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Archive - 2009

November 18th

Evolution of Highly Toxic Box Jellyfish

With thousands of stinging cells that can emit deadly venom from tentacles that can reach ten feet in length, the fifty or so species of box jellyfish have long been of interest to scientists and to the public. Yet little has been known about the evolution of this early branch in the animal tree of life. An international team of researchers has now largely unraveled the evolutionary relationships among the various species of box jellyfish, thereby providing insight into the evolution of their toxicity. “By determining the relationships among the different box jellyfish, some of which are capable of killing a healthy human, this study can help in the future development of antivenoms and treatments for their stings,” said Dr. Allen Collins, a specialist in Cnidaria, the phylum of animals that includes box jellyfish, and senior author of the report. “Researchers will now be able to make more informed choices about organisms for future venom studies, and make predictions on which species are likely to be of public health concern in addition to the known culprits.” Box jellies--also called sea wasps, stingers, or fire jellies--live primarily in warm coastal waters around the world. They are particularly well known in Australia, the Philippines and the rest of Southeast Asia, but they also occur in Hawaii and in waters off the United States Gulf and East Coasts. Their toxicity varies among species and ranges from being completely harmless to humans to causing death within minutes after a sting. Beyond their toxicity, box jellyfish have other interesting characteristics. Some species, for instance, have as many as 24 eyes, capable of sensing light and forming an image of their surroundings.

November 15th

Mouse Results Suggest Possible Drug Treatment for Huntington’s Disease

Researchers have found that normal synaptic activity in nerve cells (the electrical activity in the brain that allows nerve cells to communicate with one another) protects the brain from the misfolded proteins associated with Huntington's disease. In contrast, excessive extrasynaptic activity (aberrant electrical activity in the brain, usually not associated with communication between nerve cells) enhances the misfolded proteins' deadly effects. In addition, the scientists found that the drug Memantine, which is approved to treat Alzheimer's disease, successfully treated Huntington's disease in a mouse model by preserving normal synaptic electrical activity and suppressing excessive extrasynaptic electrical activity. "Chronic neurodegenerative diseases like Huntington's, Alzheimer's, and Parkinson's are all related to protein misfolding," said Dr. Stuart Lipton of the Burnham Institute for Medical Research, senior author of the report. "We show here, for the first time, that electrical activity controls protein folding, and if you have a drug that can adjust the electrical activity to the correct levels, you can protect against misfolding. Also, this verifies that appropriate electrical activity is protective, supporting the 'use it or lose it theory' of brain activity at the molecular level. For example, this finding may explain why epidemiologists have found that 'using' your brain by performing crossword puzzles and other games can stave off cognitive decline in diseases like Alzheimer's." A small human clinical trial of Memantine for Huntington's disease has recently shown positive effects. Larger, international clinical trials are now being planned. In addition to Dr. Lipton, the article’s authors included Dr. Michael Hayden of the University of British Columbia.

November 13th

Rasberry Ants on the March

The invasion of a new species of ant (Rasberry ants) has scientists intrigued, businesses concerned, and fire ants running for the hills, said Dr. Jerry Cook, an entomologist at Sam Houston State University. Dr. Cook and other scientists are at a loss to explain the fast and furious spread of the rapacious ant, which is named after exterminator Tom Rasberry, who discovered the ant in 2002. The ant was discovered in Houston in 2002 and has quickly spread as far north as Louisiana and Mississippi within the last year. "This is a species that we do not know much about. Presumably the ant came from the Caribbean through the Port of Houston," Dr. Cook said. "We know the ant is in the Paratrechina genus and is capable of growing a population of billions and they need to eat. They especially like other bugs, like fire ants and honey bees." The population is growing so fast, and so large, that it is potentially an ecosystem disaster, according to Dr. Cook. "If the Rasberry ant can virtually eliminate a pain like the fire ant, what else is it capable of doing?" he asked. "If bees are eliminated, plants will not be pollinated which could result in the lack of crops producing fruits and vegetables. That in turn becomes a major problem for the agriculture community. They could become more than a nuisance, they could become a danger." Dr. Cook emphasized the need for funding for research targeted at better understanding of the Rasberry ant. [Press release]

