135 research outputs found
Many-body theory of pump-probe spectra for highly excited semiconductors
We present a unified theory for pump-probe spectra in highly excited
semiconductors, which is applicable throughout the whole density regime
including the high-density electron-hole BCS state and the low-density
excitonic Bose-Einstein condensate (BEC). The analysis is based on the BCS-like
pairing theory combined with the Bethe-Salpeter (BS) equation, which first
enables us to incorporate the state-filling effect, the band-gap
renormalization and the strong/weak electron-hole pair correlations in a
unified manner. We show that the electron-hole BCS state is distinctly
stabilized by the intense pump-light, and this result strongly suggests that
the macroscopic quantum state can be observed under the strong photoexcitation.
The calculated spectra considerably deviate from results given by the BCS-like
mean field theory and the simple BS equation without electron-hole pair
correlation especially in the intermediate density states between the
electron-hole BCS state and the excitonic BEC state. In particular, we find the
sharp stimulated emission and absorption lines which originate from the optical
transition accompanied by the collective phase fluctuation mode in the
electron-hole BCS state. From the pump-probe spectral viewpoint, we show that
this fluctuation mode changes to the exciton mode with decreasing carrier
densityComment: RevTeX 11 pages, 10 figures. To appear in Phys.Rev.B1
Topological character of hydrodynamic screening in suspensions of hard spheres: an example of universal phenomenon
Although in the case of polymer solutions the existence of hydrodynamic
screening is considered as established, use of the same methods for suspensions
of hard spheres so far have failed to produce similar results. In this work we
reconsider this problem. Using superposition of topological, combinatorial and
London-style qualitative arguments, we prove the existence of screening in
suspensions. We show that the nature of hydrodynamic screening in suspensions
is analogous to that known for the Meissner effect in superconductors. The
extent of screening depends on volume fraction of hard spheres. The zero volume
fraction limit corresponds to the normal state. The case of finite volume
fractions-to the mixed state typical for superconductors of the second kind.
Such a state is becoming fully "superconducting" at some critical volume
fraction for which the (zero frequency) relative viscosity diverges. Our
analytical results describing this divergence are in accord with known scaling
results obtained by Brady and Bicerano et al which are well supported by
experimental data. We provide theoretical explanation of the divergence of
relative viscosity in terms of a topological-type transition which
mathematically can be made isomorphic to the more familiar Bose-Einstein
condensation transition. Because of this, the methods developed in this work
are not limited to suspensions only. In concluding section we mention other
applications of the developed formalism ranging from turbulence and
magnetohydrodynamics to high temperature superconductors, QCD, string models,
etc.Comment: 49 page
Coincidence analysis to search for inspiraling compact binaries using TAMA300 and LISM data
Japanese laser interferometric gravitational wave detectors, TAMA300 and
LISM, performed a coincident observation during 2001. We perform a coincidence
analysis to search for inspiraling compact binaries. The length of data used
for the coincidence analysis is 275 hours when both TAMA300 and LISM detectors
are operated simultaneously. TAMA300 and LISM data are analyzed by matched
filtering, and candidates for gravitational wave events are obtained. If there
is a true gravitational wave signal, it should appear in both data of detectors
with consistent waveforms characterized by masses of stars, amplitude of the
signal, the coalescence time and so on. We introduce a set of coincidence
conditions of the parameters, and search for coincident events. This procedure
reduces the number of fake events considerably, by a factor
compared with the number of fake events in single detector analysis. We find
that the number of events after imposing the coincidence conditions is
consistent with the number of accidental coincidences produced purely by noise.
