宽带CDMA蜂窝系统中小区容量和覆盖半径的计算

在功率控制方程中加入干扰因子后,推导了中断概率,基站接收机灵敏度,移动台最大可允许的发射功率,信干比的期望值,路径抽耗与小区覆盖半径,小区容量的关系式,在2GHz频率,宽带,各种速率时,计算了基站接收信号的信干比,小区容量和小区的覆盖半径。     

Expression of bcl-2 gene increases in apoptosis of vascular endothelial cells induced by rattlesnake venom

Apoptosis of vascular endothelial cells (VEC) has been induced by deprivation of survival factors (aFGF and serum) and by rattlesnake venom. The expression of bcl-2 gene has been examined by Northern blotting in the two apoptosis inducing systems. Our results show that the expression of bcl-2 has not been detected in normal culture cells and in apoptotic cells induced by deprivation of survival factors. But in apoptotic cells induced by rattlesnake venom (10 g/mL), the expression of bcl-2 increases, and its mRNA exhibits two bands. The data first suggest that increasing expression and splitting of bcl-2 mRNA may play an important role in apoptosis of VEC induced by rattlesnake venom, and this finding is helpful to understanding the role of bcl-2 in regulation of apoptosis.     

Asymmetric Agglomerative Hierarchical Clustering Algorithms and Their Evaluations

This paper presents asymmetric agglomerative hierarchical clustering algorithms in an extensive view point. First, we develop a new updating formula for these algorithms, proposing a general framework to incorporate many algorithms. Next we propose measures to evaluate the fit of asymmetric clustering results to data. Then we demonstrate numerical examples with real data, using the new updating formula and the indices of fit. Discussing empirical findings, through the demonstrative examples, we show new insights into the asymmetric clustering.     

Histone H2AX-dependent GABA(A) receptor regulation of stem cell proliferation

Stem cell self-renewal implies proliferation under continued maintenance of multipotency. Small changes in numbers of stem cells may lead to large differences in differentiated cell numbers, resulting in significant physiological consequences. Proliferation is typically regulated in the G1 phase, which is associated with differentiation and cell cycle arrest. However, embryonic stem (ES) cells may lack a G1 checkpoint. Regulation of proliferation in the 'DNA damage' S/G2 cell cycle checkpoint pathway is known for its role in the maintenance of chromatin structural integrity. Here we show that autocrine/paracrine gamma-aminobutyric acid (GABA) signalling by means of GABA(A) receptors negatively controls ES cell and peripheral neural crest stem (NCS) cell proliferation, preimplantation embryonic growth and proliferation in the boundary-cap stem cell niche, resulting in an attenuation of neuronal progenies from this stem cell niche. Activation of GABA(A) receptors leads to hyperpolarization, increased cell volume and accumulation of stem cells in S phase, thereby causing a rapid decrease in cell proliferation. GABA(A) receptors signal through S-phase checkpoint kinases of the phosphatidylinositol-3-OH kinase-related kinase family and the histone variant H2AX. This signalling pathway critically regulates proliferation independently of differentiation, apoptosis and overt damage to DNA. These results indicate the presence of a fundamentally different mechanism of proliferation control in these stem cells, in comparison with most somatic cells, involving proteins in the DNA damage checkpoint pathway.     

p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

Cardiac hypertrophy occurs as an adaptive response to increased workload to maintain cardiac function. However, prolonged cardiac hypertrophy causes heart failure, and its mechanisms are largely unknown. Here we show that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiac hypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure. Pressure overload initially promoted vascular growth in the heart by hypoxia-inducible factor-1 (Hif-1)-dependent induction of angiogenic factors, and inhibition of angiogenesis prevented the development of cardiac hypertrophy and induced systolic dysfunction. Sustained pressure overload induced an accumulation of p53 that inhibited Hif-1 activity and thereby impaired cardiac angiogenesis and systolic function. Conversely, promoting cardiac angiogenesis by introducing angiogenic factors or by inhibiting p53 accumulation developed hypertrophy further and restored cardiac dysfunction under chronic pressure overload. These results indicate that the anti-angiogenic property of p53 may have a crucial function in the transition from cardiac hypertrophy to heart failure.     

