Molecular gas in high-mass filament WB673

We studied the distribution of dense gas in a filamentary molecular cloud containing several dense clumps. The center of the filament is given by the dense clump WB673. The clumps are high-mass and intermediate-mass starforming regions. We observed CS (2-1), 13CO (1-0), C18O(1-0), and methanol lines at 96 GHz toward WB673 with the Onsala Space Observatory 20-m telescope. We found CS (2-1) emission in the inter-clump medium so the clumps are physically connected and the whole cloud is indeed a filament. Its total mass is 104 M⊙ and mass-to-length ratio is 360M⊙ pc−1 from 13CO (1-0) data. Mass-to-length ratio for the dense gas is 3.4 − 34M⊙ pc−1 from CS (2-1) data. The PV-diagram of the filament is V-shaped. We estimated physical conditions in the molecular gas using methanol lines. Location of the filament on the sky between extended shells suggests that it could be a good example to test theoretical models of formation of the filaments via multiple compression of interstellar gas by supersonic waves

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr–/– mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr–/– mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis