University of Tokyo

About: University of Tokyo is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Population & Gene. The organization has 134564 authors who have published 337567 publications receiving 10178620 citations. The organization is also known as: Todai & Universitas Tociensis.

The Luminosity and Color Dependence of the Galaxy Correlation Function

Abstract: Westudytheluminosityandcolordependenceofthegalaxytwo-pointcorrelationfunctionintheSloanDigitalSky Survey, starting from a sample of � 200,000 galaxies over 2500 deg 2 . We concentrate our analysis on volume-limited subsamples of specified luminosity ranges, for which we measure the projected correlation function wp(rp), which is directly related to the real-space correlation function � (r). The amplitude of wp(rp) rises continuously with luminosity from Mr �� 17: 5t oMr �� 22:5, with the most rapid increase occurring above the characteristic luminosity L� (Mr �� 20:5). Over the scales 0:1 h � 1 Mpc � 22 can be approximated, imperfectly, by power-law three-dimensional correlation functions � (r) ¼ (r/r0) � � with � � 1:8 and r0(L� ) � 5:0 h � 1 Mpc. The brightest subsample, � 23 < Mr < � 22, has a significantly steeper � (r). When we divide samples by color, redder galaxies exhibit a higher amplitude and steeper correlation function at all luminosities. The correlation amplitude of blue galaxies increases continuously with luminosity, but the luminosity dependence for red galaxies is less regular, with bright red galaxies exhibiting the strongest clustering at large scales and faint red galaxies exhibiting the strongest clustering at small scales. We interpret these results using halo occupation distribution (HOD) models assuming concordance cosmological parameters. For most samples, an HOD model with two adjustable parameters fits the wp(rp) data better than a power law, explaining inflections at rp � 1 3 h � 1 Mpc as the transition between the one-halo and two-halo regimes of � (r). The implied minimum mass for a halo hosting a central galaxy more luminous than L grows steadily, with Mmin / L at low luminosities and a steeper dependence above L� . The mass at which a halo has, on average, one satellite galaxy brighter than L is M1 � 23Mmin(L), at all luminosities. These results imply a conditional luminosity function (at fixed halo mass) in which central galaxies lie far above a Schechter function extrapolation of the satellite population. The HOD model fits nicely explain the color dependence of wp(rp) and the cross correlation between red and blue galaxies. For galaxies with Mr < � 21, halos slightly above Mmin have blue central galaxies, while more massive halos have red central galaxies and predominantly red satellite populations. The fraction of blue central galaxies increases steadily with decreasing luminosity and host halo mass. The strong clustering offaint red galaxies follows from the fact that nearly all of them are satellite systems in high-mass halos. The HOD fitting results are in good qualitative agreement with the predictions of numerical and semianalytic models of galaxy formation. Subject headingg cosmology: observations — cosmology: theory — galaxies: distances and redshifts — galaxies: halos — galaxies: statistics — large-scale structure of universe

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Abstract: Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Determination of bisphenol A concentrations in human biological fluids reveals significant early prenatal exposure

Abstract: Background There is broad human exposure to bisphenol A (BPA), an estrogenic endocrine-disrupting chemical widely used for the production of plastic products. BPA is reported to affect preimplantation embryos or fetuses and alter their postnatal development at doses typically found in the environment. We measured contamination of BPA in various kinds of human biological fluids by a novel enzyme-linked immunosorbent assay. Methods Blood samples were obtained from healthy premenopausal women, women with early and full-term pregnancy, and umbilical cord at full-term delivery. Ovarian follicular fluids obtained during IVF procedures and amniotic fluids obtained at mid-term and full-term pregnancy were also subject to BPA measurements. Results BPA was present in serum and follicular fluid at approximately 1-2 ng/ml, as well as in fetal serum and full-term amniotic fluid, confirming passage through the placenta. Surprisingly, an approximately 5-fold higher concentration, 8.3 +/- 8.7 ng/ml, was revealed in amniotic fluid at 15-18 weeks gestation, compared with other fluids. Conclusion These results suggest accumulation of BPA in early fetuses and significant exposure during the prenatal period, which must be considered in evaluating the potential for human exposure to endocrine-disrupting chemicals.

The product of the human c-erbB-2 gene: a 185-kilodalton glycoprotein with tyrosine kinase activity.

Abstract: Antibodies were raised against a synthetic peptide corresponding to 14 amino acid residues at the COOH-terminus of a protein deduced from the human c-erbB-2 nucleotide sequence. These antibodies immunoprecipitated a 185-kilodalton glycoprotein from MKN-7 adenocarcinoma cells. Incubation of the immunoprecipitates with (gamma-32P)ATP resulted in the phosphorylation of this protein on tyrosine residues. These results indicate that the human c-erbB-2 gene product is the 185-kilodalton glycoprotein that is associated with tyrosine kinase activity. Although the c-erbB-2 protein was predicted to encode a protein very similar to epidermal growth factor (EGF) receptor, EGF did not stimulate this kinase activity either in vivo or in vitro.

PPAR γ insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors

Abstract: Based on the fact that aging is associated with a reciprocal decrease of osteogenesis and an increase of adipogenesis in bone marrow and that osteoblasts and adipocytes share a common progenitor, this study investigated the role of PPARγ, a key regulator of adipocyte differentiation, in bone metabolism. Homozygous PPARγ-deficient ES cells failed to differentiate into adipocytes, but spontaneously differentiated into osteoblasts, and these were restored by reintroduction of the PPARγ gene. Heterozygous PPARγ-deficient mice exhibited high bone mass with increased osteoblastogenesis, but normal osteoblast and osteoclast functions, and this effect was not mediated by insulin or leptin. The osteogenic effect of PPARγ haploinsufficiency became prominent with aging but was not changed upon ovariectomy. The PPARγ haploinsufficiency was confirmed to enhance osteoblastogenesis in the bone marrow cell culture but did not affect the cultures of differentiated osteoblasts or osteoclast-lineage cells. This study demonstrates a PPARγ-dependent regulation of bone metabolism in vivo, in that PPARγ insufficiency increases bone mass by stimulating osteoblastogenesis from bone marrow progenitors.