Kinematics of Galactic Centre clouds shaped by shear-seeded solenoidal turbulence

The Central Molecular Zone (CMZ; the central ~ 500 pc of the Galaxy) is a kinematically unusual environment relative to the Galactic disc, with high velocity dispersions and a steep size-linewidth relation of the molecular clouds. In addition, the CMZ region has a significantly lower star formation rate (SFR) than expected by its large amount of dense gas. An important factor in explaining the low SFR is the turbulent state of the star-forming gas, which seems to be dominated by rotational modes. However, the turbulence driving mechanism remains unclear. In this work, we investigate how the Galactic gravitational potential affects the turbulence in CMZ clouds. We focus on the CMZ cloud G0.253+0.016 (`the Brick'), which is very quiescent and unlikely to be kinematically dominated by stellar feedback. We demonstrate that several kinematic properties of the Brick arise naturally in a cloud-scale hydrodynamics simulation that takes into account the Galactic gravitational potential. These properties include the line-of-sight velocity distribution, the steepened size-linewidth relation, and the predominantly solenoidal nature of the turbulence. Within the simulation, these properties result from the Galactic shear in combination with the cloud's gravitational collapse. This is a strong indication that the Galactic gravitational potential plays a crucial role in shaping the CMZ gas kinematics, and is a major contributor to suppressing the SFR by inducing predominantly solenoidal turbulent modes.Comment: 7 pages, 8 figures; accepted to MNRAS (July 24th 2023

UWISH2 -- The UKIRT Widefield Infrared Survey for H2

We present the goals and preliminary results of an unbiased, near-infrared, narrow-band imaging survey of the First Galactic Quadrant (10deg<l<65deg ; -1.3deg<b<+1.3deg). This area includes most of the Giant Molecular Clouds and massive star forming regions in the northern hemisphere. The survey is centred on the 1-0S(1) ro-vibrational line of H2, a proven tracer of hot, dense molecular gas in star-forming regions, around evolved stars, and in supernova remnants. The observations complement existing and upcoming photometric surveys (Spitzer-GLIMPSE, UKIDSS-GPS, JCMT-JPS, AKARI, Herschel Hi-GAL, etc.), though we probe a dynamically active component of star formation not covered by these broad-band surveys. Our narrow-band survey is currently more than 60% complete. The median seeing in our images is 0.73arcsec. The images have a 5sigma detection limit of point sources of K=18mag and the surface brightness limit is 10^-19Wm^-2arcsec^-2 when averaged over our typical seeing. Jets and outflows from both low and high mass Young Stellar Objects are revealed, as are new Planetary Nebulae and - via a comparison with earlier K-band observations acquired as part of the UKIDSS GPS - numerous variable stars. With their superior spatial resolution, the UWISH2 data also have the potential to reveal the true nature of many of the Extended Green Objects found in the GLIMPSE survey.Comment: 14pages, 8figures, 2tables, accepted for publication by MNRAS, a version with higher resolution figures can be found at http://astro.kent.ac.uk/~df

Mitochondrial involvement in drug-induced liver injury.

International audienceMitochondrial dysfunction is a major mechanism of liver injury. A parent drug or its reactive metabolite can trigger outer mitochondrial membrane permeabilization or rupture due to mitochondrial permeability transition. The latter can severely deplete ATP and cause liver cell necrosis, or it can instead lead to apoptosis by releasing cytochrome c, which activates caspases in the cytosol. Necrosis and apoptosis can trigger cytolytic hepatitis resulting in lethal fulminant hepatitis in some patients. Other drugs severely inhibit mitochondrial function and trigger extensive microvesicular steatosis, hypoglycaemia, coma, and death. Milder and more prolonged forms of drug-induced mitochondrial dysfunction can also cause macrovacuolar steatosis. Although this is a benign liver lesion in the short-term, it can progress to steatohepatitis and then to cirrhosis. Patient susceptibility to drug-induced mitochondrial dysfunction and liver injury can sometimes be explained by genetic or acquired variations in drug metabolism and/or elimination that increase the concentration of the toxic species (parent drug or metabolite). Susceptibility may also be increased by the presence of another condition, which also impairs mitochondrial function, such as an inborn mitochondrial cytopathy, beta-oxidation defect, certain viral infections, pregnancy, or the obesity-associated metabolic syndrome. Liver injury due to mitochondrial dysfunction can have important consequences for pharmaceutical companies. It has led to the interruption of clinical trials, the recall of several drugs after marketing, or the introduction of severe black box warnings by drug agencies. Pharmaceutical companies should systematically investigate mitochondrial effects during lead selection or preclinical safety studies