University of Graz

About: University of Graz is a education organization based out in Graz, Steiermark, Austria. It is known for research contribution in the topics: Population & Context (language use). The organization has 17934 authors who have published 37489 publications receiving 1110980 citations. The organization is also known as: Carolo Franciscea Graecensis & Karl Franzens Universität.

Die Konservierung ganzer Leichen in natürlichen Farben

Abstract: An especially low-odor embalming technique was developed over a 30-years-period using a total of 977 complete cadavers, numerous cadavers after autopsy, and in vitro series of fresh beef. The color, consistency, and transparency of the tissue were very well preserved. The technique met high standards of preservation without releasing harmful substances into the environment. Concentrations of formaldehyde in room air remained under the limit of detection by Drager capillaries. The efficacy for disinfection of the method was confirmed by bacteriologic tests. None of the cadavers or samples developed molds.

ATGL-mediated fat catabolism regulates cardiac mitochondrial function via PPAR-α and PGC-1

Abstract: Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that regulate genes involved in energy metabolism and inflammation. For biological activity, PPARs require cognate lipid ligands, heterodimerization with retinoic X receptors, and coactivation by PPAR-γ coactivator-1α or PPAR-γ coactivator-1β (PGC-1α or PGC-1β, encoded by Ppargc1a and Ppargc1b, respectively). Here we show that lipolysis of cellular triglycerides by adipose triglyceride lipase (patatin-like phospholipase domain containing protein 2, encoded by Pnpla2; hereafter referred to as Atgl) generates essential mediator(s) involved in the generation of lipid ligands for PPAR activation. Atgl deficiency in mice decreases mRNA levels of PPAR-α and PPAR-δ target genes. In the heart, this leads to decreased PGC-1α and PGC-1β expression and severely disrupted mitochondrial substrate oxidation and respiration; this is followed by excessive lipid accumulation, cardiac insufficiency and lethal cardiomyopathy. Reconstituting normal PPAR target gene expression by pharmacological treatment of Atgl-deficient mice with PPAR-α agonists completely reverses the mitochondrial defects, restores normal heart function and prevents premature death. These findings reveal a potential treatment for the excessive cardiac lipid accumulation and often-lethal cardiomyopathy in people with neutral lipid storage disease, a disease marked by reduced or absent ATGL activity.

Atmospheric Loss of Exoplanets Resulting from Stellar X-Ray and Extreme-Ultraviolet Heating

Abstract: Past studies addressing the thermal atmospheric escape of hydrogen from hot Jupiters have been based on the planet's effective temperature, which, as we show here, is not physically relevant for loss processes In consequence, these studies led to significant underestimations of the atmospheric escape rate (≤103 g s-1) and to the conclusion of long-term atmospheric stability From more realistic exospheric temperatures, determined from X-ray and extreme-ultraviolet (XUV) irradiation and thermal conduction in the thermosphere, we find that energy-limited escape and atmospheric expansion arise, leading to much higher estimations for the loss rates (≈1012 g s-1) These fluxes are in good agreement with recent determinations for HD 209458b based on observations of its extended exosphere We also show that for young solar-type stars, which emit stronger XUV fluxes, the inferred loss rates are significantly higher Thus, hydrogen-rich giant exoplanets under such strong XUV irradiances may evaporate down to their core sizes or shrink to levels at which heavier atmospheric constituents may prevent hydrodynamic escape These results could explain the apparent paucity of exoplanets so far detected at orbital distances less than 004 AU