We thus find no evidence of gravitational wave signals. We obtain an upper
limit of 0.046 /hours (CL ) to the Galactic event rate within 1kpc from
the Earth. The method used in this paper can be applied straightforwardly to
the case of coincidence observations with more than two detectors with
arbitrary arm directions.Comment: 28 pages, 17 figures, Replaced with the version to be published in
Physical Review
Belle II Technical Design Report
The Belle detector at the KEKB electron-positron collider has collected
almost 1 billion Y(4S) events in its decade of operation. Super-KEKB, an
upgrade of KEKB is under construction, to increase the luminosity by two orders
of magnitude during a three-year shutdown, with an ultimate goal of 8E35 /cm^2
/s luminosity. To exploit the increased luminosity, an upgrade of the Belle
detector has been proposed. A new international collaboration Belle-II, is
being formed. The Technical Design Report presents physics motivation, basic
methods of the accelerator upgrade, as well as key improvements of the
detector.Comment: Edited by: Z. Dole\v{z}al and S. Un
Two mechanisms of the enhanced antibody-dependent cellular cytotoxicity (ADCC) efficacy of non-fucosylated therapeutic antibodies in human blood
<p>Abstract</p> <p>Background</p> <p>Antibody-dependent cellular cytotoxicity (ADCC) has recently been identified as one of the critical mechanisms underlying the clinical efficacy of therapeutic antibodies, especially anticancer antibodies. Therapeutic antibodies fully lacking the core fucose of the Fc oligosaccharides have been found to exhibit much higher ADCC in humans than their fucosylated counterparts. However, data which show how fully non-fucosylated antibodies achieve such a high ADCC in human whole blood have not yet been disclosed. The precise mechanisms responsible for the high ADCC mediated by fully non-fucosylated therapeutic antibodies, even in the presence of human plasma, should be explained based on direct evidence of non-fucosylated antibody action in human blood.</p> <p>Methods</p> <p>Using a human <it>ex vivo </it>B-cell depletion assay with non-fucosylated and fucosylated anti-CD20 IgG1s rituximab, we monitored the binding of the therapeutic agents both to antigens on target cells (target side interaction) and to leukocyte receptors (FcγR) on effector cells (effector side interaction), comparing the intensities of ADCC in human blood.</p> <p>Results</p> <p>In the target side interaction, down-modulation of CD20 on B cells mediated by anti-CD20 was not observed. Simple competition for binding to the antigens on target B cells between fucosylated and non-fucosylated anti-CD20s was detected in human blood to cause inhibition of the enhanced ADCC of non-fucosylated anti-CD20 by fucosylated anti-CD20. In the effector side interaction, non-fucosylated anti-CD20 showed sufficiently high FcγRIIIa binding activity to overcome competition from plasma IgG for binding to FcγRIIIa on natural killer (NK) cells, whereas the binding of fucosylated anti-CD20 to FcγRIIIa was almost abolished in the presence of human plasma and failed to recruit NK cells effectively. The core fucosylation levels of individual serum IgG1 from healthy donors was found to be so slightly different that it did not affect the inhibitory effect on the ADCC of fucosylated anti-CD20.</p> <p>Conclusion</p> <p>Our results demonstrate that removal of fucosylated antibody ingredients from antibody therapeutics elicits high ADCC in human blood by two mechanisms: namely, by evading the inhibitory effects both of plasma IgG on FcγRIIIa binding (effector side interaction) and of fucosylated antibodies on antigen binding (target side interaction).</p
Role of cystine transport in intracellular glutathione level and cisplatin resistance in human ovarian cancer cell lines
The Yeast Tor Signaling Pathway Is Involved in G2/M Transition via Polo-Kinase
The target of rapamycin (Tor) protein plays central roles in cell growth. Rapamycin inhibits cell growth and promotes cell cycle arrest at G1 (G0). However, little is known about whether Tor is involved in other stages of the cell division cycle. Here we report that the rapamycin-sensitive Tor complex 1 (TORC1) is involved in G2/M transition in S. cerevisiae. Strains carrying a temperature-sensitive allele of KOG1 (kog1-105) encoding an essential component of TORC1, as well as yeast cell treated with rapamycin show mitotic delay with prolonged G2. Overexpression of Cdc5, the yeast polo-like kinase, rescues the growth defect of kog1-105, and in turn, Cdc5 activity is attenuated in kog1-105 cells. The TORC1-Type2A phosphatase pathway mediates nucleocytoplasmic transport of Cdc5, which is prerequisite for its proper localization and function. The C-terminal polo-box domain of Cdc5 has an inhibitory role in nuclear translocation. Taken together, our results indicate a novel function of Tor in the regulation of cell cycle and proliferation
A promoter-level mammalian expression atlas
