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Archive - Apr 20, 2017

Naked Mole Rat Struts More Stuff; Longest-Lived Rodent Shows Remarkable Ability to Withstand Oxygen Deprivation

Deprived of oxygen, naked mole-rats can survive by metabolizing fructose just as plants do, researchers report in the April 21, 2017 issue of Science. The article is titled “Fructose-Driven Glycolysis Supports Anoxia Resistance in the Naked Mole-Rat."Understanding how the animals do this could lead to treatments for patients suffering crises of oxygen deprivation, as in heart attacks and strokes. "This is just the latest remarkable discovery about the naked mole-rat -- a cold-blooded mammal that lives decades longer than other rodents, rarely gets cancer, and doesn't feel many types of pain," says Thomas Park, Ph.D., Professor of Biological Sciences at the University of Illinois at Chicago (UIC), who led an international team of researchers from UIC, the Max Delbrück Institute in Berlin, and the University of Pretoria in South Africa on the study. In humans, laboratory mice, and all other known mammals, when brain cells are starved of oxygen they run out of energy and begin to die. But naked mole-rats have a backup: their brain cells start burning fructose, which produces energy anaerobically through a metabolic pathway that is only used by plants - or so scientists thought. In the new study, the researchers exposed naked mole-rats to low oxygen conditions in the laboratory and found that they released large amounts of fructose into the bloodstream. The fructose, the scientists found, was transported into brain cells by molecular fructose pumps that in all other mammals are found only on cells of the intestine. "The naked mole-rat has simply rearranged some basic building-blocks of metabolism to make it super-tolerant to low oxygen conditions," said Dr. Park, who has studied the strange species for 18 years. At oxygen levels low enough to kill a human within minutes, naked mole-rats can survive for at least five hours, Dr.

Personalized Medicine 10.0 Discusses Recent Milestones and Future of Discovery Impacting Precision Management of Human Health and Disease on June 2 in San Francisco

Since 2008, the Personalized Medicine Conference has addressed challenging themes in genomic health through presentations and discussions among prominent scientific leaders in the biotechnology, pharmaceutical, and medical communities. In partnership with San Francisco State University’s Department of Biology, SF State Alumni, and the City of South San Francisco, the conference has showcased world-class science and striven to be the bellwether of the latest and greatest in personalized, genomic, and precision medicine. The conference has also been a valued networking opportunity for students and accomplished professionals alike, mirroring similar meetings serving the professional Biotech community. On June 2, 2017, San Francisco State University’s Department of Biology will host Personalized Medicine 10.0, a look back at the best topics and speakers over the last decade. The title for the upcoming meeting, (“Has It Changed Your Life?”) will review past conference topics, assess predictions of the past, and look to the future of personalized medicine in the coming decades. Aside from the stunning science itself, a wide variety of topics have been addressed, including clinical advances and applications, study design, business opportunities, regulatory issues, and the ethical and cultural impacts of personalized medicine. This year, the conference will revisit themes in bioinformatics, data management, oncology, epigenetics, genomics of rare diseases, nth-generation sequencing technologies, the microbiome, unprecedented developments in gene therapy and genome editing, and will project where the business and science of personalized medicine will be in the future.

Natural Experiment, Dogged Investigation, Yield Clue to Devastating Neurological Disease; Tubb4A Mutation Affects Myelin Production & Maintenance, Leads to Buildup of Microtubules in Oligodendrocytes

After a 29-year quest, Dr. Ian Duncan, a Professor of Veterinary Medicine at the University of Wisconsin-Madison, has finally pinpointed the cause of a serious neurologic disease in a colony of rats.” His new study, carried out with collaborators was published, online on April 10, 2017 in the journal Annals of Neurology, is more than the conclusion of a personal and intellectual odyssey, however. Dr. Duncan has just shown that the rat abnormality closely resembles a rare human mutation that results in severe neurologic dysfunction. The human disease can affect many parts of the brain and has been called H-ABC. Crucially, both abnormalities affect the production and maintenance of myelin -- the white, fatty insulation that nerves need to carry electrical signals. The deterioration of myelin in the brain causes the common neurologic disorder multiple sclerosis. Myelin defects are also at the root of the leukodystrophies -- genetic disorders that include H-ABC. Dr. Duncan's examination of nervous system tissue from both conditions revealed a telltale overgrowth of tiny tubes known as microtubules in oligodendrocytes, the cells that make myelin and deposit it on nerve fibers. The Annals study offers a window on a rare disease -- and also on the broader issue of myelin formation. "For a human disease, we have provided a model that did not exist before," Dr. Duncan says, "and we've shown that it's based on microtubule accumulation in oligodendrocytes. Now we've seen similar changes in the rats and the human cells." The new article is titled “A Mutation in the Tubb4a Gene Leads to Microtubule Accumulation With Hypomyelination and Demyelination." The roots of the new publication include a chance observation by two Chilean scientists, a couple of eyebrow-raising trips across the U.S.

New Weapon in Fight Against Antibiotic Resistance Discovered; ID of Key Sodium Pump in Chlamydia trachomatis and Development of Targeted Drug to Inhibit Pump Are “Tremendously Exciting,” Researcher Says

Scientists at St. Boniface Hospital Albrechtsen Research Centre and the University of Manitoba in Canada have developed a drug that combats two of the top ten "priority pathogens" recently defined by the World Health Organization (WHO) as antiobiotic-resistant bacteria requiring new interventions1. The drug, dubbed PEG-2S, has received a provisional patent, and its development is highlighted in a study published online on April 20, 2017 in the Canadian Journal of Physiology and Pharmacology (CJPP). Without affecting healthy cells, the drug prevents the proliferation of a harmful bacteria that possesses a specific type of energy supply shared by a number of other bacteria. The open-access article, entitled "Development of a Novel Rationally Designed Antibiotic to Inhibit A Nontraditional Bacterial Target,” revealed that a variety of bacteria share a unique respiratory sodium pump (NQR) that supplies energy vital to the bacteria's survival. The study showed that the drug in question, PEG-2S, inhibits the function of the NQR pump and the production and growth of Chlamydia trachomatis bacteria. The drug is highly targeted and only impacts bacterial cells with NQR pumps and is not toxic to normal, healthy cells. The list of NQR-possessing bacteria is growing steadily as genomic information becomes available. With more than 20 different pathogenic bacteria containing NQR, the possibility for this drug to avoid multidrug resistance through NQR inhibition represents a potential breakthrough in antibiotic design. Traditional targets for antibiotics are limited; no new antibiotics have been discovered since 1987. Only two antibiotics have received U.S. FDA approval since 2009. "New drugs are not being approved because they share the same target to which the bacteria are developing resistance.