Hydrodynamics of photoionized columns in the Eagle Nebula, M 16

We present hydrodynamical simulations of the formation, structure and evolution of photoionized columns, with parameters based on those observed in the Eagle Nebula. On the basis of these simulations we argue that there is no unequivocal evidence that the dense neutral clumps at heads of the columns were cores in the pre-existing molecular cloud. In our simulations, a variety of initial conditions leads to the formation and maintenance of near-equilibrium columns. Therefore, it is likely that narrow columns will often occur in regions with large-scale inhomogeneities, but that observations of such columns can tell us little about the processes by which they formed. The manner in which the columns in our simulations develop suggests that their evolution may result in extended sequences of radiation-induced star formation.Comment: 12 pages, 9 figures, Latex, MN macros, in press with MNRA

Time maintenance of user clocks via the tracking and data relay satellite system

A system is described which uses the Tracking and Data Relay Satellite System (TDRSS) itself to compare the user satellite clock with a clock at the White Sands station that is referenced to Universal Time Coordinated (UTC). No command of the spacecraft by the system is required, and actual on-board clock corrections are made by the spacecraft control center at its discretion. Computer models were constructed using basic orbital parameters for user and TDRS satellites. With only first-order corrections and simple averaging techniques for constant clock rates, error measurement precision of better than one microsecond was obtained. More sophisticated computations should allow considerable improvement over this

SREBF1 links lipogenesis to mitophagy and sporadic Parkinson disease

Mitochondrial quality control has an impact on many diseases, but intense research has focused on the action of 2 genes linked to heritable forms of Parkinson disease (PD), PINK1 and PARK2/parkin, which act in a common pathway to promote mitophagy. However, criticism has been raised that little evidence links this mechanism to sporadic PD. To gain a greater insight into the mechanisms of PINK1-PARK2 mediated mitophagy, we undertook a genome-wide RNAi screen in Drosophila and human cell models. Strikingly, we discovered several components of the lipogenesis pathway, including SREBF1, playing a conserved role in mitophagy. Our results suggest that lipids influence the stabilization of PINK1 during the initiation of mitophagy. Importantly, SREBF1 has previously been identified as a risk locus for sporadic PD, and thus implicates aberrant mitophagy as contributing to sporadic PD. Our findings suggest a role for lipid synthesis in PINK1-PARK2 mediated mitophagy, and propose a mechanistic link between familial and sporadic PD, supporting a common etiology

The fragmentation of expanding shells II: Thickness matters

We study analytically the development of gravitational instability in an expanding shell having finite thickness. We consider three models for the radial density profile of the shell: (i) an analytic uniform-density model, (ii) a semi-analytic model obtained by numerical solution of the hydrostatic equilibrium equation, and (iii) a 3D hydrodynamic simulation. We show that all three profiles are in close agreement, and this allows us to use the first model to describe fragments in the radial direction of the shell. We then use non-linear equations describing the time-evolution of a uniform oblate spheroid to derive the growth rates of shell fragments having different sizes. This yields a dispersion relation which depends on the shell thickness, and hence on the pressure confining the shell. We compare this dispersion relation with the dispersion relation obtained using the standard thin-shell analysis, and show that, if the confining pressure is low, only large fragments are unstable. On the other hand, if the confining pressure is high, fragments smaller than predicted by the thin-shell analysis become unstable. Finally, we compare the new dispersion relation with the results of 3D hydrodynamic simulations, and show that the two are in good agreement.Comment: 9 pages, 9 figures, accepted by MNRA

