Mass function of haloes: scale invariant models

Press-Schechter theory gives a simple, approximate functional form of the mass function of dark matter haloes. Sheth and Tormen (ST) refined this mass function to give an improved analytical fit to results of N-body simulations. These forms of the halo mass function are universal (independent of cosmology and power spectrum) when scaled in suitable variables. Using large suites of LCDM N-body simulations, studies in the last few years have shown that this universality is only approximate. We explore whether some of the deviations from universality can be attributed to the power spectrum by computing the mass function in N-body simulations of various scale-free models in an Einstein-de Sitter cosmology. This choice of cosmology does not introduce any scale into the problem. These models have the advantage of being self-similar, hence stringent checks can be imposed while running these simulations. This set of numerical experiments is designed to isolate any power spectrum dependent departures from universality of mass functions. We show explicitly that the best fit ST parameters have a clear dependence on power spectrum. Our results also indicate that an improved analytical theory with more parameters is required in order to provide better fits to the mass function.Comment: 8 pages, four figure

Formation rates of Dark Matter Haloes

We derive an estimate of the rate of formation of dark matter halos per unit volume as a function of the halo mass and redshift of formation. Analytical estimates of the number density of dark matter halos are useful in modeling several cosmological phenomena. We use the excursion set formalism for computing the formation rate of dark matter halos. We use an approach that allows us to differentiate between major and minor mergers, as this is a pertinent issue for semi-analytic models of galaxy formation. We compute the formation rate for the Press-Schechter and the Sheth-Tormen mass function. We show that the formation rate computed in this manner is positive at all scales. We comment on the Sasaki formalism where negative halo formation rates are obtained. Our estimates compare very well with N-Body simulations for a variety of models. We also discuss the halo survival probability and the formation redshift distributions using our method.Comment: 30 pages, 9 figure

Halo mass function in scale invariant models

Sheth-Tormen mass function has been widely used to quantify the abundance of dark matter halos. It is a significant improvement over the Press-Schechter mass function as it uses ellipsoidal collapse in place of spherical collapse. Both of these mass functions can be written in a form that is universal, i.e., independent of cosmology and power spectrum when scaled in suitable variables. However, cosmological simulations have shown that this universality is approximate. In this paper, we investigate the power spectrum dependence of halo mass function through a suite of dark-matter-only N-body simulations of seven power-law models in an Einstein-de Sitter cosmology. This choice of cosmology and a power-law power spectrum ensures the self-similar evolution of dark matter distribution, allowing us to isolate the power spectrum dependence of mass function. We find that the mass function shows a clear non-universality. We present fits for the parameters of the Sheth-Tormen mass function for a range of power-law power-spectrum indices. We find a mild evolution in the overall shape of the mass function with the epoch. Finally, we extend our result to LCDM cosmology. We show that the Sheth-Tormen mass function with parameter values derived from a matched power-law EdS cosmology provides a better fit to the LCDM mass function than the standard Sheth-Tormen mass function. Our results indicate that an improved analytical theory is required to provide better fits to the mass function.Comment: 11 pages, 10 figures. This is a much expanded and upgraded version of 0908.2702. Submitted to MNRA

Measurement of the small-scale structure of the intergalactic medium using close quasar pairs

The distribution of diffuse gas in the intergalactic medium (IGM) imprints a series of hydrogen absorption lines on the spectra of distant background quasars known as the Lyman-$\alpha$ forest. Cosmological hydrodynamical simulations predict that IGM density fluctuations are suppressed below a characteristic scale where thermal pressure balances gravity. We measured this pressure-smoothing scale by quantifying absorption correlations in a sample of close quasar pairs. We compared our measurements to hydrodynamical simulations, where pressure smoothing is determined by the integrated thermal history of the IGM. Our findings are consistent with standard models for photoionization heating by the ultraviolet radiation backgrounds that reionized the universe.Comment: Accepted for publication on Scienc

The correlation of high-redshift galaxies with the thermal Sunyaev-Zel’dovich effect traces reionization

