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Passive smoking increases diabetes risk
Published: Tuesday, 11-Apr-2006
1.A study published on the British Medical Journal website shows for the first time that breathing other people's smoke raises the risk of developing glucose intolerance, the precursor to diabetes.
The US research also shows that overall, white Americans are more susceptible to this effect than African-Americans.
2.Researchers examined 4572 men and women in four US cities, dividing them into four categories of smoking status: ranging from those who smoked, to those who had neither smoked nor breathed in other people's smoke. The study focussed only on those who were white or African-American.
3.The authors then tracked how many participants developed glucose intolerance - where the body can no longer produce enough insulin to regulate blood sugar - over 15 years of follow-up.
The study found that smokers had the highest risk, with 22% of them getting the disease over the study period. Non-smokers who had no exposure to second-hand smoke had the lowest risk, with less than 12% developing the condition.
But 17% of those who had never smoked themselves but were subject to second-hand smoke also developed glucose intolerance - higher than the 14% risk rate in the group who had previously smoked and given up.
4.Those breathing second-hand smoke are exposed to many toxins, say the authors. And the chemical reactions which produce second-hand smoke mean that some of those toxins may be at even higher concentrations than the levels breathed in directly by smokers. If one of these toxins particularly affects the pancreas - the organ which produces insulin - this may explain the findings, they suggest.
Until now, it had not been known that those breathing second-hand smoke faced an increased risk of diabetes, say the researchers. More studies are now needed, they conclude.
original source site:
First gene therapy human trial in the United States for a form of muscular dystrophy
First gene therapy human trial in the United States for a form of muscular dystrophy under way (PART 1)
Published: Sunday, 16-Apr-2006
1.The clinical trial for Duchenne muscular dystrophy (DMD) tests the safety and effectiveness of a therapy that was developed over two decades by scientists at the University of North Carolina Chapel Hill's School of Medicine and the University of Pittsburgh.
The trial was launched March 28, at Columbus Children's Hospital in Ohio, an affiliate of Ohio State University's School of Medicine. In the trial, six boys with DMD will receive replacement genes for an essential muscle protein.
2.Each of the boys will receive replacement genes via injection into a bicep of one arm and a placebo in the other arm. Neither the investigators nor the participants will know which muscle got the genes. After several weeks, an analysis of the injected muscle tissue's microscopic appearance, as well as extensive testing of the health and strength of the trial participants, will reveal whether gene therapy for DMD is likely to be safe and whether it's likely to result in persistent production of the essential protein in muscle cells.
3.Muscular dystrophies are genetic disorders characterized by progressive muscle wasting and weakness that begin with microscopic changes in the muscle. As muscles degenerate over time, the person's muscle strength declines.
Duchenne muscular dystrophy is a genetic disease that begins in early childhood, causes progressive loss of muscle strength and bulk, and usually leads to death in the 20s from respiratory or cardiac muscle failure. DMD occurs when a gene on the X chromosome fails to make the essential muscle protein dystrophin. One of nine types of muscular dystrophy, DMD primarily affects boys.
4.Currently, the best medical therapy can only slow the progressive muscle weakness of DMD.
5.The gene for dystrophin is one of the largest genes in the human body, and miniaturizing it, while retaining the crucial elements of its set of DNA instructions, has been among the greatest challenges to the gene therapy field.
6.The new Biostrophin therapy uses a novel combination of advanced technologies, including a miniaturized replacement dystrophin gene and nano delivery technology called biological nanoparticles. Developed from a virus known as adeno-associated virus (AAV), the nanoparticles are engineered specifically to target and carry the "minidystrophin" gene to muscle cells.
The therapy was made possible by the pioneering research in AAV by Dr. Richard Jude Samulski, professor of pharmacology and director of the Gene Therapy Center at UNC, and Dr. Xiao Xiao, a former UNC postdoctoral researcher in Samulski's laboratory now with the University of Pittsburgh Human Gene Therapy Center and associate professor of orthopedic surgery.
