University of Kiel

About: University of Kiel is a education organization based out in Kiel, Germany. It is known for research contribution in the topics: Population & Crystal structure. The organization has 27816 authors who have published 57114 publications receiving 2061802 citations. The organization is also known as: Christian Albrechts University & Christian-Albrechts-Universität zu Kiel.

The photospheric barium spectrum: solar abundance and collision broadening of Ba II lines by hydrogen

Abstract: A study of the solar Ba ii spectrum leads to a solar abundance of barium of loge ba = = 2.11±0.12, on the scale loge h = 12. The observed asymmetry of the resonance line λ4554 is consistent with an isotopic abundance ratio equal to the terrestrial one. The meteoritic Ba/Si abundance ratio found in carbonaceous chondrites appears to exceed the solar ratio by 0.1 to 0.2 dex (Section 5). The broadening by collisions with hydrogen atoms is determined from the solar spectrum (Section 4). Damping half-widths, γ h, of the three stronger Ba ii lines turn out to be larger by a factor of about 3.0 than predicted from pure van der Waals interaction of dipoles. Departures from LTE appear to be present in the cores of the resonance lines and of the lines arising from the metastable 5D levels (Section 6). The equivalent widths, however, remain practically unaffected. Equivalent widths of neutral barium lines are predicted and some new identifications of photospheric Ba i lines are suggested (Section 7).

The apoptosis/autophagy paradox: autophagic vacuolization before apoptotic death

Abstract: Autophagic cell death is morphologically characterized by an accumulation of autophagic vacuoles. Here, we show that inactivation of LAMP2 by RNA interference or by homologous recombination leads to autophagic vacuolization in nutrient-depleted cells. Cells that lack LAMP2 expression showed an enhanced accumulation of vacuoles carrying the marker LC3, yet a decreased colocalization of LC3 and lysosomes, suggesting that the fusion between autophagic vacuoles and lysosomes was inhibited. While a fraction of mitochondria from starved LAMP2-expressing cells colocalized with lysosomal markers, within autophagolysosomes, no such colocalization was found on removal of LAMP2 from the experimental system. Of note, LAMP1 depletion had no such effects and did not aggravate the phenotype induced by LAMP2-specific small interfering RNA. Serum and amino acid-starved LAMP2-negative cells exhibited an accumulation of autophagic vacuoles and then succumbed to cell death with hallmarks of apoptosis such as loss of the mitochondrial transmembrane potential, caspase activation and chromatin condensation. While caspase inhibition retarded cell death, it had no protective effect on mitochondria. Stabilization of mitochondria by overexpression of Bcl-2 or the mitochondrion-targeted cytomegalovirus protein vMIA, however, blocked all signs of apoptosis. Neither caspase inhibition nor mitochondrial stabilization antagonized autophagic vacuolization in LAMP2-deficient cells. Altogether, these data indicate that accumulation of autophagic vacuoles can precede apoptotic cell death. These findings argue against the clear-cut distinction between type 1 (apoptotic) and type 2 (autophagic) cell death.

15q13.3 microdeletions increase risk of idiopathic generalized epilepsy

Abstract: We identified 15q13.3 microdeletions encompassing the CHRNA7 gene in 12 of 1,223 individuals with idiopathic generalized epilepsy (IGE), which were not detected in 3,699 controls (joint P = 5.32 x 10(-8)). Most deletion carriers showed common IGE syndromes without other features previously associated with 15q13.3 microdeletions, such as intellectual disability, autism or schizophrenia. Our results indicate that 15q13.3 microdeletions constitute the most prevalent risk factor for common epilepsies identified to date.