quickly removed.

Two heart pumps made by Thoratec Corp (THOR.O: Quote, Profile, Research, Stock Buzz) of Pleasanton, California, were implanted to keep her blood flowing while she fought a host of ailments and recovered her strength. Doctors implanted another heart on Oct. 29.

"She essentially lived for 118 days without a heart, with her circulation supported only by the two blood pumps," said Dr. Marco Ricci, the hospital's director of pediatric cardiac surgery. During that time, Simmons was mobile but remained hospitalized.

When an artificial heart is used to sustain a patient, the patient's own heart is usually left in the body, doctors said.

In some cases, adult patients have been kept alive that way for more than a year, they said.

"This, we believe, is the first pediatric patient who has received such a device in this configuration without the heart, and possibly one of the youngest that has ... been bridged to transplantation without her native heart," Ricci said.

Simmons also suffered renal failure and had a kidney transplant the day after the second heart transplant.

Ricci said her prognosis was good. But doctors said there is a 50 percent chance that a heart transplant patient will need a new heart 12 or 13 years after the first surgery. (Editing by Cynthia Osterman)

Claudia Castillo gets windpipe tailor-made from her own stem cells

2008-11-19T14:19:00.000-08:00

A woman has been given a new section of windpipe created from her own stem cells in an operation that could revolutionise surgery.

Claudia Castillo, 30, who lives in Barcelona, has become the first person to be given a whole organ tailor-made for her in laboratories across Europe.

A graft from a donor was used, but because it has been imbued with Ms Castillo’s own cells, there is no sign that her body will reject the organ. Researchers and surgeons from Britain, Italy and Spain collaborated to grow tissue from Ms Castillo’s own bone marrow stem cells, using them to fashion the new bronchus – a branch of the windpipe. They believe that one day the approach will be used to create engineered replacements for other damaged organs, such as the bowel or bladder. In five years they hope to begin clinical trials in which laboratory-made voice boxes are implanted into patients with cancer of the larynx.

Martin Birchall, of the University of Bristol, a British member of the team, said: “This is the first time a tissue-engineered whole organ has been transplanted into a patient. I reckon in 20 years’ time it will be the commonest operation – it will transform the way we think about surgery.”

Ms Castillo, who was born in Colombia, had suffered a tuberculosis infection that ravaged her airways, leaving her unable to do simple domestic tasks. Disease had caused her windpipe, or trachea, to collapse just at the point where it entered her lung. Without the pioneering operation in June, the lung would have been removed. Today she again has a normal life and is able to look after her two children. She can walk up stairs without getting breathless and has even been dancing.

The prospect of the patient needing powerful drugs to avoid rejection had been thought to outweigh any potential benefits of trachea transplants. Four months on, Ms Castillo’s doctors have seen no sign of her immune system rejecting the transplant, even though she has had no immunosuppres-sive drugs.

Details of the transplant, performed by Paolo Macchiarini, at the Hospital Clinic of Barcelona, are published online today by The Lancet.

First a section of trachea was taken from a donor and stripped of cells that could cause an immune reaction, leaving a grey trunk of connective tissue. Stem cells were then taken from Ms Castillo’s bone marrow and grown in Professor Birchall’s laboratory. Stem cells can develop into different kinds of tissue, given the right chemical instructions, enabling researchers to cultivate cartilage and epithelial cells to cover the 7cm graft. It was then “seeded” with the new cells using a process developed in Milan. Finally the trachea, covered in cartilage and lined with epithelial cells, was cut to shape and fitted.

Professor Macchiarini said: “The probability that this lady will have rejection is almost zero. She is enjoying a normal life, which for us clinicians is the most beautiful gift.”

The researchers said that the surgery could help some patients in Britain but admitted that the procedure was too expensive to be widely available. They are seeking EU funding and commercial sponsors for trials to create and transplant a larynx, an operation that could be more cost-effective.

Ms Castillo said: “I was scared at the beginning because I was the first patient – but trusted the doctors. I am now enjoying life and am very happy that my illness has been cured.”

In Some Cultures, Cancer Stirs Shame

2008-10-03T17:36:00.000-07:00

In Some Cultures, Cancer Stirs Shame
By LUCETTE LAGNADO

When Mildred Wong received a diagnosis of breast cancer last year, she faced two tough decisions: what treatment to pursue and whom, if anyone, to tell about it.
Secret Treatment

Brooklyn's Maimonides Cancer Center takes pains to break through barriers to care among ethnic and minority groups.

In Mrs. Wong's native China, people often keep illnesses like cancer a secret. That tradition continues even here in America, where her family settled in the 1950s. Years ago, Mrs. Wong's infant daughter developed a brain tumor and her own mother insisted she tell no one. When the baby died, the grandmother tried to dissuade Mrs. Wong from attending the funeral, so great was the stigma.

Now, as she stares down her own health crisis, memories of her family's long-buried wounds are rushing in. "I came from a cultural background of stoic acceptance, saving face, keeping quiet," she explains.

Mrs. Wong, 60 years old, sought treatment at Maimonides Cancer Center, located on the edge of Brooklyn's booming Chinatown. Its patients are an ethnic tapestry of Chinese-Americans, Hasidic Jews from nearby Borough Park, Russians from Coney Island, Pakistani Muslims, as well as some Caribbean and African-Americans. Though starkly diverse, these groups often share strong beliefs about keeping a cancer diagnosis -- and possible treatments -- under wraps. The subject is such a cultural taboo that families have been known to shield loved ones from the seriousness of their condition. Some patients are reluctant to seek or heed medical advice; others even refuse to utter the word "cancer."

With ethnic minorities and immigrants fast becoming the collective U.S. majority, there is a push in medical circles to be more sensitive to cultural nuances. In 2001, the National Cancer Institute established the Center to Reduce Cancer Health Disparities to study why mortality rates for cancer can be so much higher for some groups than others. Only 71% of African-American women, for instance, survive for five years after a cancer diagnosis, compared to 86% of white women. Issues such as poverty, lack of access to care and inadequate care, are among probable reasons for the gap. But cultural factors, says the NCI center's director, Dr. Tanya Springfield, are now being recognized as a "significant" part of the problem.

