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December 21, 2005

Pain and The Brain

Pain and The Brain
Chronic pain sufferers may be able to reduce pain levels by studying their own live brain images, scientists at the Stanford University School of Medicine report in a new study.

With training and the use of high-tech imaging equipment, subjects were able to influence their pain by controlling activity in one of the pain centers of the brain through the use of mental exercises and by visualizing their own brain activity in real time.

Compare it to exercising your muscles in a top-of-the-line weight room. After repeated practice, you get better at it.

The researchers are hopeful the new technique may have potential for future use as long-term therapy for chronic pain patients-possibly even without all the high-tech equipment. They caution that significantly more work is needed before it can be thought of as a clinical therapy.

"We believe these subjects and patients really learned to control their brain and, through that, their pain," said Sean Mackey, MD, PhD, assistant professor of anesthesia and co-author of the study would be published in the Dec. 12 online issue of the Proceedings of the National Academy of Sciences.

The study posed two questions: "Can healthy subjects and patients with chronic pain learn to control activity in specific regions of their brain? And, in doing so, does this lead to an improved control of their pain?" The answer to both was a resounding "Yes." A second, larger study is under way to test the potential for long-term use in future treatment.

"Pain has a huge impact on individual patients, their families and society," said Mackey, who is also associate director of Stanford's pain management division. A recent national survey showed that more than half of all Americans suffer from chronic pain. "I got incredibly jazzed by the results [of the imaging study]," Mackey added. "We could change people's lives. However, significantly more science and testing must be done before this can be considered a therapy for chronic pain".........

Daniel      Permalink


December 21, 2005, 9:09 PM CT

Beta Blockers Not Effective in Cirrhosis

Beta Blockers Not Effective in  Cirrhosis Roberto Groszmann, M.D
Beta blockers are not effective in preventing development of varices-veins in the esophagus that can rupture and bleed-as a consequence of cirrhosis, according to a recent study by Yale School of Medicine scientists in the New England Journal of Medicine.

Cirrhosis of the liver is the seventh leading cause of death in persons between the ages of 25-65. One of the main consequences of cirrhosis is the development and rupture of varices, which account in large part for the mortality associated with cirrhosis.

One of the lead authors of the study, Roberto Groszmann, M.D, professor in the Department of Internal Medicine, Section of Digestive Diseases, said beta blockers are routinely prescribed to prevent rupture of the varices, but some practitioners also prescribe beta blockers to all patients with cirrhosis, whether or not they have varices. This study examined the effects of beta blockers in the latter situation.

The study enrolled 213 patients of which 108 received the beta blocker timolol and 105 received a placebo. The patients were followed for five years. Forty percent of the patients developed varices, but there were no differences between the beta blocker and the placebo groups.

"Additionally, patients that received the beta blocker had more side effects, a number of of which were serious," Groszmann said. "The findings of this study clearly do not support the use of beta blockers in patients who have cirrhosis without varices since the risks far outweigh the benefits".

He said another important finding of the study was that the development of varices depended on how high the portal vein pressure was at the beginning of the study and how much it could be lowered. The portal vein takes blood to the liver. The pressure is elevated in cirrhosis and leads to the development of varices.........

Scott      Permalink


December 21, 2005

Chronic Disability in Older Americans

Chronic Disability in Older Americans
The rates of chronic disability in older Americans has been substantially overestimated by about forty percent, scientists at Yale School of Medicine report in the December 12 Archives of Internal Medicine.

"Our projections yielded about two million fewer chronically disabled older Americans in 1999, relative to the published estimate of seven million," said Thomas M. Gill, M.D., who co-authored the study with Evelyne A. Gahbauer, M.D.

Gill, associate professor of medicine/geriatrics, obtained his findings using data from the "Yale PEP Study," which seeks to better understand how older persons manage day-to-day activities and remain independent at home. Titled "Epidemiology of Disability and Recovery in Older Persons," the PEP study includes 754 participants age 70 or older from the Greater New Haven area. Over the last eight years, participants have shared their experiences during a series of home assessments and monthly telephone interviews focusing on essential activities of daily living, such as bathing, dressing and walking.

