An analysis of the educational attainment and occupational composition of immigrants into Beijing.
Explore the source record for details and available documents.
Asia↗
Biomedical subjects
K Zhang
Publications and source records attributed to K Zhang.
Cloning and sequencing of cDNA encoding the complete mouse liver alcohol dehydrogenase.
The main ethanol-active alcohol dehydrogenase (ADH; alcohol:NAD+ oxidoreductase, EC 1.1.1.1) in mouse liver (ADH-AA) is similar in catalytic and molecular properties to horse liver ADH-EE and to the human class I ADHs. We have isolated cDNA clones encoding the entire mouse liver enzyme plus flanking regions. A mixture of 16 different oligonucleotides, each 14 bases long, was used to screen a liver cDNA library made from a DBA/2J mouse. A strongly hybridizing clone was found and identified as an ADH-encoding cDNA by partial DNA sequencing. This clone was used as a probe to identify others. Two overlapping cDNA clones together contained the entire protein-encoding region plus 100 nucleotides of the 5' noncoding region and 133 nucleotides of the 3' noncoding region culminating in a short poly(dA) tail. The amino acid sequence of the mouse liver enzyme deduced from this cDNA closely resembles that of horse liver ADH-E: 316 of 374 residues are identical, and 29 of the differences are conservative substitutions. The 5' region of this cDNA is interesting: the AUG that initiates the ADH polypeptide is preceded by an AUG that would encode the first amino acid of a tripeptide. Presumably termination of this tripeptide is followed by reinitiation at the AUG immediately preceding the sequence of the mature ADH polypeptide.
Alcohol Dehydrogenase↗
Population growth in Shanghai and its characteristics.
Explore the source record for details and available documents.
Age Distribution↗
The mediating role of cPLA2 in IL-1 beta and IL-6 release in LPS-induced HeLa cells.
Studies were conducted to characterize a HeLa cell model by which the roles of the 85-kDa phospholipase A2 (cPLA2) in interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) release could be evaluated. At first, untreated HeLa cells were compared with lipopolysaccharide (LPS)-treated HeLa cells. The latter resulted in cPLA2 overexpression and an increased trend of IL-1 beta and IL-6 release. The indicated doses of 85-kDa cPLA2 antisense oligonucleotide directed against the initiation site were then used to block cPLA2 in LPS-induced HeLa cells. The process led to a dose-dependent decrease in cPLA2 protein with no noticeable change of cPLA2 mRNA. Compared with that of LPS added only, a reduction of IL-1 beta and IL-6 levels in the supernatants of transfected cells following the repression of cPLA2 was observed. These results suggested that 85-kDa cPLA2 may mediate the signalling cascades by which IL-1 beta and IL-6 were released in LPS-induced HeLa cells.
HeLa Cells↗
The protective effect of bed nets impregnated with pyrethroid insecticide and vaccination against Japanese encephalitis.
A population-based case-control study to evaluate the protective effect of bed nets impregnated with pyrethroid insecticide and of vaccination against Japanese encephalitis was carried out in Gusi county, Henan province, China from June to September 1991; 50 cases and 100 matched controls were studied. Bed nets impregnated with pyrethroid insecticide greatly decreased the risk of infection among children under 10 years old, and vaccine efficacy was 78% (95% CI 16%-94%). We suggest that impregnated bed nets could be used as a quick response during outbreaks of Japanese encephalitis.
Bedding and Linens↗
Regulation of p21ras activity.
The ras genes encode GTP/GDP-binding proteins that participate in mediating mitogenic signals from membrane tyrosine kinases to downstream targets. The activity of p21ras is determined by the concentration of GTP-p21ras, which is tightly regulated by a complex array of positive and negative control mechanisms. GAP and NF1 can negatively regulate p21ras activity by stimulating hydrolysis of GTP bound to p21ras. Other cellular factors can positively regulate p21ras by stimulating GDP/GTP exchange.
Amino Acid Sequence↗
Genetic and molecular studies of macular dystrophies: recent developments.
Macular degeneration is a heterogeneous group of disorders characterized by progressive central visual loss and degeneration of the macula and underlying retinal pigment epithelium (RPE) of the eye. Age-related macular degeneration (ARMD), the most common form of the disease, is the leading cause of legal blindness in the elderly population in the United States and in the many developed countries throughout the world. Despite its prevalence, its etiology and pathogenesis are poorly understood, and effective treatment options are limited for most patients. Inherited macular dystrophies share many important features with ARMD but are more readily studied by molecular genetic approaches. Over the past few years, significant progress has been made in the molecular genetics of inherited macular dystrophies. Genes responsible for dominant and recessive Stargardt's macular dystrophy as well as Best's disease have been localized to specific chromosomal regions. The peripherin/RDS gene when defective is associated with butterfly-shaped pattern dystrophy. Molecular studies of genes involved in macular dystrophies may yield insights into the mechanisms of pathogenesis of macular degeneration and provide new rationale for the management and treatment of patients with these diseases.