Maimonides is among several hospitals nationwide attempting to hit these issues head on. In addition to dispensing medical advice to individuals, doctors routinely confer with family members, rabbis and other religious leaders as part of some patients' care. The facility has several Asian oncologists on staff who speak Chinese dialects fluently. As a nod to discretion, the center is located about a mile from the main hospital and lacks any overt signage referring to its true mission of cancer treatment. A back entrance and a special waiting room with frosted glass help visitors go undetected.
Balancing Act

Staff at the four-year-old facility balance a complicated set of cultural mores and medical responsibilities. The range of attitudes "makes our job very difficult," says Dr. Yiqing Xu, a Chinese-born oncologist.

U.S. law dictates that patients be informed about their conditions and consent to all medical treatments. Those who submit to chemotherapy or other therapies are required to sign forms that spell out the drugs they are receiving, as well as possible side effects. However, consent forms tend to be in English, as Dr. Xu points out. And many families -- especially Chinese, Russians and Muslims -- often want their loved ones to know as little as possible about their cancer.

Sze Cheng's 72-year-old grandmother, born in China, was recently found to have advanced colon cancer. But Ms. Cheng and her husband have been determined to play down the true nature of her situation -- despite advice from a Maimonides doctor.

"We try to do what is best for her," explains Ms. Cheng, who says she loves her grandmother very much. "We talked about telling her," adds her husband, Sheng Lam. "But if we tell her, she will be upset -- she will go into a depression."

Oncologist Yiwu Huang says he worked with the family to explain the consent form to his patient. He says he told the woman, who does not speak English, that she had a growth in her colon, and that the chemotherapy was a "medication to try to prevent the disease from coming back." Still, "I avoided the word 'cancer,'" he says. He beseeched the family to be more direct, he says, but to no avail. "They said, 'please don't tell her,'" the doctor recalls.

"It is not uncommon in Chinese families to hide the news," notes Dr. Xu. But while she and other doctors may defer to families, some bristle at doing so. "It is not good for the patient," says Dr. Xu. "They don't have a chance to have a say in their treatment. It should be what they want, not what their families want." She pauses, then adds: "I may be too Americanized in my views."

Alan Astrow, Maimonides's director of Hematology-Medical Oncology, says that good medical practice calls for full disclosures. "But in many traditional cultures, crucial decisions are made by the patients' family -- we treat people from all over the world. Is there a conflict? Yeah there is a conflict." While it is necessary for doctors to follow the law, he says, it is also important that clinicians be mindful of the feelings and values of both patient and family.

The center's doctors have learned to modulate their vocabulary. For example, "we don't use the term chemotherapy," says Dr. Xu. Instead, she will merely say "treatment." To get around the "C" word, she might use substitutes such as "lesion" or "mass."

Many patients welcome the edited approach. Malka Friedman, a devout Orthodox Jew, prefers to avoid all direct reference to the disease. "The word is like a sword -- this is the way we were brought up," says Mrs. Friedman. Merely to say "cancer," she believes, could somehow give malignant cells more power to spread.

Upon learning that she needed a mastectomy, Mrs. Friedman added an unofficial member to her medical team. During an appointment with her breast surgeon, she placed a call to her rabbi and had him speak to the doctor.

"It was one of my first experiences with a rabbi calling and saying 'We have been praying over this and we have gotten guidance and we don't want major surgery to be done,'" Dr. Patrick Borgen, her surgeon at Maimonides, recalls. (He agreed to perform a less-radical procedure.) Now, he says he has learned to expect that rabbis will weigh in on medical decisions.

A gentle yet strong-willed woman, Mrs. Friedman's faith dictated she cover her head with a wig even before chemotherapy. She refers to Dr. Borgen, chief of breast surgery, as "a messenger of God." Still, the 61-year-old doesn't always do what he asks.

Dr. Borgen encouraged his patient to take a test to determine if she is a carrier of a particular genetic mutation -- one way to predict if a woman might be at a high risk for developing other cancers. He further advised that her female relatives have the same test.

She refused. Instead, Mrs. Friedman says she told her daughters and other kin to go for regular medical check-ups.

Cancer is considered to be something of a social blemish in the tightly-knit Orthodox community. Merely being seen entering or leaving a cancer center might spark rumors that could have profound repercussions for a family. A young person who has suffered from the disease, for instance, is generally considered an undesirable marriage partner. Cancer in a parent or sibling also could affect one's marital prospects.

Across backgrounds, the forces of denial don't discriminate. Over the years, several hospitals have worked to try to persuade African-American women to get early screening for breast cancer -- only to find that some won't come back even when told they have a tumor.

In Atlanta, for example, the Georgia Cancer Center for Excellence reaches out to black women at churches and health fairs. Such targeted efforts have yielded results: Patients coming in with advanced, Stage Four cancers declined from 16.8% to 9% between 2001 and 2005. Even so, anywhere from 7% to 10% of women found to have cancer either fail to return or don't stay through the entire course of treatment, according to Dr. Mitchell Berger, Chief of Hematology and Oncology at the center, a division of Grady Health System.

"There are so many myths that can influence a person's tendency to seek care or refuse care -- there are many examples from Harlem to Appalachia to Native America," says Dr. Harold Freeman, founder of the Harlem-based Ralph Lauren Center for Cancer Care and Prevention. The center is a joint venture of Memorial Sloan-Kettering Cancer Center and North General, a local Harlem hospital.

"We need to be careful. It is very tough to separate race from poverty from culture, yet you need to do that," he says.
Culture Cues

Since arriving in Harlem in the 1960s, where he recalls seeing women with cancers so advanced as to be inoperable, Dr. Freeman has seen the need to address cultural points of difference.

One approach is to be mindful of patients' own myths and taboos -- then figure out ways to get them into treatment. At the Lauren center, for example, patients are assigned a "navigator" -- an employee charged with walking them through the different phases of their diagnosis and care. That can mean phoning people who don't show up for an appointment, or even knocking on their door at home if they go missing at any point during treatment.

Monica Williams, 70 years old, arrived at the Harlem center three years ago. Born in Grenada, Ms. Williams is a devout Catholic who says she had a premonition that she was ill. Years before her diagnosis, she recalls having a nightmare: "A voice said to me, 'You have cancer,' and I said, 'Get away from me, you devil.'" She remembered the dream when she learned she had colon cancer. She believed that God, not doctors, had the power to heal her.

Maud Colas, the patient navigator assigned to Ms. Williams, recalls painstaking sessions to get her to agree to treatment -- even while respecting her religious convictions. The feisty septuagenarian, herself a home health-care aide, at first wouldn't budge. Ms. Colas, who is also of Caribbean descent, appealed to Mrs. Williams to reconsider.

"I had barriers too, and I said, 'I also love God, but give our doctors a try,'" Ms. Colas recalls. She helped work out a solution: Mrs. Williams agreed to let the doctors perform surgery to remove her tumor -- while praying to God to guide them.

Ms. Williams, a proud woman who shows up to the center impeccably dressed -- she sported a pink gauze ensemble one recent afternoon -- has since endured numerous rounds of chemotherapy. All the while, she has continued her work. Yet still she harbors her secret, having told no one, not even immediate family, about her condition. When her hair started falling out as the result of chemo, she waved it off as a bad experience at the hairdresser. Asked if perhaps her husband and other relatives may have guessed the truth, she replies only: "Maybe."

Ms. Williams's cancer was fairly advanced when she was diagnosed. Then a lesion was found in her liver and she needed more surgery. As of now, says Dr. Freeman, there is no evidence of the disease. Ms. Williams says she has made her peace with human medical interventions. "I ask God to lift me up," she says.

As for Mrs. Wong, she came to a major decision this year: She would be more American than Chinese in dealing with her breast cancer. She couldn't forget how desperately alone she had felt when her baby was ill. "I didn't tell anyone, and no one came to visit," she says. In the months when the infant lay in a hospital, friends and relatives heard only that she suffered from a cold.
Difficult News

When she was first diagnosed with breast cancer, she sought a second opinion at Maimonides. The news was hard to bear. Given that the cancer had spread to a lymph node, Dr. Borgen, her surgeon, suggested treatment that would include a single mastectomy as well as chemotherapy.

Instead of keeping her fears about breast cancer bottled inside, she reached out to friends, both Chinese and American. She also leaned on members of her Baptist church where she and her husband are active. She has even attended a few meetings of a Chinese cancer support group. Without the burden of her mother's insistence on secrecy, Mrs. Wong says she was strangely liberated. "I felt totally different this time because of the love and support of my friends," she recalls. "They came over and cooked and shopped."

After surgery came a grueling round of chemotherapy. She still recalls the horror of seeing her hair fall out. She took an American step she had heard was "empowering." She shaved her head.

"You do feel better," afterwards, she says, adding that she went and bought a couple of wigs. She still wears one of them, even though her treatment is finished. "My prognosis is very good, and I am very grateful."

Firms Struggle With Varied Rules on Melamine

2008-10-03T17:23:00.000-07:00

Firms Struggle With Varied Rules on Melamine
By SKY CANAVES
*
HONG KONG -- Differing and shifting government regulations have complicated food companies' efforts to grapple with the widening Chinese tainted-milk scandal, leading to outright bans in some places for products that pass official muster in others.

U.S. regulators Friday said food products wouldn't raise health concerns if they contained levels below 2.5 parts per million of melamine, an industrial chemical at the center of the tainted-milk scandal. But they said they won't tolerate the use of melamine as a food additive, saying they couldn't determine a safe level for use in infant formula, citing gaps in scientific knowledge about its effect on babies. The agency said tainted formula hasn't been found in the U.S. (Statement)
[testing limits chart]

Meanwhile, other regulators around the world are scrambling to establish melamine limits where none previously existed. Taiwan had no standard until last week, when it set a tough limit of 0.05 parts per million. That led to a recall this week of Nestlé SA products after regulators said they found traces of melamine in Nestlé products made in China. Nestlé said that its products are safe and that the small traces found by Taiwan "exist in the natural food cycle."

Last week, Indonesian authorities announced that they had found melamine in a dozen Chinese-made products, including Nabisco Oreo wafers and Mars M&M's and Snickers, in quantities ranging from 8.5 to 945 parts per million. Mars Inc. and Kraft Foods Inc., which owns Nabisco, questioned the results, pointing to other jurisdictions where test results for the same Chinese-made products came up clean.

An Indonesia Food and Drug Control Agency spokeswoman, reached late Friday, said, "It is no surprise if the industry has complained, but that does not lessen its result." She said Indonesia follows World Health Organization guidelines for melamine levels, which are based on U.S. standards involving weight and diet. In a report issued last week, however, the WHO said that the U.S. approach "has a large uncertainty" due to the lack of data about the effects of various types of melamine and its interaction with other substances.

Multinational firms have warned that adopting tougher standards than those of the U.S. and Europe could lead to higher food costs and product unavailability. "If governments start adopting low tolerance reporting levels, that will have huge implications for many countries where most foods produced in those countries won't pass the test," said Khaled Rabbani, director of corporate and regulatory affairs for Asia Pacific for Mars.

Daniel Chan, a professor of nephrology at the University of Hong Kong, sees the justification for the tougher standards in Hong Kong and Taiwan. "Ideally, we would want none of it," he said. "But if that would have implications with the availability of choices or prices of materials involved, then we have to decide how far we're willing to be exposed to it."

Hong Kong adopted rules Sept. 23 that set a limit of one part per million for children under the age of three and women who are pregnant or breastfeeding. For others, the territory adopted the European Union's standard of 2.5 parts per million. By comparison, one brand of milk powder implicated in the scandal, made by China's Shijiazhuang Sanlu Group Co., had levels exceeding 2,500 parts per million in powdered form, according to Chinese authorities.

In Asia, parts of which import far more food from China than in the West, there's a heightened sense of vulnerability to tainted products. Thousands of products have been tested so far in a number of countries.

Melamine's presence in Chinese-made baby formula has been blamed for the deaths of as many as four infants and sickening more than 50,000 others. China is still working on national standards, and Friday it posted a notice on the Web site of the Ministry of Science and Technology inviting the public to submit methods for detecting melamine in quantities of less than two parts per million within 30 minutes.

The chemical is generally considered safe for adults in minute amounts by other agencies that follow U.S. and EU standards. But little is known about the long-term health effects of the chemical that first rose to prominence as a contaminant a year ago during a tainted pet food scandal in the U.S.