November 12th

Absence of LKB1 Gene Increases Insulin Production

Eliminating the LKB1 gene from the beta cells of the pancreas causes the production and secretion of more insulin than from normal beta cells in a mouse model, according to researchers from the Hebrew University of Jerusalem and collaborators. This results in an enhanced response to blood glucose levels. The findings have potentially significant implications for those suffering from diabetes due to insufficient production of insulin in the pancreas. Because it was shown that LKB1 negatively regulates both insulin content and secretion, the way has now been opened to possible development of a novel therapy that would limit the presence of this gene in pancreas beta cells, thus enhancing insulin secretion. This work was reported in the October 7 issue of Cell Metabolism. [Press release] [Cell Metabolism abstract]

November 11th

Preserving Ends of Chromosomes Linked to Longevity in Centenarians

Researchers at the Albert Einstein College of Medicine, and colleagues, have found a clear link between living to 100 and the inheritance of a hyperactive version of an enzyme that rebuilds telomeres. Telomeres are relatively short sections of specialized DNA that sit at the ends of all chromosomes. Telomeres have been compared to the plastic tips at the ends of shoelaces that prevent the laces from unraveling. Each time a cell divides, its telomeres erode slightly and become progressively shorter with each cell division. Eventually, telomeres become so short that their host cells stop dividing and lapse into a condition called cell senescence. As a result, vital tissues and important organs begin to fail and the classical signs of aging ensue. In investigating the role of telomeres in aging, the researchers studied Ashkenazi Jews because they are a homogeneous population that has been well studied genetically. Three groups were enrolled: 86 very old, but generally healthy, people (average age 97); 175 of their offspring; and 93 controls (offspring of parents who had lived a normal lifespan). "As we suspected, humans of exceptional longevity are better able to maintain the length of their telomeres," said Dr. Yousin Suh, senior author of the paper. "And we found that they owe their longevity, at least in part, to advantageous variants of genes involved in telomere maintenance." More specifically, the researchers found that participants who have lived to a very old age have inherited mutant genes that cause their telomerase-making system to be extra active and able to maintain telomere length more effectively. For the most part, these people were spared age-related diseases such as cardiovascular disease and diabetes, which cause most deaths among elderly people.

November 10th

Slower Pupil Response Seen in Autistic Children

Recently, University of Missouri researchers have developed a pupil response test that is 92.5 percent accurate in separating children with autism from those with typical development. The scientists used a computerized binocular infrared device, which eye doctors normally use for vision tests, to measure how pupils react to a 100-millisecond flash of light. The results showed that pupils of children diagnosed with autism were significantly slower to respond than those of a control group. "There are several potential mechanisms currently under study," said Dr. Gang Yao, senior author of the study. "If these results are successfully validated in a larger population, the pupils’ light response (PLR) might be developed into a biomarker that could have clinical implications in early screening for risks of autism. Studies have shown that early intervention will improve these children's developmental outcome." Autism is estimated to affect 1 in 150 children today, making it more common than childhood cancer, juvenile diabetes, and pediatric AIDS combined. Despite its widespread effect, autism is not well understood and there are currently no objective medical tests to diagnose it. This new report was published in the November issue of the Journal of Autism and Developmental Disorders. [Press release] [JADD article]

November 9th

Genes Distinguish Rare Long Survivors of Advanced Melanoma

Although the chances of surviving advanced melanoma are not very good with current therapies, some patients can live for years with melanoma that has spread beyond the skin to other organs. Now it may be possible to identify which patients are more likely to survive by analyzing the activity of hundreds of genes involved in the immune response and gene proliferation, according New York University Langone Medical Center scientists and collaborators. In a new study, the researchers used DNA microarray technology to find 266 genes associated with shorter or longer survival among 38 patients whose melanomas had recurred after being surgically removed. Such genetic information may someday help decide the best course of treatment for patients with advanced disease. "If we could actually understand what was happening in those patients, within the tumor itself, perhaps we'd be able to help them in terms of what therapy they might go on," said Dr. Nina Bhardwaj, the study's senior author. The collaborative study, led by graduate student Dusan Bogunovic, provided some hints about the underlying mechanism of melanoma. "We found that patients who survived longer had gene activity consistent with an immune response," Dr. Bhardwaj said. "Patients who didn't survive as long didn't have an up-regulation of those genes, but tended to have higher levels of genes associated with cell proliferation, suggesting that if your cells are growing more actively, the tumor is going to grow faster." She cautioned, however, that the study must still be validated with a much larger, independent group of patients. The study is to be published online in PNAS during the week of November 9. [Press release]

