Minutes-duration optical flares with supernova luminosities

In recent years, certain luminous extragalactic optical transients have been observed to last only a few days1. Their short observed duration implies a different powering mechanism from the most common luminous extragalactic transients (supernovae), whose timescale is weeks2. Some short-duration transients, most notably AT2018cow (ref. 3), show blue optical colours and bright radio and X-ray emission4. Several AT2018cow-like transients have shown hints of a long-lived embedded energy source5, such as X-ray variability6,7, prolonged ultraviolet emission8, a tentative X-ray quasiperiodic oscillation9,10 and large energies coupled to fast (but subrelativistic) radio-emitting ejecta11,12. Here we report observations of minutes-duration optical flares in the aftermath of an AT2018cow-like transient, AT2022tsd (the ‘Tasmanian Devil’). The flares occur over a period of months, are highly energetic and are probably nonthermal, implying that they arise from a near-relativistic outflow or jet. Our observations confirm that, in some AT2018cow-like transients, the embedded energy source is a compact object, either a magnetar or an accreting black hole

Horticultural traditions and the emergence of the flower garden in Italy

SIGLEAvailable from British Library Document Supply Centre- DSC:DXN002741 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

The Lin28/let-7 Axis Regulates Glucose Metabolism

The let-7 tumor suppressor microRNAs are known for their regulation of oncogenes, while the RNA-binding proteins Lin28a/b promote malignancy by inhibiting let-7 biogenesis. We have uncovered unexpected roles for the Lin28/let-7 pathway in regulating metabolism. When overexpressed in mice, both Lin28a and LIN28B promote an insulin-sensitized state that resists high-fat-diet induced diabetes. Conversely, muscle-specific loss of Lin28a or overexpression of let-7 results in insulin resistance and impaired glucose tolerance. These phenomena occur, in part, through the let-7-mediated repression of multiple components of the insulin-PI3K-mTOR pathway, including IGF1R, INSR, and IRS2. In addition, the mTOR inhibitor, rapamycin, abrogates Lin28a-mediated insulin sensitivity and enhanced glucose uptake. Moreover, let-7 targets are enriched for genes containing SNPs associated with type 2 diabetes and control of fasting glucose in human genome-wide association studies. These data establish the Lin28/let-7 pathway as a central regulator of mammalian glucose metabolism.National Institutes of Health (U.S.)Singapore. Agency for Science, Technology and Research (NSS Scholarship)American Cancer Society (Postdoctoral Fellowship)National Institutes of Health (U.S.) (NIH NIDDK Diseases Career Development Award)American Diabetes Association (Postdoctoral Fellowship)National Human Genome Research Institute (U.S.)National Institute of General Medical Sciences (U.S.)Pew Charitable Trusts (Pew Research Scholar)Doris Duke Charitable Foundation (Distinguished Clinical Scholar)Burroughs Wellcome Fund (Clinical Scientist Award in Translational Research)Leukemia & Lymphoma Society of America (Clinical Scientist Award in Translational Research)Howard Hughes Medical Institute (Investigator)Boston Children's Hospital (Manton Center for Orphan Disease Research, Investigator)American Cancer Society (Graduate Training in Cancer Research Grant