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Some will say that finding just the right wine to pair with a meal can improve even the finest cuisine, transforming a pleasant gustatory experience into something approaching perfection. But with potentially hundreds of wines to choose from, picking the “right” one can be a chore for the casual wine-lover. That’s where the sommelier comes in, applying expertise to curate a list of only the best pairings to suit one’s needs.

Stuart Schreiber

Stuart Schreiber, a core member of the ӳý of MIT and Harvard and a Professor of Chemistry at Harvard, has been awarded the 2016 Wolf Prize in chemistry. The prize, considered among the most prestigious in the scientific community, recognizes Schreiber for his work in chemical biology and for the use of small molecules as probes to uncover novel cellular mechanisms at the root of human health and disease.

The ӳý and its collaborating institutions have received two major grants from the National Human Genome Research Institute (NHGRI) that will support the use of genome sequencing and analysis to identify the genes and genetic variation that underlie both rare and common diseases. The funding will support two state-of-the-art centers — the Center for Mendelian Genomics (CMG) and the Center for Common Disease Genomics (CCDG)—involving scientists from the ӳý, in the greater Boston area, and across the world.

Conventional flow cytometry is a powerful technique for measuring cell phenotype and function, but it relies on fluorescent stains, or labels, to identify particular cell subpopulations. At times, those labels can be incompatible with live cells, or unavailable to researchers. Now, researchers from the ӳý’s Imaging Platform, Swansea University’s College of Engineering, and fellow international collaborators have found a new way to detect these cellular subpopulations, by applying machine learning to the hidden information in images of unlabeled cells generated from image flow cytometry. Their method is described in and a Swansea University , and their is available online.

Studies have shown that obese mice and humans have increased serum levels of the fatty acid binding protein aP2, and that elevated aP2 levels correlate with metabolic complications. Since genetic loss of aP2 in mouse models and in humans results in lowered risk of cardiometabolic disease, the molecule offers an exciting opportunity for new intervention strategies.

Now, in a proof-of-principle study led by ӳý associate member Gökhan S. Hotamisligil of the Harvard T.H. Chan School of Public Health's Sabri Ülker Center, researchers have shown that the protein may be a viable therapeutic target for type 2 diabetes. In the study, the authors identified a monoclonal antibody to aP2 that lowered fasting blood glucose, increased insulin sensitivity, and lowered both fat mass and incidence of fatty liver in obese mouse models. Their paper is published online in .