We explore a potential new probe of reionization: the cross-correlation of high-redshift galaxies with maps of the thermal Sunyaev-Zel’dovich (tSZ) effect. We consider two types of high redshift galaxies: Lyman break galaxies (LBGs) and Lyman-α emitters (LAEs). LBGs and LAEs will be detected in large numbers at high redshift (z ≈ 4 – 7) by ongoing and future surveys. We consider a future LBG sample from The Rubin Observatory Legacy Survey of Space and Time (LSST), and a selection of LAEs modelled after the Subaru SILVERRUSH program, but covering a much larger sky fraction. The tSZ effect is sensitive to a line-of-sight integral of the ionized gas pressure, and is measured across large patches of sky using multi-frequency CMB surveys. We consider forecast tSZ maps from CMB Stage 4 and more futuristic observations. Using a suite of hydrodynamical simulations, we show that LBGs and LAEs are correlated with the tSZ signal from reionization. The cross-spectra between LBGs/LAEs with tSZ maps contain information about the reionization history of the Universe, such as the distribution of bubble sizes, and could be used to directly measure the timing of reionization. The amplitude of the signal is small, however, and its detectability is hindered by low-redshift contributions to tSZ maps and by instrumental noise. If the low-redshift contribution to the observed tSZ signal is suppressed by masking of massive halos, a combination of overlapping futuristic CMB and galaxy surveys could probe this signal

A comprehensive framework for evaluation of high pacing frequency and arrhythmic optical mapping signals

Introduction: High pacing frequency or irregular activity due to arrhythmia produces complex optical mapping signals and challenges for processing. The objective is to establish an automated activation time-based analytical framework applicable to optical mapping images of complex electrical behavior.Methods: Optical mapping signals with varying complexity from sheep (N = 7) ventricular preparations were examined. Windows of activation centered on each action potential upstroke were derived using Hilbert transform phase. Upstroke morphology was evaluated for potential multiple activation components and peaks of upstroke signal derivatives defined activation time. Spatially and temporally clustered activation time points were grouped in to wave fronts for individual processing. Each activation time point was evaluated for corresponding repolarization times. Each wave front was subsequently classified based on repetitive or non-repetitive events. Wave fronts were evaluated for activation time minima defining sites of wave front origin. A visualization tool was further developed to probe dynamically the ensemble activation sequence.Results: Our framework facilitated activation time mapping during complex dynamic events including transitions to rotor-like reentry and ventricular fibrillation. We showed that using fixed AT windows to extract AT maps can impair interpretation of the activation sequence. However, the phase windowing of action potential upstrokes enabled accurate recapitulation of repetitive behavior, providing spatially coherent activation patterns. We further demonstrate that grouping the spatio-temporal distribution of AT points in to coherent wave fronts, facilitated interpretation of isolated conduction events, such as conduction slowing, and to derive dynamic changes in repolarization properties. Focal origins precisely detected sites of stimulation origin and breakthrough for individual wave fronts. Furthermore, a visualization tool to dynamically probe activation time windows during reentry revealed a critical single static line of conduction slowing associated with the rotation core.Conclusion: This comprehensive analytical framework enables detailed quantitative assessment and visualization of complex electrical behavior

Generation, annotation, and analysis of ESTs from midgut tissue of adult female Anopheles stephensi mosquitoes

<p>Abstract</p> <p>Background</p> <p>Malaria is a tropical disease caused by protozoan parasite, <it>Plasmodium</it>, which is transmitted to humans by various species of female anopheline mosquitoes. <it>Anopheles stephensi </it>is one such major malaria vector in urban parts of the Indian subcontinent. Unlike <it>Anopheles gambiae</it>, an African malaria vector, transcriptome of <it>A. stephensi </it>midgut tissue is less explored. We have therefore carried out generation, annotation, and analysis of expressed sequence tags from sugar-fed and <it>Plasmodium yoelii </it>infected blood-fed (post 24 h) adult female <it>A. stephensi </it>midgut tissue.</p> <p>Results</p> <p>We obtained 7061 and 8306 ESTs from the sugar-fed and <it>P. yoelii </it>infected mosquito midgut tissue libraries, respectively. ESTs from the combined dataset formed 1319 contigs and 2627 singlets, totaling to 3946 unique transcripts. Putative functions were assigned to 1615 (40.9%) transcripts using BLASTX against UniProtKB database. Amongst unannotated transcripts, we identified 1513 putative novel transcripts and 818 potential untranslated regions (UTRs). Statistical comparison of annotated and unannotated ESTs from the two libraries identified 119 differentially regulated genes. Out of 3946 unique transcripts, only 1387 transcripts were mapped on the <it>A. gambiae </it>genome. These also included 189 novel transcripts, which were mapped to the unannotated regions of the genome. The EST data is available as ESTDB at <url>http://mycompdb.bioinfo-portal.cdac.in/cgi-bin/est/index.cgi</url>.</p> <p>Conclusion</p> <p>3946 unique transcripts were successfully identified from the adult female <it>A. stephensi </it>midgut tissue. These data can be used for microarray development for better understanding of vector-parasite relationship and to study differences or similarities with other malaria vectors. Mapping of putative novel transcripts from <it>A. stephensi </it>on the <it>A. gambiae </it>genome proved fruitful in identification and annotation of several genes. Failure of some novel transcripts to map on the <it>A. gambiae </it>genome indicates existence of substantial genomic dissimilarities between these two potent malaria vectors.</p

Systematic review and meta-analysis on trimodal therapy versus radical cystectomy for muscle-invasive bladder cancer: Does the current quality of evidence justify definitive conclusions?