In the U.S., the FDA has limited recall power, and it relies on manufacturers to pull questionable products off shelves. Since it warned against selling or eating one brand of Chinese-made candy called White Rabbit Creamy Candy, state officials in California, Connecticut and others have found it on shelves and warned consumers.

After promising to take a "zero tolerance" approach to melamine, on Sept. 24 Taiwan's health authorities said they would adopt the EU standard.

Hearing Aids Go Hi-Tech

2008-09-07T05:40:00.000-07:00

PURE from Siemens is the latest in hearing aid technology that not only boasts a discreet design, but it is also unparalleled in sound amplification and signal-processing technology. This new device enables wearers to access Bluetooth-enabled devices wirelessly, including phones and MP3 players.

Patients 'free from cancer' after immune-boost treatment

2008-09-03T16:26:00.000-07:00

Cancer patients have been left free of the disease after being treated with a new drug which harnesses the power of their own immune cells.
# Cancer and immunotherapy Q and A
# Immunotherapy: could it be the cure for cancer?
# Cancer patient recovers after injection of immune cells

Four of 38 patients with non-Hodgkin's lymphoma have seen "complete regressions" following treatment, while five others saw reductions of 50 per cent in their tumours.

Immunotherapy for cancer
While the trials were only carried out on patients with blood cancer, it is hoped the methods can be adapted to tackle other cancers

The drug, which could prove cheaper than other therapies that try to achieve the same effect with cells, works by activating the body's own defences to attack the cancer.

The results have been described as an "exciting" and "significant" development in the use of immunotherapy, the process of using the body's own immune system to fight disease.

While the trials were only carried out on patients with the blood cancer, it is hoped the methods can be adapated to tackle other cancers.

The disease claims the lives of more than 150,000 people in the UK every year and more than one million people are suffering from cancer at any one time.
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Earlier this year doctors announced that a patient with advanced skin cancer was free of the disease two years after they injected him with billions of his own immune cells using a different method. However, experts warned at the time that the process could prove extremely expensive.

The development of the drug could prove a much cheaper alternative way of providing immunotherapy treatments.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "These exciting preliminary results come from using them to harness the body's own immune response in a new way. Although the side effects need to be monitored carefully, we hope that this type of treatment will prove to be active in larger trials in the future"

"This a significant study," said Dr Cassian Yee, Fred Hutchinson Cancer Research Center, Seattle, who has had significant results using the alternative method of treating patients with white blood cells grown in the lab.

"It remains to be seen if most of the responses are longlasting. Certainly the results are very promising."

The drug, which has been developed by Micromet, in Bethesda, Maryland, was trialled by a team led by Dr Ralf Bargou at University of Würzburg in Würzburg, German.

The results, published in the journal Science, are encouraging because they suggest that the bigger the dose, the bigger the effect.

Coauthor of the study Dr Patrick Baeuerle, of Micromet, said all seven who received the highest dose responded to the drug.

"Two of the seven had a complete response, and five a partial regression (greater than 50 per cent reduction of tumour).".

The longest duration of a response was so far seen in a patient who received one quarter of their dose. After 13 months, he remains free of the blood cancer.

There are adverse side effects involved, however, such as fevers and chills, occasionally with confusion and tremor, though all stopped after treatment ceased.

Now a further trial is investigating how the drugs works in patients with another form of blood cancer, called acute lymphoblastic leukaemia.

Trials with a similar drug are also under way on patients with another type of cancer, which affects glandular tissue and can appear in the lungs, prostate, breast, colon and elsewhere in the body.

Micromet targets the body's own white blood cells on the cancer, using a fraction of a millionth of a gram of a specialised protein called a "bispecific antibody".

The company has created antibodies, called BiTE antibodies, which are able to stick to sites with exquisite precision, in this case to activate specialised white blood cells ( T cells) to attack cancer.

The antibodies overcome a key problem with immunotherapy that as tumours become more advanced they become more "invisible" to the T cells because the cancer cells lack molecules for white blood cells to hang on to and stage their attack.

Normal antibodies are designed to latch on to one molecular target but the bispecific antibody developed by Micromet, given the name blinatumomab, binds to two, the cancer cell and the T cell, and bring the two together to target the immune system on the cancer.

The team tried varying doses of blinatumomab in patients, and found that among 38 patients, at doses from 0.0005 to 0.06 milligrams (millionths of a gram) per square metre of body surface per day, 11 of them exhibited major responses and tumour shrinking. The disease was cleared from bone marrow, spleen and liver too.

Killer Carbs: Scientist Finds Key To Overeating As We Age

2008-08-25T05:59:00.000-07:00

ScienceDaily (Aug. 22, 2008) — A Monash University scientist has discovered key appetite control cells in the human brain degenerate over time, causing increased hunger and potentially weight-gain as we grow older. The research by Dr Zane Andrews, a neuroendocrinologist with Monash University's Department of Physiology, has been published in Nature.

Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars.

"The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more," Dr Andrews said.

Dr Andrews said the attack on appetite suppressing cells creates a cellular imbalance between our need to eat and the message to the brain to stop eating.

"People in the age group of 25 to 50 are most at risk. The neurons that tell people in the crucial age range not to over-eat are being killed-off.

"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMC's kick in.

"However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied," Dr Andrews said.

The free radicals also try to attack the hunger neurons, but these are protected by the uncoupling protein 2 (UCP2).

Dr Andrews said the reduction in the appetite-suppressing cells could be one explanation for the complex condition of adult-onset obesity.

"A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration," Dr Andrews said.

Dr Andrews' next research project will focus on finding if a diet rich in carbohydrates and sugars has other impacts on the brain, such as the increased incidences of neurological conditions like Parkinson's disease.

Japanese create stem cells from wisdom teeth

2008-08-23T05:14:00.000-07:00

Japanese scientists said Friday they had derived stem cells from wisdom teeth, opening another way to study deadly diseases without the ethical controversy of using embryos.

Researchers at the government-backed National Institute of Advanced Industrial Science and Technology said they created stem cells of the type found in human embryos using the removed wisdom teeth of a 10-year-old girl.

"This is significant in two ways," team leader Hajime Ogushi told AFP. "One is that we can avoid the ethical issues of stem cells because wisdom teeth are destined to be thrown away anyway.

"Also, we used teeth that had been extracted three years ago and had been preserved in a freezer. That means that it's easy for us to stock this source of stem cells."