Patients were classified as having chronic disability based on the presence of disability during consecutive monthly interviews immediately before or after the fourth comprehensive assessment. Of the 552 participants, 16.1 to 17.2 percent met criteria for chronic disability, leading to a national estimate ranging from 4.9 to 5.3 million chronically disabled older Americans.

Gill said accurate estimates of chronic disability are important for a variety of reasons. From a policy perspective, these estimates are often used to inform decisions regarding the current and future health care needs of older persons and to forecast the likely demand for long-term care. From an epidemiologic perspective, the causes of chronic disability, including pre-disposing risk factors and subsequent precipitants, may differ from those of short-term disability.........

Janet      Permalink


December 21, 2005

Novel mechanism for blood disease

Novel mechanism for blood disease
Approximately 80,000 to 100,000 people in the United States suffer from myeloproliferative disease, a broad category of ailments characterized by overproduction of different types of blood cells. Often these diseases lead to cancers of blood cells. Scientists at Whitehead Institute for Biomedical Research and Brigham and Women's Hospital have discovered an unusual mechanism underlying this condition, and their findings may lay the foundation for future drug development.

As people age, their genes acquire mutations. In a patient with myeloproliferative disease, a mutation occurs in a specific kind of protein called a kinase, that is, a protein that adds a small molecule called a phosphate to other proteins, in this case proteins involved in blood-cell growth. But the mutation alone will not produce the disease. The mutant kinase, named JAK2V617F, causes the condition only after binding to another molecule. This makes myeloproliferative disease an unusual disease of overproduction of cells, since a number of other kinase mutations lead directly to cell proliferation.

"Surprisingly, this mutant kinase is completely dependent on a cell-surface protein for its transforming potential," says Whitehead Member Harvey Lodish, whose lab made the discovery in collaboration with D. Gary Gilliland of Brigham and Women's. Their results will be published online in Proceedings of the National Academy of Sciences during the week of December 19.

"This paper provides new and important insights into how this gene contributes to the development of myeloproliferative disease and it should provide an important foundation for subsequent development of new drugs," says Gilliland, who is also a Howard Hughes Medical Institute investigator.

Gilliland's lab was one of several to identify the precise genetic mutation responsible for myeloproliferative disease when they discovered that the exact same genetic mutation in a kinase called JAK2 causes many distinct disorders that fall under the myeloproliferative disease umbrella. After publishing this finding in Cancer Cell in April, Gilliland turned to Lodish lab researchers, who designed experiments that shed light on the mechanism behind the disease.........

Daniel      Permalink


December 21, 2005

Light-sensing cells in retina

Light-sensing cells in retina
Investigators at Washington University School of Medicine in St. Louis have found that cells making up a non-visual system in the eye are in place and functioning long before the rods and cones that process light into vision. The discovery should help researchers learn more about the eye's non-visual functions such as the synchronization of the body's internal, circadian clock, the pupil's responses to light and light-regulated release of hormones.

The scientists report in the Dec. 22 issue of Neuron that in the mouse retina, intrinsically photosensitive retinal ganglion cells (ipRGCs) are active and functioning at birth. That was surprising because the mouse retina doesn't develop fully until a mouse is almost three weeks old, and the first rod cells don't appear until about 10 days after birth.

"We were stunned to find these photoreceptors were firing action potentials on the day of birth," says Russell N. Van Gelder, M.D., Ph.D., associate professor of ophthalmology and visual sciences and of molecular biology and pharmacology. "Mice are very immature when they're born. It takes about three weeks after birth for the retina to fully develop. No one previously had detected light-dependent cell firing in a mouse before 10 days."

Van Gelder says the ganglion cells react to light in two ways, sending messages to parts of the brain that control circadian rhythms, and (on the first day or two of life) also setting off a wave of activity that spreads through the retina, possibly helping visual cells develop.

Van Gelder and his colleagues have spent the last few years learning how blind animals (and people) can sense light and use it to set their circadian clocks. The ipRGCs were first identified in 2002 - by David M. Berson, Ph.D., and his colleagues at Brown University - as the cells that could sense light even in visually blind eyes. But it was very difficult and time consuming to isolate and study the cells, requiring precise injection of a tracing dye into the brains of animals to label and identify the ipRGCs.........

