442 research outputs found

    Mechanisms for High-frequency QPOs in Neutron Star and Black Hole Binaries

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    We explain the millisecond variability detected by Rossi X-ray Timing Explorer (RXTE) in the X-ray emission from a number of low mass X-ray binary systems (Sco X-1, 4U1728-34, 4U1608-522, 4U1636-536, 4U0614+091, 4U1735-44, 4U1820-30, GX5-1 and etc) in terms of dynamics of the centrifugal barrier, a hot boundary region surrounding a neutron star. We demonstrate that this region may experience the relaxation oscillations, and that the displacements of a gas element both in radial and vertical directions occur at the same main frequency, of order of the local Keplerian frequency. We show the importance of the effect of a splitting of the main frequency produced by the Coriolis force in a rotating disk for the interpretation of a spacing between the QPO peaks. We estimate a magnitude of the splitting effect and present a simple formula for the whole spectrum of the split frequencies. It is interesting that the first three lowest-order overtones fall in the range of 200-1200 Hz and match the kHz-QPO frequencies observed by RXTE. Similar phenomena should also occur in Black Hole (BH) systems, but, since the QPO frequency is inversely proportional to the mass of a compact object, the frequency of the centrifugal-barrier oscillations in the BH systems should be a factor of 5-10 lower than that for the NS systems. The X-ray spectrum formed in this region is a result of upscattering of a soft radiation (from a disk and a NS surface) off relatively hot electrons in the boundary layer. We also briefly discuss some alternative QPO models, including a possibility of acoustic oscillations in the boundary layer, the proper stellar rotation, and g-mode disk oscillations.Comment: The paper is coming out in the Astrophysical Journal in the 1st of May issue of 199

    New Analytical Formula for Supercritical Accretion Flows

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    We examine a new family of global analytic solutions for optically thick accretion disks, which includes the supercritical accretion regime. We found that the ratio of the advection cooling rate, QadvQ_{\rm adv}, to the viscous heating rate, QvisQ_{\rm vis}, i.e., f=Qadv/Qvisf=Q_{\rm adv}/Q_{\rm vis}, can be represented by an analytical form dependent on the radius and the mass accretion rate. The new analytic solutions can be characterized by the photon-trapping radius, \rtrap, inside which the accretion time is less than the photon diffusion time in the vertical direction; the nature of the solutions changes significantly as this radius is crossed. Inside the trapping radius, ff approaches fr0f \propto r^0, which corresponds to the advection-dominated limit (f1f \sim 1), whereas outside the trapping radius, the radial dependence of ff changes to fr2f \propto r^{-2}, which corresponds to the radiative-cooling-dominated limit. The analytical formula for ff derived here smoothly connects these two regimes. The set of new analytic solutions reproduces well the global disk structure obtained by numerical integration over a wide range of mass accretion rates, including the supercritical accretion regime. In particular, the effective temperature profiles for our new solutions are in good agreement with those obtained from numerical solutions. Therefore, the new solutions will provide a useful tool not only for evaluating the observational properties of accretion flows, but also for investigating the mass evolution of black holes in the presence of supercritical accretion flows.Comment: 14 pages, 7 figures, accepted for publication in the Astrophysical Journa

    Glutamate May Be an Efferent Transmitter That Elicits Inhibition in Mouse Taste Buds

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    Recent studies suggest that l-glutamate may be an efferent transmitter released from axons innervating taste buds. In this report, we determined the types of ionotropic synaptic glutamate receptors present on taste cells and that underlie this postulated efferent transmission. We also studied what effect glutamate exerts on taste bud function. We isolated mouse taste buds and taste cells, conducted functional imaging using Fura 2, and used cellular biosensors to monitor taste-evoked transmitter release. The findings show that a large fraction of Presynaptic (Type III) taste bud cells (∼50%) respond to 100 µM glutamate, NMDA, or kainic acid (KA) with an increase in intracellular Ca2+. In contrast, Receptor (Type II) taste cells rarely (4%) responded to 100 µM glutamate. At this concentration and with these compounds, these agonists activate glutamatergic synaptic receptors, not glutamate taste (umami) receptors. Moreover, applying glutamate, NMDA, or KA caused taste buds to secrete 5-HT, a Presynaptic taste cell transmitter, but not ATP, a Receptor cell transmitter. Indeed, glutamate-evoked 5-HT release inhibited taste-evoked ATP secretion. The findings are consistent with a role for glutamate in taste buds as an inhibitory efferent transmitter that acts via ionotropic synaptic glutamate receptors

