“Our Brains Have The Amazing Ability To Be Energy Efficient! - Med India” plus 4 more |
- Our Brains Have The Amazing Ability To Be Energy Efficient! - Med India
- Mother's cancer spread to baby in the womb - Sydney Morning Herald
- A biology teacher from Des Lacs-Burlington is a finalist for this year ... - KFYR-TV
- Fish vision discovery makes waves in natural selection - Genetic Engineering News
- Skin Cells May Provide Early Warning For Cancer Risk Elsewhere In Body - Science Daily
Our Brains Have The Amazing Ability To Be Energy Efficient! - Med India Posted: 15 Oct 2009 10:03 PM PDT The amount of energy needed for action potentials was previously estimated using a giant nerve cell from squid. Now, researchers at the Max-Planck Institute for Brain Research in Germany show that squid cell studies overestimated the amount of energy necessary to generate an action potential by almost a factor of four, suggesting human brains have the same potential to be energy efficient. The researchers used a novel technique to record the voltage generated by nerve cells to "show that a rather subtle separation between the timing of sodium entry and potassium exit during action potentials can determine how much energy is expended to maintain the ionic gradients," Murthy says. Murthy goes on to say that "[these results] are important, not just for a basic understanding of brain metabolism, but also for interpreting signals detected by non-invasive brain imaging techniques." Sorensen concludes that "the amazing thing is that we didn't realize the result a long time ago!" Source-Eurekalert This content has passed through fivefilters.org. | |
Mother's cancer spread to baby in the womb - Sydney Morning Herald Posted: 14 Oct 2009 05:51 AM PDT SCIENTISTS have established beyond doubt that cancer can be transmitted from mother to baby in the womb, but Australian women have been told the incidence is ''extraordinarily rare'' and no cause for alarm. The discovery was made by scientists in Britain when a baby developed cancer a few months after her mother died from leukaemia. The girl, born to a Japanese woman, 28, developed lymphoma, but a team at the Institute of Cancer Research, a college of the University of London, found that leukaemia cells had crossed the placenta and spread from the mother to her unborn baby, defying accepted theories of biology. The scientific adviser to Cancer Council Australia, Nik Zeps, said yesterday that there had been anecdotal evidence for more than 100 years that cancer could spread from mother to baby, but this case gave scientists the first hard evidence that the phenomenon existed. ''We need to stress that it is very rare, extraordinarily rare, for a pregnant woman to contract cancer and additionally rare for that to ever be passed on to an infant, but the most interesting part of this case for researchers is how the cells escaped the baby's immune system,'' Dr Zeps said. Publishing their findings in the Proceedings of the National Academy of Sciences, researchers said about 17 cases of suspected mother-to-child transmission had been noted throughout the world - usually leukaemia or melanoma - although Dr Zeps said he was unaware of any cases in Australia. If the cells crossed the placental barrier the baby's immune system should have recognised them as foreign invaders and destroyed them. In the latest case no one knew the mother had cancer during her pregnancy. She had a normal delivery in hospital, giving birth to an apparently healthy baby girl. But a month later the mother was diagnosed with advanced leukaemia and died. When the baby was 11 months old she was taken to hospital with a swollen right cheek. Tests showed she had a tumour in her jaw and the cancer had spread to her lungs. Researchers then found the cancer cells of mother and baby carried the identical mutated cancer gene, called BCR-ABL1, but the infant had not inherited this gene. This meant that the cells must have come from the mother. Scientists then looked for evidence of some form of immunological acceptance or tolerance of the foreign cells by the foetus. They examined the genes of the cancer cells in the infant and found a deletion mutation - some DNA missing in the region that controls expression of the major histo-compatibility locus. This was significant because HLA molecules primarily distinguish one individual, and his or her cells, from another, so the absence of these on the cancer cells meant the infant's immune system would not have recognised that they were foreign. ''Hopefully, this case will now open up new avenues of research into how targeting immune systems can prevent or treat cancer,'' Dr Zeps said. with Guardian News & Media This content has passed through fivefilters.org. | |
A biology teacher from Des Lacs-Burlington is a finalist for this year ... - KFYR-TV Posted: 12 Oct 2009 04:52 PM PDT A biology teacher from Des Lacs-Burlington is a finalist for this year`s North Dakota Teacher of the Year award. | Mary Eldredge-Sandbo is in her 27th year at Des Lacs-Burlington high school. Sanbo is among four other finalists which were announced today by the state Department of Public Instruction. KMOT featured Sanbo in an Education in Action story last December. With Sandbo`s help Des Lacs-Burlington high school has received $340,000 dollars through grants. With the money, the school has been able to purchase computers, projectors, smart boards and other teaching equipment. The award winner will be announced at the North Dakota Education Association conference Oct. 22 in Grand Forks. This content has passed through fivefilters.org. |