The announcement follows the groundbreaking discovery by US and Japanese scientists last year that they could produce stem cells from skin, a finding that was hailed by the Vatican and US President George W. Bush.

Research involving embryonic stem cells -- which can develop into various organs or nerves -- is seen as having the potential to save lives by helping find cures for diseases such as cancer and diabetes.

But studies on embryos are strongly opposed by religious conservatives, who argue that such research destroys human life, albeit at its earliest stage of development.

In the new research, cells were extracted from the wisdom teeth and developed for about 35 days.

The researchers then tested them and found that they were stem cells, which can develop into various other kinds of human cells, Ogushi said.

As with last year's skin cell discovery, the Japanese researchers said it would take time to put the use of wisdom teeth into practical use.

Ogushi estimated it would take at least five years to put the method into clinical use such as trial treatments of congenital bone disease.

"Because extractions of wisdom teeth are commonly operated in dental clinics, we can expect a lot of donors of stem cells," he said.

"That enable us to create stem cells of various genetic codes, eliminating the risk that a body of a patient would reject transplanted tissues or organs," he added.

He was hopeful that the method would produce stem cells of various genetic codes -- reducing the risk that patients' bodies would reject transplanted tissues or organs.

Theoretically, people who give up their wisdom teeth in their youth could use the stem cells later in life if they need treatment.

The research takes points from last year's skin cell breakthrough, which was a collaborative effort by researchers at Kyoto University and the University of Wisconsin at Madison.

The Kyoto University team, led by Shinya Yamanaka, generated human stem cells by introducing four genes into a sample of human skin.

Ogushi introduced three of of the four genes identified by Yamanaka into the wisdom teeth.

Japan, the largest spender on scientific research after the United States, in December announced a 10 billion-yen (92 million-dollar) plan to advance stem cell research over five years.

Sleep on It: How Snoozing Makes You Smarter

2008-08-08T06:09:00.000-07:00

During slumber, our brain engages in data analysis, from strengthening memories to solving problems

By Robert Stickgold and Jeffrey M. Ellenbogen

In 1865 Friedrich August Kekulé woke up from a strange dream: he imagined a snake forming a circle and biting its own tail. Like many organic chemists of the time, Kekulé had been working feverishly to describe the true chemical structure of benzene, a problem that continually eluded understanding. But Kekulé’s dream of a snake swallowing its tail, so the story goes, helped him to accurately realize that benzene’s structure formed a ring. This insight paved the way for a new understanding of organic chemistry and earned Kekulé a title of nobility in Germany.

Although most of us have not been ennobled, there is something undeniably familiar about Kekulé’s problem-solving method. Whether deciding to go to a particular college, accept a challenging job offer or propose to a future spouse, “sleeping on it” seems to provide the clarity we need to piece together life’s puzzles. But how does slumber present us with answers?

The latest research suggests that while we are peacefully asleep our brain is busily processing the day’s information. It combs through recently formed memories, stabilizing, copying and filing them, so that they will be more useful the next day. A night of sleep can make memories resistant to interference from other information and allow us to recall them for use more effectively the next morning. And sleep not only strengthens memories, it also lets the brain sift through newly formed memories, possibly even identifying what is worth keeping and selectively maintaining or enhancing these aspects of a memory. When a picture contains both emotional and unemotional elements, sleep can save the important emotional parts and let the less relevant background drift away. It can analyze collections of memories to discover relations among them or identify the gist of a memory while the unnecessary details fade—perhaps even helping us find the meaning in what we have learned.

Not Merely Resting
If you find this news surprising, you are not alone. Until the mid-1950s, scientists generally assumed that the brain was shut down while we snoozed. Although German psychologist Hermann Ebbinghaus had evidence in 1885 that sleep protects simple memories from decay, for decades researchers attributed the effect to a passive protection against interference. We forget things, they argued, because all the new information coming in pushes out the existing memories. But because there is nothing coming in while we get shut-eye, we simply do not forget as much.

Then, in 1953, the late physiologists Eugene Aserinsky and Nathaniel Kleitman of the University of Chicago discovered the rich variations in brain activity during sleep, and scientists realized they had been missing something important. Aserinsky and Kleitman found that our sleep follows a 90-minute cycle, in and out of rapid-eye-movement (REM) sleep. During REM sleep, our brain waves—the oscillating electromagnetic signals that result from large-scale brain activity—look similar to those produced while we are awake. And in subsequent decades, the late Mircea Steriade of Laval University in Quebec and other neuroscientists discovered that individual collections of neurons were independently firing in between these REM phases, during periods known as slow-wave sleep, when large populations of brain cells fire synchronously in a steady rhythm of one to four beats each second. So it became clear that the sleeping brain was not merely “resting,” either in REM sleep or in slow-wave sleep. Sleep was doing something different. Something active.

Sleep to Remember
The turning point in our understanding of sleep and memory came in 1994 in a groundbreaking study. Neurobiologists Avi Karni, Dov Sagi and their colleagues at the Weizmann Institute of Science in Israel showed that when volunteers got a night of sleep, they improved at a task that involved rapidly discriminating between objects they saw—but only when they had had normal amounts of REM sleep. When the subjects were deprived of REM sleep, the improvement disappeared. The fact that performance actually rose overnight negated the idea of passive protection. Something had to be happening within the sleeping brain that altered the memories formed the day before. But Karni and Sagi described REM sleep as a permissive state—one that could allow changes to happen—rather than a necessary one. They proposed that such unconscious improvements could happen across the day or the night. What was important, they argued, was that improvements could only occur during part of the night, during REM.

It was not until one of us (Stickgold) revisited this question in 2000 that it became clear that sleep could, in fact, be necessary for this improvement to occur. Using the same rapid visual discrimination task, we found that only with more than six hours of sleep did people’s performance improve over the 24 hours following the learning session. And REM sleep was not the only important component: slow-wave sleep was equally crucial. In other words, sleep—in all its phases—does something to improve memory that being awake does not do.

To understand how that could be so, it helps to review a few memory basics. When we “encode” information in our brain, the newly minted memory is actually just beginning a long journey during which it will be stabilized, enhanced and qualitatively altered, until it bears only faint resemblance to its original form. Over the first few hours, a memory can become more stable, resistant to interference from competing memories. But over longer periods, the brain seems to decide what is important to remember and what is not—and a detailed memory evolves into something more like a story.

