On the Initial Mass Function of Population III Stars

The collapse and fragmentation of filamentary primordial gas clouds are explored using 1D and 2D hydrodynamical simulations coupled with the nonequilibrium processes of H2 formation. The simulations show that depending upon the initial density,there are two occasions for the fragmentation of primordial filaments. If a filament has relatively low initial density, the radial contraction is slow due to less effective H2 cooling. This filament tends to fragment into dense clumps before the central density reaches $10^{8-9}$ cm$^{-3}$, where H2 cooling by three-body reactions is effective and the fragment mass is more massive than some tens $M_\odot$. In contrast, if a filament is initially dense, the more effective H2 cooling with the help of three-body reactions allows the filament to contract up to $n\sim 10^{12}$ cm$^{-3}$. After the density reaches $n\sim 10^{12}$ cm$^{-3}$, the filament becomes optically thick to H2 lines and the radial contraction subsequently almost stops. At this final hydrostatic stage, the fragment mass is lowered down to $\approx 1M_\odot$ because of the high density of the filament. The dependence of the fragment mass upon the initial density could be translated into the dependence on the local amplitude of random Gaussian density fields or the epoch of the collapse of a parent cloud. Hence, it is predicted that the initial mass function of Population III stars is likely to be bimodal with peaks of $\approx 10^2 M_\odot$ and $\approx 1M_\odot$, where the relative heights could be a function of the collapse epoch.Comment: Accepted by Ap

Specific Functions for ERK/MAPK Signaling during PNS Development

We have established functions of the stimulus dependent MAPKs, ERK1/2 and ERK5 in DRG, motor neuron, and Schwann cell development. Surprisingly, many aspects of early DRG and motor neuron development were found to be ERK1/2 independent and Erk5 deletion had no obvious effect on embryonic PNS. In contrast, Erk1/2 deletion in developing neural crest resulted in peripheral nerves that were devoid of Schwann cell progenitors, and deletion of Erk1/2 in Schwann cell precursors caused disrupted differentiation and marked hypomyelination of axons. The Schwann cell phenotypes are similar to those reported in neuregulin-1 and ErbB mutant mice and neuregulin effects could not be elicited in glial precursors lacking Erk1/2. ERK/MAPK regulation of myelination was specific to Schwann cells, as deletion in oligodendrocyte precursors did not impair myelin formation, but reduced precursor proliferation. Our data suggest a tight linkage between developmental functions of ERK/MAPK signaling and biological actions of specific RTK-activating factors

Lysophosphatidic Acid Acyltransferase β (LPAATβ) Promotes the Tumor Growth of Human Osteosarcoma

Osteosarcoma is the most common primary malignancy of bone with poorly characterized molecular pathways important in its pathogenesis. Increasing evidence indicates that elevated lipid biosynthesis is a characteristic feature of cancer. We sought to investigate the role of lysophosphatidic acid acyltransferase β (LPAATβ, aka, AGPAT2) in regulating the proliferation and growth of human osteosarcoma cells. LPAATβ can generate phosphatidic acid, which plays a key role in lipid biosynthesis as well as in cell proliferation and survival. Although elevated expression of LPAATβ has been reported in several types of human tumors, the role of LPAATβ in osteosarcoma progression has yet to be elucidated.Endogenous expression of LPAATβ in osteosarcoma cell lines is analyzed by using semi-quantitative PCR and immunohistochemical staining. Adenovirus-mediated overexpression of LPAATβ and silencing LPAATβ expression is employed to determine the effect of LPAATβ on osteosarcoma cell proliferation and migration in vitro and osteosarcoma tumor growth in vivo. We have found that expression of LPAATβ is readily detected in 8 of the 10 analyzed human osteosarcoma lines. Exogenous expression of LPAATβ promotes osteosarcoma cell proliferation and migration, while silencing LPAATβ expression inhibits these cellular characteristics. We further demonstrate that exogenous expression of LPAATβ effectively promotes tumor growth, while knockdown of LPAATβ expression inhibits tumor growth in an orthotopic xenograft model of human osteosarcoma.Our results strongly suggest that LPAATβ expression may be associated with the aggressive phenotypes of human osteosarcoma and that LPAATβ may play an important role in regulating osteosarcoma cell proliferation and tumor growth. Thus, targeting LPAATβ may be exploited as a novel therapeutic strategy for the clinical management of osteosarcoma. This is especially attractive given the availability of selective pharmacological inhibitors

Technical note: A study of Hersey and Blanchard\u27s situational leadership theory

This study empirically tested Hersey and Blanchard’s situational leadership theory (SLT) among 151 senior executives within service and manufacturing businesses of a large Fortune 100 company. SLT focuses on the interaction of the leader’s behaviour and follower readiness to determine leader effectiveness. SLT suggests that the appropriate level of task and relationship behaviour is the one that “matches” the level of follower readiness. A variety of statistical techniques were used to test the central hypotheses of SLT and the matching concept. The study produced 18 matches and 126 mismatches. One statistical technique, the partitioned test, was found to provide the most insight about SLT and the concept of matching. The researchers recommend its utilization in future research of SLT. The researchers conclude that SLT remains intuitively appealing and empirically contradictory. The concepts of SLT and matching are engaging and further research is recommended

Francisella tularensis Genes Required for Inhibition of the Neutrophil Respiratory Burst and Intramacrophage Growth Identified by Random Transposon Mutagenesis of Strain LVS▿

Francisella tularensis is a facultative intracellular pathogen and the causative agent of tularemia. We have shown that F. tularensis subspecies holarctica strain LVS prevents NADPH oxidase assembly and activation in human neutrophils, but how this is achieved is unclear. Herein, we used random transposon mutagenesis to identify LVS genes that affect neutrophil activation. Our initial screen identified carA, carB, and pyrB, which encode the small and large subunits of carbamoylphosphate synthase and aspartate carbamoyl transferase, respectively. These strains are uracil auxotrophs, and their growth was attenuated on cysteine heart agar augmented with sheep blood (CHAB) or in modified Mueller-Hinton broth. Phagocytosis of the uracil auxotrophic mutants triggered a respiratory burst in neutrophils, and ingested bacteria were killed and fragmented in phagosomes that contained superoxide. Conversely, phagocytosis did not trigger a respiratory burst in blood monocytes or monocyte-derived macrophages (MDM), and phagosomes containing wild-type or mutant bacteria lacked NADPH oxidase subunits. Nevertheless, the viability of mutant bacteria declined in MDM, and ultrastructural analysis revealed that phagosome egress was significantly inhibited despite synthesis of the virulence factor IglC. Other aspects of infection, such as interleukin-1β (IL-1β) and IL-8 secretion, were unaffected. The cultivation of carA, carB, or pyrB on uracil-supplemented CHAB was sufficient to prevent neutrophil activation and intramacrophage killing and supported escape from MDM phagosomes, but intracellular growth was not restored unless uracil was added to the tissue culture medium. Finally, all mutants tested grew normally in both HepG2 and J774A.1 cells. Collectively, our data demonstrate that uracil auxotrophy has cell type-specific effects on the fate of Francisella bacteria