November 8th

Deletion of a Nicotinic Receptor Gene Could Lead to Learning Defects

The loss of a particular gene (CHRNA7) through deletion of genetic material on chromosome 15 appears to be associated with significant abnormalities in learning and behavior, according to a recent report by Baylor College of Medicine (BCM) researchers and colleagues. "This research goes about 95 percent of the way to pinning these problems in a specific group of individuals to this gene," said Dr. Arthur Beaudet, chair of molecular and human genetics at BCM and an author of the report. Dr. Beaudet believes that the deletion will be identified in other people with behavioral problems, as well as schizophrenia, developmental delay, and epilepsy. The gene's role in schizophrenia has been under study for some time. "This gene encodes a subunit of a nicotinic receptor," Dr. Beaudet said. "It is a gene that mediates the response to nicotine via a receptor whose normal ligand is acetylcholine." The gene encodes a protein called an ion channel, which allows ions to flow in and out of neurons in the brain. Defects in ion channels have previously been associated with forms of epilepsy or seizure disorder. "If insufficient expression of the nicotinic receptor causes most or all of the problems associated with deletions in this particular area of chromosome 15, then it offers a target for drug treatment," said Dr. Pawel Stankiewicz, senior author of the report. One such drug mentioned in the paper is Chantix, a medicine now used in smoking cessation efforts. This work was published online on November 8 in Nature Genetics. [Press release] [Nature Genetics abstract]

November 6th

Simple Blood Test May Identify Women at Risk of Alzheimer’s

Middle-aged women with high levels of a specific amino acid (homocysteine) in their blood are twice as likely to suffer from Alzheimer's disease many years later, according to a recent thesis from the Sahlgrenska Academy at the University of Gothenburg, Sweden. This discovery could lead to a new and simple way of determining who is at risk long before there are any signs of the illness. The thesis is based on the Prospective Population Study of Women in Gothenburg, which was started at the end of the 1960s when almost 1,500 women between the ages of 38 and 60 were examined, asked questions about their health, and had blood samples taken. Nearly all of the samples have now been analyzed and compared with information on who went on to suffer from Alzheimer's and dementia much later. "Alzheimer's disease was more than twice as common among the women with the highest levels of homocysteine than among those with the lowest, and the risk for any kind of dementia was 70 per cent higher," said Dr. Dimitri Zylberstein, author of the thesis. Historically, elevated homocysteine levels have been related to certain vitamin deficiencies (B12 and folate). Today we know that high homocysteine levels might be present even with perfectly normal vitamin status. "These days we in our clinical practice use homocysteine analyses mainly for assessment of vitamin status. However, our results mean that we could use the very same analysis for assessment of an individual's risk profile for dementia development. This opens the possibility for future preventive treatment at a very early stage," said Dr. Zylberstein. [Press release]

November 4th

Scientists Target DNA Quadruplexes in Battle Against Cancer

Some designers of anti-cancer drugs are investigating mysterious chunks of the genetic material DNA that may play a key role in preventing the growth and spread of cancer cells, according to an article in the November 2 issue of Chemical & Engineering News, the weekly newsmagazine of the American Chemical Society. In the article, C&EN Deputy Assistant Managing editor Stu Borman notes that the DNA structures, which scientists term "quadruplexes" because they have four-sided structures, are a genre of folded DNA that may help control whether genes are switched on or off. Quadruplexes sometimes form near genes that foster the growth of cancer cells. Some scientists thus regard them as promising targets for developing new anti-cancer drugs. Drugs that interact with quadruplexes could help kill cancer cells without harming healthy cells. In addition, they may side-step the serious problem of drug resistance, in which some drugs gradually lose their effectiveness against cancer. The C&EN article describes research on quadruplex-targeted drugs and explores the mysteries about how quadruplexes form, disappear, and function. [Press release] [C&EN article]