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Archive - Jan 31, 2013

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Autism Risk Linked to Prenatal Inflammation

Maternal inflammation during early pregnancy may be related to an increased risk of autism in children, according to new findings supported by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. Researchers found this in children of mothers with elevated C-reactive protein (CRP), a well-established marker of systemic inflammation. The risk of autism among children in the study was increased by 43 percent among mothers with CRP levels in the top 20th percentile, and by 80 percent for maternal CRP in the top 10th percentile. The findings appeared online on January 22, 2013 in the journal Molecular Psychiatry and add to mounting evidence that an overactive immune response can alter the development of the central nervous system in the fetus. "Elevated CRP is a signal that the body is undergoing a response to inflammation from, for example, a viral or bacterial infection," said the lead scientist on the study, Alan Brown, M.D., professor of clinical psychiatry and epidemiology at Columbia University College of Physicians and Surgeons, New York State Psychiatric Institute, and Mailman School of Public Health. "The higher the level of CRP in the mother, the greater the risk of autism in the child." Dr. Brown cautioned that the results should be viewed in perspective because the prevalence of inflammation during pregnancy is substantially higher than the prevalence of autism. "The vast majority of mothers with increased CRP levels will not give birth to children with autism," Dr. Brown said.

Deficiencies in Two Genes Combine to Contribute to Hirschprung Disease

Mutations in single genes can cause catastrophic diseases, such as Huntington's disease or sickle cell anemia. However, many conditions, including cancer, diabetes, and birth defects are multigenic, arising from the collective failure of the function of more than one gene. Researchers know that mutations in at least twelve individual genes are associated with the congenital defect Hirschprung Disease (HSCR), in which children are born lacking nerves that innervate the large intestine. Now two companion studies published in Human Molecular Genetics by Paul Trainor, Ph.D., Investigator at the Stowers Institute for Medical Research, identify a new gene associated with HSCR and show how the migration of cells that form the gut nervous system is impeded when the combined doses of two candidate genes are low. Understanding the genetic basis of HSCR offers hope for better diagnostics and treatment for it and other developmental defects caused by failure of cell migration. The cells that go awry in HSCR are a subset of what are called neural crest cells, embryonic cells that spring from the developing brain and spinal cord in mice or humans and then travel long distances to form, among other structures, structures in the face and heart, smooth muscle, and neurons of the peripheral nervous system, including those that innervate the gut. Dr. Trainor has been interested in neural crest cells since he was a graduate student, often focusing on developmental defects caused by their malfunction. "Neural crest cells have to be born in the right place, migrate an incredibly long distance, survive the migration, multiply and then differentiate into a mature cell type," says Dr.

Diffusion Coefficients for Complete Proteome of E. coli Determined for First Time

Understanding of the chemical foundations of life requires knowledge about the rate of chemical reactions in cells. The rates of these reactions depend on how fast the molecules taking part in reactions move (diffuse) in the cytoplasm. Professor Robert Hołyst's research team from the Institute of Physical Chemistry of the Polish Academy of Sciences in Warsaw (IPC PAS) managed to determine – for the first time – the diffusion coefficients for virtually all the proteins occurring in Escherichia coli. The method developed by the researchers can also be used for other cells. The movements of molecules in cells resemble a bit what's going on in railway stations. But the differences are obvious at first glance. "Regular trains leave stations at fixed times, whereas in cells transport processes take place virtually all the time. That's why it doesn't make sense to ask what time does the train with specific molecules leave the station. But it definitely makes sense to ask how fast the train with specific molecules is moving!” explains Professor Hołyst. Transport efficiency of chemical compounds in cells became inspiring for many transport companies. There's talk of biologistics as modelling vehicle or rail transport by looking up to what's going on inside the cells. Professor Hołyst, however, has no illusions about that: "Everyone is delighted, for in cells the transport is so wonderfully resistant to perturbations. They forget, however, that the transport results from random fluctuations, in addition occurring in a small volume, where viscosity depends not only on the medium, but also on the size of the viscosity probe! I wish good luck to all those who want to transfer processes occurring in physically so different environment to our roads.