In 2006 we demonstrated the powerful ability of sleep to stabilize memories and provided further evidence against the myth that sleep only passively (and, therefore, transiently) protects memories from interference. We reasoned that if sleep merely provides a transient benefit for memory, then memories after sleep should be, once again, susceptible to interference. We first trained people to memorize pairs of words in an A-B pattern (for example, “blanket-window”) and then allowed some of the volunteers to sleep. Later they all learned pairs in an A-C pattern (“blanket-sneaker”), which were meant to interfere with their memories of the A-B pairs. As expected, the people who slept could remember more of the A-B pairs than people who had stayed awake could. And when we introduced interfering A-C pairs, it was even more apparent that those who slept had a stronger, more stable memory for the A-B sets. Sleep changed the memory, making it robust and more resistant to interference in the coming day.

But sleep’s effects on memory are not limited to stabilization. Over just the past few years, a number of studies have demonstrated the sophistication of the memory processing that happens during slumber. In fact, it appears that as we sleep, the brain might even be dissecting our memories and retaining only the most salient details. In one study we created a series of pictures that included either unpleasant or neutral objects on a neutral background and then had people view the pictures one after another. Twelve hours later we tested their memories for the objects and the backgrounds. The results were quite surprising. Whether the subjects had stayed awake or slept, the accuracy of their memories dropped by 10 percent for everything. Everything, that is, except for the memory of the emotionally evocative objects after night of sleep. Instead of deteriorating, memories for the emotional objects actually seemed to improve by a few percent overnight, showing about a 15 percent improvement relative to the deteriorating backgrounds. After a few more nights, one could imagine that little but the emotional objects would be left. We know this culling happens over time with real-life events, but now it appears that sleep may play a crucial role in this evolution of emotional memories.

Precisely how the brain strengthens and enhances memories remains largely a mystery, although we can make some educated guesses at the basic mechanism. We know that memories are created by altering the strengths of connections among hundreds, thousands or perhaps even millions of neurons, making certain patterns of activity more likely to recur. These patterns of activity, when reactivated, lead to the recall of a memory—whether that memory is where we left the car keys or a pair of words such as “blanket-window.” These changes in synaptic strength are thought to arise from a molecular process known as long-term potentiation, which strengthens the connections between pairs of neurons that fire at the same time. Thus, cells that fire together wire together, locking the pattern in place for future recall.

During sleep, the brain reactivates patterns of neural activity that it performed during the day, thus strengthening the memories by long-term potentiation. In 1994 neuroscientists Matthew Wilson and Bruce McNaughton, both then at the University of Arizona, showed this effect for the first time using rats fitted with implants that monitored their brain activity. They taught these rats to circle a track to find food, recording neuronal firing patterns from the rodents’ brains all the while. Cells in the hippocampus—a brain structure critical for spatial memory—created a map of the track, with different “place cells” firing as the rats traversed each region of the track [see “The Matrix in Your Head,” by James J. Knierim; Scientific American Mind, June/July 2007]. Place cells correspond so closely to exact physical locations that the researchers could monitor the rats’ progress around the track simply by watching which place cells were firing at any given time. And here is where it gets even more interesting: when Wilson and McNaughton continued to record from these place cells as the rats slept, they saw the cells continuing to fire in the same order—as if the rats were “practicing” running around the track in their sleep.

As this unconscious rehearsing strengthens memory, something more complex is happening as well—the brain may be selectively rehearsing the more difficult aspects of a task. For instance, Matthew P. Walker’s work at Harvard Medical School in 2005 demonstrated that when subjects learned to type complicated sequences such as 4-1-3-2-4 on a keyboard (much like learning a new piano score), sleeping between practice sessions led to faster and more coordinated finger movements. But on more careful examination, he found that people were not simply getting faster overall on this typing task. Instead each subject was getting faster on those particular keystroke sequences at which he or she was worst.

The brain accomplishes this improvement, at least in part, by moving the memory for these sequences overnight. Using functional magnetic resonance imaging, Walker showed that his subjects used different brain regions to control their typing after they had slept. The next day typing elicited more activity in the right primary motor cortex, medial prefrontal lobe, hippocampus and left cerebellum—places that would support faster and more precise key-press movements—and less activity in the parietal cortices, left insula, temporal pole and frontopolar region, areas whose suppression indicates reduced conscious and emotional effort. The entire memory got strengthened, but especially the parts that needed it most, and sleep was doing this work by using different parts of the brain than were used while learning the task.

Solutions in the Dark
These effects of sleep on memory are impressive. Adding to the excitement, recent discoveries show that sleep also facilitates the active analysis of new memories, enabling the brain to solve problems and infer new information. In 2007 one of us (Ellenbogen) showed that the brain learns while we are asleep. The study used a transitive inference task; for example, if Bill is older than Carol and Carol is older than Pierre, the laws of transitivity make it clear that Bill is older than Pierre. Making this inference requires stitching those two fragments of information together. People and animals tend to make these transitive inferences without much conscious thought, and the ability to do so serves as an enormously helpful cognitive skill: we discover new information (Bill is older than Pierre) without ever learning it directly.

The inference seems obvious in Bill and Pierre’s case, but in the experiment, we used abstract colored shapes that have no intuitive relation to one another, making the task more challenging. We taught people so-called premise pairs—they learned to choose, for example, the orange oval over the turquoise one, turquoise over green, green over paisley, and so on. The premise pairs imply a hierarchy—if orange is a better choice than turquoise and turquoise is preferred to green, then orange should win over green. But when we tested the subjects on these novel pairings 20 minutes after they learned the premise pairs, they had not yet discovered these hidden relations. They chose green just as often as they chose orange, performing no better than chance.

When we tested subjects 12 hours later on the same day, however, they made the correct choice 70 percent of the time. Simply allowing time to pass enabled the brain to calculate and learn these transitive inferences. And people who slept during the 12 hours performed significantly better, linking the most distant pairs (such as orange versus paisley) with 90 percent accuracy. So it seems the brain needs time after we learn information to process it, connecting the dots, so to speak—and sleep provides the maximum benefit.