CD38 is critical for social behaviour by regulating oxytocin secretion

CD38, a transmembrane glycoprotein with ADP-ribosyl cyclase activity, catalyses the formation of Ca2+ signalling molecules, but its role in the neuroendocrine system is unknown. Here we show that adult CD38 knockout (CD38-/-) female and male mice show marked defects in maternal nurturing and social behaviour, respectively, with higher locomotor activity. Consistently, the plasma level of oxytocin (OT), but not vasopressin, was strongly decreased in CD38-/- mice. Replacement of OT by subcutaneous injection or lentiviral-vector-mediated delivery of human CD38 in the hypothalamus rescued social memory and maternal care in CD38-/- mice. Depolarization-induced OT secretion and Ca2+ elevation in oxytocinergic neurohypophysial axon terminals were disrupted in CD38-/- mice; this was mimicked by CD38 metabolite antagonists in CD38+/+ mice. These results reveal that CD38 has a key role in neuropeptide release, thereby critically regulating maternal and social behaviours, and may be an element in neurodevelopmental disorders.     

Magnetic properties of perpendicularly orientated L1<Subscript>0</Subscript> FePt nanoparticles

L10 FePt films were deposited on MgO (001) substrates heated to 700°C by magnetron sputtering.Assisted by the misfit of lattice between film and substrate,strong (001) texture was formed.The film at nominal thickness t N=5 nm was composed of nanoparticles with a size of～70 nm,and showed a high coercivity of～105 kOe at 4.2 K.At t N=～50 nm,as the film changed from discontinuous to continuous,the coercivity dropped about one order of magnitude.Micromagnetic simulation implies that the magnetization reversal is...     

Effects of the metals,Be, Fe,Cu and Al,on the mobility of immunoglobulin receptors

Summary Cap formation in mouse spleen cells induced by antiimmunoglobulin was inhibited by the metals Be, Fe, Cu and Al. Be was especially strong as an inhibitor of cap formation. It is suggested that these metals might change the mobility of the membrane and have some biological effects on the cross association of antigen receptors when B lymphocytes are attached by them.     

Formation and branch migration of Holliday junctions mediated by eukaryotic recombinases

Holliday junctions (HJs) are key intermediates in homologous recombination and are especially important for the production of crossover recombinants. Bacterial RecA family proteins promote the formation and branch migration of HJs in vitro by catalysing a reciprocal DNA-strand exchange reaction between two duplex DNA molecules, one of which contains a single-stranded DNA region that is essential for initial nucleoprotein filament formation. This activity has been reported only for prokaryotic RecA family recombinases, although eukaryotic homologues are also essential for HJ production in vivo. Here we show that fission yeast (Rhp51) and human (hRad51) RecA homologues promote duplex-duplex DNA-strand exchange in vitro. As with RecA, a HJ is formed between the two duplex DNA molecules, and reciprocal strand exchange proceeds through branch migration of the HJ. In contrast to RecA, however, strand exchange mediated by eukaryotic recombinases proceeds in the 3'-->5' direction relative to the single-stranded DNA region of the substrate DNA. The opposite polarity of Rhp51 makes it especially suitable for the repair of DNA double-strand breaks, whose repair is initiated at the processed ends of breaks that have protruding 3' termini.     

Structure of the DNA deaminase domain of the HIV-1 restriction factor APOBEC3G

The human APOBEC3G (apolipoprotein B messenger-RNA-editing enzyme, catalytic polypeptide-like 3G) protein is a single-strand DNA deaminase that inhibits the replication of human immunodeficiency virus-1 (HIV-1), other retroviruses and retrotransposons. APOBEC3G anti-viral activity is circumvented by most retroelements, such as through degradation by HIV-1 Vif. APOBEC3G is a member of a family of polynucleotide cytosine deaminases, several of which also target distinct physiological substrates. For instance, APOBEC1 edits APOB mRNA and AID deaminates antibody gene DNA. Although structures of other family members exist, none of these proteins has elicited polynucleotide cytosine deaminase or anti-viral activity. Here we report a solution structure of the human APOBEC3G catalytic domain. Five alpha-helices, including two that form the zinc-coordinating active site, are arranged over a hydrophobic platform consisting of five beta-strands. NMR DNA titration experiments, computational modelling, phylogenetic conservation and Escherichia coli-based activity assays combine to suggest a DNA-binding model in which a brim of positively charged residues positions the target cytosine for catalysis. The structure of the APOBEC3G catalytic domain will help us to understand functions of other family members and interactions that occur with pathogenic proteins such as HIV-1 Vif.