Biomedical subjects

D Zhou

Publications and source records attributed to D Zhou.

At least 145 records · Page 8Linked to original sources

PubMed1999

[Clinical application of expandable metal stent for palliation of malignant biliary obstruction].

OBJECTIVE: To investigated the long-term result of expandable metallic biliary stent implantation and evaluated preliminarily the factors that might impact the therapeutic effectiveness. METHODS: 134 patients with malignant choledochal stenosis were treated with metallic endo-prosthesis (128 transpapillary endoscopically and 6 transhepatic percutaneously). The follow-up results were compared with those of 97 patients with conventional plastic stents during the same period. RESULTS: The success rate was 95.7%, and the procedure related complications were found in 6.4% of patients. The jaundice was eliminated completely in 85.6% patients. During long-term follow-up, the metal stents were shown patent for a mean duration of 300 days, which was significantly longer than 80 days of polyethylene endoprostheses (P < 0.01). The mean survival was 210 days. From classified data assessment, the stent patency in primary bile duct neoplasm group was almost similar to that in metastatic group, but the median survival of the former was slightly longer than that of the latter. There were flow differences in patancy and survival rates between the hilar obstruction group and the middle and low obstruction group. CONCLUSIONS: The median patancy of expandable metal stents was significantly longer than that of conventional plastic prostheses. To get the highest benefit, however, the indication should be strictly selected.

Adult↗

PubMed1999

[Roles of bifidobacterium on prevention of experimental colorectal carcinoma and induction of apoptosis].

OBJECTIVE: To explore the effect of bifidobacterium adolescence on prevention from experimental colorectal carcinoma and its antitumor mechanism. METHODS: An animal model of nude mouse tumor transplanted from colorectal carcinoma was set up. Bifidobacteria adolescence were intraperitoneally injected into nude mice in advance. The growth rate, ultrastructure, density of apoptotic cells, rate of bcl-2 and bax oncoprotein expression and its positive cell density in transplanted tumor of nude mice from colorectal carcinoma were investigated by employing transmission microscopy, in situ end labeling technique and immunohistochemical staining. RESULTS: The growth rate of transplanted tumors from colorectal carcinoma in the group with bifidobacterium prevention was slower than that in the control group. Many tumor cells at varied apoptotic stages could be observed in transplantation tumor tissue in the bifidobacterium prevention group and their density of apoptotic cells, rate of bcl-2 and bax oncoprotein expression and its positive cell density were significantly higher in the group with bifidobacterium prevention, as compared with the control group (P < 0.01). But, expression rate of bcl-2 oncoprotein turned contrary to that of bax oncoprotein. CONCLUSION: Bifidobacteria adolescence could markedly prevent from occurrence and development of colorectal carcinoma in vivo and induce apoptosis of tumor.

Animals↗

PubMed1999

[Effect of transforming growth factor-beta on proliferation cycle of epiphyseal chondrocyte].

In order to investigate the effect of transforming growth factor-beta (TGF-beta) on chondrocyte proliferation cycle, we used flow-cytometry to assess the epiphyseal chondrocyte of embryonic chick femora which was cultured in free-serum media and treated with TGF-beta. The results showed that after treated with TGF-beta for 24 h, the proliferation indexes(PIs) of experimental groups(0.11 ng, 0.33 ng, 1.00 ng/ml) were lower than the PIs of the control groups, but the PI of 3.00 ng/ml group was higher than that of the control group (P < 0.001). After treated for 48 h, except the 0.11 ng/ml group, the PIs of experimental groups were lower than those of the control (P < 0.001). And after treated for 96 h, the PIs of all groups were higher than those of the control; the PI of the 0.33 ng/ml group was the highest (P < 0.001). These suggest that after treated in varied time and dosage, the effect of TGF-beta on epiphyseal chondrocyte is obvious, and TGF-beta on epiphyseal chondrocyte is obvious, and TGF-beta can inhibit chondrocyte proliferation first, and then its effect on chondrocyte can transform from inhibition into proliferation.

Animals↗

PubMed1999

[Breeding of yeast for beer manufacturing by inactivated protoplast fusion].

QSB-XI6, one of fusants, was obtained by PEG-induced fusion between UV-inactivated protoplasts of Saccharomyces cerevisiae LQ16 (Ile-, Datr) and heat-inactivated protoplasts of S. cerevisiae QSB7(Ala-, H2S-). The cell volume, bicmass, genotype and DNA content of the fusant were measured in comparison with of its parents and the results showed that QSB-XI6 was a fusant. The fermentation ability and the flocculent capacity of this fusant were higher than those of its parents. The diacetyl content of the beer produced by the fusant was measured and some other compositions of the beer was also analysed by gas chromatography. The sensory evaluation of the beer was much better and the flavour was distinctive. The results of many production trials in succession showed that all good characteristics of QSB-XI6 were stable.

Cell Fusion↗

PubMed1999

[Bilateral acoustic neuromas].

OBJECTIVE: To investigate the clinical course, growth character and treatment of bilateral acoustic neuromas (BANs). METHODS: Five cases of BANs were reported. RESULTS: From 1986 to 1996, 92 patients with acoustic tumors were managed. Of them, 5(5%) bilateral acoustic neuromas were observed. All patients were males, the age at the time of testing ranged from 16 to 31 years (mean 23.8 years). In all patients, progressive hearing loss and tinnitus were the most common initial symptoms. In addition, signs of other cranial nerve deficits were detected in all patients. Two cases had cafe au lait spots and all cases had neurofibromas of varying sizes and shapes in subcutaneous tissues. Four had unilateral acoustic tumors operated on, one by the translabyrinthine approach, 3 by the suboccipital approach. One patient died due to encephaledema and hernia of brain after operation. According to the MRI data in one case, the average growth rate of acoustic tumor was 1.1 cm (superior/inferior) and 0.7 cm (medical/lateral) per year. CONCLUSION: The management of BANs patients presents challenging problems different from the unilateral acoustic tumors.

