Discovery and Observations of ASASSN-13db, an EX Lupi-Type Accretion Event on a Low-Mass T Tauri Star

We discuss ASASSN-13db, an EX Lupi-type ("EXor") accretion event on the young stellar object (YSO) SDSS J051011.01$-$032826.2 (hereafter SDSSJ0510) discovered by the All-Sky Automated Survey for SuperNovae (ASAS-SN). Using archival photometric data of SDSSJ0510 we construct a pre-outburst spectral energy distribution (SED) and find that it is consistent with a low-mass class II YSO near the Orion star forming region ($d \sim 420$ pc). We present follow-up photometric and spectroscopic observations of the source after the $\Delta V \sim-$5.4 magnitude outburst that began in September 2013 and ended in early 2014. These data indicate an increase in temperature and luminosity consistent with an accretion rate of $\sim10^{-7}$ $\rm{M}_\odot$ yr$^{-1}$, three or more orders of magnitude greater than in quiescence. Spectroscopic observations show a forest of narrow emission lines dominated by neutral metallic lines from Fe I and some low-ionization lines. The properties of ASASSN-13db are similar to those of the EXor prototype EX Lupi during its strongest observed outburst in late 2008.Comment: 14 pages, 4 figures, 1 table. Updated May 2014 to reflect changes in the final version published in ApJL. Photometric data presented in this submission are included as ancillary files. For a brief video explaining this paper, see http://youtu.be/yRCCrNJnvt

The choline transporter Slc44a2 controls platelet activation and thrombosis by regulating mitochondrial function

Genetic factors contribute to the risk of thrombotic diseases. Recent genome wide association studies have identified genetic loci including SLC44A2 which may regulate thrombosis. Here we show that Slc44a2 controls platelet activation and thrombosis by regulating mitochondrial energetics. We find that Slc44a2 null mice (Slc44a2(KO)) have increased bleeding times and delayed thrombosis compared to wild-type (Slc44a2(WT)) controls. Platelets from Slc44a2(KO) mice have impaired activation in response to thrombin. We discover that Slc44a2 mediates choline transport into mitochondria, where choline metabolism leads to an increase in mitochondrial oxygen consumption and ATP production. Platelets lacking Slc44a2 contain less ATP at rest, release less ATP when activated, and have an activation defect that can be rescued by exogenous ADP. Taken together, our data suggest that mitochondria require choline for maximum function, demonstrate the importance of mitochondrial metabolism to platelet activation, and reveal a mechanism by which Slc44a2 influences thrombosis

Track D Social Science, Human Rights and Political Science

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138414/1/jia218442.pd

The distribution of Cryptosporidium in livestock and wild animal populations on a Warwickshire farm

SIGLEAvailable from British Library Document Supply Centre-DSC:DXN007265 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Crystal structures of BMPRII extracellular domain in binary and ternary receptor complexes with BMP10

Heterozygous mutations in BMPR2 (bone morphogenetic protein (BMP) receptor type II) cause pulmonary arterial hypertension. BMPRII is a receptor for over 15 BMP ligands, but why BMPR2 mutations cause lung-specific pathology is unknown. To elucidate the molecular basis of BMP:BMPRII interactions, we report crystal structures of binary and ternary BMPRII receptor complexes with BMP10, which contain an ensemble of seven different BMP10:BMPRII 1:1 complexes. BMPRII binds BMP10 at the knuckle epitope, with the A-loop and beta 4 strand making BMPRII-specific interactions. The BMPRII binding surface on BMP10 is dynamic, and the affinity is weaker in the ternary complex than in the binary complex. Hydrophobic core and A-loop interactions are important in BMPRII-mediated signalling. Our data reveal how BMPRII is a low affinity receptor, implying that forming a signalling complex requires high concentrations of BMPRII, hence mutations will impact on tissues with highest BMPR2 expression such as the lung vasculature.Mutations in BMPR2 is the major genetic cause for pulmonary arterial hypertension (PAH). Here by solving crystal structures of BMPRII in binary and ternary receptor complexes with BMP10, the authors report the molecular recognition between BMPRII and BMP10, and its implication in PAH.Cancer Signaling networks and Molecular Therapeutic