Base Sequence↗
Nigrostriatal dopaminergic denervation enhances dopamine D(4) receptor binding in rat caudate-putamen.
Radioligand binding to dopamine (DA) D(4) receptors was examined in adult rat forebrain 5 weeks after unilateral 6-hydroxydopamine (6-OHDA) lesioning of substantia nigra to remove ascending nigrostriatal dopaminergic projections. D(4) receptor binding was increased by up to 47% in denervated caudate-putamen (CPu) in rats that rotated away from the lesioned side with apomorphine challenge, with lesser changes in rats that failed to rotate with apomorphine. Functional significance of D(4) receptor upregulation induced by the lesions was investigated by examining behavioral effects of the highly selective D(4) agonist CP-226,269 and antagonist CP-293,019. Neither agent induced rotation at doses as high as 30 mg/kg ip. Pretreatment with the D(4) antagonist CP-293,019 did not affect rotation induced by either a D(1)-like (SKF-38393) or D(2)-like receptor (quinpirole) agonist. These findings provide the first evidence that D(4) receptors can be upregulated by nigrostriatal dopaminergic denervation. They also suggest that, unlike D(1) and D(2) receptors, D(4) receptors do not play a pivotal role in rotational behavior in rats with unilateral dopaminergic lesions.
Animals↗
A computational study of intramolecular proton transfer in gaseous protonated glycine.
The minimum energy paths for intramolecular proton transfer between the amino nitrogen and carbonyl oxygen atoms in gaseous protonated glycine were estimated at the Hartree-Fock (HF) and second-order Møller-Plesset Perturbation (MP2) levels of theory. Potential energy profiles and their associated reactant, transition state, and product species calculated at the MP2/6-31G* level were shown to differ significantly from those obtained at the HF/6-31G* level. Effects of electron correlation and basis functions on the calculated geometries and energies of relevant species were examined at the HF, MP2, MP4, CCSD, and B3LYP levels using the 6-31G*, 6-31G**, 6-31+G**, 6-311+G**, 6-31+G(2d,2p), 6-311+G(3df,2p), cc-pVDZ, aug-cc-pVDZ, and cc-pVTZ basis sets. The HF and MP2 optimized levels with the 6-31G*, 6-31G**, 6-31+G**, and 6-311+G** bases were used to calculate the thermodynamic and kinetic properties of the proton transfer reaction at 298.15 K and 1 atm, which include enthalpy, entropy, Gibbs free energy, equilibrium constant, potential energy barriers, tunneling transmission coefficients, and rate constants. Results indicate that the proton in a carbonyl O-protonated glycine undergoes a rapid migration to the amino nitrogen atom, while the reverse process is extremely unfavorable. The objective of this work is to develop practical theoretical procedures for studying proton transfer reactions in amino acids and peptides and to assemble physical data from these model calculations for future references.
Electrochemistry↗
Cytokines and pulmonary fibrosis.
In the past several years, significant progress in many aspects of pulmonary fibrosis research has been made. Among them, the finding that a variety of cytokines play important roles in the complex process appears most intriguing. These cytokines include at least transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), platelet-derived growth factor, fibroblast growth factors, (TGF-alpha), interleukin-1, monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha. These cytokines have been demonstrated to be produced at the sites of active fibrosis where they appear to be expressed by activated inflammatory cells, such as macrophages and eosinophils. More interestingly, other noninflammatory lung cells including mesenchymal cells, such as myofibroblasts, and epithelial cells, have been found to be significant sources as well, albeit in most instances at somewhat different time points than those by inflammatory cells. Study of the individual cytokines in vitro has revealed a variety of potential roles for these cytokines in the regulation of the fibrotic process in vivo, including chemoattractant, mitogenic activities for fibroblasts, stimulation of extracellular matrix and alpha-smooth muscle actin gene expression, alteration of the contractile phenotype of fibroblasts and regulation of diverse functions of lung inflammatory and epithelial cells which can further impact on the fibrotic process by autocrine and paracrine mechanisms. Of these cytokines, it appears that TGF-beta is probably the most important cytokine in terms of the direct stimulation of lung matrix expression which typifies fibrosis. Recently however, there is accumulating evidence to indicate that the situation is much more complex than any one single cytokine being solely responsible for the fibrotic response. The concept of complex lung cytokine networks, orchestrated by a few key cytokines, such as TNF-alpha, being responsible for this response has received strong support from recent studies. This means that it is the balance of positive (profibrogenic) and negative (antifibrogenic) forces generated from interaction among the various cytokines constituting these networks, which may finally determine the outcome of lung injury and inflammation. The importance of these cytokines also suggests new potential targets for designing new therapies for progressive pulmonary fibrosis, and perhaps their utility in prognostication as well.
Animals↗
Alternative RNA of epsilon transcripts produces mRNAs encoding two membrane and four secreted IgE isoforms.
