By Ross Weale
Health magazine contributor Roshini Raj, MD, discusses the connection between caffeine and miscarriage on the Today show on Jan. 21.
DR. ROSHINI RAJ
Roshini Raj, MD, a Health magazine contributor and part of the magazine’s Health Expert Network, is board-certified in gastroenterology and internal medicine with degrees from the New York University School of Medicine and Harvard University. Currently Dr. Raj is an attending physician at NYU Medical Center’s Tisch Hospital in New York City. She also serves as an assistant professor at the NYU School of Medicine, and she has a special interest in women’s health and cancer screening. She has also published several research articles on colon-cancer screening.
Dr. Raj has discussed health topics on numerous television outlets including NBC’s Today show, ABC’s Good Morning America, CNN, FOX News, and Discovery Health. She has been quoted in publications such as the New York Times, the Wall Street Journal, Men’s Health, Women’s Health, and Fitness on the state of health care and other health news of the day. Dr. Raj is often called upon to explain and demystify complicated health topics.
Showing posts with label Cause. Show all posts
Showing posts with label Cause. Show all posts
Saturday, August 02, 2008
Monday, July 07, 2008
Breakthroughs Offer Hope to MS Patients
(HealthDay News) -- There's no one single way to suffer from multiple sclerosis.Every patient exhibits different symptoms as the disease gnaws away at the nerve endings in the brain, the spinal cord and even the eyes.
Doctors aren't even sure what causes MS, or what makes one person more likely to get it than another.
"I have a patient who is 6 years old," said Dr. Daniel Kantor, director of the Comprehensive Multiple Sclerosis Center at the University of Florida. "I have a patient who is 71 years old. I have patients from all walks of life, all ages."
But, the recent discovery of a second gene linked to Multiple sclerosis -- hailed as a major breakthrough -- is giving researchers hope that they are zeroing in on useful treatments -- and, ultimately, a cure.
In what is considered the most significant genetic breakthrough in MS research in three decades, scientists last year announced they had found a gene that increases the risk of developing the disease by 30 percent.
"This discovery is very significant, because it is hopefully the first of many, and after more than 30 years of finding nothing," said Dr. Jennie Q. Lou, professor of public health and internal medicine at Nova Southeastern University in Fort Lauderdale, Fla.
"We will expect to find many more of these genes over the next few years. Either these genes, or genes related to them, may be an excellent target that researchers can use to develop treatments and cures for MS," she added.
The symptoms of multiple sclerosis are many and varied, as the disease attacks different parts of the nervous system.
One MS patient may have trouble walking, while another is wheelchair-bound. One person may experience terrible fatigue, while another might struggle with blurred or double vision. Still another might have slurred speech, tremors, stiffness and bladder problems, according to the National Multiple Sclerosis Society.
"A lot of the symptoms are invisible symptoms to an outsider," Kantor said. "Pain, extreme fatigue, memory problems -- these are problems you just can't see."
Multiple sclerosis is considered an autoimmune disease, because it attacks the central nervous system.
The nerve fibers of the central nervous system are surrounded and protected by a fatty tissue called myelin, which helps the fibers conduct electrical impulses. With MS, myelin is lost in multiple areas, leaving scar tissue called sclerosis. Sometimes, the fiber itself is harmed.
When myelin or the nerve fiber is destroyed or damaged, the ability of the nerves to conduct electrical impulses to and from the brain is disrupted, producing the various symptoms of MS.
Most people with MS are diagnosed between the ages of 20 and 50, and twice as many women as men have the disease. About 400,000 Americans are known to have MS, and every week about 200 new cases are diagnosed. Worldwide, the MS toll may run as high as 2.5 million people, according to the National Multiple Sclerosis Society.
The exact cause of MS is unknown, but doctors suspect it comes from some combination of genetic and environmental factors, Kantor said.
"There's a genetic predisposition and then something happens, they are exposed to something, and it makes the body's defense system attack itself versus attacking a foreign invader," he said.
That's why the discovery of the second gene is so important. Researchers now know they have to cast a wider net.
"We've been looking at one gene the whole time, and we thought that was going to be the answer to understanding MS," Kantor said. "This is just telling us there's another part of the immune system that is important as well. It's made things more complicated, but if it's true, it's true."
The gene discovery is one of a number of advances that are occurring at a rapid pace.
Lou noted that new research has successfully used stem cells to help replace myelin in the brains of mice. "This discovery has shed light on the great potential of using stem cells in MS treatment," she said.
And last year, researchers proved that an experimental DNA vaccine to fight multiple sclerosis is safe and stands a good chance of being effective. The vaccine works by thwarting the immune system's attack on the myelin sheaths protecting nerve fibers.
Other advances noted by Lou include:
- Better and earlier diagnosis owing to advances in imaging technology.
- Improved drugs to reduce the frequency and severity of symptoms, and the accumulation of lesions in the brain and spinal cord.
- More aggressive rehabilitation programs developed specifically for MS patients.
"Every time we get our Journal of Neurology, more than half of it is about MS and how we can treat MS," Kantor said. "The MS of today is not the MS of even 15 years ago. We are learning more about it at a rapid rate."
More information
To learn more, visit the National Multiple Sclerosis Society.
Sunday, June 01, 2008
Green Tea Antioxidant May Help Prevent Alzheimer's
(HealthDay News) -- An antioxidant found in green tea appears to prevent the development of amyloid fibrils, a toxic protein associated with Alzheimer's and Parkinson's disease, a new study finds.Amyloid plaque is commonly seen in the brains of Alzheimer's patients and appears to disrupt the function of cells. Strategies to prevent the development of amyloid plaque are one avenue being explored in the prevention and treatment of Alzheimer's.
Now, a German team says the tea antioxidant, called epigallocatechin gallate (EGCG), has potent anti-plaque ability.
"We can use small molecules like EGCG to convert certain misfolded structures of a protein into a new type of molecule, which is less toxic or not toxic for cells," said lead researcher Erich Wanker, from the Max Delbrueck Center for Molecular Medicine in Berlin.
The findings are published in the May 30 online edition of Nature Structural & Molecular Biology.
The accumulation of amyloid plaque in Alzheimer's and other neurodegenerative diseases, such as Parkinson's, are thought to be caused by the misfolding of certain proteins, which then become toxic to cells. The way proteins fold is key to their function, the researchers explained.
In experiments in the laboratory, the German team found that EGCG seems to change potentially harmful proteins into proteins that are not detrimental to brain cells. "We are able to convert a toxic structure into a less toxic structure," Wanker explained.
Because EGCG binds to unfolded proteins -- which are not associated with Alzheimer's -- the discovery could lead to medications that recognize the more troublesome proteins and convert them to harmless substances.
"This method could be more generally used to get rid of or remove the concentration of misfolded proteins in cells," Wanker said. "This strategy should be tested with patients. If treated early on, it could prevent the formation of amyloid plaque," he speculated.
Whether this type of treatment could reverse plaques that have already formed in the brain isn't known, Wanker said.
He noted that the study remains basic science, and he was cautious about recommending green tea as a way of preventing Alzheimer's disease. "I don't want to do a lot of speculating which could point people in the direction that could be harmful," Wanker said. "We have to go step-by-step."
One expert believes the approach could yield real results, however.
"Red wine, yellow curry and green tea have suspected health benefits because of high content of antioxidants," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System, and associate director of the Alzheimer's Disease Research Center at UCLA David Geffen School of Medicine. He was not involved in the study.
"This study provides evidence that a compound called EGCG, one of the major polyphenols in green tea, may be useful for diseases like Parkinson's and Alzheimer's, because it can block the formation of the filament-forming protein aggregates implicated in causing disease," Cole said.
One novel aspect of the study is the authors' demonstration that EGCG prevents toxic filament formation by redirecting the aggregating proteins to make non-toxic proteins, Cole said.
"This is surprising, because similar protein aggregate spheres called amyloid oligomers can be highly toxic to neurons and synapses," Cole said. "It will be important for the authors to prove that the EGCG-directed proteins also lack toxicity to synapses which were not present in the systems used to test toxicity," he said.
Assuming that the green tea compound has a stable effect and chronically blocks toxicity to real neurons and synapses, it could have genuine potential for Alzheimer's patients, Cole said.
"The major caveat is the very poor absorption and delivery of EGCG seen in some studies," Cole said. The fact that EGCG isn't available for patenting by pharmaceutical companies might be a problem, too, he said, since it could "limit the investment needed for clinical trials of sufficient size to prove that it really works."
In related research, a team of American scientists said that interrupting a key signaling pathway in immune system cells allowed those cells to enter the brain and attack and remove amyloid plaque.
Reporting May 30 in Nature Medicine, a team led by research scientist Terrence Town, of Cedars-Sinai Medical Center, Los Angeles, conducted their study in genetically engineered mice. The group blocked a molecule that typically suppresses a portion of the immune response. Once the system was freed up, immune cells called macrophages made their way to the brains and devoured up to 90 percent of amyloid plaques, the team said.
"If these experimental animals are representative of the clinical syndrome of Alzheimer's disease, we may have a therapeutic target that we did not have before," study co-author Dr. Jun Tan, of the University of South Florida, said in a statement.
More information
For more about Alzheimer's disease, visit the Alzheimer's Association.
Thursday, April 24, 2008
Why Belly Fat Is Bad for Your Brain
Turns out, it's a very special kind of fat, and it may even be linked to dementiaby Theresa Tamkins
The news just keeps getting worse for the potbellied. Not only does belly fat put you at risk for diabetes and heart disease, but a study suggests it may make you lose your mind as well.
It seems that your sagittal abdominal diameter, or SAD—your belly size—is associated with risk of dementia in old age, according to a recent study in Neurology. The bigger the SAD in your 40s, the greater the chance you'll have mental deterioration in old age.
It seems that your sagittal abdominal diameter, or SAD—your belly size—is associated with risk of dementia in old age, according to a recent study in Neurology. The bigger the SAD in your 40s, the greater the chance you'll have mental deterioration in old age.
How much of a chance? If you're overweight or obese and don't have a potbelly, your dementia risk is 1.8 times higher than that of your slender peers. If you are overweight or obese and do have an apple shape, your risk is 2.3 to 3.6 times greater than that of wasp-waisted folks.
