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January 4, 2006

Two New Stem Cell Lines In Animal Cell-free Culture

Two New Stem Cell Lines In Animal Cell-free Culture Lab manager Jessica Antosiewicz removes a tray of stem cell cultures from an incubator
Researchers working at the WiCell Research Institute, a private laboratory affiliated with UW-Madison, have developed a precisely defined stem cell culture system free of animal cells and used it to derived two new human embryonic stem cell lines.

The new work, which is reported today (Jan. 1, 2006) in the journal Nature Biotechnology, helps move stem cells a small step closer to clinical reality by completely ridding the culture medium in which they are grown of animal products that could harbor viruses or other deleterious agents.

Successfully growing living cells outside the body generally requires providing the cells in a lab dish with the right mix of nutrients, hormones, growth factors and blood serum. But those methods have often depended on animal cells - such as those obtained from mouse embryos in the case of embryonic stem cells - and other animal products to keep the cells alive and thriving in culture. Some researchers worry that animal viruses and other problematic agents might be taken up in the human cells and infect human patients, should those cells be used for treatment.

"All of the concerns about contaminating proteins in existing stem cell lines can essentially be removed using this medium," says the Nature Biotechnology paper's lead author, Tenneille Ludwig, a UW-Madison research scientist working at WiCell who led the effort to develop the new culture media. "This work helps us clear some of the major hurdles for using these cells therapeutically".

"We've been optimizing (culture) media on the existing stem cell lines since 1998, but it has only been recently that there have been dramatic improvements," says James Thomson, the senior author of the new study and a UW-Madison professor of anatomy who seven years ago was the first to successfully grow human embryonic stem cells in the lab. "This is the first time it has been possible for us to derive new cell lines in completely defined conditions in medium that completely lacks animal products".........

Scott      Permalink


January 3, 2006

Night eating syndrome among psychiatric patients

Night eating syndrome among psychiatric patients
As per a studythat appears in the January 1 issue of The American Journal of Psychiatry, scientists at the University of Pennsylvania School of Medicine and the University of Minnesota found that night eating syndrome is a common disorder among psychiatric outpatients and is associated with substance use and obesity.

Typically typically typically night eating syndrome is a condition that is characterized by two main features: excessive eating in the evening (hyperphagia) and nocturnal awakening with ingestion of food. Its prevalence has been estimated to be 1.5% in the general population and 8.9% in an obesity clinic.

"This is the first study that looks at the connection between psychiatric conditions and night eating syndrome," said Jennifer D. Lundgren, PhD, lead author of the paper and postdoctoral research associate in Penn's Department of Psychiatry, Division of Weight and Eating Disorders. "Night eating syndrome is often associated with life stress and depression, so we were especially interested in looking at the prevalence of the condition in this population," said Lundgren.

The research was supported by the National Institute of Mental Health and the National Institute of Diabetes and Digestive and Kidney Disease.

Study Protocol.

The study consisted of 399 participants from psychiatric outpatient clinics. Participants were screened using a questionnaire to assess hunger and craving patterns, percentage of calories consumed following the evening meal, insomnia and awakenings, nocturnal food cravings and ingestions, and mood. Those who scored above cutoff on the questionnaire were then interviewed by phone and diagnosed with night eating syndrome if one or both of the following criteria were met: 1) evening hyperphagia and/or 2) nocturnal awakenings with ingestions of food occurring three or more times per week.........

JoAnn      Permalink


January 3, 2006

Hyperbaric Oxygen Treatments Mobilize Stem Cells

Hyperbaric Oxygen Treatments Mobilize Stem Cells
As per a studywould be published in The American Journal of Physiology-Heart and Circulation Physiology, a typical course of hyperbaric oxygen therapys increases by eight-fold the number of stem cells circulating in a patient's body. Stem cells, also called progenitor cells are crucial to injury repair. The study currently appears on-line and is scheduled for publication in the April 2006 edition of the American Journal.

Stem cells exist in the bone marrow of human beings and animals and are capable of changing their nature to become part of a number of different organs and tissues. In response to injury, these cells move from the bone marrow to the injured sites, where they differentiate into cells that assist in the healing process. The movement, or mobilization, of stem cells can be triggered by a variety of stimuli - including pharmaceutical agents and hyperbaric oxygen therapys. Where as drugs are associated with a host of side effects, hyperbaric oxygen therapys carry a significantly lower risk of such effects.

