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January 22, 2006, 10:08 PM CT

Two New Stem Cell Lines In Animal Cell-free Culture

Two New Stem Cell Lines In Animal Cell-free Culture Photo: Jeff Miller, University of Wisconsin
Lab manager Jessica Antosiewicz removes a tray of stem cell cultures from an incubator in researcher James Thomson's lab at the University of Wisconsin-Madison. Thomson, a developmental biologist and professor of anatomy, directed the research group that reported the first isolation of embryonic stem cell lines from a nonhuman primate in 1995, work that led his group to the first successful isolation of human embryonic stem cell lines in 1998.

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.........

Posted by: Scott      Permalink


January 16, 2006, 11:45 PM CT

Boosting Stem Cells to Treat Diabetes

Boosting Stem Cells to Treat Diabetes
For diabetes patients, who can't produce their own insulin, human stem cell-based transplants that produce insulin would be a major breakthrough.

But current laboratory methods of culturing human stem cells result in very limited quantities, far short of the quantities necessary for therapeutic applications.

For that reason, Emmanuel (Manolis) Tzanakakis, Ph.D., is striving to boost the numbers of stem cells produced in the laboratory, expanding the pool of cells that eventually can be differentiated into insulin-producing cells.

Tzanakakis, assistant professor in the Department of Chemical and Biological Engineering in the University at Buffalo School of Engineering and Applied Sciences, has received a $200,000 James D. Watson Investigator Grant award to support his studies from the New York State Office of Science, Technology and Academic Research (NYSTAR). He is one of six scientists throughout the state to receive the award this year.

His ultimate goal is to conduct research to develop methods that will allow sufficient quantities of differentiated cells that secrete insulin to be produced from the stem cells. Such cells could be used for diabetes therapies, including transplantation into patients, freeing them from the lifelong necessity of daily insulin injections.........

Posted by: JoAnn      Permalink


January 9, 2006, 11:49 PM CT

Gene Mutation Means Poor Outcomes In Thyroid Cancer

Gene Mutation Means With Poor Outcomes In Thyroid Cancer Thyroid gland is located on both sides of the neck
Researchers at Johns Hopkins have found that a mutation in the gene that triggers production of a tumor growth protein is linked to poorer outcomes for patients with papillary thyroid cancer (PTC). A report on the study is published in the recent issue of The Journal of Clinical Endocrinology and Metabolism.

Mingzhao Xing, M.D., Ph.D., an assistant professor in the Division of Endocrinology and Metabolism at The Johns Hopkins University School of Medicine, led the multi-center study. "This discovery should help physicians rate risk levels for patients with PTC," he says.

The gene, called BRAF, is part of a signaling pathway that, when activated, is known to cause tumor growth, and mutations in BRAF have been linked to a variety of human cancers, the scientists say.

For the study, Xing and his colleagues looked at information from 219 PTC patients from 1990 to 2004. The relationship among BRAF mutations, initial tumor characteristics, cancer recurrence and clinical outcomes was analyzed.

Results showed a "significant association" between BRAF mutation and spread of the cancer from the thyroid, lymph node metastasis, and advanced tumor stage at the time of surgery to remove the malignant thyroid gland. The thyroid, a gland located beneath the voice box (larynx) that produces thyroid hormone, helps regulate body cell growth and metabolism. Results also showed that, given an average follow-up of three to four years, 25 percent of patients with BRAF mutations experienced tumor recurrence compared to 9 percent without evidence of BRAF mutations.........

Posted by: Emily      Permalink


January 9, 2006, 11:29 PM CT

Molecule From The Sea Kills Cancer Cells

Molecule From The Sea Kills Cancer Cells 
Sea sponge porifera one type of sea sponge
A natural chemical made by a New Zealand sea sponge exerts its deadly effects on cancer cells by preventing the cells' protein-building machinery from turning on, Johns Hopkins researchers report in the Dec. 9 issue of Molecular Cell.

The chemical's anti-cancer effects have been known since 1991, but this is the first comprehensive report to show how the molecule, known as pateamine A (PatA), stalls the growth of so-called eukaryotic cells -- cells that have membranes and a nucleus.

"Agents that interfere with protein production in bacteria are already useful antibiotics, but this is the first small molecule found to interfere specifically with the earliest steps of protein production in human cells," says the study's leader, Jun Liu, Ph.D., a professor of pharmacology and molecular sciences in the Johns Hopkins Institute for Basic Biomedical Sciences.