7.Samulski has long pioneered methodologies for making viruses deliver genes. As a graduate student at the University of Florida in the early 1980s, his thesis project was developing the AAV as a vector for therapeutic genes. This work eventually led to isolation of type-2 AAV, which has been used for gene therapy trials in cystic fibrosis and in several other settings, Samulski said.
"It's what we would call the parent virus that everybody started with."
Samulski moved to the University of Pittsburgh in 1986, joining the biology department as an assistant professor with his own laboratory. His first graduate student was Xiao, who had just come from China. Xiao focused on the lab's AAV vector project. "We've continued to have productive collaborations ever since he graduated from my lab," Samulski said.
First gene therapy human trial in the United States...(PART 2)
First gene therapy human trial in the United States for a form of muscular dystrophy under way (PART 2)
8.In 1993, Samulski moved to the University of North Carolina at Chapel Hill, becoming director of UNC's new Gene Therapy Center. Xiao moved first into industry, then to UNC as a postdoctoral researcher in Samulski's gene therapy center. In 1996, the team published a report of the first muscle gene delivery involving an AAV vector.
Xiao then returned to Pittsburgh in 1998, where he worked on muscle biology with an eye toward gene transfer, while Samulski remained focused on the vector aspects of AAV, the delivery system.
At Pittsburgh, Xiao had developed a miniaturized version of the gene for dystrophin, the muscle protein needed by people with DMD. Eager to test it in a vector, he contacted his former mentor.
9."The dystrophy gene is like a long picket fence. It's the largest gene in the human body, occupying 1 percent of the X chromosome," Samulski said. "Xiao Xiao began removing pegs, or pickets, from the fence, making it smaller and smaller but kept testing to see if it would still perform its function," Samulski said.
10.Xiao then began looking for a way he might move his minidystrophin gene forward clinically.
"We had just finished demonstrating that we could make clinical-grade virus for another genetic disorder called Canavan's disease, an enzyme deficiency disorder," Samulski said. "We were the first academic institution to ever make FDA-certified AAV vectors to go into the brains of children with Canavan's disease. So we had cut our teeth and had a bit of a track record by 2002, and that's when Xiao approached me."
11.Xiao told Samulski he wanted to put his new minidystrophin gene into an AAV vector and test it.
"He wanted to know if UNC could make the virus, and that's when I told him that we were using this virus for Canavan's disease and for other efforts. We had started improving the vectors, and we had developed some new ones that we thought were better for muscle."
12.Xiao and Samulski put their projects together and formed Asklepios BioPharmaceutical Inc. (AskBio) in 2003. Along with the rights granted by UNC to Samulski's vector technology, AskBio acquired the intellectual property rights to Xiao's uniquely miniaturized dystrophin gene.
In July 2004, the Muscular Dystrophy Association (MDA) awarded $1.6 million to AskBio to develop gene therapy strategies for DMD.
Rounding out the AskBio team clinically is neurologist Dr. Jerry R. Mendell, co-director of the MDA clinic at Columbus Children's Hospital; professor of pediatrics, neurology and pathology at Ohio State University's School of Medicine; and head of the neuromuscular research program and Center for Gene Therapy at Columbus Children's Research Institute. In the clinical trial at the Columbus Children's Hospital's MDA clinic, Mendell will administer the injections.
13.Following extensive laboratory toxicity experiments required by the U.S. Food and Drug Administration demonstrating that minidystrophin gene transfer was unlikely to harm and could ultimately benefit muscles affected by DMD, approval was granted March 3, 2006, to proceed with the human trial.
"After years of encouraging pre-clinical results, I'm excited that AskBio will help bring this promising new therapy into the clinic, and look forward with a great deal of optimism to offering this initial step toward hope for the DMD community," Samulski said.
Emphysema patients benefit from one-sided lung reduction (1)
By Gwen Ericson
April 4, 2006 -- In many cases of advanced emphysema a chronic, progressive lung condition that interferes with breathing reducing the size of the lungs by surgically removing lobes from both sides has been shown to improve both survival and quality of life. But some emphysema patients can't tolerate this bilateral operation.