Fish vision discovery makes waves in natural selection - Genetic Engineering News Posted: 16 Oct 2009 09:37 AM PDT Oct 16 2009, 12:20 PM EST Fish vision discovery makes waves in natural selectionEUREKALERT Contact: Beverly Clarkbeverly.clark@emory.edu 404-712-8780 Emory University Emory University researchers have identified the first fish known to have switched from ultraviolet vision to violet vision, or the ability to see blue light. The discovery is also the first example of an animal deleting a molecule to change its visual spectrum. Their findings on scabbardfish, linking molecular evolution to functional changes and the possible environmental factors driving them, were published Oct. 13 in the Proceedings of the National Academy of Sciences. "This multi-dimensional approach strengthens the case for the importance of adaptive evolution," says evolutionary geneticist Shozo Yokoyama, who led the study. "Building on this framework will take studies of natural selection to the next level." The research team included Takashi Tada, a post-doctoral fellow in biology, and Ahmet Altun, a post-doctoral fellow in biology and computational chemistry. Vision 'like a painting' For two decades, Yokoyama has done groundbreaking work on the adaptive evolution of vision in vertebrates. Vision serves as a good study model, since it is the simplest of the sensory systems. For example, only four genes are involved in human vision. "It's amazing, but you can mix together this small number of genes and detect a whole color spectrum," Yokoyama says. "It's just like a painting." The common vertebrate ancestor possessed UV vision. However, many species, including humans, have switched from UV to violet vision, or the ability to sense the blue color spectrum. From the ocean depths Fish provide clues for how environmental factors can lead to such vision changes, since the available light at various ocean depths is well quantified. All fish previously studied have retained UV vision, but the Emory researchers found that the scabbardfish has not. To tease out the molecular basis for this difference, they used genetic engineering, quantum chemistry and theoretical computation to compare vision proteins and pigments from scabbardfish and another species, lampfish. The results indicated that scabbardfish shifted from UV to violet vision by deleting the molecule at site 86 in the chain of amino acids in the opsin protein. "Normally, amino acid changes cause small structure changes, but in this case, a critical amino acid was deleted," Yokoyama says. More examples likely "The finding implies that we can find more examples of a similar switch to violet vision in different fish lineages," he adds. "Comparing violet and UV pigments in fish living in different habitats will open an unprecedented opportunity to clarify the molecular basis of phenotypic adaptations, along with the genetics of UV and violet vision." Scabbardfish spend much of their life at depths of 25 to 100 meters, where UV light is less intense than violet light, which could explain why they made the vision shift, Yokoyama theorizes. Lampfish also spend much of their time in deep water. But they may have retained UV vision because they feed near the surface at twilight on tiny, translucent crustaceans that are easier to see in UV light. A framework for evolutionary biology Last year, Yokoyama and collaborators completed a comprehensive project to track changes in the dim-light vision protein opsin in nine fish species, chameleons, dolphins and elephants, as the animals spread into new environments and diversified over time. The researchers found that adaptive changes occur by a small number of amino acid substitutions, but most substitutions do not lead to functional changes. Their results provided a reference framework for further research, and helped bring to light the limitations of studies that rely on statistical analysis of gene sequences alone to identify adaptive mutations in proteins. "Evolutionary biology is filled with arguments that are misleading, at best," Yokoyama says. "To make a strong case for the mechanisms of natural selection, you have to connect changes in specific molecules with changes in phenotypes, and then you have to connect these changes to the living environment." For more Emory University news: www.emory.edu/esciencecommons. This content has passed through fivefilters.org. | |