"This is the safest way clinically to increase stem cell circulation, far safer than any of the pharmaceutical options," said Stephen Thom, MD, PhD, Professor of Emergency Medicine at the University of Pennsylvania School of Medicine and lead author of the study. "This study provides information on the fundamental mechanisms for hyperbaric oxygen and offers a new theoretical therapeutic option for mobilizing stem cells".

"We reproduced the observations from humans in animals in order to identify the mechanism for the hyperbaric oxygen effect," added Thom. "We found that hyperbaric oxygen mobilizes stem/progenitor cells because it increases synthesis of a molecule called nitric oxide in the bone marrow. This synthesis is thought to trigger enzymes that mediate stem/progenitor cell release".........

Daniel      Permalink


January 3, 2006

New Class Of Anti-cancer Drugs Based On Platinum

New Class Of Anti-cancer Drugs Based On Platinum Platinum like this used in the coin has been used for the production of various chemotherapy drugs.
Scientists at Virginia Commonwealth University's Massey Cancer Center have created a new platinum-based, anti-cancer agent able to overcome acquired drug resistance by first modifying the way it is absorbed into cancer cells and then attacking the DNA of those cancer cells.

The findings may help scientists design a new generation of anti-cancer drugs that selectively target cancer cells, reduce resistance and side effects and expand the range of tumors that can be treated by platinum.

In the Dec. 26 issue of the journal Inorganic Chemistry scientists reported on the design of a new trinuclear platinum compound and demonstrated that its cellular absorption is significantly greater than that of neutral cisplatin, as well as other multi-nuclear platinum compounds. The enhanced uptake into cancer cells takes advantage of weak molecular interactions on the cells' surface. These results underscore the importance of the new compound's "non-covalent" interactions, previous to the attack on DNA. Non-covalent interactions minimize potential side reactions and produce changes in the structure of proteins and DNA, which is different from currently used drugs. This research was selected as the cover article for the print version of the journal, Issue 26.

Scientists compared the cytotoxicity and cellular concentrations of three anti-cancer drugs including the phase II clinical drug, BBR 3464, cisplatin and the new trinuclear platinum compound. In a laboratory model, human ovary cancer cells were exposed to each drug.

"In platinum antitumor chemistry our objective is to design and develop complexes acting by new mechanisms of action," said Nicholas Farrell, Ph.D., professor and chair in the Department of Chemistry at VCU, and lead author of the study. "Resistance to current drugs is due to poor cellular absorption and an increased ability of the cell to process or repair the damage caused by the chemotherapeutic agent".........

Daniel      Permalink


January 2, 2006, 10:16 PM CT

Research Effort Will Help Troops And Veterans

Research Effort Will Help Troops And Veterans
The San Francisco VA Medical Center, the Department of Defense, and the Northern California Institute for Research and Education have joined together to establish a new SFVAMC Neuroscience Center of Excellence.

The goal of the Center is to investigate new approaches to diagnosing and treating neurological injuries and illnesses suffered by US military personnel - especially fighters stationed in the Iraq and Afghanistan theaters of war - as well as veterans and the general public.

Research will be a collaborative effort involving a range of scientific disciplines.

"This is the only joint VA-DOD program with a neuroscience focus in the United States," observed Michael Weiner, MD, director of the Center for Imaging of Neurodegenerative Disease at SFVAMC and the principal investigator of the overall research program. "We expect that the results of our research will lead to improvements in the neurological and mental health of active duty war fighters, post-active duty veterans, and the general population." Weiner is also professor of radiology, medicine, psychiatry, and neurology at UCSF.

The 19 principal researchers at the Center, whose research grants are administered by NCIRE, will conduct research on topics including posttraumatic stress disorder (PTSD), Gulf War Illness, brain and spinal cord injury, wound healing, bladder dysfunction, and other combat-related neurological injuries and syndromes. Projects represent a spectrum of investigation ranging from basic laboratory science to clinical diagnosis and therapy (see list below).