Overall, about 15% of the people in the study developed dementia, as did 21% of people with potbellies. The 6,583 participants had their midsections measured in the late 1960s and early 1970s, when they were 40 to 45 years old, and then again around age 70 by researchers at the Kaiser Permanente Division of Research in Oakland, California.
So why is belly fat so bad for your brain? Although it makes up less than 5% of total body fat, belly or visceral fat is nestled around the heart, pancreas, and other organs, according to Tongjian You, PhD, an assistant professor in the department of exercise and nutrition sciences at the University at Buffalo in Buffalo, New York.
And it's different from other types of fat because it produces all kinds of inflammatory compounds that can contribute to heart disease, diabetes, and now, potentially, dementia.
"Visceral fat releases higher amounts of those cytokines, especially interleukin 6, that cause cardiovascular disease and diabetes," says Dr. You, who was not involved in the dementia study. But what's the brain connection? "Inflammation is a contributing factor to dementia, so that's a reasonable link," he says.
You don't have to be wearing gigantic pants to be potbellied. The American Heart Association's guideline for a too-generous waistline is 102 centimeters (40 inches) or more for men and 88 centimeters (34.5 inches) for women, says Dr. You. It's not clear if diet alone is enough to whittle your abdominal fat. From his own and other research, he believes that exercise is important for shrinking belly fat, particularly in those who are relatively lean.
"If a person is overweight and obese, that person should change both diet and exercise," he says. However, if someone is lean or just a little overweight and has excess weight in their midsection, "exercise may be the perfect treatment."
Sunday, April 20, 2008
Chemotherapy Has Turned Me Into a Bloodhound
Cancer drugs scramble the signals that the nose and tongue send to the brain, with bizarre results by Jason Carpenter
When one of the doctors offhandedly mentioned that my sense of taste or smell could be affected by the high-dose chemotherapy treatments I was getting in my battle against multiple myeloma, I didn't pay much attention. Not until I found I could detect the slightest whiff of anything from 20 feet. Not until anything I put in my mouth had a taste so intense that I vomited every meal for two weeks.
It was a horrible cycle that I could not break: When a meal came back up, it smelled awful and made me puke more. My mom, who spent some time at the hospital with me and at my house after I was discharged, developed a two-puke-pan routine: She would remove one pan on my command, then slip another one under me so I didn't have to endure the output.
While in the hospital, I developed a vomit association with just about everything the institution stocked for supplies: bathroom soap, hand soap, paper towels, hand sanitizer, toilet paper, and even facial tissue (I could smell tissues rippling in the air across the room). Clearly, some of this was in my head, but a good portion of it was not, according to breastcancer.com.
Thirty-two days after my transplant, I cannot smell hospital supplies without gagging. Because I need to constantly disinfect my hands and face (trying to banish germs that could attack my weakened immune system), I've had to switch to neutral-smelling antibacterial baby wipes. Things are somewhat better: I gag but don’t usually vomit, though I do risk hurling on my laptop just writing this down. I'm told this will slowly ebb over the next weeks or months.
Even my sense of touch has been affected. For the first few post-op visits to the hospital, I nearly jumped out of my skin with pain when the nurse drew blood. I have had my blood drawn hundreds of times, and it's never hurt like this. The nurse noticed and said, "Your nerves are sensitive because of the chemo. It's completely normal."
Normal, my ass. I'm a bloodhound; my food tastes as if someone turned the volume to 11; and I screech like a little girl when I have my blood drawn. But I’ll say it again: I'll take all these wacky side effects over cancer.
As to my progress, I went to the doctor today and my white blood count is back up to 4.1 (close to the low end of normal), my platelets are good, and my red blood cells are charging back. The doctor is so pleased with my recovery that I don't need to see her for three weeks. She even said that I can start to ease the restrictions of being around people. Which means I’m planning to play poker again, tonight, latex gloves and all.
See Jason Carpenter's ongoing video postings about his life with cancer. Warning: Some expletives.
When one of the doctors offhandedly mentioned that my sense of taste or smell could be affected by the high-dose chemotherapy treatments I was getting in my battle against multiple myeloma, I didn't pay much attention. Not until I found I could detect the slightest whiff of anything from 20 feet. Not until anything I put in my mouth had a taste so intense that I vomited every meal for two weeks.
It was a horrible cycle that I could not break: When a meal came back up, it smelled awful and made me puke more. My mom, who spent some time at the hospital with me and at my house after I was discharged, developed a two-puke-pan routine: She would remove one pan on my command, then slip another one under me so I didn't have to endure the output.
While in the hospital, I developed a vomit association with just about everything the institution stocked for supplies: bathroom soap, hand soap, paper towels, hand sanitizer, toilet paper, and even facial tissue (I could smell tissues rippling in the air across the room). Clearly, some of this was in my head, but a good portion of it was not, according to breastcancer.com.
Thirty-two days after my transplant, I cannot smell hospital supplies without gagging. Because I need to constantly disinfect my hands and face (trying to banish germs that could attack my weakened immune system), I've had to switch to neutral-smelling antibacterial baby wipes. Things are somewhat better: I gag but don’t usually vomit, though I do risk hurling on my laptop just writing this down. I'm told this will slowly ebb over the next weeks or months.
Even my sense of touch has been affected. For the first few post-op visits to the hospital, I nearly jumped out of my skin with pain when the nurse drew blood. I have had my blood drawn hundreds of times, and it's never hurt like this. The nurse noticed and said, "Your nerves are sensitive because of the chemo. It's completely normal."
Normal, my ass. I'm a bloodhound; my food tastes as if someone turned the volume to 11; and I screech like a little girl when I have my blood drawn. But I’ll say it again: I'll take all these wacky side effects over cancer.
As to my progress, I went to the doctor today and my white blood count is back up to 4.1 (close to the low end of normal), my platelets are good, and my red blood cells are charging back. The doctor is so pleased with my recovery that I don't need to see her for three weeks. She even said that I can start to ease the restrictions of being around people. Which means I’m planning to play poker again, tonight, latex gloves and all.
See Jason Carpenter's ongoing video postings about his life with cancer. Warning: Some expletives.
Stem Cell Transplant Update: Advice On Hair Falling Out
Thursday, April 10, 2008
Caffeine May Block High Cholesterol Linked to Alzheimer's
(HealthDay News) -- A little caffeine every day could offer some protection from Alzheimer's disease for people with high cholesterol.Rabbits given the daily caffeine equivalent of one cup of coffee and fed a cholesterol-rich diet for 12 weeks suffered relatively little damage in their blood-brain barrier (BBB), which protects the central nervous system from the rest of the body's circulation, new research found.
The findings were published in the open-access publication Journal of Neuroinflammation.
Previous studies have shown that high levels of cholesterol break down the BBB, exposing the central nervous system to damage from blood-borne contamination. BBB leakage occurs in a variety of neurological disorders such as Alzheimer's disease.
"High levels of cholesterol are a risk factor for Alzheimer's disease, perhaps by compromising the protective nature of the blood-brain barrier. For the first time, we have shown that chronic ingestion of caffeine protects the BBB from cholesterol-induced leakage," Jonathan Geiger, of the University of North Dakota School of Medicine and Health Sciences, said in a prepared statement.
Caffeine appears to offer protection by helping proteins maintain the tight binding of the cells in the BBB, so they stop unwanted molecules from entering the central nervous system.
The findings also confirm previous studies showing that caffeine protects against memory loss in aging and in Alzheimer's disease.
"Caffeine is a safe and readily available drug, and its ability to stabilize the blood-brain barrier means it could have an important part to play in therapies against neurological disorders," Geiger said.
More information
The U.S. National Institute on Aging has more about Alzheimer's medications.
Friday, April 04, 2008
The Feel-Good-Enough Drugs
Antidepressants are widely prescribed because they restore balance. But balance isn’t happinessby Walter Armstrong
I’ve been taking antidepressants since 1994. That may seem like a long time, but since I expect to pop these pills every morning until I die, I’ve stopped keeping count. You could say I’m reconciled to the fact that I was born with bad brain chemistry and need a little extra push to reach that state familiar to everyone but the chronically depressed as well-being. I like it there and have no intention of leaving.
I remember vividly the moment when Prozac first kicked in, like switching from black-and-white to color. I was talking on the phone to a friend who was telling me about her problems, which included taking care of a husband who was dying of AIDS. I heard in the familiar tone of her sad voice how hopeless she felt, but for the first time it failed to find an echo inside me. I proceeded to deliver my first-ever pep talk to her, with all the annoying sincerity of a fresh convert to hope.
The novelty wore off soon enough.
Continue reading "The Feel-Good-Enough Drugs" »
Tuesday, March 11, 2008
Health Tip: Your Diet and Sleep
(HealthDay News) -- If you've noticed that you feel particularly sleepy or more energized after eating certain foods, that's because what you eat can have an impact on how well you sleep and how awake you are during the day.Here are examples of foods that can affect your sleep, courtesy of the National Sleep Foundation:
- Carbohydrate-rich foods, such as pastas and breads, can make you more sleepy.
- Carbohydrates work well with proteins to induce sleepiness, which makes combinations such as peanut butter on toast, cereal with milk, or cheese and crackers good bedtime snacks.
- A large meal can make you more tired, especially one with a lot of carbohydrates.
Caffeine in foods and beverages is a stimulant that blocks hormones in the brain that make you feel sleepy. - While alcohol may help you relax and fall asleep in the short term, over the course of the night it inhibits the sleep process and can prevent you from getting deep, restful sleep.
Balancing Your Hormones Without Drugs... You Can Feel Good Again$19.95  Hormone imbalance can be reversed! Look and feel better than ever, just take the time to learn about yourself and read the information contained in this just released e-book about reversing hormone imbalance. Are you ready to finally look and feel great? If so... read on... - E-Book Version.(BH) |
Monday, February 25, 2008
New Stroke Therapies Show Promise
(HealthDay News) -- Several new studies point to the promise of new ways to treat different types of stroke.
The research was presented during a teleconference Friday at the American Stroke Association's International Stroke Conference in New Orleans.