1.Lung volume reduction surgery showing the stapler and the typical location of resection of the lung
Now a study conducted by researchers at Washington University School of Medicine in St. Louis and the University of Pennsylvania Health System has shown that unilateral, or one-sided, lung volume reduction surgery has significant benefits for some emphysema patients, offering help to those who are not candidates for the bilateral surgery.
2.The researchers described their work in January at the 42nd annual meeting of the Society of Thoracic Surgeons, a not-for-profit educational organization representing more than 4,800 chest surgeons worldwide.
"A certain subset of emphysema patients are poor candidates for bilateral surgery," says Bryan Meyers, M.D., associate professor of surgery. "Patients who have scarring on one side of their chest from past surgery, patients with coexisting heart conditions and the small segment of patients whose emphysema affects only one side of their lungs these are all candidates for a unilateral lung volume reduction procedure."
3.The presentation at the annual meeting discussed outcomes for 49 emphysema patients who underwent unilateral lung volume reduction surgery at the School of Medicine and Barnes-Jewish Hospital. After the procedure, the patients on average had over 30 percent increased lung function as measured by how much air they could blow out with a vigorous breath in one second. Although the improvement in function gradually decreased, as expected with this incurable and progressive disease, the benefits lasted at least three years for the average patient.
4.Tests also showed that the unilateral surgery patients had lower amounts of air left in the lung after exhalation, indicating they could exhale more thoroughly. This improvement also gradually decreased but lasted at least five years for the average patient.
In addition, requirements for supplemental oxygen declined substantially after the operation....continues
Emphysema patients benefit from one-sided lung reduction (2)
"We saw not only a functional benefit but also a survival benefit from the unilateral surgery," Meyers says. "After three years, 83 percent of the patients who had the unilateral procedure were still alive and after five years, 55 percent had survived. That's a significant increase in survival rate compared to emphysema patients who don't have surgery."
6.Survival for patients who had the unilateral procedure was the same as for a similar group of patients who had the bilateral procedure, and a national trial of lung volume reduction surgery clearly demonstrated that the bilateral procedure increases survival.
7.The current bilateral lung volume reduction procedure was pioneered at the School of Medicine in 1993 to treat end-stage emphysema. Removal of 20 percent to 30 percent of the lung on each side allows the remaining, less-diseased portion of the lung to function better, giving patients an improved quality of life.
8."Try taking a deep breath and then another breath without exhaling the first, and you'll get a feel for what happens in emphysema," Meyers says. "The lungs of emphysema patients are maximally expanded because the lung's air sacs have lost their elasticity and can't push air out. With the expansion of the lungs and chest, the patients don't have much ability to move air back and forth. But we found if we remove part of the lungs, we make it possible for the ribs and diaphragm to return to a more normal position, and it becomes easier for the patients to breathe."
Early reported successes led to the lung volume reduction procedure's rapid spread, but concerns about the safety and effectiveness led to a systematic evaluation of patient selection criteria and long-term outcomes in the National Emphysema Treatment Trial (NETT), which ran from 1996 to 2002.
9.Excluding patients at high risk of dying after surgery or with little chance of functional benefit, NETT researchers found that on average, patients with severe emphysema who undergo lung volume reduction are more likely to function better and don't face an increased risk of death compared to those who receive only medical therapy. Overall, patients who had the surgery were more likely than those who were treated only medically to improve in function, symptoms and quality of life.
"As the result of NETT, Medicare now pays for bilateral lung volume reduction surgery for qualified emphysema patients," Meyers says. "But they need more data on the efficacy of the unilateral procedure before they will approve coverage, and we believe this study helps provide that."
Sultan PK, Meyers BF, Guthrie TJ, Davis GE, Yusen RD, Lefrak SS, Patterson GA, Cooper JD. Unilateral lung volume reduction: Long-term outcome in 49 emphysema patients. Presented at the 42nd annual meeting of the Society of Thoracic Surgeons. January 2006.