Mike      Permalink


December 21, 2005

Links Between Kidney Function And Bone

Links Between Kidney Function And Bone Keith A. Hruska, MD
Multitasking might seem like a modern invention, but in biology it's been an established technique for millennia.

The organs of the human body, for example, all have their well-known primary specialties, but a number of of them also play secondary roles in support of each other.

One such moonlighter is the human kidney, which purifies waste from the blood, but also has a more recently identified role as a contributor to the structural integrity of the human skeleton.

Keith A. Hruska, MD, professor of pediatrics, medicine and of cell biology and physiology at the School of Medicine and head of pediatric nephrology at St. Louis Children's Hospital, has developed several new insights into the connections between the kidney and the skeleton and hopes to put them to use soon in new therapys for kidney patients that will ease the harmful effects their condition inflicts on both the skeleton and the heart.

To recognize the connections between the kidney and the skeleton, doctors first had to understand that the skeleton isn't the dry and unchanging place it .

was once thought to be.

"In the past, the skeleton has been viewed as mostly a dead structure, but that's not the case at all," Hruska explains. "The adult skeleton is very active tissue that is continually remodeling, dismantling damaged bone and replacing it with new bone".

Cells inside the bone marrow accomplish this task, regularly destroying and rebuilding bone structure to adjust for wear, injury and changes in the mechanical loads and pressures placed on the bones.

Kidney disease's direct connection to bone health was initially masked by a complication of chronic kidney disease (CKD) known as secondary hyperparathyroidism. This complication, which afflicts about 100,000 new patients with kidney disease each year, raises bloodstream levels of the parathyroid hormone.........

Daniel      Permalink


December 21, 2005

Impediments For Overweight People From Exercising

Impediments For Overweight People From Exercising
Doctors treating overweight or obese patients often prescribe exercise as part of a regime to take off pounds. However, a new study indicates that some people's ability to exercise may be hampered by a variety of gastrointestinal problems that frequently affect individuals who are overweight.

A team of scientists studying nearly 1,000 men and women participating in a randomized trial evaluating three weight-loss programs in Minnesota found that associations between gastrointestinal symptoms, diet and exercise may have implications for the therapy of both obesity and gastrointestinal problems. The physiological mechanisms linking gastrointestinal symptoms, obesity and exercise still need to be determined, said psychology expert Rona Levy, lead author of the study and a University of Washington professor of social work whose research focuses on common gastrointestinal disorders such as irritable bowel syndrome in adults.

"Our main finding is that the amount of exercise people in a weight loss program do is related to gastrointestinal symptoms. In statistical terms, this means exercise is protective against gastrointestinal symptoms. This isn't surprising, but it has not been demonstrated before with this population. Science has now validated what people have been guessing," she said.

"But we don't know if this is a 'did the chicken or the egg come first' kind of a thing. We are not sure which is the key, exercise or gastrointestinal symptoms. It is plausible that if a doctor put a patient on an exercise program to lose weight the GI problems experienced might hamper the patient's ability to exercise".

People in the study reported experiencing a variety of problems: 19 percent said they had abdominal pain, 13 percent had irritable bowel syndrome, 25 percent had diarrhea and 20 percent had bloating.........

JoAnn      Permalink


December 21, 2005

Emotional Recovery From Breast Cancer

Emotional Recovery From Breast Cancer
Contrary to psychology experts' expectations, breast cancer survivors don't experience an extended emotional crisis after their therapy regimens end, according to a new study by scientists at Washington University School of Medicine in St. Louis. The study appears in the recent issue of Supportive Care in Cancer.

"We thought we'd find that women do worse psychologically after therapy," says Washington University psychology expert, Teresa L. Deshields, Ph.D., assistant professor of medicine. "That's the clinical lore. After all, a number of of the patients referred to us are the ones struggling at the end of therapy. But our study shows that within two weeks most women adjust very well to survivorship".