Regulated transcription controls the diversity, developmental pathways and spatial organization of the hundreds of cell types that make up a mammal. Using single-molecule cDNA sequencing, we mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body. We find that few genes are truly â ̃ housekeepingâ TM, whereas many mammalian promoters are composite entities composed of several closely separated TSSs, with independent cell-type-specific expression profiles. TSSs specific to different cell types evolve at different rates, whereas promoters of broadly expressed genes are the most conserved. Promoter-based expression analysis reveals key transcription factors defining cell states and links them to binding-site motifs. The functions of identified novel transcripts can be predicted by coexpression and sample ontology enrichment analyses. The functional annotation of the mammalian genome 5 (FANTOM5) project provides comprehensive expression profiles and functional annotation of mammalian cell-type-specific transcriptomes with wide applications in biomedical research. © 2014 Macmillan Publishers Limited
The Constrained Maximal Expression Level Owing to Haploidy Shapes Gene Content on the Mammalian X Chromosome
X chromosomes are unusual in many regards, not least of which is their nonrandom gene content. The causes of this bias are commonly discussed in the context of sexual antagonism and the avoidance of activity in the male germline. Here, we examine the notion that, at least in some taxa, functionally biased gene content may more profoundly be shaped by limits imposed on gene expression owing to haploid expression of the X chromosome. Notably, if the X, as in primates, is transcribed at rates comparable to the ancestral rate (per promoter) prior to the X chromosome formation, then the X is not a tolerable environment for genes with very high maximal net levels of expression, owing to transcriptional traffic jams. We test this hypothesis using The Encyclopedia of DNA Elements (ENCODE) and data from the Functional Annotation of the Mammalian Genome (FANTOM5) project. As predicted, the maximal expression of human X-linked genes is much lower than that of genes on autosomes: on average, maximal expression is three times lower on the X chromosome than on autosomes. Similarly, autosome-to-X retroposition events are associated with lower maximal expression of retrogenes on the X than seen for X-to-autosome retrogenes on autosomes. Also as expected, X-linked genes have a lesser degree of increase in gene expression than autosomal ones (compared to the human/Chimpanzee common ancestor) if highly expressed, but not if lowly expressed. The traffic jam model also explains the known lower breadth of expression for genes on the X (and the Z of birds), as genes with broad expression are, on average, those with high maximal expression. As then further predicted, highly expressed tissue-specific genes are also rare on the X and broadly expressed genes on the X tend to be lowly expressed, both indicating that the trend is shaped by the maximal expression level not the breadth of expression per se. Importantly, a limit to the maximal expression level explains biased tissue of expression profiles of X-linked genes. Tissues whose tissue-specific genes are very highly expressed (e.g., secretory tissues, tissues abundant in structural proteins) are also tissues in which gene expression is relatively rare on the X chromosome. These trends cannot be fully accounted for in terms of alternative models of biased expression. In conclusion, the notion that it is hard for genes on the Therian X to be highly expressed, owing to transcriptional traffic jams, provides a simple yet robustly supported rationale of many peculiar features of X’s gene content, gene expression, and evolution
Differential roles of epigenetic changes and Foxp3 expression in regulatory T cell-specific transcriptional regulation
Naturally occurring regulatory T (Treg) cells, which specifically express the transcription factor forkhead box P3 (Foxp3), are engaged in the maintenance of immunological self-tolerance and homeostasis. By transcriptional start site cluster analysis, we assessed here how genome-wide patterns of DNA methylation or Foxp3 binding sites were associated with Treg-specific gene expression. We found that Treg-specific DNA hypomethylated regions were closely associated with Treg up-regulated transcriptional start site clusters, whereas Foxp3 binding regions had no significant correlation with either up- or down-regulated clusters in nonactivated Treg cells. However, in activated Treg cells, Foxp3 binding regions showed a strong correlation with down-regulated clusters. In accordance with these findings, the above two features of activation-dependent gene regulation in Treg cells tend to occur at different locations in the genome. The results collectively indicate that Treg-specific DNA hypomethylation is instrumental in gene up-regulation in steady state Treg cells, whereas Foxp3 down-regulates the expression of its target genes in activated Treg cells. Thus, the two events seem to play distinct but complementary roles in Treg-specific gene expression
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