    Different level of population differentiation among human genes

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    <p>Abstract</p> <p>Background</p> <p>During the colonization of the world, after dispersal out of African, modern humans encountered changeable environments and substantial phenotypic variations that involve diverse behaviors, lifestyles and cultures, were generated among the different modern human populations.</p> <p>Results</p> <p>Here, we study the level of population differentiation among different populations of human genes. Intriguingly, genes involved in osteoblast development were identified as being enriched with higher <it>F</it><sub>ST </sub>SNPs, a result consistent with the proposed role of the skeletal system in accounting for variation among human populations. Genes involved in the development of hair follicles, where hair is produced, were also found to have higher levels of population differentiation, consistent with hair morphology being a distinctive trait among human populations. Other genes that showed higher levels of population differentiation include those involved in pigmentation, spermatid, nervous system and organ development, and some metabolic pathways, but few involved with the immune system. Disease-related genes demonstrate excessive SNPs with lower levels of population differentiation, probably due to purifying selection. Surprisingly, we find that Mendelian-disease genes appear to have a significant excessive of SNPs with high levels of population differentiation, possibly because the incidence and susceptibility of these diseases show differences among populations. As expected, microRNA regulated genes show lower levels of population differentiation due to purifying selection.</p> <p>Conclusion</p> <p>Our analysis demonstrates different level of population differentiation among human populations for different gene groups.</p

    Evidence for Positive Selection on the Osteogenin (BMP3) Gene in Human Populations

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    BACKGROUND: Human skeletal system has evolved rapidly since the dispersal of modern humans from Africa, potentially driven by selection and adaptation. Osteogenin (BMP3) plays an important role in skeletal development and bone osteogenesis as an antagonist of the osteogenic bone morphogenetic proteins, and negatively regulates bone mineral density. METHODOLOGY/PRINCIPAL FINDINGS: Here, we resequenced the BMP3 gene from individuals in four geographically separated modern human populations. Features supportive of positive selection in the BMP3 gene were found including the presence of an excess of nonsynonymous mutations in modern humans, and a significantly lower genetic diversity that deviates from neutrality. The prevalent haplotypes of the first exon region in Europeans demonstrated features of long-range haplotype homogeneity. In contrast with findings in European, the derived allele SNP Arg192Gln shows higher extended haplotype homozygosity in East Asian. The worldwide allele frequency distribution of SNP shows not only a high-derived allele frequency in Asians, but also in Americans, which is suggestive of functional adaptation. CONCLUSIONS/SIGNIFICANCE: In conclusion, we provide evidence for recent positive selection operating upon a crucial gene in skeletal development, which may provide new insight into the evolution of the skeletal system and bone development