Funding from the National Institutes of Health supported this research.
article taken from the Washington University School website...
New treatment against persistent ulcer-inducing bacteria successful
Published: Monday, 1-May-2006
For those who suffer from stomach ulcers, the daily routine of breakfast, lunch and dinner can be painful. A common cause of these ulcers, as well as other gastric malignancies, is a bacterium called Helicobacter pylori . For some, this infection can be persistent and difficult to treat.
Many approaches have been taken in an attempt to clear such infections, but with limited or unsuccessful outcomes. In a recent meta-analysis of therapies published in the April issue of The American Journal of Gastroenterology, Levofloxacin-based triple therapy was found to be better tolerated and more effective than bismuth-based quadruple therapy for patients with persistent H. pylori despite previous treatment attempts. Levofloxacin is commonly prescribed to treat such infections as pneumonia, bronchitis and urinary tract infections.
According to author William D. Chey, "Helicobacter pylori is a highly prevalent chronic infection with a worldwide prevalence of nearly 50% and U.S. prevalence of 20-40%." This bacterial infection is particularly difficult to treat because of its ability to adapt to the harsh environment in the stomach. The bacterium guards itself in the lining of the stomach, which prevents the body's natural defenses (Killer T Cells) from attacking it.
Levofloxacin-based triple therapy may offer an effective and safe treatment option for patients with persistent H. pylori infection, according to researchers. With so many people living with this infection, it has become increasingly important to achieve effective methods of treatment. Levofloxacin-based therapy may prove to be this method.
Kidney patients warned away from potassium
Published: Tuesday, 2-May-2006
Many kidney failure patients are increasing their chance of nerve damage in their legs and feet by simply having too much potassium in their diet, according to research carried out by the University of New South Wales (UNSW), the Prince of Wales Medical Research Institute (POWMRI) and the Prince of Wales Hospital.
The researchers found that high levels of potassium, which is found in foods such as bananas and peanuts, is responsible for causing nerve damage in these patients, which in extreme cases can lead to people being forced to use a wheelchair.
One in three Australian adults have an increased risk of developing kidney disease, which is commonly caused by diabetes. In end stage kidney disease, the kidneys function at less than ten percent of normal capacity and cannot sustain life of the patient without dialysis or a kidney transplant. 52,000 Australians have severe kidney function impairment or kidney failure (Kidney Health Australia).
"The majority of people with end-stage renal failure have nerve damage, in their legs and arms. This can mean they have difficulty walking or in feeling their feet," said Dr Arun Krishnan, a Neurologist and PhD candidate in the Faculty of Medicine at UNSW. "Once nerve damage develops, it cannot be reversed unless the patient undergoes renal transplantation. But our research indicates that patients do have some control over their situation.
"We found that higher levels of potassium in renal failure patients cause that nerve damage," said Dr Krishnan. "The clear health message is that anyone with kidney failure or chronic kidney problems should regulate their intake of potassium in an attempt to preserve nerve function."
Potassium is found in foods such as bananas, peanuts, soybeans, apricots and sultanas.
The research Sensory nerve excitability and neuropathy in end stage kidney disease has just been published in the Journal of Neurology, Neurosurgery and Psychiatry.
"Scientists have known for a long time that potassium was an important substance in terms of regulating nerve function, but until now no-one has made the connection between kidney function and nerve function," said co-author UNSW Associate Professor Matthew Kiernan, a neurologist based at the Prince of Wales Hospital.
"Until now, kidney specialists have been less concerned about higher levels of potassium amongst these patients, unless they were affecting the heart," said Professor Kiernan. "The clear message is that potassium levels need to be monitored in terms of nerve function too."
The other authors are R K S Phoon, B Pussell and J Charlesworth, all from the Department of Nephrology at the Prince of Wales Hospital.
The research was supported by the Australian Association of Neurologists Research Fellowship and the NHMRC. Grant support from the Brain Foundation, the Sylvia and Charles Viertel Charitable Foundation and the Ramaciotti Foundation.
