201 research outputs found

    Large excess of heavy nitrogen in both hydrogen cyanide and cyanogen from comet 17P/Holmes

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    From millimeter and optical observations of the Jupiter-family comet 17P/Holmes performed soon after its huge outburst of October 24, 2007, we derive 14 N/15N = 139 +/- 26 in HCN, and 14N/15N = 165 +/- 40 in CN, establishing that HCN has the same non-terrestrial isotopic composition as CN. The same conclusion is obtained for the long-period comet C/1995 O1 (Hale-Bopp) after a reanalysis of previously published measurements. These results are compatible with HCN being the prime parent of CN in cometary atmospheres. The 15N excess relative to the Earth atmospheric value indicates that N-bearing volatiles in the solar nebula underwent important N isotopic fractionation at some stage of Solar System formation. HCN molecules never isotopically equilibrated with the main nitrogen reservoir in the solar nebula before being incorporated in Oort-cloud and Kuiper-belt comets. The 12C/13C ratios in HCN and CN are measured to be consistent with the terrestrial value.Comment: Accepted for publication in the Astrophysical Journal (Letters) 4 page

    Experimental and Analytical Research of the Heat Transfer Process in the Package of Perforated Plates

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    The need for compact heat exchangers has led to the development of many types of surfaces that enhance the rate of heat transfer, among them the perforated plate heat exchangers, also known as matrix heat exchangers. The perforated plate heat exchangers consist of a series of perforated plates that are separated by a series of spacers. The present study investigates the heat transfer characteristics of the package of perforated plates. Perforated plates were 2 mm thick, with holes with 2 mm in diameter and porosity of 25.6%. The package of one, two, and three perforated plates was set in the channel of the experimental chamber at which entrance was a thrust fan with the ability to control the flow rate. The fluid flow rates, the temperatures of the fluids at the inlet and outlet of the chamber and the temperature of the air between the plates, were measured at the pre-defined locations in the package and the experimental chamber. Based on the measurements, heat transfer coefficients for the individual plates, as well as for the packages of perforated plates were determined. In further research, an iterative analytical procedure for investigation of the heat transfer process and the overall heat transfer coefficient for the package of perforated plates were developed. Based on these analytical and experimental results, conclusions were drawn about the heat transfer in a package of perforated plates.17th Symposium of the Society-of-Thermal-Engineers-of-Serbia (SIMTERM), Oct 20-23, 2015, Sokobanja, Serbi

    A High-Velocity Narrow Absorption Line Outflow in the Quasar J212329.46-005052.9

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    We report on a variable high-velocity narrow absorption line outflow in the redshift 2.3 quasar J2123-0050. Five distinct outflow systems are detected with velocity shifts from -9710 to -14,050 km/s and CIV 1548,1551 line widths of FWHM = 62-164 km/s. These data require five distinct outflow structures with similar kinematics, physical conditions and characteristic sizes of order 0.01-0.02 pc. The most likely location is ~5 pc from the quasar. The coordinated line variations in <0.63 yr (rest) are best explained by global changes in the outflow ionization caused by changes in the quasar's ionizing flux. The absence of strong X-ray absorption shows that radiative shielding is not needed to maintain the moderate ionizations and therefore, apparently, it is not needed to facilitate the radiative acceleration to high speeds. The kinetic energy yield of this flow is at least two orders of magnitude too low to be important for feedback to the host galaxy's evolution.Comment: 20 pages. In press with MNRA

    A single intranasal dose of human mesenchymal stem cell-derived extracellular vesicles after traumatic brain injury eases neurogenesis decline, synapse loss, and BDNF-ERK-CREB signaling

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    An optimal intranasal (IN) dose of human mesenchymal stem cell-derived extracellular vesicles (hMSC-EVs), 90 min post-traumatic brain injury (TBI), has been reported to prevent the evolution of acute neuroinflammation into chronic neuroinflammation resulting in the alleviation of long-term cognitive and mood impairments. Since hippocampal neurogenesis decline and synapse loss contribute to TBI-induced long-term cognitive and mood dysfunction, this study investigated whether hMSC-EV treatment after TBI can prevent hippocampal neurogenesis decline and synapse loss in the chronic phase of TBI. C57BL6 mice undergoing unilateral controlled cortical impact injury (CCI) received a single IN administration of different doses of EVs or the vehicle at 90 min post-TBI. Quantifying neurogenesis in the subgranular zone-granule cell layer (SGZ-GCL) through 5′-bromodeoxyuridine and neuron-specific nuclear antigen double labeling at ~2 months post-TBI revealed decreased neurogenesis in TBI mice receiving vehicle. However, in TBI mice receiving EVs (12.8 and 25.6 × 109 EVs), the extent of neurogenesis was matched to naive control levels. A similar trend of decreased neurogenesis was seen when doublecortin-positive newly generated neurons were quantified in the SGZ-GCL at ~3 months post-TBI. The above doses of EVs treatment after TBI also reduced the loss of pre-and post-synaptic marker proteins in the hippocampus and the somatosensory cortex. Moreover, at 48 h post-treatment, brain-derived neurotrophic factor (BDNF), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated cyclic AMP response-element binding protein (p-CREB) levels were downregulated in TBI mice receiving the vehicle but were closer to naïve control levels in TBI mice receiving above doses of hMSC-EVs. Notably, improved BDNF concentration observed in TBI mice receiving hMSC-EVs in the acute phase was sustained in the chronic phase of TBI. Thus, a single IN dose of hMSC-EVs at 90 min post-TBI can ease TBI-induced declines in the BDNF-ERK-CREB signaling, hippocampal neurogenesis, and synapses

    Treg-driven tumour control by PI3Kδ inhibition limits myeloid-derived suppressor cell expansion

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    Background Recent studies have demonstrated that blocking the PI3Kδ signalling enzyme (by administering a small molecule inhibitor, PI-3065) can potently improve the anti-tumour T-cell response through direct inhibition of Tregs. This treatment also has a negative impact on MDSC numbers but the primary mechanism driving this effect has remained unclear. Methods The 4T1 breast cancer mouse model was used in combination with PI-3065 to gain insights into the effect of PI3Kδ inhibition on MDSCs. Results PI-3065 treatment resulted in a concomitant reduction in MDSC expansion and tumour size. However, targeting Tregs independent of PI-3065 was also associated with reduced tumour volume and MDSC numbers. Surgical removal of tumours resulted in a rapid and significant decline in MDSC numbers, whilst ex vivo studies using cells from PI-3065-treated mice demonstrated no direct effect of the inhibitor on MDSC activity. Conclusions Our data suggest that MDSCs are not inhibited directly by PI-3065 treatment but that their reduced recruitment and immunosuppression within the tumour microenvironment is an indirect consequence of PI3Kδ-inhibition-driven tumour control. This indicates that PI3Kδ inhibition drives tumour immunity by breaking down multiple immunosuppressive pathways through both direct mechanisms (on Treg) and indirect mechanisms, secondary to tumour control (on MDSCs)

    Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

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    The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline
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