Skin Cells May Provide Early Warning For Cancer Risk Elsewhere In Body - Science Daily Posted: 16 Oct 2009 08:11 AM PDT ScienceDaily (Oct. 16, 2009) While some scientists have argued that cancer is such a complex genetic disease that you'd have to sequence a person's complete genome in order to predict his or her cancer risk, a University of California, Berkeley, cell biologist suggests that the risk may be more simply determined by inexpensively culturing a few skin cells. Harry Rubin, professor emeritus of molecular and cell biology at UC Berkeley, acknowledges that cancer cells have mutations in hundreds of genes, making it hard to determine which are the key triggers and making prognosis and treatment equally difficult. Even normal tissue differs from person to person because of a myriad of less disruptive mutations and because of different environmental exposures, both of which affect future cancer risk. But in the September issue of the journal Cancer Epidemiology, Biomarkers and Prevention, Rubin argues that, while it may be hard to dissect the role of each of these mutations, their collective effect should be observable in tissue before any cancers develop. Specifically, increases in how densely the cells grow, which Rubin argues are a prelude to cancer, may be detectable even before the cancer appears, warning of risks that could be lessened by behavioral changes. "Over a 50-year career, I've worked with cells transforming (into cancer) in culture and seen the first step in a dynamic way, seen cells continuing to multiply when they should have stopped," Rubin said. "This is the first step in cancer, though not yet cancer, and you can measure these changes quantitatively." The problem, of course, is that it is impractical to test all the body's tissues to determine whether they have abnormal cell growth. But Rubin has found evidence from other studies that, in some cases, skin fibroblasts show these early changes even before cancer appears in other tissues, such as the colon. "The abnormal growth behavior of skin fibroblasts in cancer-prone individuals has suggested that, at least in some cases, cancer can be considered a systemic disease and that this difference in the behavior of skin fibroblast cells from such individuals may be a practical basis for prevention, diagnosis and management of the disease," he concluded in his paper. "It's a great idea, scientifically; the question is, 'Is it there clinically?'" said Douglas Brash, professor of therapeutic radiology, genetics and dermatology at Yale School of Medicine. "This is interesting enough that someone should look to see whether it is clinically reliable." Dr. Stuart H. Yuspa, co-chief of the Laboratory of Cancer Biology and Genetics at the National Cancer Institute, agreed. "Harry's ideas are always amazing, and I admired the paper," he said. "His idea has scientific support, and if it turned out to be correct, it could be extremely valuable for people, assuming they would want to know their risk." Rubin bases his argument on various studies over the past 50+ years that show that cancers grow from a larger "field" of abnormally multiplying cells that otherwise look normal. These "field" cells are generally ignored by surgeons when they remove solid cancers - in fact, the large size of the field would make its total removal impossible - but pathologists have shown that the cells are capable of again giving rise to cancers. "These cells have early mutations that could lead to cancer," Rubin said. "Even though they look normal, they multiply in places where they shouldn't and eventually accumulate enough mutations to form a carcinoma. They are the first stage in cancer, but not cancer." The inappropriate growth - called cancerization - is a sign that the normal processes that stop growth when cells contact one another have been disrupted, though not fully, because otherwise the cells would invade the underlying connective tissue and become cancerous. Rubin showed in experiments 15 years ago that if you take cells that grow normally in cell culture and encourage mutations, then select for behavioral abnormalities involving growth, you can get proliferation of cells that behave like cancerization field cells. Similarly, while normal skin fibroblast cells grow to a certain density and stop, fibroblasts from cancer-susceptible individuals grow to an unusually high density in a Petri dish. That difference between fibroblasts from normal and cancer-susceptible individuals can be amplified to improve identification of those at risk of cancer, Rubin said. Rubin suspects that the growth change in skin fibroblasts heralds a general change in all the body's epithelial tissue, that is, the tissues that line all the body organs. The most prevalent cancers - including colon, breast, lung, skin, head and neck - arise from epithelial tissue. In certain cancer-prone families, for example, the same mutated gene is found in all tissues, and the fibroblasts grow to high densities in culture, just like epithelial cells in a precancerous field do in the body. "If this works out after studying a large number of cases, then the people who are found to have a high probability of developing cancer would be more likely to pay attention to their diet, exercise, weight, smoking and behaviors that are known to contribute to an increased risk of cancer," he said. "Basic studies of a cell culture model for field cancerization should reveal the conditions that drive or delay the process and could be applied in prevention of cancer." This content has passed through fivefilters.org. |
You are subscribed to email updates from Biology - Bing News To stop receiving these emails, you may unsubscribe now. | Email delivery powered by Google |
Google Inc., 20 West Kinzie, Chicago IL USA 60610 |
0 comments:
Post a Comment