We elucidated a series of alternatively spliced human epsilon mRNAs by employing a human epsilon-specific RT-PCR strategy. Two mRNA isoforms provide for the expression of distinct membrane IgE proteins, the common form of which contains a novel 56-amino-acid sequence after the last epsilon constant-region domain. Other mRNAs encode, in addition to the classic secreted epsilon chain, at least three novel epsilon secreted proteins that lack a transmembrane domain and possess distinctive C-terminal features. Furthermore, the expression of these epsilon mRNA isoforms is differentially regulated by stimuli such as interleukin-10, Fc epsilon RII cross-linking and aromatic hydrocarbons found in diesel exhaust.
B-Lymphocytes↗
Quercetin-induced apoptosis in the monoblastoid cell line U937 in vitro and the regulation of heat shock proteins expression.
Quercetin, a widely distributed plant flavonoid, inhibits the growth of tumor cells and the expression of heat shock proteins. In this study, we examined quercetin-induced apoptosis of U937 cells in vitro and the regulation of heat shock proteins expression. The quercetin-induced apoptosis was demonstrated to be dose- and time-dependent. Flow cytometry analysis revealed that sub-G1 peak appeared at 12 hours, 24 hours and 48 hours respectively when treated with 50 mM of quercetin and at 6 hours, 12 hours, 24 hours and 48 hours with 100 mM of quercetin. Agarose gel electrophoresis demonstrated a typical ladder-like pattern of DNA fragments in the same time intervals with 50 mM of quercetin and at 6 hours only with 100 mM of quercetin. The distribution of DNA contents showed that U937 cells were accumulated mainly at G2/M phase when incubated with 50 mM of quercetin for 24 hours and 48 hours. There was no specific effect on cell cycle distribution at 100 mM of quercetin. On exposure to 100 mM of quercetin, the inhibition of hsp27 and hsp70 expression was observed from 12 hours to 48 hours and 6 hours to 48 hours respectively. The inhibition of hsp90 expression was not found eiyher at 50 mM or 100 mM of quercetin exposure. When incubated with 50 mM of quercetin, there was no inhibitory effect on hsp27, hsp70 and hsp90 expression by the Western blot analysis. These results suggested that it is dependent on the dose and exposure time of quercetin to induce apoptosis of U937 cells in vitro, to affect the cell cycle distribution and to regulate the expression of hsp27 and hsp70.
Apoptosis↗
Metabolic chiral inversion of stiripentol in the rat. I. Mechanistic studies.
To study enantioselective aspects of the disposition of stiripentol (STP), a chiral allylic alcohol undergoing development as an antiepileptic drug, a stereoselective synthesis was developed and the configuration of the two enantiomers determined to be (R)-(+) and (S)-(-). Following a single oral dose (300 mg kg-1) of the individual enantiomers to adult male Sprague-Dawley rats, it was found that (R)-STP was transformed extensively to its antipode, whereas little inversion was detected when (S)-STP was administered. Studies on the mechanism of this apparently unidirectional chiral inversion revealed that the phenomenon was dependent on the presence of the side-chain C==C double bond, because the enantiomers of the corresponding saturated alcohol (D2602) did not interconvert in vivo. Experiments with analogs of STP labeled with deuterium or oxygen-18 at the chiral center showed that, whereas the deuterium was retained in vivo, partial loss of the 18O occurred from both enantiomers of the drug. Pretreatment of rats with pentachlorophenol (40 mumol kg-1 i.p.), an inhibitor of sulfation (and possibly other conjugation reactions), led to a marked decrease in the rate of conversion of (R)-STP to its antipode, suggesting that the chiral inversion phenomenon may be mediated, at least in part, by an enantioselective conjugation process.
Administration, Oral↗
Metabolic chiral inversion of stiripentol in the rat. II. Influence of route of administration.
As described in the accompanying study, it was found that when the S enantiomer of stiripentol [(S)-STP] was given orally to rats, blood specimens contained only (S)-STP, whereas following administration of an equivalent dose of (R)-STP, both R and S forms of the drug were detected in the systemic circulation. In the present study, we investigated the influence of route of administration on this apparently unidirectional chiral inversion of (R)-STP in the rat. When (R)-STP was given either intravenously (60 mg kg-1) or intraperitoneally (300 mg kg-1), the inversion phenomenon was not observed, indicating that the process must take place presystemically. Following oral administration of either enantiomer of STP, it was found that the drug present at various points along the gastrointestinal tract became progressively enriched in molecules of R configuration, such that the free STP in cecum, large intestine, and feces consisted largely of the R enantiomer, regardless of the configuration of the administered drug. In a parallel in vitro study, it was demonstrated that STP undergoes acid-catalyzed racemization, the rate of which is appreciable at the pH value of the rat stomach (pH approximately 4). On the basis of these observations, it is proposed that the apparent metabolic chiral inversion of (R)-STP results from the combination of at least two factors: 1) partial acid-catalyzed racemization in gastric acid (that affects both enantiomers equally), and 2) enantioselectivity in one or more of the processes involved in the absorption, first pass metabolism or biliary excretion of STP, such that the S isomer appears selectively in the systemic circulation, whereas the R enantiomer is eliminated preferentially in the feces.
Administration, Oral↗