    Characterizing Dynamic Changes in the Human Blood Transcriptional Network

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    Gene expression data generated systematically in a given system over multiple time points provides a source of perturbation that can be leveraged to infer causal relationships among genes explaining network changes. Previously, we showed that food intake has a large impact on blood gene expression patterns and that these responses, either in terms of gene expression level or gene-gene connectivity, are strongly associated with metabolic diseases. In this study, we explored which genes drive the changes of gene expression patterns in response to time and food intake. We applied the Granger causality test and the dynamic Bayesian network to gene expression data generated from blood samples collected at multiple time points during the course of a day. The simulation result shows that combining many short time series together is as powerful to infer Granger causality as using a single long time series. Using the Granger causality test, we identified genes that were supported as the most likely causal candidates for the coordinated temporal changes in the network. These results show that PER1 is a key regulator of the blood transcriptional network, in which multiple biological processes are under circadian rhythm regulation. The fasted and fed dynamic Bayesian networks showed that over 72% of dynamic connections are self links. Finally, we show that different processes such as inflammation and lipid metabolism, which are disconnected in the static network, become dynamically linked in response to food intake, which would suggest that increasing nutritional load leads to coordinate regulation of these biological processes. In conclusion, our results suggest that food intake has a profound impact on the dynamic co-regulation of multiple biological processes, such as metabolism, immune response, apoptosis and circadian rhythm. The results could have broader implications for the design of studies of disease association and drug response in clinical trials

    Physicochemical Characterization of Passive Films and Corrosion Layers by Differential Admittance and Photocurrent Spectroscopy

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    Two different electrochemical techniques, differential admittance and photocurrent spectroscopy, for the characterization of electronic and solid state properties of passive films and corrosion layers are described and critically evaluated. In order to get information on the electronic properties of passive film and corrosion layers as well as the necessary information to locate the characteristic energy levels of the passive film/electrolyte junction like: flat band potential (Ufb), conduction band edge (EC) or valence band edge (EV), a wide use of Mott-Schottky plots is usually reported in corrosion science and passivity studies. It has been shown, in several papers, that the use of simple M-S theory to get information on the electronic properties and energy levels location at the film/electrolyte interface can be seriously misleading and/or conflicting with the physical basis underlying the M-S theory. A critical appraisal of this approach to the study of very thin and thick anodic passive film grown on base-metals (Cr, Ni, Fe, SS etc..) or on valve metals (Ta, Nb, W etc..) is reported in this work, together with possible alternative approach to overcome some of the mentioned inconsistencies. At this aim the theory of amorphous semiconductor Schottky barrier, introduced several years ago in the study of passive film/electrolyte junction, is reviewed by taking into account some of the more recent results obtained by the present authors. Future developments of the theory appears necessary to get more exact quantitative information on the electronic properties of passive films, specially in the case of very thin film like those formed on base metals and their alloys. The second technique described in this chapter, devoted to the physico-chemical characterization of passive film and corrosion layers, is a more recent technique based on the analysis of the photo-electrochemical answer of passive film/electrolyte junction under illumination with photons having suitable energy. Such a technique usually referred to as Photocurrent Spectroscopy (PCS) has been developed on the basis of the large research effort carried out by several groups in the 1970’s and aimed to investigate the possible conversion of solar energy by means of electrochemical cells. In this work the fundamentals of semiconductor/electrolyte junctions under illumination will be highlighted both for crystalline and amorphous materials. The role of amorphous nature and film thickness on the photo-electrochemical answer of passive film/solution interface is reviewed as well the use of PCS for quantitative analysis of the film composition based on a semi-empirical correlation between optical band gap and difference of electronegativity of film constituents previously suggested by the present authors. In this frame the results of PCS studies on valve metal oxides and valve metal mixed oxides will be discussed in order to show the validity of the proposed method. The results of PCS studies aimed to get information on passive film composition and carried out by different authors on base metals (Fe, Cr, Ni) and their alloys, including stainless steel, will be also compared with compositional analysis carried out by well-established surface analysis techniques

    Advances in tenascin-C biology

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    Tenascin-C is an extracellular matrix glycoprotein that is specifically and transiently expressed upon tissue injury. Upon tissue damage, tenascin-C plays a multitude of different roles that mediate both inflammatory and fibrotic processes to enable effective tissue repair. In the last decade, emerging evidence has demonstrated a vital role for tenascin-C in cardiac and arterial injury, tumor angiogenesis and metastasis, as well as in modulating stem cell behavior. Here we highlight the molecular mechanisms by which tenascin-C mediates these effects and discuss the implications of mis-regulated tenascin-C expression in driving disease pathology
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