The first trial found some benefit when tPA, the only approved therapy for acute ischemic stroke, was given outside the usual three-hour treatment window. Patients in this Australian trial who were given tPA three to six hours after having a stroke had increased restoration of blood flow and a smaller area of the brain was deprived of blood. The study was expected to be published in the April issue of The Lancet Neurology, but was released Friday to coincide with the meeting presentation.
Ischemic stroke involves an obstruction in one of the vessels supplying blood to the brain. Currently, "clot busters" are only considered effective for the first three hours after a stroke.
"The issue is that we've got a three-hour label, and can we extend that to six hours," said study author Dr. Stephen M. Davis, of Royal Melbourne Hospital. "Based on our results, it gives a lot of encouragement that you can enrich that population. A lot of people arrive too late, and these are ones we would be targeting."
The findings are enough to warrant further trials but not to change current clinical guidelines just yet.
"This should be viewed as very encouraging, as an intermediate step that's leading to the formation hopefully of a larger study that can be more definitive and that could impact our guidelines significantly," said Dr. Philip Gorelick, moderator of the teleconference and head of the department of neurology and rehabilitation at the University of Illinois at Chicago.
A second study looked at patients in China, South Korea and Australia with acute cerebral hemorrhage, the most serious form of stroke.
"High blood pressure is a cause of intercerebral hemorrhage and is also very common at [the] acute state, and we don't know what to do about it," said study author Dr. Craig Anderson, from the University of Sydney in Australia. "We believe that having high blood pressure causes extra bleeding and expansion of blood in the brain. If we can bring blood pressure down, we may be able to arrest bleeding in the brain and bring it under control."
In fact, intensive lowering of blood pressure arrested about half a teaspoon of blood and, Anderson said, "in real life, it might have a bigger treatment effect."
Again, the authors hope the findings will lead to funding for larger trials.
A third trial found that reducing blood pressure in the 60 percent to 70 percent of patients who have elevated levels following acute stroke resulted in reduced dysphasia (communication problems) and some mortality benefits.
"These are very small numbers, and I don't want to hang too much on those results, but I think it's very encouraging, so we can probably go forward and do a much larger phase 3 study," said British study author Dr. John Potter.
For now, Gorelick said, "we continue to recommend that physicians follow American Heart Association/American Stroke Association guidelines. The blood pressure [issue] has not been resolved, and there are important questions of what to do with blood pressure. . . [although] it would be nice to have a definitive plan here and get people on blood pressure-lowering medicine."
Other studies being presented at the conference found that:
The research was presented during a teleconference Friday at the American Stroke Association's International Stroke Conference in New Orleans.
The first trial found some benefit when tPA, the only approved therapy for acute ischemic stroke, was given outside the usual three-hour treatment window. Patients in this Australian trial who were given tPA three to six hours after having a stroke had increased restoration of blood flow and a smaller area of the brain was deprived of blood. The study was expected to be published in the April issue of The Lancet Neurology, but was released Friday to coincide with the meeting presentation.
Ischemic stroke involves an obstruction in one of the vessels supplying blood to the brain. Currently, "clot busters" are only considered effective for the first three hours after a stroke.
"The issue is that we've got a three-hour label, and can we extend that to six hours," said study author Dr. Stephen M. Davis, of Royal Melbourne Hospital. "Based on our results, it gives a lot of encouragement that you can enrich that population. A lot of people arrive too late, and these are ones we would be targeting."
The findings are enough to warrant further trials but not to change current clinical guidelines just yet.
"This should be viewed as very encouraging, as an intermediate step that's leading to the formation hopefully of a larger study that can be more definitive and that could impact our guidelines significantly," said Dr. Philip Gorelick, moderator of the teleconference and head of the department of neurology and rehabilitation at the University of Illinois at Chicago.
A second study looked at patients in China, South Korea and Australia with acute cerebral hemorrhage, the most serious form of stroke.
"High blood pressure is a cause of intercerebral hemorrhage and is also very common at [the] acute state, and we don't know what to do about it," said study author Dr. Craig Anderson, from the University of Sydney in Australia. "We believe that having high blood pressure causes extra bleeding and expansion of blood in the brain. If we can bring blood pressure down, we may be able to arrest bleeding in the brain and bring it under control."
In fact, intensive lowering of blood pressure arrested about half a teaspoon of blood and, Anderson said, "in real life, it might have a bigger treatment effect."
Again, the authors hope the findings will lead to funding for larger trials.
A third trial found that reducing blood pressure in the 60 percent to 70 percent of patients who have elevated levels following acute stroke resulted in reduced dysphasia (communication problems) and some mortality benefits.
"These are very small numbers, and I don't want to hang too much on those results, but I think it's very encouraging, so we can probably go forward and do a much larger phase 3 study," said British study author Dr. John Potter.
For now, Gorelick said, "we continue to recommend that physicians follow American Heart Association/American Stroke Association guidelines. The blood pressure [issue] has not been resolved, and there are important questions of what to do with blood pressure. . . [although] it would be nice to have a definitive plan here and get people on blood pressure-lowering medicine."
Other studies being presented at the conference found that:
- The recently approved Penumbra device, a "vacuum cleaner" which sucks clots out of the brain, was effective for eight hours after the onset of a stroke, adding five hours to a patient's treatment window.
- Aricept (donepezil) improved several measures of executive function and processing speed in patients with a subcortical form of vascular dementia but did not improve overall cognitive scores, according to researchers from the University of Muenchen in Muenchen, Germany.
- Certain chromosomal regions may harbor genes important in assessing individuals at risk for aneurysms. "This is a critical first step if you want to find genes," said study author Dr. Tatiana Foroud, of Medical & Molecular Genetics in Indianapolis. "The ultimate goal is a genetic test to identify individuals at higher risk for aneurysm, and those individuals could have targeted and more costly screening pursued on a regular basis."
More information
Visit the American Stroke Association for more on different types of stroke.
Friday, February 22, 2008
Stem Cells Repair Stroke Damage in Rats
(HealthDay News) -- Human stem cells helped repair stroke-related brain damage in rats, Stanford University researchers report.
The use of neural cells derived from human embryonic stem cells led to improvements in the rats' physical abilities, according to the study, which is published in the Feb. 20 issue of Public Library of Science ONE. The stroke damage induced by the researchers left the rats with a weakened forelimb.
This is the first time that scientists have used human embryonic stem cells to generate neural cells that grow well in the lab, repair stroke damage in rats, and don't consistently form tumors after transplantation, according to the researchers.
While the findings show the potential of using stem cell therapies to treat stroke, the researchers noted this is a small study, and more research is needed to determine if this approach could work in humans.
In the laboratory, the researchers grew embryonic stem cells in a combination of growth hormones that prodded the cells to mature into stable neural stem cells. This was an important step, because immature cells tend to grow uncontrollably into tumors.
The neural stem cells were then transplanted into the brains of 10 rats with stroke-related brain damage. After two months, the transplanted neural stem cells had migrated to the damaged area of the brain and incorporated into the surrounding tissue. None of the transplanted cells formed tumors.
The rats that received the transplants were better able to use their forelimbs than rats that had similarly damaged brain regions but weren't given stem cell transplants.
Each year, about 780,000 people in the United States suffer strokes, according to the American Stroke Association.
More information
The U.S. National Institute of Neurological Disorders and Stroke has more about stroke.
The use of neural cells derived from human embryonic stem cells led to improvements in the rats' physical abilities, according to the study, which is published in the Feb. 20 issue of Public Library of Science ONE. The stroke damage induced by the researchers left the rats with a weakened forelimb.
This is the first time that scientists have used human embryonic stem cells to generate neural cells that grow well in the lab, repair stroke damage in rats, and don't consistently form tumors after transplantation, according to the researchers.
While the findings show the potential of using stem cell therapies to treat stroke, the researchers noted this is a small study, and more research is needed to determine if this approach could work in humans.
In the laboratory, the researchers grew embryonic stem cells in a combination of growth hormones that prodded the cells to mature into stable neural stem cells. This was an important step, because immature cells tend to grow uncontrollably into tumors.
The neural stem cells were then transplanted into the brains of 10 rats with stroke-related brain damage. After two months, the transplanted neural stem cells had migrated to the damaged area of the brain and incorporated into the surrounding tissue. None of the transplanted cells formed tumors.
The rats that received the transplants were better able to use their forelimbs than rats that had similarly damaged brain regions but weren't given stem cell transplants.
Each year, about 780,000 people in the United States suffer strokes, according to the American Stroke Association.
More information
The U.S. National Institute of Neurological Disorders and Stroke has more about stroke.
Balancing Your Hormones Without Drugs... You Can Feel Good Again$19.95 Hormone imbalance can be reversed! Look and feel better than ever, just take the time to learn about yourself and read the information contained in this just released e-book about reversing hormone imbalance. Are you ready to finally look and feel great? If so... read on... - E-Book Version.(BH) |
Thursday, February 14, 2008
Marijuana Use Among MS Patients Raises Risk for Cognitive, Mood Problems
(HealthDay News) -- Multiple sclerosis patients who smoke marijuana in search of symptom relief are more likely to suffer cognitive shortfalls and mood disorders, new Canadian research suggests.
A slowing down in the ability to process and remember information is one significant side effect, as is a rise in the rate of depression and anxiety.
"This is a small study, so our findings are preliminary, but the bottom line is that multiple sclerosis patients who smoke cannabis appear to be at an increased risk for cognitive issues, particularly with respect to the speed of their thinking," said study author Dr. Anthony Feinstein, a professor of psychiatry with the Sunnybrook Health Sciences Centre's department of psychiatry at the University of Toronto.
Feinstein's observations are published in the Feb. 13 online edition of Neurology and are focused exclusively on the impact of smoking marijuana illegally obtained by patients themselves. Medically prescribed marijuana was not studied.
The authors noted that a "significant minority" of multiple sclerosis patients smoke marijuana to combat the tingling, numbness, blindness and paralysis that can accompany the progressive and often disabling nervous system disease.
However, Feinstein's team stressed that scientists have yet to definitively prove that the psychoactive substance -- long linked to psychosis, anxiety and delirium among healthy users -- provides a measurable benefit to the more than 400,000 Americans and 2.5 million people worldwide who suffer from the disease.