Eventhough any clinical applications of PatA or related molecules are likely a number of years away, Liu notes, PatA's abilities offers researchers the chance to probe the earliest steps in protein production and the biology of so-called "suicide" in human cells.

"The whole idea of chemical biology is that we can use active molecules like PatA as bait to fish out their biological targets, which sheds light on normal biology and can clarify why the molecules' interaction is important," says Liu, whose research has focused on using chemical biology to study the regulation of the immune system. "This is incredibly powerful as researchers begin creating networks, not just linear pathways, of biological understanding".........

Posted by: Emily      Permalink


January 9, 2006, 11:00 PM CT

Telomerase And More

Telomerase And More
With seed money from Johns Hopkins Institute of Cell Engineering, a Johns Hopkins geneticist and her team have discovered a critical link between the health of stem cells and the length of the chromosome ends within them.

Chromosome ends, or telomeres, are repetitive stretches of DNA that protect chromosomes in much the same way as plastic tips on shoelaces prevent the fabric from fraying. Each time a cell divides, its chromosome ends get a little shorter, and eventually the cell can no longer divide because its critical genetic information is exposed. In stem cells, however, a protein called telomerase normally maintains the telomeres' length, allowing the cells to divide indefinitely.

Now, the Hopkins scientists report that mice engineered to have just half the normal amount of telomerase can't maintain their stem cells' chromosome ends, showing that a little telomerase isn't enough. In these "half-telomerase" mice, their telomeres shortened over time, bringing an early demise to stem cells that replenish the blood supply, immune system and intestine, the scientists report. Moreover, offspring of these mice bred to have normal levels of telomerase still exhibited early loss of stem cells, the scientists report in the Dec. 16 issue of Cell.

"These offspring have what we have called 'occult' genetic disease -- their genetic make-up is perfectly normal, but they still have the physical problems of their parents," says Carol Greider, Ph.D., director and professor of molecular biology and genetics in the Johns Hopkins Institute of Basic Biomedical Sciences. "This phenomenon could complicate the hunt for disease genes."........

Posted by: Emily      Permalink


January 9, 2006, 10:55 PM CT

Integrating New Neurons In To Adult Brain

Integrating New Neurons In To  Adult Brain
In experiments with mice, researchers from Johns Hopkins' Institute for Cell Engineering have discovered the steps mandatory to integrate new neurons into the brain's existing operations.

For more than a century, researchers thought the adult brain could only lose nerve cells, not gain them, but in fact, new neurons do form during adulthood in all mammals, including humans, and become a working part of the adult brain in mice at the very least.

In the first study to show how these "baby" neurons are integrated into the brain's existing networks, the Johns Hopkins scientists show that a brain chemical called GABA readies baby neurons to make connections to old ones. The discovery is described in the Dec. 11 advance online section of Nature.

"GABA is important during fetal development, but most researchers thought it would have the same role it has with adult neurons, which is to inhibit the cells' signals," says Hongjun Song, Ph.D., an assistant professor in the Neuroregeneration and Repair Program within ICE. "We've shown that GABA instead excites new neurons and that this is the first step toward their integration into the adult brain".

Song added that their discovery might help efforts to increase neuron regeneration in the brain or to make transplanted stem cells form connections more efficiently.........

Posted by: Daniel      Permalink


January 9, 2006, 9:48 PM CT

Optimizing Immune Response Viral Infections

Optimizing Immune Response Viral Infections Gordon Freeman, PhD
Like boxers wearied by a 15-round bout, the immune system's CD8 T cells eventually become "exhausted" in their battle against persistent viral infection, and less effective in fighting the disease.

In a study would be published Dec. 28 on the journal Nature's website, scientists at Dana-Farber Cancer Institute and Emory University have traced the problem to a gene that turns off the infection-fighting drive of CD8 T cells in mice. The discovery raises the possibility that CD8 cell exhaustion can be reversed in human patients, reinvigorating the immune system's defenses against chronic viral infections ranging from hepatitis to HIV, the virus that causes AIDS.

"CD8 T cells that have fought viral infections retain a 'memory' of the viruses they've encountered, so they can rapidly respond to new infections from those viruses," says the study's author, Gordon Freeman, PhD, of Dana-Farber. In the case of chronic infection, however, senior author Rafi Ahmed, PhD, of Emory, has shown that memory cells become exhausted and lose the capacity to respond to the virus. Why this occurs, on a molecular level, has been unclear.

To find the cause, Freeman and colleagues conducted a "microarray" experiment measuring the activity of thousands of genes in normal memory CD8 T cells in mice and in "exhausted" versions of those cells. They found that a gene known as PD-1 was much more active in the exhausted cells.........