"The Neuroscience Center of Excellence is clearly on a trajectory to provide national leadership in neurological health and therapy," predicted Col. Karl Friedl, PhD, commander of the US Army Research Institute of Environmental Medicine, which is funding the work of the Center. "This research program is beautifully focused on issues of great importance to soldiers returning from current deployments and veterans of all eras".........

Scott      Permalink


January 2, 2006, 10:09 PM CT

New Drug Target For Alzheimer's Disease

New Drug Target For Alzheimer's Disease
Gladstone scientists identify new drug target for Alzheimer's disease.

Scientists at the Gladstone Institute of Neurological Disease have identified a potential new way to stop brain cell death related to Alzheimer's disease.

Working with cell cultures, the researchers investigated how amyloid beta (A?) proteins, which build up in the brain tissue of people with Alzheimer's disease, kill neurons. The cell cultures were established from brain tissue of laboratory rats. Study findings showed that A? could be prevented from causing neuronal cell death with a compound called resveratrol, which is also found as a natural ingredient in red wine.

"Our study suggests that resveratrol and related compounds may protect against neuronal loss associated with Alzheimer's disease," explains senior author Li Gan, PhD, a staff research investigator at the Gladstone Institute of Neurological Disease and an assistant professor of neurology at UC San Francisco. "This could certainly open up new avenues for drug development".

The research results are reported in the December 2 issue of the Journal of Biological Chemistry.

According to the research team, it was especially interesting that the beneficial effect of resveratrol was not due to a direct effect on A? or on neurons but on other types of brain cells, called microglia.

Microglia are the immune cells of the brain. They can protect or hurt neurons, depending on which of their powerful defense or attack pathways are activated. The researchers found that A? triggers a pathway in microglia that makes them attack neurons with poisonous chemicals.

A key mediator in this pathway is a protein called NF?B, which resveratrol happens to block. Without resveratrol, A??activates NF?B in microglia, turning them into powerful neuron killing machines.........

Scott      Permalink


January 2, 2006, 9:59 PM CT

How Brain Understands Language

How Brain Understands Language
UC Irvine cognitive neuroscientist has been awarded a National Institutes of Health grant for $2.4 million over five years to unlock the secrets of how the brain translates sound waves into meaningful language.

Greg Hickok, professor of cognitive sciences, will lead a team of researchers from UCI, UC San Diego, the University of Southern California and the University of Iowa in this research that may one day help those with language disorders caused by stroke, Alzheimer's disease and autism. The grant is a renewal from the National Institute on Deafness and Other Communication Disorders (NIDCD), a component of the NIH, and will allow Hickok to continue the work he has done in this field since 1999.

"When we listen to speech, what hits our ears is nothing more than tiny fluctuations in air pressure, or sound waves," Hickok said. "The ability of humans to turn these sound waves into meaningful language is a complex task, one that we have not managed to replicate yet with computer voice recognition systems. This project will help us better understand how brain circuits can do what computers circuits so far cannot".

It is estimated that acquired language disorders, also known as aphasia, affect approximately 1 million people in the U.S., with 80,000 new cases diagnosed each year. Aphasia generally results from a stroke. Language ability is also often affected in those who suffer from neurodegenerative diseases such as Alzheimer's and from disorders such as autism. Understanding the basic circuitry of how speech is processed could help in treating these disorders.

Following on his prior work, Hickok, along with his colleagues, will use functional magnetic resonance imaging (fMRI) technology, which measures blood flow and allows researchers to map which brain regions become active during a task involving speech or language use. The team plans to conduct 200 fMRIs on healthy subjects, primarily at UCI.........

Scott      Permalink


January 2, 2006, 9:37 PM CT

Clinical Trials Urged For Paediatric Stroke

Clinical Trials Urged For Paediatric Stroke
Scientists at The Hospital for Sick Children (SickKids), Stollery Children's Hospital and Chedoke McMaster have advised that randomized clinical trials are urgently needed to equip diagnosing physicians with the most effective therapy options for paediatric stroke. This research is published in the January 2006 issue of the journal Stroke.

"There is a lot of uncertainty for clinicians when identifying the best therapy options for different types of paediatric stroke, as there is little to no evidence from clinical trials to support therapy decisions," said Dr. Gabrielle deVeber, the study's principal investigator, a paediatric neurologist and scientist at SickKids and an associate professor of Paediatrics at the University of Toronto. "By compiling data on the largest number of children with stroke and the clinicians treating them, we were able to identify the most significant therapy issues facing physicians when dealing with paediatric stroke".