The researchers therefore assessed the experience of 140 Toronto-based MS outpatients, 10 of whom had smoked the drug at least once in the previous month and were considered regular marijuana users.
All the patients -- three-quarters of them women -- underwent cognitive and mental health exams by a neurologist and a neuro-psychiatrist. Interviews were also conducted to assess disease severity and course, medications being used, and current disability.
Feinstein and his team observed that while pot smokers were younger, there were no differences between marijuana users and nonusers in terms of gender, education, or MS disease course or duration.
However, MS patients who used marijuana were found to perform 50 percent slower on tests tracking information-processing speed and were more likely than nonusers to have a mental disability of some kind.
Marijuana use was also associated with a greater risk for being depressed or experiencing anxiety. However, the authors were not able to determine whether the drug had triggered such conditions, or if patients had sought out marijuana to help deal with a preexisting emotional issue.
They nonetheless cautioned that smoking marijuana might further raise the risk for experiencing the kind of neuro-psychological impairment that typically occurs among 40 percent to 65 percent of all MS patients.
Feinstein said that he next hopes to gather a much larger pool of patients, while exploring possible differences in the health impact of street-purchased marijuana versus prescribed cannabis.
Meanwhile, Dr. Marshall Keilson, director of neurology at Maimonides Medical Center in Brooklyn, N.Y., said he thinks it best to proceed on a case-by-case basis.
"There are some MS patients who are emotionally disabled from their disease, and if we can use cannabis to help them feel better about the world or life, we should," he said. "We need to always err on the side of doing what's best for our patients. And I don't necessarily believe there is a permanent damage to the brain, based on occasional marijuana use. If they're smoking 10 times a day, yes, there will be damage done. But this goes for excessive alcohol use, too. So, I think we're going to end up somewhere in the middle with this."
More information
For more on multiple sclerosis, visit the National Multiple Sclerosis Society.
A slowing down in the ability to process and remember information is one significant side effect, as is a rise in the rate of depression and anxiety.
"This is a small study, so our findings are preliminary, but the bottom line is that multiple sclerosis patients who smoke cannabis appear to be at an increased risk for cognitive issues, particularly with respect to the speed of their thinking," said study author Dr. Anthony Feinstein, a professor of psychiatry with the Sunnybrook Health Sciences Centre's department of psychiatry at the University of Toronto.
Feinstein's observations are published in the Feb. 13 online edition of Neurology and are focused exclusively on the impact of smoking marijuana illegally obtained by patients themselves. Medically prescribed marijuana was not studied.
The authors noted that a "significant minority" of multiple sclerosis patients smoke marijuana to combat the tingling, numbness, blindness and paralysis that can accompany the progressive and often disabling nervous system disease.
However, Feinstein's team stressed that scientists have yet to definitively prove that the psychoactive substance -- long linked to psychosis, anxiety and delirium among healthy users -- provides a measurable benefit to the more than 400,000 Americans and 2.5 million people worldwide who suffer from the disease.
The researchers therefore assessed the experience of 140 Toronto-based MS outpatients, 10 of whom had smoked the drug at least once in the previous month and were considered regular marijuana users.
All the patients -- three-quarters of them women -- underwent cognitive and mental health exams by a neurologist and a neuro-psychiatrist. Interviews were also conducted to assess disease severity and course, medications being used, and current disability.
Feinstein and his team observed that while pot smokers were younger, there were no differences between marijuana users and nonusers in terms of gender, education, or MS disease course or duration.
However, MS patients who used marijuana were found to perform 50 percent slower on tests tracking information-processing speed and were more likely than nonusers to have a mental disability of some kind.
Marijuana use was also associated with a greater risk for being depressed or experiencing anxiety. However, the authors were not able to determine whether the drug had triggered such conditions, or if patients had sought out marijuana to help deal with a preexisting emotional issue.
They nonetheless cautioned that smoking marijuana might further raise the risk for experiencing the kind of neuro-psychological impairment that typically occurs among 40 percent to 65 percent of all MS patients.
Feinstein said that he next hopes to gather a much larger pool of patients, while exploring possible differences in the health impact of street-purchased marijuana versus prescribed cannabis.
Meanwhile, Dr. Marshall Keilson, director of neurology at Maimonides Medical Center in Brooklyn, N.Y., said he thinks it best to proceed on a case-by-case basis.
"There are some MS patients who are emotionally disabled from their disease, and if we can use cannabis to help them feel better about the world or life, we should," he said. "We need to always err on the side of doing what's best for our patients. And I don't necessarily believe there is a permanent damage to the brain, based on occasional marijuana use. If they're smoking 10 times a day, yes, there will be damage done. But this goes for excessive alcohol use, too. So, I think we're going to end up somewhere in the middle with this."
More information
For more on multiple sclerosis, visit the National Multiple Sclerosis Society.
Saturday, February 02, 2008
Quit-Smoking Drug May Raise Suicide Risk
(HealthDay News) -- There's increasing evidence that the smoking-cessation drug Chantix is linked to serious "neuropsychiatric" side effects, including agitation, depressed mood and even suicide, U.S. health officials said Friday.
The U.S. Food and Drug Administration has asked Chantix's manufacturer, Pfizer Inc., to make the warning about these potential problems more prominent on prescribing information and on the drug's label. The agency is also working with Pfizer to produce a Medication Guide for patients, officials said.
"We have become increasingly concerned as we have seen a number of compelling cases that truly look as if they are the result of exposure to the drug and not to other causes," Dr. Bob Rappaport, director of the FDA's Division of Anesthesia, Analgesia and Rheumatology Products, said during an afternoon teleconference.
"These cases involve abnormal behaviors, changes in mood, and suicidal ideation and suicide," Rappaport said.
The FDA knows of 491 cases of suicidal behavior associated with Chantix, said Dr. Celia Winchell, a team leader in the FDA's Division of Anesthesia, Analgesia and Rheumatology Products.
"Of these, 420 are from the United States," Winchell said. "There are 39 that involve completed suicides, 34 in the United States."
According to Pfizer, 5 million patients have taken Chantix, whose generic name is varenicline.
Friday's warning follows a Nov. 20 FDA statement that the agency was "evaluating post-marketing adverse event reports on Chantix related to changes in behavior, agitation, depressed mood, suicidal ideation, and actual suicidal behavior."
At that time, Pfizer said there had never been a cause-and-effect relationship shown between Chantix and these symptoms. The company also said that part of the problem may be due to nicotine withdrawal.
Last month, Pfizer agreed, after consulting with the FDA, to update packages of Chantix sold in the United States to more prominently display a warning that users should be monitored for suicidal behavior, depressed mood, and other mental health symptoms.
The FDA approved Chantix in May 2006 as a smoking-cessation drug. It acts in areas of the brain affected by nicotine and may ease withdrawal symptoms and block the effects of nicotine if users resume smoking.
On Friday, FDA officials advised patients to tell their doctor about any history of psychiatric illness before starting Chantix. The drug can cause current psychiatric illness to get worse even if it is under control. Chantix may also cause the recurrence of an old psychiatric illness, the officials warned.
Patients should also report changes in mood and behavior to their doctor. Symptoms to look out for include anxiety, nervousness, tension, depressed mood, unusual behaviors and thinking about or attempting suicide, the FDA officials said.
In most cases, these symptoms developed while taking Chantix, but they can also appear after stopping the drug, the officials noted.
"We are continuing with the review process over the next several months as we try to pin down to what extent these problems are being seen with Chantix," Rappaport said.
Vivid, unusual, or strange dreams may occur while taking the drug. Patients may also experience impaired ability to drive or operate heavy machinery, the officials said.
More information
For more on quitting smoking, visit Smokefree.gov.
The U.S. Food and Drug Administration has asked Chantix's manufacturer, Pfizer Inc., to make the warning about these potential problems more prominent on prescribing information and on the drug's label. The agency is also working with Pfizer to produce a Medication Guide for patients, officials said.
"We have become increasingly concerned as we have seen a number of compelling cases that truly look as if they are the result of exposure to the drug and not to other causes," Dr. Bob Rappaport, director of the FDA's Division of Anesthesia, Analgesia and Rheumatology Products, said during an afternoon teleconference.
"These cases involve abnormal behaviors, changes in mood, and suicidal ideation and suicide," Rappaport said.
The FDA knows of 491 cases of suicidal behavior associated with Chantix, said Dr. Celia Winchell, a team leader in the FDA's Division of Anesthesia, Analgesia and Rheumatology Products.
"Of these, 420 are from the United States," Winchell said. "There are 39 that involve completed suicides, 34 in the United States."
According to Pfizer, 5 million patients have taken Chantix, whose generic name is varenicline.
Friday's warning follows a Nov. 20 FDA statement that the agency was "evaluating post-marketing adverse event reports on Chantix related to changes in behavior, agitation, depressed mood, suicidal ideation, and actual suicidal behavior."
At that time, Pfizer said there had never been a cause-and-effect relationship shown between Chantix and these symptoms. The company also said that part of the problem may be due to nicotine withdrawal.
Last month, Pfizer agreed, after consulting with the FDA, to update packages of Chantix sold in the United States to more prominently display a warning that users should be monitored for suicidal behavior, depressed mood, and other mental health symptoms.
The FDA approved Chantix in May 2006 as a smoking-cessation drug. It acts in areas of the brain affected by nicotine and may ease withdrawal symptoms and block the effects of nicotine if users resume smoking.
On Friday, FDA officials advised patients to tell their doctor about any history of psychiatric illness before starting Chantix. The drug can cause current psychiatric illness to get worse even if it is under control. Chantix may also cause the recurrence of an old psychiatric illness, the officials warned.
Patients should also report changes in mood and behavior to their doctor. Symptoms to look out for include anxiety, nervousness, tension, depressed mood, unusual behaviors and thinking about or attempting suicide, the FDA officials said.
In most cases, these symptoms developed while taking Chantix, but they can also appear after stopping the drug, the officials noted.
"We are continuing with the review process over the next several months as we try to pin down to what extent these problems are being seen with Chantix," Rappaport said.
