Strange stars with different quark mass scalings

We investigate the stability of strange quark matter and the properties of the corresponding strange stars, within a wide range of quark mass scaling. The calculation shows that the resulting maximum mass always lies between 1.5 solor mass and 1.8 solor mass for all the scalings chosen here. Strange star sequences with a linear scaling would support less gravitational mass, and a change (increase or decrease) of the scaling around the linear scaling would lead to a larger maximum mass. Radii invariably decrease with the mass scaling. Then the larger the scaling, the faster the star might spin. In addition, the variation of the scaling would cause an order of magnitude change of the strong electric field on quark surface, which is essential to support possible crusts of strange stars against gravity and may then have some astrophysical implications.Comment: 5 pages, 6 figures, 1 table. accepted by M

Gas kinematics and star formation in the filamentary molecular cloud G47.06+0.26

We performed a multi-wavelength study toward the filamentary cloud G47.06+0.26 to investigate the gas kinematics and star formation. We present the 12CO (J=1-0), 13CO (J=1-0) and C18O (J=1-0) observations of G47.06+0.26 obtained with the Purple Mountain Observation (PMO) 13.7 m radio telescope to investigate the detailed kinematics of the filament. The 12CO (J=1-0) and 13CO (J=1-0) emission of G47.06+0.26 appear to show a filamentary structure. The filament extends about 45 arcmin (58.1 pc) along the east-west direction. The mean width is about 6.8 pc, as traced by the 13CO (J=1-0) emission. G47.06+0.26 has a linear mass density of about 361.5 Msun/pc. The external pressure (due to neighboring bubbles and H II regions) may help preventing the filament from dispersing under the effects of turbulence. From the velocity-field map, we discern a velocity gradient perpendicular to G47.06+0.26. From the Bolocam Galactic Plane Survey (BGPS) catalog, we found nine BGPS sources in G47.06+0.26, that appear to these sources have sufficient mass to form massive stars. We obtained that the clump formation efficiency (CFE) is about 18% in the filament. Four infrared bubbles were found to be located in, and adjacent to, G47.06+0.26. Particularly, infrared bubble N98 shows a cometary structure. CO molecular gas adjacent to N98 also shows a very intense emission. H II regions associated with infrared bubbles can inject the energy to surrounding gas. We calculated the kinetic energy, ionization energy, and thermal energy of two H II regions in G47.06+0.26. From the GLIMPSE I catalog, we selected some Class I sources with an age of about 100000 yr, which are clustered along the filament. The feedback from the H II regions may cause the formation of a new generation of stars in filament G47.06+0.26.Comment: 10 pages, 11 figures, accepted for publication in A&

mGluR5 antagonism inhibits cocaine reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.

Metabotropic glutamate receptor 5 (mGluR5) antagonism inhibits cocaine self-administration and reinstatement of drug-seeking behavior. However, the cellular and molecular mechanisms underlying this action are poorly understood. Here we report a presynaptic glutamate/cannabinoid mechanism that may underlie this action. Systemic or intra-nucleus accumbens (NAc) administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) dose-dependently reduced cocaine (and sucrose) self-administration and cocaine-induced reinstatement of drug-seeking behavior. The reduction in cocaine-taking and cocaine-seeking was associated with a reduction in cocaine-enhanced extracellular glutamate, but not cocaine-enhanced extracellular dopamine (DA) in the NAc. MPEP alone, when administered systemically or locally into the NAc, elevated extracellular glutamate, but not DA. Similarly, the cannabinoid CB1 receptor antagonist, rimonabant, elevated NAc glutamate, not DA. mGluR5s were found mainly in striatal medium-spiny neurons, not in astrocytes, and MPEP-enhanced extracellular glutamate was blocked by a NAc CB1 receptor antagonist or N-type Ca++ channel blocker, suggesting that a retrograde endocannabinoid-signaling mechanism underlies MPEP-induced glutamate release. This interpretation was further supported by our findings that genetic deletion of CB1 receptors in CB1-knockout mice blocked both MPEP-enhanced extracellular glutamate and MPEP-induced reductions in cocaine self-administration. Together, these results indicate that the therapeutic anti-cocaine effects of mGluR5 antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid-CB1 receptor disinhibition mechanism

The study of neutron spectra in water bath from Pb target irradiated by 250MeV/u protons

The spallation neutrons were produced by the irradiation of Pb with 250 MeV protons. The Pb target was surrounded by water which was used to slow down the emitted neutrons. The moderated neutrons in the water bath were measured by using the resonance detectors of Au, Mn and In with Cd cover. According to the measured activities of the foils, the neutron flux at different resonance energy were deduced and the epithermal neutron spectra were proposed. Corresponding results calculated with the Monte Carlo code MCNPX were compared with the experimental data to check the validity of the code.Comment: 6 pages,9 figure

Aldose reductase regulates microglia/macrophages polarization through the cAMP response element-binding protein after spinal cord injury in mice.

Inflammatory reactions are the most critical pathological processes occurring after spinal cord injury (SCI). Activated microglia/macrophages have either detrimental or beneficial effects on neural regeneration based on their functional polarized M1/M2 subsets. However, the mechanism of microglia/macrophage polarization to M1/M2 at the injured spinal cord environment remains unknown. In this study, wild-type (WT) or aldose reductase (AR)-knockout (KO) mice were subjected to SCI by a spinal crush injury model. The expression pattern of AR, behavior tests for locomotor activity, and lesion size were assessed at between 4 h and 28 days after SCI. We found that the expression of AR is upregulated in microglia/macrophages after SCI in WT mice. In AR KO mice, SCI led to smaller injury lesion areas compared to WT. AR deficiency-induced microglia/macrophages induce the M2 rather than the M1 response and promote locomotion recovery after SCI in mice. In the in vitro experiments, microglia cell lines (N9 or BV2) were treated with the AR inhibitor (ARI) fidarestat. AR inhibition caused 4-hydroxynonenal (HNE) accumulation, which induced the phosphorylation of the cAMP response element-binding protein (CREB) to promote Arg1 expression. KG501, the specific inhibitor of phosphorylated CREB, could cancel the upregulation of Arg1 by ARI or HNE stimulation. Our results suggest that AR works as a switch which can regulate microglia by polarizing cells to either the M1 or the M2 phenotype under M1 stimulation based on its states of activity. We suggest that inhibiting AR may be a promising therapeutic method for SCI in the future

ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors

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