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Duchenne Muscular Dystrophy, Lobbying Campaign At 10 Downing Street, UK
On 16 June, boys living with Duchenne Muscular Dystrophy, their families and supporters will be lobbying MPs and marching to No. 10 Downing Street to bring an end to the continuing serious under-funding for research into the condition. Results from recent clinical trials into the effectiveness of Exon Skipping as a gene therapy for the treatment of Duchenne have been very promising and scientists say that a cure is tantalisingly close, but more funding is needed. The lobby action is being organised by Action Duchenne, the only UK charity dedicated solely to raising awareness and raising funds for research into treatments and finding a cure, and providing support for families living with Duchenne.
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MicroRNAs Grease The Cell's Circadian Clockwork
Most of our cells possess an internal clock, a group of genes displaying a cyclic expression pattern that reaches a peak once a day. A large number of circadian genes are expressed by organs such as the liver, whose activity needs to be precisely regulated over the course of the day. A team of researchers of the National Centre of Competence in Research Frontiers in Genetics, based at the University of Geneva, Switzerland, reveals that an important regulator of this molecular oscillator is a specific microRNA. The latter belongs to a class of small RNA molecules that regulate the production of proteins in our cells. Thus far, little was known about their function within the circadian clockwork. The study by Ueli Schibler"s team, published in the 1st June edition of Genes & Development, fills in this important gap.
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Bone From Blood: Circulating Cells Form Bone Outside The Normal Skeleton
The accepted dogma has been that bone-forming cells, derived from the body"s connective tissue, are the only cells able to form the skeleton. However, new research shows that specialized cells in the blood share a common origin with white blood cells derived from the bone marrow and that these bloodstream cells are capable of forming bone at sites distant from the original skeleton. This work, published online this month in the journal Stem Cells, represents the first example of how circulating cells may contribute to abnormal bone formation.
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Sleep And Weight Gain: A Molecular Link

There appears to be a link between sleep and weight control, with some studies indicating that sleep disruption can increase weight gain and others that diet affects sleep. Victor Uebele and colleagues, at Merck Research Laboratories, West Point, have now provided further evidence to support this association by showing that T-type calcium channels regulate body weight maintenance and sleep in mice. These data suggest that sleep and circadian treatment approaches may be of benefit in the fight against obesity. Previous studies have shown that mice lacking the CaV3.1 T-type calcium channel have disrupted sleep/wake activity. In this study, the researchers found that these mice were resistant to weight gain when fed a high-fat diet. Consistent with these data, when normal-weight rodents were administered a drug that specifically antagonized T-type calcium channels during their inactive phase they showed increased sleep and were protected from weight gain due to a high-fat diet. Further, when the same drug was given to obese rodents it reduced body weight and fat mass. The authors conclude that the benefits of the drug are likely to be a result of better alignment of feeding patterns and the circadian rhythm, and that targeting T-type calcium channels might provide a new avenue of research for those developing drugs to treat obesity. TITLE: Antagonism of T-type calcium channels inhibits high-fat diet-induced weight gain in mice AUTHOR CONTACT: Victor N. Uebele Merck Research Laboratories, West Point, Pennsylvania, USA. View the PDF of this article at: https://www.the-jci.org/article.php?id=36954 Karen Honey Journal of Clinical Investigation


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