Vivid, unusual, or strange dreams may occur while taking the drug. Patients may also experience impaired ability to drive or operate heavy machinery, the officials said.
More information
For more on quitting smoking, visit Smokefree.gov.
Monday, January 07, 2008
Breast Is Best for Reducing Stress
(HealthDay News) -- Breast-feeding is considered a great way for a mother to form a close bond with her infant. And now there's evidence to suggest it may also help kids be more resilient to stress.
Researchers in Sweden and the United Kingdom examined data on almost 9,000 children born in Great Britain in 1970. Relevant information was collected at birth and again at ages 5 and 10 from parents, teachers, health-care workers and midwives.
Teachers were asked to rate the kids' anxiety levels on a zero-to-50 scale at age 10. And parents were asked about major life events -- including divorce or separation -- that occurred when their children were between 5 and 10 years old.
Not surprisingly, children whose parents had divorced or separated were more likely to have high anxiety. But what the researchers found striking was the difference in stress levels between breast-fed and bottle-fed kids. Breast-fed children were significantly less anxious than kids who hadn't nursed at their mother's breast.
Lead author Scott Montgomery, an associate professor at the Karolinska Institutet in Stockholm, said the research team was interested in examining whether there are any specific early-life exposures that make children better able to cope with stress later in life. The study attempted to replicate animal studies that showed close physical contact between a mother and her offspring may have a positive impact on the development of the offspring's stress response, he said.
"The best marker of maternal physical contact in the first month of life that we could find among the research information at our disposal was breast-feeding," Montgomery said.
The American Academy of Pediatrics recommends that healthy women exclusively breast-feed their infants for at least the first six months of life and continue breast-feeding "for at least the first year of life and beyond for as long as mutually desired by mother and child."
Breast-feeding offers many health and development benefits for baby, says the National Institute of Child Health & Human Development. Kids get the right balance of nutrients to support optimal growth, fatty acids to promote brain development and protection against many childhood illnesses. And there are important emotional and physical benefits for moms as well.
"There is no question that breast-feeding is better for the health of mothers and children," said Nicole Else-Quest, an assistant professor of psychology at Villanova University in Pennsylvania, "but it is less clear how breast-feeding affects the mother-child relationship." Breast-feeding may help to establish an early bond, she added, but "it is only one of many ways to do so."
As for why there might be differences in stress between breast-fed and bottle-fed kids, Else-Quest said it is difficult to speculate "given that many factors influence the decisions to breast-feed in the first place."
The research team considered factors that might affect a child's reaction to stress and ability to cope, such as maternal depression, parental education levels, social class, and smoking habits. Even after accounting for those factors, breast-fed children were less anxious than their peers. In addition, bottle-fed children whose parents divorced were more anxious than breast-fed kids.
Yet the study findings don't prove that breast-feeding itself reduces anxiety. It may be a mark of close, early physical contact, the researchers noted.
"A child without such regular contact may perceive greater danger reacting to stress -- indicating a potentially dangerous situation -- with a more reactive and less well-controlled stress response," Montgomery said.
It's also possible, he added, that mothers who breast-fed simply have a better relationship with their child.
"The parent-child relationship influences the child's health and development in many ways," Montgomery said. "A good relationship with parents is important, and this relationship begins in infancy, so good early contact with the child is important."
The study findings were published in the journal Archives of Disease in Childhood.
More information
The National Institute of Child Health & Human Development has the latest research on breast-feeding.
Researchers in Sweden and the United Kingdom examined data on almost 9,000 children born in Great Britain in 1970. Relevant information was collected at birth and again at ages 5 and 10 from parents, teachers, health-care workers and midwives.
Teachers were asked to rate the kids' anxiety levels on a zero-to-50 scale at age 10. And parents were asked about major life events -- including divorce or separation -- that occurred when their children were between 5 and 10 years old.
Not surprisingly, children whose parents had divorced or separated were more likely to have high anxiety. But what the researchers found striking was the difference in stress levels between breast-fed and bottle-fed kids. Breast-fed children were significantly less anxious than kids who hadn't nursed at their mother's breast.
Lead author Scott Montgomery, an associate professor at the Karolinska Institutet in Stockholm, said the research team was interested in examining whether there are any specific early-life exposures that make children better able to cope with stress later in life. The study attempted to replicate animal studies that showed close physical contact between a mother and her offspring may have a positive impact on the development of the offspring's stress response, he said.
"The best marker of maternal physical contact in the first month of life that we could find among the research information at our disposal was breast-feeding," Montgomery said.
The American Academy of Pediatrics recommends that healthy women exclusively breast-feed their infants for at least the first six months of life and continue breast-feeding "for at least the first year of life and beyond for as long as mutually desired by mother and child."
Breast-feeding offers many health and development benefits for baby, says the National Institute of Child Health & Human Development. Kids get the right balance of nutrients to support optimal growth, fatty acids to promote brain development and protection against many childhood illnesses. And there are important emotional and physical benefits for moms as well.
"There is no question that breast-feeding is better for the health of mothers and children," said Nicole Else-Quest, an assistant professor of psychology at Villanova University in Pennsylvania, "but it is less clear how breast-feeding affects the mother-child relationship." Breast-feeding may help to establish an early bond, she added, but "it is only one of many ways to do so."
As for why there might be differences in stress between breast-fed and bottle-fed kids, Else-Quest said it is difficult to speculate "given that many factors influence the decisions to breast-feed in the first place."
The research team considered factors that might affect a child's reaction to stress and ability to cope, such as maternal depression, parental education levels, social class, and smoking habits. Even after accounting for those factors, breast-fed children were less anxious than their peers. In addition, bottle-fed children whose parents divorced were more anxious than breast-fed kids.
Yet the study findings don't prove that breast-feeding itself reduces anxiety. It may be a mark of close, early physical contact, the researchers noted.
"A child without such regular contact may perceive greater danger reacting to stress -- indicating a potentially dangerous situation -- with a more reactive and less well-controlled stress response," Montgomery said.
It's also possible, he added, that mothers who breast-fed simply have a better relationship with their child.
"The parent-child relationship influences the child's health and development in many ways," Montgomery said. "A good relationship with parents is important, and this relationship begins in infancy, so good early contact with the child is important."
The study findings were published in the journal Archives of Disease in Childhood.
More information
The National Institute of Child Health & Human Development has the latest research on breast-feeding.
Wednesday, November 21, 2007
Scientists Turn Human Skin Cells Into Stem Cells
(HealthDay News) -- Two separate groups of scientists have succeeded in turning human skin cells into cells that are very similar -- but not identical -- to embryonic stem cells.
The two teams, one based in Japan and the other in Wisconsin, used slightly different methods to achieve essentially identical goals, researchers said.
"Embryonic stem cells can divide forever, and there has never been good evidence for such cells in adults, but this new paper shows a method to make cells essentially identical to embryonic stem cells," said James Thomson, senior author of the Wisconsin study and a professor in the departments of medicine and public health at the University of Wisconsin-Madison. "This will change the ethical debate," he said at a teleconference held Tuesday.
"We are now in a position to be able to generate patient- and disease-specific stem cells, without using human eggs or embryos," added Dr. Shinya Yamanaka, senior author of the first paper, who is affiliated with Kyoto University in Japan and the Gladstone Institute of Cardiovascular Disease in San Francisco. "These cells should be useful in understanding disease mechanisms, searching for effective and safe drugs, and treating patients with cell therapy," he said.
One outside exert agreed the achievement could shift research away from embryonic stem cells.
"Here's verification of another source of multipotent cells that could be useful for treating disease and would get around some of the ethical issues related to embryonic sources," Paul Sanberg, distinguished professor of neurosurgery and director of the University of South Florida Center for Aging and Brain Repair in Tampa, told HealthDay. "It also demonstrates that there are many cells that can be reprogrammed in the body, and this is not going to be the last time we hear of other types of cells and other ways we can make multipotent."
Multipotency or pluripotency refers to the ability of stem cells to grow into a variety of cell types.
However, the journey from laboratory to patient therapy is still a long one, experts said.
"This is a proof of principle, but, in terms of application, there are many steps in between," said Dr. Robert Tsai, assistant professor in the Center for Cancer and Stem Cell Biology at Texas A&M Health Science Center Institute of Biosciences and Technology in Houston.
The achievements followed closely on the heels of another breakthrough: Last week, U.S. scientists announced that they had created dozens of cloned embryos from a 10-year-old male macaque, a primate. This puts science one step closer to human cloning, those authors stated.
Embryonic stem cells are pluripotent, meaning they have the ability to develop into virtually any cell type in the body. The hope is that such cells may one day yield treatments or cures for diseases such as diabetes, liver failure, spinal injury, stroke, Alzheimer's disease and heart disease.
However, harvesting embryonic stem cells involves destroying a viable embryo, stirring much political debate. In the United States, embryonic stem cell research has been severely limited since August 2001, when President George W. Bush placed limits on federal funding of the field and restricted the number of embryonic stem cell lines that could be used.
Since that time, researchers have been racing to find other sources of viable stem cells. The approach documented in these two studies would circumvent the need for embryos and, thus, would bypass any controversy. The findings of Yamanaka's team are detailed in the Nov. 30 print issue of Cell, and the Wisconsin group's work was released online Tuesday by Science.
Last year, Yamanaka's team transformed mouse skin cells into pluripotent stem cells.
This year, the researchers tried the same method in humans: using a retrovirus to activate specific transcription genes in the skin cells. Transcription genes regulate gene expression, explained Yamanaka.
Using this method, his group generated about 10 cell clones from 50,000 human facial skin cells.
The new "induced pluripotent stem" (iPS) cells were identical to embryonic stem cells in terms of appearance and behavior in cell culture. They also expressed genetic markers that were the same as those observed in embryonic stem cells.
The iPS cells could also differentiate into other tissue types, the team found.
However, a screen of more than 30,000 genes showed that the iPS cells were not actually indistinguishable from embryonic stem cells. In fact, roughly 1,000 genes were expressed differently.
"Human iPS cells are similar, but not identical, to human embryonic stem cells, Yamanaka said. "DNA microarray analyses identified differentially expressed genes between the two stem cell lines. Further studies are required to determine whether human iPS cells can replace human ES cells."