Massive star formation via high accretion rates and early disk-driven outflows

We present an investigation of massive star formation that results from the gravitational collapse of massive, magnetized molecular cloud cores. We investigate this by means of highly resolved, numerical simulations of initial magnetized Bonnor-Ebert-Spheres that undergo collapse and cooling. By comparing three different cases - an isothermal collapse, a collapse with radiative cooling, and a magnetized collapse - we show that massive stars assemble quickly with mass accretion rates exceeding 10^-3 Msol/yr. We confirm that the mass accretion during the collapsing phase is much more efficient than predicted by selfsimilar collapse solutions, i.e. dM/dt ~ c^3/G. We find that during protostellar assembly the mass accretion reaches 20 - 100 c^3/G. Furthermore, we determined the self-consistent structure of bipolar outflows that are produced in our three dimensional magnetized collapse simulations. These outflows produce cavities out of which radiation pressure can be released, thereby reducing the limitations on the final mass of massive stars formed by gravitational collapse. Moreover, we argue that the extraction of angular momentum by disk-threaded magnetic fields and/or by the appearance of bars with spiral arms significantly enhance the mass accretion rate, thereby helping the massive protostar to assemble more quickly.Comment: 22 pages, 12 figures, aastex style, accepted for publication in ApJ, see http://www.ita.uni-heidelberg.de/~banerjee/publications/MassiveStars.pdf for high resolution figure

Harnessing the senga institution of adolescent sex education for the control of HIV and STDs in rural Uganda.

Senga (father's sister) is a traditional channel of communication about sexual behaviour for adolescent females in rural Uganda. We evaluated a modification of this approach as an intervention for HIV and STDs in a pilot study in two intervention villages and one control village over 12 months. Eleven adult women and three adolescent girls were chosen and trained to become sengas. Adolescent girls were encouraged to visit the sengas for sexual health information. Adult sengas saw an average of 21 clients; adolescent sengas saw five. Adolescent girls made 45% of visits. The expected reasons for attending the sengas accounted for 51% of visits. Knowledge about HIV/AIDS, sexual communication skills, consistent condom use and family planning service use increased in the intervention group of girls over the study period and compared to control girls. Symptomatic STDs decreased in the intervention group. This intervention was readily accepted by the community; members of all ages and both sexes attended for a wider variety of reasons than anticipated. Adolescent girls in the intervention group showed improved knowledge, attitudes and practices related to HIV and STDs. This promising intervention warrants further testing in larger studies and other settings

VPS35 pathogenic mutations confer no dominant toxicity but partial loss of function in Drosophila and genetically interact with parkin.

Mutations in VPS35 (PARK17) cause autosomal dominant, late onset Parkinson's disease (PD). VPS35 forms a core component of the retromer complex that mediates the retrieval of membrane proteins from endosomes back to either the Golgi or plasma membrane. While aberrant endosomal protein sorting has been linked to several neurodegenerative diseases the mechanisms by which VPS35 mutations and retromer function contribute to PD pathogenesis are not clear. To address this we generated transgenic Drosophila that express variant forms of human VPS35 found in PD cases and the corresponding variants of the Drosophila ortholog. We did not find evidence of dominant toxicity from any variant form including the pathogenic D620N mutation, even with aging. However, assessing the ability of Vps35 variants to rescue multiple vps35 mutant phenotypes we found that the D620N mutation confers a partial loss of function. Recently, VPS35 has been linked to the formation of mitochondria derived vesicles, which mediate the degradation of mitochondrial proteins and contribute to mitochondrial quality control. This process is also promoted by two other PD-lined genes parkin (PARK2) and PINK1 (PARK6). We demonstrate here that vps35 genetically interacts with parkin but interestingly not with pink1. Strikingly, Vps35 overexpression is able to rescue several parkin mutant phenotypes. Together these findings provide in vivo evidence that the D620N mutation likely confers pathogenicity through a partial loss of function mechanism, and that this may be linked to other known pathogenic mechanisms such as mitochondrial dysfunction

Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin

Loss of the E3 ubiquitin ligase Parkin causes early onset Parkinson's disease, a neurodegenerative disorder of unknown etiology. Parkin has been linked to multiple cellular processes including protein degradation, mitochondrial homeostasis, and autophagy; however, its precise role in pathogenesis is unclear. Recent evidence suggests that Parkin is recruited to damaged mitochondria, possibly affecting mitochondrial fission and/or fusion, to mediate their autophagic turnover. The precise mechanism of recruitment and the ubiquitination target are unclear. Here we show in Drosophila cells that PINK1 is required to recruit Parkin to dysfunctional mitochondria and promote their degradation. Furthermore, PINK1 and Parkin mediate the ubiquitination of the profusion factor Mfn on the outer surface of mitochondria. Loss of Drosophila PINK1 or parkin causes an increase in Mfn abundance in vivo and concomitant elongation of mitochondria. These findings provide a molecular mechanism by which the PINK1/Parkin pathway affects mitochondrial fission/fusion as suggested by previous genetic interaction studies. We hypothesize that Mfn ubiquitination may provide a mechanism by which terminally damaged mitochondria are labeled and sequestered for degradation by autophagy

Unbalanced Activation of Glutathione Metabolic Pathways Suggests Potential Involvement in Plant Defense against the Gall Midge Mayetiola destructor in Wheat

Citation: Liu, X. M., Zhang, S. Z., Whitworth, R. J., Stuart, J. J., & Chen, M. S. (2015). Unbalanced Activation of Glutathione Metabolic Pathways Suggests Potential Involvement in Plant Defense against the Gall Midge Mayetiola destructor in Wheat. Scientific Reports, 5, 7. doi:10.1038/srep08092Glutathione, gamma-glutamylcysteinylglycine, exists abundantly in nearly all organisms. Glutathione participates in various physiological processes involved in redox reactions by serving as an electron donor/acceptor. We found that the abundance of total glutathione increased up to 60% in resistant wheat plants within 72 hours following attack by the gall midge Mayetiola destructor, the Hessian fly. The increase in total glutathione abundance, however, is coupled with an unbalanced activation of glutathione metabolic pathways. The activity and transcript abundance of glutathione peroxidases, which convert reduced glutathione (GSH) to oxidized glutathione (GSSG), increased in infested resistant plants. However, the enzymatic activity and transcript abundance of glutathione reductases, which convert GSSG back to GSH, did not change. This unbalanced regulation of the glutathione oxidation/reduction cycle indicates the existence of an alternative pathway to regenerate GSH from GSSG to maintain a stable GSSG/GSH ratio. Our data suggest the possibility that GSSG is transported from cytosol to apoplast to serve as an oxidant for class III peroxidases to generate reactive oxygen species for plant defense against Hessian fly larvae. Our results provide a foundation for elucidating the molecular processes involved in glutathione-mediated plant resistance to Hessian fly and potentially other pests as well

Genetic structure of Tribolium castaneum populations in mills

We investigated the genetic diversity and differentiation among nine populations of Tribolium castaneum using eight polymorphic loci, including microsatellites and other insertion-deletion polymorphisms (=”indels”). Samples were collected in food processing/storage facilities located in Kansas, Nebraska, California, Louisiana, Florida and Puerto Rico. Standard population genetic analysis was applied, and an assignment test was used to assign individuals to their genetic population. All loci were polymorphic across populations, with the number of alleles per locus-population combination varying from three to fourteen. Among 72 locus-by-population combinations, 31 deviated significantly from Hardy-Weinberg equilibrium, which was associated with a deficiency in heterozygosity. Tribolium castaneum populations show some level of genetic structuring. Genetic differentiation between populations, using FST estimates, was significant, with FST varying from 0.018 to 0.149. AMOVA indicated that 8.32% of the variation in allele frequency resulted from comparisons among populations. Genetic distance was not significantly correlated with geographic distance. Correct assignment to the genetic population was possible in only 56% of all individuals. Together, these results revealed that geographically distinct populations of T. castaneum had low to moderate levels of genetic differentiation that was not correlated with geographic distance, and the genotypic profile of the individuals did not provide enough information for fingerprinting them with their source population. Keywords: Tribolium castaneum, Population genetics, Genetic structure, FST, Genetic fingerprintin