Chemical reactions in protoplanetary accretion disks. Pt. 4 Multicomponent dust mixture

We consider the different major components of the dust mixture in protostellar accretion disks and the development of their structure and chemical composition as the disk material slowly migrates inwards during the viscous phase of the disk evolution. It is shown that the amorphous structure of the dust grains from the parent molecular cloud is converted by annealing at about 800 K into a well ordered crystalline lattice structure accompanied by a chemical differentiation by solid state diffusion processes. The chemical composition of the abundant refractory dust components formed from silicon, magnesium, iron, aluminium, and calcium is discussed on the basis of chemical equilibrium considerations. Convenient approximations for calculating the equilibrium abundance of the major dust components are derived. These are used to calculate a self consistent model for a stationary accretion disk around a one solar mass protosun in the one zone approximation and to derive the radial variation of the abundance of the different dust species. The model takes properly into account the strong coupling between disk structure, opacity, and the chemical composition and abundance of the major dust species, i.e. amorphous silicates in the cool parts of the disk, and olivine, orthopyroxene, iron, and aluminium compounds in the warm parts. (orig.)SIGLEAvailable from TIB Hannover: RR 1606(98-13) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

The Origin of Mercury

Mercury’s unusually high mean density has always been attributed to special circumstances that occurred during the formation of the planet or shortly thereafter, and due to the planet’s close proximity to the Sun. The nature of these special circumstances is still being debated and several scenarios, all proposed more than 20 years ago, have been suggested. In all scenarios, the high mean density is the result of severe fractionation occurring between silicates and iron. It is the origin of this fractionation that is at the centre of the debate: is it due to differences in condensation temperature and/or in material characteristics (e.g. density, strength)? Is it because of mantle evaporation due to the close proximity to the Sun? Or is it due to the blasting off of the mantle during a giant impact? In this paper we investigate, in some detail, the fractionation induced by a giant impact on a proto-Mercury having roughly chondritic elemental abundances. We have extended the previous work on this hypothesis in two significant directions. First, we have considerably increased the resolution of the simulation of the collision itself. Second, we have addressed the fate of the ejecta following the impact by computing the expected reaccretion timescale and comparing it to the removal timescale from gravitational interactions with other planets (essentially Venus) and the Poynting–Robertson effect. To compute the latter, we have determined the expected size distribution of the condensates formed during the cooling of the expanding vapor cloud generated by the impact. We find that, even though some ejected material will be reaccreted, the removal of the mantle of proto-Mercury following a giant impact can indeed lead to the required long-term fractionation between silicates and iron and therefore account for the anomalously high mean density of the planet. Detailed coupled dynamical–chemical modeling of this formation mechanism should be carried out in such a way as to allow explicit testing of the giant impact hypothesis by forthcoming space missions (e.g. MESSENGER and BepiColombo)

A hepatic GAbp-AMPK axis links inflammatory signaling to systemic vascular damage.

Increased pro-inflammatory signaling is a hallmark of metabolic dysfunction in obesity and diabetes. Although both inflammatory and energy substrate handling processes represent critical layers of metabolic control, their molecular integration sites remain largely unknown. Here, we identify the heterodimerization interface between the α and β subunits of transcription factor GA-binding protein (GAbp) as a negative target of tumor necrosis factor alpha (TNF-α) signaling. TNF-α prevented GAbpα and β complex formation via reactive oxygen species (ROS), leading to the non-energy-dependent transcriptional inactivation of AMP-activated kinase (AMPK) β1, which was identified as a direct hepatic GAbp target. Impairment of AMPKβ1, in turn, elevated downstream cellular cholesterol biosynthesis, and hepatocyte-specific ablation of GAbpα induced systemic hypercholesterolemia and early macro-vascular lesion formation in mice. As GAbpα and AMPKβ1 levels were also found to correlate in obese human patients, the ROS-GAbp-AMPK pathway may represent a key component of a hepato-vascular axis in diabetic long-term complications