OBJECTIVES To systematically review and meta-analyze the current literature in a methodologically rigorous and transparent manner for quantitative evidence on survival outcomes among patients diagnosed with muscle-invasive bladder cancer that were treated by either trimodal therapy or radical cystectomy. MATERIALS AND METHODS MEDLINE, EMBASE, CENTRAL were systematically searched for comparative observational studies reporting disease-specific survival and/or overall survival on adult patients diagnosed with localized muscle-invasive bladder cancer that were exposed to either trimodal therapy or radical cystectomy. Studies qualified for meta-analysis (random effects model) if they were not at critical risk of bias (RoB). RESULTS The literature search identified 12 eligible studies. Three (all rated as "moderate RoB") out of 6 studies reporting on disease-specific survival qualified for quantitative analysis and yielded a pooled hazard ratio (trimodal therapy versus radical cystectomy) of 1.39 (95% confidence interval: 1.03-1.88). Four (mainly rated as "serious RoB") out of 12 studies were included in the meta-analysis of overall survival and estimated a hazard ratio of 1.39 (1.20-1.59). CONCLUSION Pooled results were significant in favor of radical cystectomy. The conclusion is mainly driven by large population-based studies that are at high RoB. Hence, the certainty of these treatment estimates can be considered very low and further research will likely have an important impact on these estimates. At present, the ultimate decision between trimodal therapy and radical cystectomy should be left to the patient based on individual preferences and on the recommendation of a multidisciplinary provider team experienced with both approaches

Genetic Deficiency of Glycogen Synthase Kinase-3β Corrects Diabetes in Mouse Models of Insulin Resistance

Despite treatment with agents that enhance β-cell function and insulin action, reduction in β-cell mass is relentless in patients with insulin resistance and type 2 diabetes mellitus. Insulin resistance is characterized by impaired signaling through the insulin/insulin receptor/insulin receptor substrate/PI-3K/Akt pathway, leading to elevation of negatively regulated substrates such as glycogen synthase kinase-3β (Gsk-3β). When elevated, this enzyme has antiproliferative and proapoptotic properties. In these studies, we designed experiments to determine the contribution of Gsk-3β to regulation of β-cell mass in two mouse models of insulin resistance. Mice lacking one allele of the insulin receptor (Ir+/−) exhibit insulin resistance and a doubling of β-cell mass. Crossing these mice with those having haploinsufficiency for Gsk-3β (Gsk-3β+/−) reduced insulin resistance by augmenting whole-body glucose disposal, and significantly reduced β-cell mass. In the second model, mice missing two alleles of the insulin receptor substrate 2 (Irs2−/−), like the Ir+/− mice, are insulin resistant, but develop profound β-cell loss, resulting in early diabetes. We found that islets from these mice had a 4-fold elevation of Gsk-3β activity associated with a marked reduction of β-cell proliferation and increased apoptosis. Irs2−/− mice crossed with Gsk-3β+/− mice preserved β-cell mass by reversing the negative effects on proliferation and apoptosis, preventing onset of diabetes. Previous studies had shown that islets of Irs2−/− mice had increased cyclin-dependent kinase inhibitor p27kip1 that was limiting for β-cell replication, and reduced Pdx1 levels associated with increased cell death. Preservation of β-cell mass in Gsk-3β+/−Irs2−/− mice was accompanied by suppressed p27kip1 levels and increased Pdx1 levels. To separate peripheral versus β-cell–specific effects of reduction of Gsk3β activity on preservation of β-cell mass, mice homozygous for a floxed Gsk-3β allele (Gsk-3F/F) were then crossed with rat insulin promoter-Cre (RIP-Cre) mice to produce β-cell–specific knockout of Gsk-3β (βGsk-3β−/−). Like Gsk-3β+/− mice, βGsk-3β−/− mice also prevented the diabetes of the Irs2−/− mice. The results of these studies now define a new, negatively regulated substrate of the insulin signaling pathway specifically within β-cells that when elevated, can impair replication and increase apoptosis, resulting in loss of β-cells and diabetes. These results thus form the rationale for developing agents to inhibit this enzyme in obese insulin-resistant individuals to preserve β-cells and prevent diabetes onset