Genetic testing can improve newborn screening tests for hearing defects
Published: Wednesday, 17-May-2006
1.Researchers have identified several changes that could be made to existing newborn screening tests for hearing defects that could advance the standard of care in detecting deaf infants, according to an article in the New England Journal of Medicine.
Walter E. Nance, M.D., Ph.D., professor of human genetics in Virginia Commonwealth University's School of Medicine, and Cynthia C. Morton, Ph.D., a professor of human genetics at the Harvard Medical School, have summarized four important criteria to be considered for screening programs throughout the country for newborn hearing defects. These include the prompt confirmation of abnormal results from screening tests; adoption of an etiologic focus to determine the cause of the deafness; initiation of molecular genetic testing for all newborns; and better recognition of infants at risk for late-onset hearing loss occurring prior to speech and language development.
2.Molecular genetic testing of blood spots from all newborn infants for the presence of the CMV virus, connexin deafness, Pendred syndrome and mitochondrial mutations in the 12S rRNA gene would allow the immediate diagnosis of the commonest forms of genetic and environmental deafness that are expressed at birth, according to the article, published in the May 18 issue of the New England Journal of Medicine. In addition, these tests would allow for the identification of infants at risk for the commonest genetic, environmental and preventable causes of delayed onset prelingual deafness.
3."If hearing loss is detected at birth and appropriate intervention is promptly initiated the educational outcome for deaf infants can be dramatically improved," said Nance, who is the corresponding author of the article. "Although newborn hearing screening programs have improved the lives of infants throughout the world, our report suggests several specific ways in which these programs can be improved, including the screening of all newborns for a limited number of the major genetic and environmental causes of hearing loss."
According to Nance, who has been studying genetic deafness for more than 30 years, identifying the actual cause of the deafness can be just as important as detecting the hearing loss. He said that data from genetic testing would provide a powerful supplement to audiologic testing that could greatly improve the overall effectiveness of these programs.
4.In 1964, Marion Downes, a distinguished audiologist, first showed that profound deafness could be recognized in newborn infants by painstaking observations of their response to sounds. Since that time, advances in technology now allow the automated screening of infants by trained technicians. At the same time, dramatic advances have been made in understanding the causes of deafness.
5.In addition to many environmental causes of deafness, researchers have identified more than 100 genes that are linked to deafness. Nance said that approximately 50 percent to 60 percent of childhood hearing loss in developed countries is due to genetic factors.
6.Hearing is essential for the normal acquisition of speech. According to Nance, if oral or sign language is not acquired during a critical developmental stage, deaf children may never achieve their full developmental potential. Other studies have indicated that early detection of hearing loss and intervention can improve the educational and social outcomes of these newborns.
original site of the article:
Mood swings and irritability no fun for anyone!
From women to women.
Mood swings and irritability are closely related. We use mood swing to describe a reaction that isnt appropriate to what triggered it. Irritability to most of us means an angry or impatient reaction to something that happens.
What causes mood swings and irritability? In both cases, the physiology is based on hormonal imbalance. The underlying cause may be fatigue and if youre having hot flashes or insomnia, you are very fatigued! But it can also be the sudden shifts in hormonal balance so characteristic of perimenopause, especially when your body doesn't have enough support to maintain its natural balance.
Mood swings and irritability have an emotional aspect as well. Perimenopause is a time when many women find their true voices. Thats a good and natural process. You may note the resurfacing of old emotional issues that remain unresolved. This work is important, not just to relieve your mood swings, but for your very health.
Women often come to us saying, I thought I was losing my mind! because theyre shocked by their mood swings and irritability. For them its a relief to know that their moods have a physical basis and can be relieved. Theres usually nothing wrong with you that you cant fix by taking better care of yourself.
Weve been very successful in our Personal Program in helping women find relief from their mood swings and irritability. Even severe mood swings can be alleviated by providing your body with the support it needs to achieve hormonal balance. So heres what we recommend you do next:
If youd like to get started, the first step is to take our on-line Hormonal Balance Profile. Its easy, informative, and free.