In a 2004 study Ullrich Wagner and others in Jan Born’s laboratory at the University of Lübeck in Germany elegantly demonstrated just how powerful sleep’s processing of memories can be. They taught subjects how to solve a particular type of mathematical problem by using a long and tedious procedure and had them practice it about 100 times. The subjects were then sent away and told to come back 12 hours later, when they were instructed to try it another 200 times.

What the researchers had not told their subjects was that there is a much simpler way to solve these problems. The researchers could tell if and when subjects gained insight into this shortcut, because their speed would suddenly increase. Many of the subjects did, in fact, discover the trick during the second session. But when they got a night’s worth of sleep between the two sessions, they were more than two and a half times more likely to figure it out—59 percent of the subjects who slept found the trick, compared with only 23 percent of those who stayed awake between the sessions. Somehow the sleeping brain was solving this problem, without even knowing that there was a problem to solve.

The Need to Sleep
As exciting findings such as these come in more and more rapidly, we are becoming sure of one thing: while we sleep, our brain is anything but inactive. It is now clear that sleep can consolidate memories by enhancing and stabilizing them and by finding patterns within studied material even when we do not know that patterns might be there. It is also obvious that skimping on sleep stymies these crucial cognitive processes: some aspects of memory consolidation only happen with more than six hours of sleep. Miss a night, and the day’s memories might be compromised—an unsettling thought in our fast-paced, sleep-deprived society.

But the question remains: Why did we evolve in such a way that certain cognitive functions happen only while we are asleep? Would it not seem to make more sense to have these operations going on in the daytime? Part of the answer might be that the evolutionary pressures for sleep existed long before higher cognition—functions such as immune system regulation and efficient energy usage (for instance, hunt in the day and rest at night) are only two of the many reasons it makes sense to sleep on a planet that alternates between light and darkness. And because we already had evolutionary pressure to sleep, the theory goes, the brain evolved to use that time wisely by processing information from the previous day: acquire by day; process by night.

Or it might have been the other way around. Memory processing seems to be the only function of sleep that actually requires an organism to truly sleep—that is, to become unaware of its surroundings and stop processing incoming sensory signals. This unconscious cognition appears to demand the same brain resources used for processing incoming signals when awake. The brain, therefore, might have to shut off external inputs to get this job done. In contrast, although other functions such as immune system regulation might be more readily performed when an organism is inactive, there does not seem to be any reason why the organism would need to lose awareness. Thus, it may be these other functions that have been added to take advantage of the sleep that had already evolved for memory.

Many other questions remain about our nighttime cognition, however it might have evolved. Exactly how does the brain accomplish this memory processing? What are the chemical or molecular activities that account for these effects? These questions raise a larger issue about memory in general: What makes the brain remember certain pieces of information and forget others? We think the lesson here is that understanding sleep will ultimately help us to better understand memory.

The task might seem daunting, but these puzzles are the kind on which scientists thrive—and they can be answered. First, we will have to design and carry out more and more experiments, slowly teasing out answers. But equally important, we are going to have to sleep on it.

Doctors Find Promise To Help Cure Leukemia

2008-08-07T17:18:00.000-07:00

New York - German doctors seeking a cure for leukemia see promise in an unexpected source - methadone.

The drug, used to treat people addicted to heroin and other opioids, kills leukemia cells without harming healthy blood cells, University of Ulm researchers report in the journal Cancer Research.

And methadone may attack other cancers, too.

“[It] also can kill solid tumors,” said study chief Dr. Claudia Friesen.

The Exercise Pill

2008-08-01T08:43:00.000-07:00

A pill that can replace exercise? Sounds too good to be true, right? For the time being, it is — unless you’re a lab mouse. (Stupid mice, they get all the cool drugs before we do.) But according to Scientific American, promising test results mean it might not be long before an “exercise pill” is in the works for humans.
So how does it work? “It tricks the muscle into ‘believing’ it’s been exercised daily,” says Ronald Evans, a developmental biologist at the Salk Institute for Biological Studies, in La Jolla, Calif., and co-author of a study published in Cell. “It proves you can have a pharmacologic equivalent to exercise.” (That’s pretty definitive language; usually scientists mumble about the results “suggesting” that something “might” work in humans … but this study proves it? We’re impressed … and maybe a little skeptical, too.) What it does it “reprogram” muscle cells, switching them from being sugar-burning, fast-twitching machines that are built for power and sudden bursts of speed but tire quickly — not so necessary if you’re a desk jockey/couch potato — to fat-burning, slow-twitching muscles that enjoy increased endurance and stamina.

You read right: not only would the pill help you lose weight, it also increases your endurance, meaning that if you do decide to work out (even while taking the pill), like lab mice, you may find you can rock the Stairmaster 40-50% longer without becoming exhausted. (I have a feeling this is going to be a hit with middle-aged men; kill that gut and cancel your Viagra presecription as well.)

The key to this transformation is a protein called PPARdelta, which the team previously showed could create so-called high-endurance “marathon mice” when the animals were genetically engineered to make a lot of it. But, a drug that targeted only PPARdelta—although having metabolic benefits like lowering fatty acids and blood sugar—had no effect on endurance unless the mice were running regularly.

Enter AICAR, which targets a protein called adenosine monophosphate-activated protein kinase (AMPK). AMPK is produced when cells need more energy, as they do when we’re exercising. It also interacts with PPARdelta, effectively turbo-boosting that protein’s activity. So, by using AICAR, the scientists thought they might be able to trick the body into thinking it was exercising.

After four weeks of treatment with AICAR alone, the mice that took it could run on treadmills nearly 1.5 times as long as untreated animals—and without any training.

That does sound too good to be true, doesn’t it? Naturally, some contrarian scientists agree, maintaining that there’s no way a pill can replace the multitude of benefits that actual sweat-through-your-shirt exercise provides your body (not to mention your mental health). Here’s hoping the naysayers are wrong!

Drugs may offer some hope in autism cases

2008-07-28T13:37:00.000-07:00

By Blythe Bernhard
ST. LOUIS POST-DISPATCH
07/25/2008

ST. LOUIS — New treatments for a rare genetic disorder may hold clues for treating autism, researchers said Thursday at the International Fragile X Conference held at Union Station.

Fragile X syndrome is a common inherited cause of cognitive impairments, including about 5 percent of autism cases. Symptoms can include hyperactivity, seizures, learning disabilities and speech delays.