The team at the University of Wisconsin-Madison also used human skin cells, then added two of the same genes as Yamanaka's team and two different genes in their approach. The outcome was essentially the same.
"The actual combination of the factors they put in are different, the rationale is the same," Tsai explained. "There are some tiny differences between the two different combinations."
The advent of the new cells does not render embryonic stem cells unnecessary, however.
"This does not mean that it is the end of embryonic stem cell research, if only that we need a gold standard to compare to," the University of Wisconsin's Thomson told reporters. "Over time, I believe embryonic stem cells will be used by fewer and fewer labs. These new stem cells would not have been derived if it had not been for the last 10 years of research on embryonic stem cell lines. I do, nonetheless, think that the world has changed."
Can the newly designed cells be used to clone humans? "Any cell in the body can do that," Thomson said. "It's probably true of these cells, if you manipulate them enough, but not if you put them in the body as they are."
It's not clear in either of the two new studies if the cells are completely pluripotent or if one line is more efficient than the other. "Will they have the ability to fully differentiate?" Tsai asked. "There's some evidence that they can move from a differentiated state to an undifferentiated state, but will they be able to reverse back?"
"We have to be sure the cells are safe," Yamanaka said. "One of the difficulties about human embryonic stem cells is their tumorigenicity [propensity to develop tumors]. Because of the usage of retroviruses, iPS cells may be more tumorigenic than human embryonic stem cells. We will have to find a way to avoid retroviruses."
But for the more immediate purposes of drug discovery and toxicology, the use of retroviruses is not a big problem, Yamanaka added.
iPS may present their own ethical concerns, however, if they are used to generate sperm and egg cells. "This might help people with infertility problems, but it will be essential to have proper regulation regarding the generation and usage of human iPS cells to avoid misusages of this technology," Yamanaka said.
More information
Learn more about stem cells at the International Society for Stem Cell Research.
The two teams, one based in Japan and the other in Wisconsin, used slightly different methods to achieve essentially identical goals, researchers said.
"Embryonic stem cells can divide forever, and there has never been good evidence for such cells in adults, but this new paper shows a method to make cells essentially identical to embryonic stem cells," said James Thomson, senior author of the Wisconsin study and a professor in the departments of medicine and public health at the University of Wisconsin-Madison. "This will change the ethical debate," he said at a teleconference held Tuesday.
"We are now in a position to be able to generate patient- and disease-specific stem cells, without using human eggs or embryos," added Dr. Shinya Yamanaka, senior author of the first paper, who is affiliated with Kyoto University in Japan and the Gladstone Institute of Cardiovascular Disease in San Francisco. "These cells should be useful in understanding disease mechanisms, searching for effective and safe drugs, and treating patients with cell therapy," he said.
One outside exert agreed the achievement could shift research away from embryonic stem cells.
"Here's verification of another source of multipotent cells that could be useful for treating disease and would get around some of the ethical issues related to embryonic sources," Paul Sanberg, distinguished professor of neurosurgery and director of the University of South Florida Center for Aging and Brain Repair in Tampa, told HealthDay. "It also demonstrates that there are many cells that can be reprogrammed in the body, and this is not going to be the last time we hear of other types of cells and other ways we can make multipotent."
Multipotency or pluripotency refers to the ability of stem cells to grow into a variety of cell types.
However, the journey from laboratory to patient therapy is still a long one, experts said.
"This is a proof of principle, but, in terms of application, there are many steps in between," said Dr. Robert Tsai, assistant professor in the Center for Cancer and Stem Cell Biology at Texas A&M Health Science Center Institute of Biosciences and Technology in Houston.
The achievements followed closely on the heels of another breakthrough: Last week, U.S. scientists announced that they had created dozens of cloned embryos from a 10-year-old male macaque, a primate. This puts science one step closer to human cloning, those authors stated.
Embryonic stem cells are pluripotent, meaning they have the ability to develop into virtually any cell type in the body. The hope is that such cells may one day yield treatments or cures for diseases such as diabetes, liver failure, spinal injury, stroke, Alzheimer's disease and heart disease.
However, harvesting embryonic stem cells involves destroying a viable embryo, stirring much political debate. In the United States, embryonic stem cell research has been severely limited since August 2001, when President George W. Bush placed limits on federal funding of the field and restricted the number of embryonic stem cell lines that could be used.
Since that time, researchers have been racing to find other sources of viable stem cells. The approach documented in these two studies would circumvent the need for embryos and, thus, would bypass any controversy. The findings of Yamanaka's team are detailed in the Nov. 30 print issue of Cell, and the Wisconsin group's work was released online Tuesday by Science.
Last year, Yamanaka's team transformed mouse skin cells into pluripotent stem cells.
This year, the researchers tried the same method in humans: using a retrovirus to activate specific transcription genes in the skin cells. Transcription genes regulate gene expression, explained Yamanaka.
Using this method, his group generated about 10 cell clones from 50,000 human facial skin cells.
The new "induced pluripotent stem" (iPS) cells were identical to embryonic stem cells in terms of appearance and behavior in cell culture. They also expressed genetic markers that were the same as those observed in embryonic stem cells.
The iPS cells could also differentiate into other tissue types, the team found.
However, a screen of more than 30,000 genes showed that the iPS cells were not actually indistinguishable from embryonic stem cells. In fact, roughly 1,000 genes were expressed differently.
"Human iPS cells are similar, but not identical, to human embryonic stem cells, Yamanaka said. "DNA microarray analyses identified differentially expressed genes between the two stem cell lines. Further studies are required to determine whether human iPS cells can replace human ES cells."
The team at the University of Wisconsin-Madison also used human skin cells, then added two of the same genes as Yamanaka's team and two different genes in their approach. The outcome was essentially the same.
"The actual combination of the factors they put in are different, the rationale is the same," Tsai explained. "There are some tiny differences between the two different combinations."
The advent of the new cells does not render embryonic stem cells unnecessary, however.
"This does not mean that it is the end of embryonic stem cell research, if only that we need a gold standard to compare to," the University of Wisconsin's Thomson told reporters. "Over time, I believe embryonic stem cells will be used by fewer and fewer labs. These new stem cells would not have been derived if it had not been for the last 10 years of research on embryonic stem cell lines. I do, nonetheless, think that the world has changed."
Can the newly designed cells be used to clone humans? "Any cell in the body can do that," Thomson said. "It's probably true of these cells, if you manipulate them enough, but not if you put them in the body as they are."
It's not clear in either of the two new studies if the cells are completely pluripotent or if one line is more efficient than the other. "Will they have the ability to fully differentiate?" Tsai asked. "There's some evidence that they can move from a differentiated state to an undifferentiated state, but will they be able to reverse back?"
"We have to be sure the cells are safe," Yamanaka said. "One of the difficulties about human embryonic stem cells is their tumorigenicity [propensity to develop tumors]. Because of the usage of retroviruses, iPS cells may be more tumorigenic than human embryonic stem cells. We will have to find a way to avoid retroviruses."
But for the more immediate purposes of drug discovery and toxicology, the use of retroviruses is not a big problem, Yamanaka added.
iPS may present their own ethical concerns, however, if they are used to generate sperm and egg cells. "This might help people with infertility problems, but it will be essential to have proper regulation regarding the generation and usage of human iPS cells to avoid misusages of this technology," Yamanaka said.
More information
Learn more about stem cells at the International Society for Stem Cell Research.
Friday, September 21, 2007
Brain Defect Helps Drive Fragile X Syndrome
(HealthDay News) -- A newly discovered brain defect might be a target for the treatment of the inherited mental disorder known as fragile X syndrome, researchers report.
The discovery in rats provides an understanding of how the gene mutation responsible for the condition changes the way brain cells communicate, according to the report in this week's issue of the Proceedings of the National Academy of Sciences.
"Fragile X syndrome is the most common form of inherited mental retardation," explained co-author Gary J. Bassell, a professor of cell biology at Emory University in Atlanta. "It has strong links to autism and epilepsy."
Fragile X syndrome occurs in approximately one in 4,000 males and one in 8,000 females, Bassell noted.
Working with rat brain cells, the team found that synapses between brain cells in the part of the brain called the hippocampus are defective in animals with fragile X, Bassell said.
"We discovered what the specific underlying defect is," he said. "It is actually a defect in the mGluR5 receptor, which is on the surface of neurons. The defect is that there is excessive signaling."
Children with fragile X have difficulty in processing information, because these receptors allow too much signaling and change the function of other receptors, Bassell theorized.
When his team treated the receptor with an mGluR5 antagonist called MPEP, they were able to reverse the effects of the mutation. "When you quiet down this receptor, it corrects the defects that occur in other receptors as well," he noted.
Bassell stressed that MPEP is not a suitable drug for humans. However, the discovery should help researchers find other drugs that do the same thing safely.
Any drug that targets the receptor will not be a cure for fragile X, Bassell cautioned. "These children have a permanent defect in their DNA," he said. "The goal here is to improve the quality of life for these children. We are going to decrease the severity of episodes to help them focus better on learning tasks and help with the behavior problems and improve their cognitive function," he said.
One expert hailed the finding.
"This is a very important paper," said Dr. Randi Hagerman, a professor of pediatrics and medical director of the M.I.N.D. Institute at the University of California, Davis. "It proves that mGluR5 antagonists will be helpful in kids with fragile X syndrome," she added. "We are looking forward to a new age of treatment in fragile X syndrome."
Hagerman noted that trials with mGluR5 antagonists on adults with fragile X syndrome will be starting this fall. "If things go well with adults, then we will move to pediatric trials," she said.
"This is a very hopeful message," Hagerman said. "This means that there will be very specific treatments that will have an impact in the very near future."
Another expert agreed that the discovery should lead to new treatments for children with fragile X.
"This is a very exciting paper, which is a powerful confirmation of the mGluR theory of fragile X," said Dr. Michael Tranfaglia, medical director of the FRAXA Research Foundation. "Since FRAXA Research Foundation is currently working with several pharmaceutical companies to bring mGluR5 antagonists into clinical trials for fragile X, we are delighted to see this elegant proof of the therapeutic potential of this class of drugs."