Posted by: Scott      Permalink


January 7, 2006, 4:55 PM CT

Mysterious Eye Cells Adapt To Light

Mysterious Eye Cells Adapt To Light
A new retinal photoreceptor adjusts its sensitivity in different lighting conditions, according to researchers at Brown University, where the rare eye cells were discovered.

The results, published in Neuron, are a surprise. Though rods and cones, their biological cousins in the retina, clearly adjust to light levels, these new cells - intrinsically photosensitive retinal ganglion cells, or ipRGCs - were assumed not to adapt this way. Still, the adaptation process in ipRGCs is weaker and slower than it is in rods and cones.

The findings provide further evidence that the eye has complementary brain-signaling systems at work. Rods and cones rapidly communicate changes in brightness, signals which allow us to glimpse a baseball streaking across the sky or a deer darting into a darkened road. But ipRGCs work differently. They send signals about overall brightness, telling the brain when it is night and when it is day.

"These cells operate like a light meter on a camera," said David Berson, the Sidney A. Fox and Dorothea Doctors Fox Professor of Ophthalmology and Visual Sciences. "They tell the brain to constrict the pupil based on the amount of light registered over time".

Berson discovered ipRGCs in his Brown neuroscience lab three years ago. These cells number no more than 2,000 in the eye and have a direct link to the brain, sending electrical messages to an area regulating the pupil as well as a region controlling the body clock. This circadian rhythm controls alertness, sleep, hormone production, body temperature and organ function.........

Posted by: Mike      Permalink


January 7, 2006, 3:55 PM CT

Gene Therapy For Muscular Dystrophy

Gene Therapy For Muscular Dystrophy Gene defects are often the cause of muscular dystrophy
A new gene treatment technique that has shown promise in skin disease and hemophilia might one day be useful for treating muscular dystrophy, according to a new study by scientists at Stanford University School of Medicine.

In the study, published online in the Proceedings of the National Academy of Sciences the week of Jan. 2, the scientists used gene treatment to introduce a healthy copy of the gene dystrophin into mice with a condition that mimics muscular dystrophy. The dystrophin gene is mutated and as a result produces a defective protein in the roughly 20,000 people in the United States with the most common form of the disease.

Using gene treatment to treat muscular dystrophy isn't a new idea. Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences, said that scientists have tried several different techniques with variable success. One hurdle is getting genes into muscle cells all over the body. Another is convincing those cells to permanently produce the therapeutic protein made by those genes.

The gene treatment technique Rando and postdoctoral fellow Carmen Bertoni, PhD, used was developed by Michele Calos, PhD, associate professor of genetics. One of the main advantages of this method is that it could potentially provide a long-term fix for a variety of genetic diseases, including muscular dystrophy.........

Posted by: Daniel      Permalink


January 4, 2006

Brain Cell Activity Increases Amyloid Beta

Brain Cell Activity Increases Amyloid Beta
Increased communication between brain cells increases levels of amyloid beta, the key ingredient in Alzheimer's brain plaques, researchers at Washington University School of Medicine in St. Louis have found.

The findings showed that turning up brain cell firing rates drove up levels of amyloid beta in the spaces between brain cells. Corresponding drops in amyloid beta levels occurred when brain cells' ability to send messages was dampened or blocked completely.

The results, produced in mouse models of Alzheimer's, will appear in the journal Neuron on Dec. 22. They complement a Washington University study published earlier this year that used functional brain imaging to show that the brain areas that develop Alzheimer's plaques are also the regions that are the most active in healthy young people who are daydreaming or not carrying out a specific cognitive task (http://news-info.wustl.edu/news/page/normal/5621.html).

The two papers have scientists considering the possibility of someday slowing or preventing the development of Alzheimer's disease by using pharmaceuticals to selectively reduce some communication between brain cells. However, scientists still have to determine if increased levels of amyloid beta can be partially linked to particular classes of the nerve cell messengers and receptors that cells use to communicate with each other.

"Ideally, we will be hoping to find a drug or mechanism that could very specifically target the processes that lead to increased amyloid beta levels," says lead author John Cirrito, Ph.D., a postdoctoral research associate in neurology and psychology. "If we can identify these and find ways to modulate them, we'd have new ways of intervening in Alzheimer's disease."

Senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, says that the results do not contradict earlier studies that suggested crossword puzzles, exercise and other mental stimulation can reduce the chances of developing Alzheimer's disease.........

Daniel      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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