3,458 research outputs found
Imprint of Inhomogeneous Reionization on the Power Spectrum of Galaxy Surveys at High Redshifts
We consider the effects of inhomogeneous reionization on the distribution of
galaxies at high redshifts. Modulation of the formation process of the ionizing
sources by large scale density modes makes reionization inhomogeneous and
introduces a spread to the reionization times of different regions with the
same size. After sources photo-ionize and heat these regions to a temperature
\ga 10^4K at different times, their temperatures evolve as the ionized
intergalactic medium (IGM) expands. The varying IGM temperature makes the
minimum mass of galaxies spatially non-uniform with a fluctuation amplitude
that increases towards small scales. These scale-dependent fluctuations modify
the shape of the power spectrum of low-mass galaxies at high redshifts in a way
that depends on the history of reionization. The resulting distortion of the
primordial power spectrum is significantly larger than changes associated with
uncertainties in the inflationary parameters, such as the spectral index of the
scalar power spectrum or the running of the spectral index. Future surveys of
high-redshift galaxies will offer a new probe of the thermal history of the IGM
but might have a more limited scope in constraining inflation.Comment: 8 pages, 5 figures, replaced to match version accepted by Ap
Eco-Evolutionary Feedback and the Invasion of Cooperation in Prisoner's Dilemma Games
Unveiling the origin and forms of cooperation in nature poses profound challenges in evolutionary ecology. The prisoner's dilemma game is an important metaphor for studying the evolution of cooperation. We here classified potential mechanisms for cooperation evolution into schemes of frequency- and density-dependent selection, and focused on the density-dependent selection in the ecological prisoner's dilemma games. We found that, although assortative encounter is still the necessary condition in ecological games for cooperation evolution, a harsh environment, indicated by a high mortality, can foster the invasion of cooperation. The Hamilton rule provides a fundamental condition for the evolution of cooperation by ensuring an enhanced relatedness between players in low-density populations. Incorporating ecological dynamics into evolutionary games opens up a much wider window for the evolution of cooperation, and exhibits a variety of complex behaviors of dynamics, such as limit and heteroclinic cycles. An alternative evolutionary, or rather succession, sequence was proposed that cooperation first appears in harsh environments, followed by the invasion of defection, which leads to a common catastrophe. The rise of cooperation (and altruism), thus, could be much easier in the density-dependent ecological games than in the classic frequency-dependent evolutionary games
Nanorice Particles: Hybrid Plasmonic Nanostructures
A new hybrid nanoparticle, i.e., a nanorice particle, which combines the intense local fields of nanorods with the highly tunable plasmon resonances of nanoshells, is described herein. This geometry possesses far greater structural tunability than previous nanoparticle geometries, along with much larger local field enhancements and far greater sensitivity as a surface plasmon resonance (SPR) nanosensor than presently known dielectric-conductive material nanostructures. In an embodiment, a nanoparticle comprises a prolate spheroid-shaped core having a first aspect ratio. The nanoparticle also comprises at least one conductive shell surrounding said prolate spheroid-shaped core. The nanoparticle has a surface plasmon resonance sensitivity of at least 600 nm RIU(sup.-1). Methods of making the disclosed nanorice particles are also described herein
Molecular regulation of the PAIâ1 gene by hypoxia: contributions of Egrâ1, HIFâ1 α, and C/EBPα
Hypoxia, as occurs during tissue ischemia, tips the natural anticoagulant/procoagulant balance of the endovascular wall to favor activation of coagulation. Plasminogen activator inhibitorâ1 (PAIâ1) is an important factor suppressing fibrinolysis under conditions of low oxygen tension. We previously reported that hypoxia induced PAIâ1 mRNA and antigen expression in murine macrophages secondary to increased de novo transcription as well as increased mRNA stability. We now show in RAW264.7 murine macrophages that the transcription factors early growth response geneâ1 (Egrâ1), hypoxiaâinducible factorâ1α (HIFâ1α), and CCAAT/enhancer binding protein α (C/EBPα) are quickly activated in hypoxia and are responsible for transcription and expression of PAIâ1. Murine PAIâ1 promoter constructs, including Egr, HIFâ1α, and/or C/EBPα binding sites, were transfected into RAW 264.7 murine macrophages. To identify the relative importance of each of these putative hypoxiaâresponsive elements, cells were exposed to normobaric hypoxia, and transcriptional activity was recorded. At 16 h of hypoxic exposure, murine PAIâ1 promoter deletion constructs that included Egr, HIFâ1α, and/or C/EBPα binding sites demonstrated increased tranâscriptional activity. Mutation of each of these three murine PAIâ1 promoter sites (or a combination of them) resulted in a marked reduction in hypoxia sensitivity as detected by transcriptional analysis. Functional data obtained using 32Pâlabeled Egr, HIFâ1 α response element (HRE), and C/EBPα oligonucleotides revealed induction of DNA binding activity in nuclear extracts from hypoxic RAW cells, with supershift analysis confirming activation of Egrâ1, HIFâ1 α, or C/EBPα. ChIP analysis confirmed the authenticity of these interactions as each of these transcription factors binds to chromatin under hypoxic conditions. Further, the induction of PAIâ1 by Egrâ1, HIFâ1 α, or C/EBPα was replicated in primary peritoneal macrophages. These data suggest that although HIFâ1 α appears to dominate the PAIâ1 transcriptional response in hypâoxia, Egrâ1 and C/EBPα greatly augment this response and can do so independent of HIFâ1α or each other. These studies are relevant to ischemic upâregulation of the PAIâ1 gene and consequent accrual of microâvascular thrombus under ischemic conditions.âLiao, H., Hyman, M. C., Lawrence, D. A., Pinsky, D. J. Molecular regulation of the PAIâ1 gene by hypoxia: contributions of Egrâ1, HIFâ1α, and C/EBPα. FASEB J. 21, 935â949 (2007)Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154298/1/fsb2fj066285com.pd
In vivo reconstitution of autophagy in Saccharomyces cerevisiae
Autophagy is a major intracellular degradative pathway that is involved in various human diseases. The role of autophagy, however, is complex; although the process is generally considered to be cytoprotective, it can also contribute to cellular dysfunction and disease progression. Much progress has been made in our understanding of autophagy, aided in large part by the identification of the autophagy-related (ATG) genes. Nonetheless, our understanding of the molecular mechanism remains limited. In this study, we generated a Saccharomyces cerevisiae multiple-knockout strain with 24 ATG genes deleted, and we used it to carry out an in vivo reconstitution of the autophagy pathway. We determined minimum requirements for different aspects of autophagy and studied the initial protein assembly steps at the phagophore assembly site. In vivo reconstitution enables the study of autophagy within the context of the complex regulatory networks that control this process, an analysis that is not possible with an in vitro system
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