More information
For more information on fragile X syndrome, visit the Fragile X Research Foundation.
The discovery in rats provides an understanding of how the gene mutation responsible for the condition changes the way brain cells communicate, according to the report in this week's issue of the Proceedings of the National Academy of Sciences.
"Fragile X syndrome is the most common form of inherited mental retardation," explained co-author Gary J. Bassell, a professor of cell biology at Emory University in Atlanta. "It has strong links to autism and epilepsy."
Fragile X syndrome occurs in approximately one in 4,000 males and one in 8,000 females, Bassell noted.
Working with rat brain cells, the team found that synapses between brain cells in the part of the brain called the hippocampus are defective in animals with fragile X, Bassell said.
"We discovered what the specific underlying defect is," he said. "It is actually a defect in the mGluR5 receptor, which is on the surface of neurons. The defect is that there is excessive signaling."
Children with fragile X have difficulty in processing information, because these receptors allow too much signaling and change the function of other receptors, Bassell theorized.
When his team treated the receptor with an mGluR5 antagonist called MPEP, they were able to reverse the effects of the mutation. "When you quiet down this receptor, it corrects the defects that occur in other receptors as well," he noted.
Bassell stressed that MPEP is not a suitable drug for humans. However, the discovery should help researchers find other drugs that do the same thing safely.
Any drug that targets the receptor will not be a cure for fragile X, Bassell cautioned. "These children have a permanent defect in their DNA," he said. "The goal here is to improve the quality of life for these children. We are going to decrease the severity of episodes to help them focus better on learning tasks and help with the behavior problems and improve their cognitive function," he said.
One expert hailed the finding.
"This is a very important paper," said Dr. Randi Hagerman, a professor of pediatrics and medical director of the M.I.N.D. Institute at the University of California, Davis. "It proves that mGluR5 antagonists will be helpful in kids with fragile X syndrome," she added. "We are looking forward to a new age of treatment in fragile X syndrome."
Hagerman noted that trials with mGluR5 antagonists on adults with fragile X syndrome will be starting this fall. "If things go well with adults, then we will move to pediatric trials," she said.
"This is a very hopeful message," Hagerman said. "This means that there will be very specific treatments that will have an impact in the very near future."
Another expert agreed that the discovery should lead to new treatments for children with fragile X.
"This is a very exciting paper, which is a powerful confirmation of the mGluR theory of fragile X," said Dr. Michael Tranfaglia, medical director of the FRAXA Research Foundation. "Since FRAXA Research Foundation is currently working with several pharmaceutical companies to bring mGluR5 antagonists into clinical trials for fragile X, we are delighted to see this elegant proof of the therapeutic potential of this class of drugs."
More information
For more information on fragile X syndrome, visit the Fragile X Research Foundation.
Tuesday, September 18, 2007
Gene Mutation Linked to Parkinson's Disease
(HealthDay News) -- People who carry a certain gene mutation appear to have a greater risk for getting Parkinson's disease and for getting it at a relatively early age, new research suggests.The study authors also found that because Ashkenazi Jews -- those with an Eastern European background-- are more likely to carry this gene mutation, this population may run an even higher risk for the disease. An estimated 90 percent of American Jews are of Ashkenazi lineage.
Study lead author Lorraine N. Clark, a researcher at Columbia University, described her team's findings as "unique and different."
"We specifically compared patients who had an early onset Parkinson's before age 50 with patients who had a later onset after age 50, and also with patients with and without Jewish ancestry," she said. "And we showed that mutations are twice as common among early onset Parkinson's and also that they're more frequent among patients with Jewish ancestry."
Clark serves as an assistant professor in the department of clinical pathology with the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, as well as the Center for Human Genetics, both at Columbia University.
The findings are published in the Sept. 18 issue of the journal Neurology.
Parkinson's disease is a brain disorder that affects 1.5 million Americans, according to National Parkinson Foundation estimates. Approximately 60,000 news cases occur each year, striking men and women equally, usually over the age of 65.
The disease is characterized by widespread damage to dopamine-producing nerve cells, impeding their ability to regulate body movement and muscle control. Key signs of the disease include tremors, stiffness, balance problems, and slowness of movement. Patients may also experience difficulty with speech and depression. There is no known cure.
To explore potential genetic underpinnings to the onset of Parkinson's, Clark and her colleagues decided to focus on the GBA gene. Mutations of this gene have already been identified as the cause of Gaucher disease, a rare fat-storage disorder that disrupts spleen and brain function.
Gaucher's and Parkinson's have some links, the study authors noted. In some cases, Gaucher's patients have a family history of Parkinson's, while others actually develop neurological features of Parkinson's. It is also one of the most prevalent genetic illnesses among Ashkenazi Jews.
For the new study, the researchers conducted a sequencing analysis of the GBA gene among 278 Parkinson's patients, 178 of who were of Jewish ancestry dating back to all four grandparents. A similar analysis was done among 179 men and women without Parkinson's.
Clark and her team found that 14 percent of the Parkinson's patients had GBA mutations, compared to just 5 percent of the healthy patients. And, while GBA mutations were found among 22 percent of Parkinson's patients who were diagnosed with their illness before the age of 50, only 10 percent of patients diagnosed after 50 had such abnormalities.
Teasing out information on Jewish patients, the researchers found that while nearly 17 percent of Jewish Parkinson's patients had GBA mutations, the figure was 8 percent among non-Jewish Parkinson's patients.
Clark called the study findings preliminary, and she cautioned that it remains unclear whether a single GBA mutation is a cause of Parkinson's or merely a part of a larger puzzle.
Still, she believes the findings could prove helpful in opening up new avenues of research into the disease.
"This is a gene we hadn't really thought about before," she said. "And it implicates new pathways that might be important in the pathogenesis of Parkinson's disease which could lead to the development of new treatment strategies. I do think, however, that further studies are needed in larger patient populations before we could use this work in diagnostic testing and counseling."
Robin Elliott, executive director of the Parkinson's Disease Foundation in New York City, called the new research "very interesting and very worthwhile, solid work in one of the most fruitful areas of Parkinson's research.
"Genetics and the study of genetics has been one of the most exciting areas of Parkinson's in the last 10 years," he said. "In 1996, we had not a single gene associated with the disease, and now it's up to 12 or 13. So, this is a very important study that pushes the science even further, and gives us the basis for more work."
More information
To learn more, visit the Parkinson's Disease Foundation.
Thursday, August 30, 2007
Saline Reduces Mortality for Brain Injury Patients
(HealthDay News) -- A simple change in the way people with traumatic brain injuries are treated initially might make a big difference in their survival odds, a new Australian study suggests.
The study found that using saline rather than albumin fluid to maintain normal fluid volume levels in people with severe brain injuries resulted in nearly double the survival rate at 24 months after the injury.
"We determined that the 2-year mortality rate was significantly high in those patients who received albumin-based fluids compared to those who received saline, particularly those patients with severe brain injuries who presented with traumatic coma," said the study's lead author, Dr. John Myburgh, director of the division of critical care and trauma at the George Institute for International Health, in Sydney.
"Given the significant difference in mortality that we observed, we recommend that albumin-based fluids be avoided for the acute fluid resuscitation of patients with traumatic brain injury," added Myburgh, who's also a professor of critical care at the University of New South Wales.
Results of the study are published in the Aug. 30 issue of the New England Journal of Medicine.
Traumatic brain injury is caused by a sharp blow to the head that often occurs in falls, motor vehicle crashes or from physical assault, according to the U.S. Centers for Disease Control and Prevention. The CDC estimates that about 1.4 million traumatic brain injuries occur annually in the United States, and about 50,000 of those people die as a result of the injury each year.
Those who survive may have lifelong disabilities.
Some of the most serious damage to the brain occurs at the time of the injury, and soon after, when the brain swells in response to the injury. Because the brain is an enclosed system, if swelling occurs, brain tissue becomes damaged.
Fluid resuscitation is a common part of traumatic brain injury treatment to ensure normal blood circulation in the brain, according to the study. However, there's been some debate as to what type of fluid would most benefit people with traumatic brain injuries -- saline or albumin fluid.
Albumin is the main protein component of human blood.
"Albumin is a very expensive product that has to be purified," explained Dr. Keith Siller, medical director of the Comprehensive Stroke Care Center at New York University Medical Center in New York City. "If they're equally effective, you'd pick the cheaper fluid."
And, in fact, a previous study had compared the two fluids and found no statistically significant difference in the rates of death after 28 days.
But, Myburgh and his colleagues re-analyzed the original data to assess results at 24 months after injury. In the original study, 460 people with traumatic brain injuries were randomly selected to receive either saline or albumin fluid. Slightly more than two-thirds of the participants in each group were classified as having a severe traumatic brain injury.
After two years, the researchers behind the new study found that people with traumatic brain injuries who received albumin had a 63 percent higher risk of dying than those given saline. For those with severe brain injuries, the albumin group had an 88 percent increased risk of death compared to the saline group.
"These are people in very bad shape," said Siller. "If there's anything that can help them have better outcomes, we have to pay attention."
Dr. James Goodrich, director of pediatric neurosurgery at the Children's Hospital at Montefiore in New York City, said, "This is a great study that definitely found a significant difference in the sense of outcomes." But, he added, it just confirms what's already going on in the treatment of people with serious brain injury. "Albumin has pretty much been given up on," he said.
As to why saline might offer some benefit over albumin, Myburgh said the researchers can't explain the difference. "The exact mechanism by which the difference in mortality between saline and albumin remains unclear," he said.
"It's probably one of two things," said Siller. "Either albumin is making the brain swelling worse, or somehow the saline is doing something beneficial that albumin can't."
More information
To learn more about traumatic brain injury, visit the National Institute of Neurological Disorders and Stroke.
The study found that using saline rather than albumin fluid to maintain normal fluid volume levels in people with severe brain injuries resulted in nearly double the survival rate at 24 months after the injury.
"We determined that the 2-year mortality rate was significantly high in those patients who received albumin-based fluids compared to those who received saline, particularly those patients with severe brain injuries who presented with traumatic coma," said the study's lead author, Dr. John Myburgh, director of the division of critical care and trauma at the George Institute for International Health, in Sydney.
