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Archive - Mar 17, 2011

New Research Tool Targets MicroRNA Expression

A new research tool for studying microRNA expression in zebrafish will help researchers analyze the effects of microRNA (miRNA) on the early development of this model organism and better understand developmental and disease mechanisms in humans, as described in Zebrafish, a peer-reviewed journal published by Mary Ann Liebert, Inc. The article is available free online ahead of print. Researchers from University of Oregon (Eugene) have developed a novel, cost-effective method for measuring the expression of miRNAs in specific tissues in developing zebrafish embryos. miRNAs play an important role in regulating embryonic development. They are difficult to detect because they are very short strands of oligonucleotide and are often present in cells at low levels. Drs. Xinjun He, Yi-Lin Yan, April DeLaurier, and John Postlethwait describe the efficient technique they devised using digoxigenin-labeled riboprobes (oligonucleotide-based probe sequences capable of binding to a complementary miRNA sequence) in in situ hybridization (ISH) experiments. "This is a terrific new addition to the zebrafish toolbox, opening the door to an array of new experiments focused on the biology of non-coding RNAs using this superb model system," said Dr. Stephen Ekker, Editor-in-Chief of Zebrafish and Professor of Medicine at the Mayo Clinic, Rochester, Minnesota. [Press release] [Zebrafish abstract]

New Clinical Guidelines on Diagnosis and Management of Idiopathic Pulmonary Fibrosis

The American Thoracic Society has released new official clinical guidelines on the diagnosis and management of idiopathic pulmonary fibrosis (IPF). The statement replaces ATS guidelines published in 2000, and reviews current knowledge in the epidemiology, etiology, diagnosis and management of IPF, as well as available treatment options, including pharmacologic and non-pharmacologic therapies and palliative care. The statement appears in the March 15, 2011 issue of American Journal of Respiratory and Critical Care Medicine. IPF is a chronic, progressive, fatal form of fibrotic lung disease, characterized by shortness of breath during exertion, which occurs primarily in relatively older adults. The etiology of IPF is unclear. The disease occurs when injury to the lungs is triggered by an unknown cause, resulting in the formation of scar tissue that causes the lungs to become thickened and stiff. IPF may progress slowly over several years and may be punctuated by episodes of acute respiratory decline. Lung transplantation is a feasible treatment option in highly selected patients. A subgroup of patients with IPF has a genetic predisposition to the disease. "In the decade since the publication of the previous statement on IPF, studies have used the criteria for the diagnosis of IPF and recommendations published in the previous consensus-based statement to further our understanding of the clinical manifestations and course of IPF, and there has been an increasing body of evidence pertinent to its clinical management," said Dr. Ganesh Raghu, director of the Interstitial Lung Disease/Sarcoid/Pulmonary Fibrosis Program at the University of Washington Medical Center in Seattle and chair of the collaborative committee that drafted the statement.

Bacteria More Likely to Adopt “Loner” Genes

A new study of more than three dozen bacteria species — including the microbes responsible for pneumonia, meningitis, stomach ulcers and plague — settles a longstanding debate about why bacteria are more likely to steal some genes than others. While most organisms get their genes from their parents just as people do, bacteria and other single-celled creatures also regularly pick up genes from more distant relatives. This ability to 'steal' snippets of DNA from other species — known as lateral gene transfer — is responsible for the rapid spread of drug resistance among disease-causing bacteria. "By understanding why some genes are more likely to spread from one species to the next, we can better understand how new virulent bacterial strains emerge," said co-author Dr. Tal Pupko, a visiting scientist at the National Evolutionary Synthesis Center in Durham, North Carolina. Scientists have proposed several theories to explain why some bacterial genes are more likely to jump into other genomes. One theory, Dr. Pupko explained, is that it depends on what the gene does in the cell. Genes involved in core functions, like converting RNA into protein, are much less likely to make the leap. "If a species already has the basic molecular machinery for transcription and translation, there's no advantage to taking in another set of genes that do the same thing," Pupko said. Other studies suggest it's not what the gene does that matters, but how many proteins it interacts with – a network researchers have dubbed the 'interactome.' Genes involved in transcription and translation, for example, must work in concert with many partners to do their job.