About one in 4,000 boys and one in 6,000 to 8,000 girls are born with the Fragile X, according to the Centers for Disease Control and Prevention.
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Because the disorder can be linked to a defect in a singular gene, it's a promising field of study for researchers. At the weeklong conference sponsored by the National Fragile X Foundation, St. Louis hosts several hundred parents, physicians and researchers looking for the latest developments in treatments and patient support.

Typically, treatment for Fragile X includes medications that treat behavioral symptoms. Researchers are now working on the underlying disorder that over-stimulates the nerve pathways in the brains of people with the syndrome and those with autism.

Drug therapies that block those pathways are still experimental. To date, there have been no large clinical trials in Fragile X patients. The small studies have shown some promise, however.

"It's been the first conference where the promise of powerful new treatments is literally around the corner," said Robert Miller, the foundation's executive director. "There's just a lot of hope and excitement because everybody's picked up on the buzz."

One drug, the mood stabilizer lithium, corrected hyperactivity and reduced seizures in mice. In a two-month trial in 15 children, behavioral symptoms improved in 13 patients after two months, but IQ levels did not change.

Other drugs mentioned at the conference included oxytocin, a mood-enhancing hormone, and minocycline, an antibiotic that shows promise in reducing symptoms of mice treated in infancy.

Another drug, fenobam, has also shown reductions in seizures in mice affected with Fragile X. In a human trial of 12 adult patients at Rush University Medical Center in Chicago and the University of California, Davis, half of the patients showed improved eye contact and one-third experienced calmer behavior, researchers said.

With that anecdotal data, researchers feel future trials are worthwhile in adults and kids, and are awaiting approval from the Food and Drug Administration for a larger study to start as soon as January. Researchers theorize that the drugs could work even better in children because their brains are still developing and more adaptable.

There's a "strong possibility that non-Fragile X autism patients may also improve" on Fenobam, said Dr. Randi Hagerman of the MIND Institute at the University of California, Davis.

The future for treatment of Fragile X and autism will probably include combinations of these drugs, Hagerman said.

Still, the researchers cautioned parents and researchers that the drugs are not overnight cures. Patients with Fragile X and autism will still need behavioral therapy and help from a team of family members, teachers, psychologists and doctors.

Tilapia May Be Risky

2008-07-12T11:53:00.000-07:00

Winston-Salem, NC - Researchers from Wake Forest University Medical Center say you’re better of with a big juicy burger than with this mild, low-fat fish, which turns out to be high in an unhealthful form of fat called long-chain omega-6 fatty acids, especially when it’s produced by fish farms.
Long chain omega-6 fats promote inflammation associated with heart disease, asthma, some cancers, Alzheimer’s disease, stroke and other conditions, said Floyd Chilton, professor of physiology at Wake Forest and head of the study.
Is there anything left that the experts say we should eat? Not much, said Chilton, thanks to a large-scale corruption of the American food chain with cheap corn feed. That has altered the composition of fats found in beef, chicken, eggs and farmed fish, such as catfish and tilapia.
In tests, the researchers found that grain-fed tilapia concentrated even more of the worst fats than did grain-fed beef.
One animal-based food that Chilton recommends is wild-caught fish, such as salmon and sardines, since they contain inflammation-fighting omega-3 fatty acids.
Unfortunately, he said, public health officials have been wrongly telling people to get more of this important nutrient by eating more fish without specifying what kind.

The Fattest States

2008-07-05T13:08:00.000-07:00

Calorie Lab’s Fattest States rankings for 2008 are out, and Mississippi is number one for the third year in a row. Colorado has the smallest percentage of obese people.

West Virginia passed Alabama to become the second fattest state in 2008. The four states of Mississippi, West Virginia, Alabama, and Louisiana have obese populations that exceed 30 percent over a three-year average and two-thirds of the citizens of Mississippi and West Virginia were either overweight or obese by CDC standards in 2007.

7 Tips for quality sleep

2008-07-05T06:13:00.000-07:00

Sleeping can be made efficient too? That’s right — getting 10 hours of sleep is useless if it isn’t good sleep! I’m sure you’ve spent entire nights tossing and turning without actually falling asleep and waking up feeling just as exhausted as the night before. This happens to everyone but there are several methods to try to prevent this and to make sure you really are getting the best sleep you can get.

1. Sleep - Quality over QuantityGet a Comfortable Bed
The definition of comfort is different for everyone, but I would suggest trying different beds. It’s been proven that really soft mattresses aren’t good for the spine but neither are hard ones so it’s up to the individual to find something that suits them.
2. Avoid sugar and caffeine right before bed
Both of these things are stimulants and won’t let your body relax properly. If you’re thirsty right before bed, water is the best bet (in fact water is the best bet for almost all situations).
3. Don’t exercise right before bed
If you’re going to do 50 sit-ups before you sleep, make sure you do it a few hours in advance. Exercise, like sugar, stimulates the body and hinders it from properly relaxing.
4. Don’t drink too much water
On that last note, drinking too much water isn’t good. Depending on your bladder size you may have to get up to urinate in the middle of the night!
5. Keep a good constant temperature
If it’s cold outside, stay warm; if it’s hot, stay cool. Try to keep a constant temperature so you aren’t constantly kicking your blanket off and pulling it back on. Also, you may want to avoid sleeping naked since it is harder to maintain a constant temperature without the benefit of a layer of clothing.
6. Ambient noises
This is another personal preference. Some people prefer music, some prefer the quiet hum of their computer fan, others prefer dead silence. Figure out what works for you and stick with it.
7. Maintain a regular sleep pattern
By keeping a stable biological clock, your body will know when it is time for sleep so it can prepare itself adequately. Unless you really need to pull that all-nighter, try your best to sleep at the same time every night. Waking up at the same time every day regardless of when your day actually starts is great too — my best tip is to keep your window blinds open to let in the morning sun.

With most of these points, consistency is the key. Once you’ve figured out a combination that works for you then try to replicate the exact situations every day. That way your body gets conditioned to sleep under those environmental conditions.

How do you know if you’ve gotten quality sleep?

* If you wake up on your own before your alarm goes off.
* If your joints aren’t aching when you get up.
* If you feel relaxed and ready to start your day.
* If you wake up smiling :)

And guess what, getting a good night’s rest can increase metabolism and help you stay in shape and lower heart disease.