From January 1995 to January 1, 2005 physicians worldwide consulted the 1-800-NOCLOTS toll-free paediatric stroke telephone consultation service. The consultation service, run out of SickKids in Toronto , Stollery Children's Hospital in Edmonton and the Children's Hospital at Chedoke McMaster in Hamilton provided telephone support and therapy suggestions to physicians dealing with paediatric stroke. The paediatric neurologists and haematologists operating the line documented caller and patient characteristics, antithrombotic therapys and caller's questions for entry into a computerized database.

"While we were collecting data, physicians were also provided with patient-specific support by a consultation service through the use of an annually updated published paediatric stroke protocol," said Dr. deVeber, who is also director of the Children's Stroke Program at SickKids.........

JoAnn      Permalink


December 28, 2005

More Noise In Gene Expression

More Noise In Gene Expression Jennifer Marciniak and Dmitri Volfson
Human identical twins have different fingerprints and march to the beat of subtly different phenotypes, an indication of heterogeneity which led bioengineering scientists at the University of California, San Diego (UCSD) to devised computer algorithms that identify the underlying sources of variation at the basic level of life: unscripted fluctuations within individual cells and variations between identical cells.

"Researchers might assume that natural selection would prune any sloppiness at the level of gene expression, but recent studies by our group at UCSD and others have shown that is definitely not the case," said Jeff Hasty, a bioengineering professor at UCSD's Jacobs School of Engineering. "A number of individual genes produce less than 10 copies of regulatory messenger molecules, which is such a small number that it makes clockwork-like regularity of downstream cellular circuits statistically impossible. Our group and others have detected and classified significant downstream fluctuations that result from this source of 'intrinsic noise' in gene expression."

Hasty leads a team of scientists at UCSD that will report in a Dec. 21 advanced online publication by Nature a mathematical description of "extrinsic noise," an even larger component of variation in gene expression. This second type of noise results because no two geneticcally identical cells can keep the same time. The measurement of extrinsic noise was based on experiments involving baker's yeast, Saccharomyces cerevisiae, but the phenomenon and the way it is described mathematically would apply to other types of cells and other species.

"Individual yeast cells exist at various stages of their growth cycle, and this extrinsic variability explains a large component of the noise that must be accounted for in creating a mathematical model of the cell," said Dmitri Volfson, project scientist and a co-author of the study. "In this case, one yeast cell may be preparing to divide, another may be the result of a recent division, and the phenotypes of these two otherwise identical cells can be very different."........

Scott      Permalink


December 28, 2005

Defeating Malarial Parasite Defense

Defeating Malarial Parasite Defense
The world's deadliest malaria parasite, Plasmodium falciparum, sneaks past the human immune system with the help of a wardrobe of invisibility cloaks. If a person's immune cells learn to recognize one of the parasite's a number of camouflage proteins, the surviving invaders can swap disguises and slip away again to cause more damage. Malaria kills an estimated 2.7 million people annually worldwide, 75 percent of them children in Africa.

Howard Hughes Medical Institute (HHMI) international research scholars in Australia have determined how P. falciparum can turn on one cloaking gene and keep dozens of others silent until each is needed in turn. Their findings, published in the December 28, 2005, issue of Nature, reveal the mechanism of action of the genetic machinery thought to be the key to the parasite's survival.

A DNA sequence near the start of a cloaking gene, known as the gene's promoter, not only turns up production of its protein, but also keeps all other cloaking genes under wraps, according to Alan Cowman and Brendan Crabb, HHMI international research scholars at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and their co-authors. "The promoter is all you need for activation and silencing," Cowman said. "It's the main site of action where everything is happening."

Malaria parasites enter human blood from infected mosquitoes. The organisms invade and promptly remodel red blood cells. They decorate the surface of the cells they occupy with a protein called PfEMP1, made by the var gene family.

Using this versatile surface protein, the parasite evades the host's immune system using two basic strategies. First, the protein sticks infected red blood cells to the blood vessel lining, removing the infected cells from circulation, where they would probably be destroyed.........

Mark      Permalink



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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