The research team surveyed 94 women drawn from patients of the radiation oncology practice at the Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital. The women, averaging 55 years of age, had stage 0, I, II or III breast cancer and at the start of the study were completing the last of a six- to seven-week course of daily radiation therapys.

The women were surveyed five times: on their last day of radiation therapy, two weeks later, several days before their first follow-up appointment (four to six weeks post-treatment) and at three and six months. The survey measured patients' depressive symptoms and quality of life (the quality of life measurement quantifies a set of attributes that include physical, social/family, emotional and functional well-being, and breast-cancer-specific concerns). For the group of breast-cancer survivors, the average score for indications of depression was heightened at the end of therapy compared to a group of healthy men and women. A higher score on the depression index indicates more severe depressive symptoms.........

Emily      Permalink


December 20, 2005

Promise For Mending Broken Heart

Promise For Mending Broken Heart
More Stem Cell research news from UW-MadisonWorking with heart attack-stricken mice, a team of UW-Madison researchers has shown that embryonic stem cells may one day live up to their clinical promise.

In a paper would be published in the January 2006 issue of the Journal of Molecular and Cellular Cardiology, a team led by UW-Madison stem cell researcher and heart specialist Timothy J. Kamp reports that all-purpose embryonic stem cells, transplanted into mouse hearts damaged by experimentally induced heart attacks, shift gears and morph into functional forms of the major types of cells that compose the healthy heart.

The study's results are important because they demonstrate that blank-slate embryonic stem cells can be introduced to damaged heart tissue, develop into heart muscle and into cells that form the heart's blood vessels. If perfected, such treatment could provide a practical, less-invasive alternative to current therapies such as surgery, improve the quality of life for a number of patients and reduce the number of deaths attributed to heart disease, now estimated at about 700,000 deaths per year in the United States.

"Typically, when that heart muscle dies (as the result of heart attack), it is gone for good," says Kamp, a professor of medicine and physiology in the UW-Madison School of Medicine and Public Health.

In their experiments, when stem cells were introduced directly to tissue damaged by a heart attack, three critical types of cells formed: cardiomyocytes or heart muscle; vascular smooth muscle, the muscle that forms the bulk of the walls of blood vessels; and endothelial cells, the flat cells that line the interior surfaces of blood vessels in the heart and throughout the body's circulatory system.

"There are multiple components," Kamp explains. "But (in these experiments) we see the three most important types of cells forming. It didn't completely repair the heart, but it was encouraging."........

Scott      Permalink


December 20, 2005

Sneaking Drugs Into The Brain

Sneaking Drugs Into The Brain
One of the great challenges for treating Parkinson's diseases and other neurodegenerative disorders is getting medicine to the right place in the brain.

The brain is a complex organ with a number of different types of cells and structures, and it is fortified with a protective barrier erected by blood vessels and glial cells - the brain's structural building blocks - that effectively blocks the delivery of most drugs from the bloodstream.

But now researchers have found a new way to sneak drugs past the blood-brain barrier by engineering and implanting progenitor brain cells derived from stem cells to produce and deliver a critical growth factor that has already shown clinical promise for treating Parkinson's disease.

Writing today in the journal Gene Therapy, UW-Madison neuroscientist Clive Svendsen and colleagues describe experiments that demonstrate that engineered human brain progenitor cells, transplanted into the brains of rats and monkeys, can effectively integrate into the brain and deliver medicine where it is needed.

The Wisconsin team obtained and grew large numbers of progenitor cells from human fetal brain tissue. They then engineered the cells to produce a growth factor known as glial cell line-derived neurotrophic factor (GDNF). In some small but promising clinical trials, GDNF showed a marked ability to provide relief from the debilitating symptoms of Parkinson's. But the drug, which is expensive and hard to obtain, had to be pumped directly into the brains of Parkinson's patients for it to work, as it is unable to cross the blood-brain barrier.

In an effort to develop a less invasive strategy to effectively deliver the drug to the brain, Svendsen's team implanted the GDNF secreting cells into the brains of rats and elderly primates. The cells migrated within critical areas of the brain and produced the growth factor in quantities sufficient for improving the survival and function of the defective cells at the root of Parkinson's.........

Daniel      Permalink




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