"Given the significant difference in mortality that we observed, we recommend that albumin-based fluids be avoided for the acute fluid resuscitation of patients with traumatic brain injury," added Myburgh, who's also a professor of critical care at the University of New South Wales.
Results of the study are published in the Aug. 30 issue of the New England Journal of Medicine.
Traumatic brain injury is caused by a sharp blow to the head that often occurs in falls, motor vehicle crashes or from physical assault, according to the U.S. Centers for Disease Control and Prevention. The CDC estimates that about 1.4 million traumatic brain injuries occur annually in the United States, and about 50,000 of those people die as a result of the injury each year.
Those who survive may have lifelong disabilities.
Some of the most serious damage to the brain occurs at the time of the injury, and soon after, when the brain swells in response to the injury. Because the brain is an enclosed system, if swelling occurs, brain tissue becomes damaged.
Fluid resuscitation is a common part of traumatic brain injury treatment to ensure normal blood circulation in the brain, according to the study. However, there's been some debate as to what type of fluid would most benefit people with traumatic brain injuries -- saline or albumin fluid.
Albumin is the main protein component of human blood.
"Albumin is a very expensive product that has to be purified," explained Dr. Keith Siller, medical director of the Comprehensive Stroke Care Center at New York University Medical Center in New York City. "If they're equally effective, you'd pick the cheaper fluid."
And, in fact, a previous study had compared the two fluids and found no statistically significant difference in the rates of death after 28 days.
But, Myburgh and his colleagues re-analyzed the original data to assess results at 24 months after injury. In the original study, 460 people with traumatic brain injuries were randomly selected to receive either saline or albumin fluid. Slightly more than two-thirds of the participants in each group were classified as having a severe traumatic brain injury.
After two years, the researchers behind the new study found that people with traumatic brain injuries who received albumin had a 63 percent higher risk of dying than those given saline. For those with severe brain injuries, the albumin group had an 88 percent increased risk of death compared to the saline group.
"These are people in very bad shape," said Siller. "If there's anything that can help them have better outcomes, we have to pay attention."
Dr. James Goodrich, director of pediatric neurosurgery at the Children's Hospital at Montefiore in New York City, said, "This is a great study that definitely found a significant difference in the sense of outcomes." But, he added, it just confirms what's already going on in the treatment of people with serious brain injury. "Albumin has pretty much been given up on," he said.
As to why saline might offer some benefit over albumin, Myburgh said the researchers can't explain the difference. "The exact mechanism by which the difference in mortality between saline and albumin remains unclear," he said.
"It's probably one of two things," said Siller. "Either albumin is making the brain swelling worse, or somehow the saline is doing something beneficial that albumin can't."
More information
To learn more about traumatic brain injury, visit the National Institute of Neurological Disorders and Stroke.
Saturday, July 28, 2007
Health Tip: Causes of Fainting
(HealthDay News) -- Fainting occurs due to a sudden drop in blood flow to the brain, resulting in brief loss of consciousness. Fainting can be accompanied by dizziness or nausea.
Here are some common triggers, courtesy of the U.S. National Library of Medicine:
Here are some common triggers, courtesy of the U.S. National Library of Medicine:
- Straining during urination or a bowel movement.
- Excessive coughing.
- Standing for too long in the same position, or quickly standing up from a lying position.
- Severe pain, stress, fear or emotional distress.
- Excessive bleeding or dehydration.
- Medications used to treat conditions like high blood pressure, anxiety, allergies and nasal congestion.
- Use of drugs or alcohol.
- Low blood sugar.
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Thursday, June 28, 2007
CDC Panel Recommends Meningitis Vaccine for All Teens
(HealthDay News) -- Advisers to the U.S. Centers for Disease Control and Prevention recommended Wednesday that all teens between the ages of 11 and 18 be routinely vaccinated against potentially deadly bacterial meningitis.
The recommendation, issued by the CDC's Advisory Committee on Immunization Practices, broadens the current guidelines for vaccinating adolescents and will be adopted by the agency, experts said.
"The prior recommendation had focused on different age groups," said Dr. Carol Baker, chairwoman of the committee's Meningococcal Working Group. "The new recommendation will be routine vaccination of all adolescents 11 through 18 years of age."
The earlier recommendation, which targeted only 15- to 18-year-olds, was made because vaccine supplies were limited, added Baker, who is president of the National Foundation for Infectious Diseases.
"The vaccine supply to be able to immunize this many adolescents is now sufficient," she said. "Now we will prevent many more infections."
Meningococcal meningitis is a rare but sometimes fatal bacterial infection that often strikes pre-adolescents, adolescents and young adults. The disease strikes quickly and has devastating complications, including hearing loss, brain damage, limb amputations and, in some cases, death.
"Vaccination is going to do a whole lot to reduce the incidence of this disease," said Lynn Bozof, executive director of the National Meningitis Association.
"The CDC's action will raise awareness ... among parents and adolescents that this disease is out there and it is potentially vaccine-preventable," she added.
The committee recommended that teens be routinely vaccinated with Menactra, the meningococcal conjugate vaccine (MCV4) made by Sanofi Pasteur.
The vaccine has been proven to protect against up to 83 percent of meningococcal cases among adolescents, according to the National Meningitis Association.
"The CDC recognizes that all adolescents are at risk for this disease, and they are doing what is in the best interest of the public," Bozof, who lost a son to meningitis, said. "If this recommendation had been in place nine years ago, my son would be alive."
Meningitis is spread through the exchange of respiratory droplets, which can come from sharing a drink or utensils, kissing, or coughing and sneezing. Adolescents and young adults are at increased risk for the disease, which can be contracted in crowded living situations, such as dormitories, boarding schools and sleep-away camps.
Bozof believes all adolescents should be vaccinated. "You have a vaccine that can prevent the killer disease," she said. "To me it's a no-brainer -- you just go and protect your children."
More information
For more information on meningitis, visit the National Meningitis Association.
The recommendation, issued by the CDC's Advisory Committee on Immunization Practices, broadens the current guidelines for vaccinating adolescents and will be adopted by the agency, experts said.
"The prior recommendation had focused on different age groups," said Dr. Carol Baker, chairwoman of the committee's Meningococcal Working Group. "The new recommendation will be routine vaccination of all adolescents 11 through 18 years of age."
The earlier recommendation, which targeted only 15- to 18-year-olds, was made because vaccine supplies were limited, added Baker, who is president of the National Foundation for Infectious Diseases.
"The vaccine supply to be able to immunize this many adolescents is now sufficient," she said. "Now we will prevent many more infections."
Meningococcal meningitis is a rare but sometimes fatal bacterial infection that often strikes pre-adolescents, adolescents and young adults. The disease strikes quickly and has devastating complications, including hearing loss, brain damage, limb amputations and, in some cases, death.
"Vaccination is going to do a whole lot to reduce the incidence of this disease," said Lynn Bozof, executive director of the National Meningitis Association.
"The CDC's action will raise awareness ... among parents and adolescents that this disease is out there and it is potentially vaccine-preventable," she added.
The committee recommended that teens be routinely vaccinated with Menactra, the meningococcal conjugate vaccine (MCV4) made by Sanofi Pasteur.
The vaccine has been proven to protect against up to 83 percent of meningococcal cases among adolescents, according to the National Meningitis Association.
"The CDC recognizes that all adolescents are at risk for this disease, and they are doing what is in the best interest of the public," Bozof, who lost a son to meningitis, said. "If this recommendation had been in place nine years ago, my son would be alive."
Meningitis is spread through the exchange of respiratory droplets, which can come from sharing a drink or utensils, kissing, or coughing and sneezing. Adolescents and young adults are at increased risk for the disease, which can be contracted in crowded living situations, such as dormitories, boarding schools and sleep-away camps.
Bozof believes all adolescents should be vaccinated. "You have a vaccine that can prevent the killer disease," she said. "To me it's a no-brainer -- you just go and protect your children."
More information
For more information on meningitis, visit the National Meningitis Association.
Friday, June 22, 2007
Helmets Might Help Skiers
(HealthDay News) -- Many snowboarders and skiers who pursue their pastime off the main slopes are going slow enough so that a helmet would give significant protection from head injuries, a new study finds.
Currently, ski/snowboard helmets offer only limited protection in a direct collision at speeds greater than 15 mph. On open slopes, skiers and snowboarders can reach speeds of 25 mph to 30 mph.
But in this study, U.S. researchers clocked the speeds of expert skiers and snowboarders as they went through non-traditional ski areas such as terrain parks and gladed areas.
They found that the participants' speeds were below 15 mph 87.6 percent of the time.
At these slower speeds -- which result from the variation and change of direction needed to navigate non-traditional ski areas -- helmets would offer significant protection, the researchers concluded.
Each year, about 139,000 skiers and snowboarders suffer injuries that are serious enough to require treatment in an emergency department. While traumatic brain injury is the leading cause of death and serious injury among skiers and snowboarders, rates of helmet use are low, particularly among adults, according to background information in the study.
The findings are published in the latest issue of Wilderness Medicine magazine.
More information
The American Orthopaedic Society for Sports Medicine has more about helmet use in snow sports.
Currently, ski/snowboard helmets offer only limited protection in a direct collision at speeds greater than 15 mph. On open slopes, skiers and snowboarders can reach speeds of 25 mph to 30 mph.
But in this study, U.S. researchers clocked the speeds of expert skiers and snowboarders as they went through non-traditional ski areas such as terrain parks and gladed areas.
They found that the participants' speeds were below 15 mph 87.6 percent of the time.
At these slower speeds -- which result from the variation and change of direction needed to navigate non-traditional ski areas -- helmets would offer significant protection, the researchers concluded.
Each year, about 139,000 skiers and snowboarders suffer injuries that are serious enough to require treatment in an emergency department. While traumatic brain injury is the leading cause of death and serious injury among skiers and snowboarders, rates of helmet use are low, particularly among adults, according to background information in the study.
The findings are published in the latest issue of Wilderness Medicine magazine.
More information
The American Orthopaedic Society for Sports Medicine has more about helmet use in snow sports.
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