If youd like to learn more about the biology behind the Personal Program, go to How It Works.
If you have questions about whether the Program will work for you, call us toll-free at 1-800-254-1734 . Were here to listen and help.
Explaining food cravings
An enormous percentage of women crave sugar, carbohydrates, or alcohol. In most cases, these food cravings are not true eating disorders, but instead are signs of hormonal imbalance caused by a lack of healthy nutrition.
Your personal issue may be the afternoon snack (often chocolate or candy or a food thats also heavy in carbohydrates), too many potato chips, the extra glass of wine at night, or a hundred other variations. But the underlying mechanism, and the way to curb cravings, is the same. And it has nothing to do with willpower, or your lack thereof!
What food cravings mean
Food cravings mean that the body has its signals mixed up. When we are exhausted or blue, we have low blood sugar and/or low serotonin, and the body signals the brain that it needs a pick-me-up. This signal causes a sugar craving or carbohydrate craving.
Serotonin is our basic feel-good hormone. If serotonin is low, we feel sad or depressed. And hormonal imbalance or weak digestion can lead to low serotonin. Unfortunately, sugars and simple carbohydrates release a short burst of serotonin we feel good for a moment, but soon return to our low-serotonin state then crave more sugar and simple carbohydrates. Its a downward spiral.
If you eat a low-fat diet in the hope of losing weight, you unintentionally make the problem worse. If, like millions of women, you have eaten a low-fat, high-carbohydrate diet for many years, or followed fad diets, the odds are good that you have become at least partially insulin resistant.
Insulin is responsible for maintaining stable blood sugar levels by telling the bodys cells when to absorb glucose from the bloodstream. Being insulin resistant means your body stops responding to insulin, and instead grabs every calorie it can and deposits it as fat. So no matter how little you eat, you will gradually gain weight.
At the same time, your cells cannot absorb the glucose they need, so they signal your brain that you need more carbohydrates or sugars. The result is persistent food cravings.
Even worse, insulin resistance leads directly to obesity, diabetes, and heart disease. Many experts believe it is the root cause of the epidemic of those diseases in America today. And a low-fat diet makes it far more likely you will suffer from this condition.
Millions of American women are now trying the Atkins Diet or the South Beach Diet. While these diets are an improvement over the conventional low-fat, high-carbohydrate diet, they can worsen your metabolic problems, because dieting itself is stressful to the body. So many women need to heal their metabolism first before even considering weight loss.
Another cause of food cravings is adrenal fatigue. If you are under a great deal of stress, or suffer from insomnia or sleep deprivation, you are probably exhausted much of the time. This leads to adrenal fatigue or outright adrenal exhaustion, which in turn signals the body it needs a pick-me-up. You may resort to sugar or carbohydrate snacks or coffee during the day and carbohydrates or alcohol at night, all of which exacerbate the problem.
How to curb cravings
Women who blame themselves for their food cravings only worsen their mood and increase their need for serotonin. Thats when a pattern of emotional eating can develop. Remember, there are biological causes of sugar cravings, and your carbohydrate craving is rarely just a behavioral problem. The root problem is more likely inadequate nutrition.
How to break this vicious cycle? To reduce food cravings, the body needs real support and lots of it. We have seen over and over that eating healthy foods, adding pharmaceuticalgrade nutritional supplements and moderate exercise can almost miraculously curb cravings. Your metabolism will heal itself when provided with the necessary nutritional support. If it has been damaged, the process can take some time, but it will happen. The good news is you dont have to give up chocolate!
Weve been very successful in our Personal Program in resolving cravings of all kinds. So heres what we recommend you do next:
If youre ready to get started, consider joining the Personal Program. The first step is to complete our on-line Hormonal Balance Profile. Its easy and informative.
If youd like to learn more about the biology behind the Program, go to How It Works.
If you have questions about whether the Program will work for you, call us toll-free at 1-800-254-1734 . Were here to listen and help.
If youre under a lot of stress and feel exhausted much of the time, be sure to read our article on adrenal fatigue.
Click here to return to Symptoms.
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