Adolescent↗

PubMed1999

[Study on the molar absorption coefficients of Bi(III)-thiocyanate complexes in UV spectrum].

The absorption spectra of bismuth(II)-thiocyanate in the Tween-80-H2O solution were studied in this paper, in which the maximum wavelength lambdamax = 335 nm and the molar extinction coefficient epsilon335 = 2.61 x 10(4), similar to those of complexes of bismuth with PAR or azoarsenic(III), epsilon610 = 2.70 x 10(4). A new tribasic complex was found and used to explain that bismuth(III)-thiocyanate is a sensitive colour reaction in the Tween-80-H2O solution.

English Abstract↗

PubMed1998

Modulation of aromatase expression in the breast tissue by ERR alpha-1 orphan receptor.

We have previously identified a silencer element (S1) that is situated between promoters I.3 and II of the human aromatase gene and that down-regulates the action of these promoters. We recently applied the yeast one-hybrid approach to screen a human breast tissue hybrid cDNA expression library for genes encoding the proteins binding to the silencer region. Most proteins identified from this approach belong to the nuclear receptor superfamily. Fifty % of the positive clones encode for ERR alpha-1, and other positive clones include EAR-2, EAR-3 (COUP-TF1), RAR gamma, and p120E4F. Because ERR alpha-1 was found to be the major protein interacting with S1, we decided to examine the regulatory action of ERR alpha-1 on promoter I.3 of the human aromatase gene. Using a reporter plasmid that includes the aromatase genomic fragment containing promoter I.3 and S1, ERR alpha-1 was found to have a positive regulatory function in breast cancer SK-BR-3 cells. Gel mobility shift assays have confirmed that ERR alpha-1 binds to S1 in a dose-dependent manner, and DNase I footprinting analysis has revealed that ERR alpha-1 binds to a region, 5'-AAGGTCAGAAAT-3', which is within S1 and between 96 and 107 bp relative to the transcriptional start site of promoter I.3. In addition, despite the fact that the nuclear receptor SF1 was shown previously to bind to the same site and to mediate a cAMP response in ovary, our yeast one-hybrid screening did not find any SF-1 clones. Gel mobility shift assays further revealed that SF-1 can bind to the silencer element with an affinity comparable with ERR alpha-1. Because our reverse transcription-PCR analysis was not able to detect SF1 mRNA in breast cancer tissue or in SK-BR-3 cells, it is thought that SF1 protein is not expressed in breast cancer tissue. Two ERR alpha-1 RNA variants with differences at the 5'-end have been reported. Our reverse transcription-PCR analysis identified the shorter variant in 28 of 32 breast tumor specimens and the longer variant in only 1 specimen. In addition, the shorter variant was detected in breast cancer SK-BR-3 cells as well as in a breast tumor fibroblast line WS3TF. The results suggest that ERR alpha-1 is one of the nuclear proteins interacting with S1 in breast cancer tissue. It is thought that the silencer element in the human aromatase gene may function differently in different tissues because of distinct expression patterns of transcription factors.

Aromatase↗

PubMed1998

AnkyrinG is required for clustering of voltage-gated Na channels at axon initial segments and for normal action potential firing.

Voltage-gated sodium channels (NaCh) are colocalized with isoforms of the membrane-skeletal protein ankyrinG at axon initial segments, nodes of Ranvier, and postsynaptic folds of the mammalian neuromuscular junction. The role of ankyrinG in directing NaCh localization to axon initial segments was evaluated by region-specific knockout of ankyrinG in the mouse cerebellum. Mutant mice exhibited a progressive ataxia beginning around postnatal day P16 and subsequent loss of Purkinje neurons. In mutant mouse cerebella, NaCh were absent from axon initial segments of granule cell neurons, and Purkinje cells showed deficiencies in their ability to initiate action potentials and support rapid, repetitive firing. Neurofascin, a member of the L1CAM family of ankyrin-binding cell adhesion molecules, also exhibited impaired localization to initial segments of Purkinje cell neurons. These results demonstrate that ankyrinG is essential for clustering NaCh and neurofascin at axon initial segments and is required for physiological levels of sodium channel activity.

Action Potentials↗

PubMed1998

Nervous system defects of AnkyrinB (-/-) mice suggest functional overlap between the cell adhesion molecule L1 and 440-kD AnkyrinB in premyelinated axons.

The L1 CAM family of cell adhesion molecules and the ankyrin family of spectrin-binding proteins are candidates to collaborate in transcellular complexes used in diverse contexts in nervous systems of vertebrates and invertebrates. This report presents evidence for functional coupling between L1 and 440-kD ankyrinB in premyelinated axons in the mouse nervous system. L1 and 440-kD ankyrinB are colocalized in premyelinated axon tracts in the developing nervous system and are both down-regulated after myelination. AnkyrinB (-/-) mice exhibit a phenotype similar to, but more severe, than L1 (-/-) mice and share features of human patients with L1 mutations. AnkyrinB (-/-) mice exhibit hypoplasia of the corpus callosum and pyramidal tracts, dilated ventricles, and extensive degeneration of the optic nerve, and they die by postnatal day 21. AnkyrinB (-/-) mice have reduced L1 in premyelinated axons of long fiber tracts, including the corpus callosum, fimbria, and internal capsule in the brain, and pyramidal tracts and lateral columns of the spinal cord. L1 was evident in the optic nerve at postnatal day 1 but disappeared by postnatal day 7 in mutant mice while NCAM was unchanged. Optic nerve axons of ankyrinB (-/-) mice become dilated with diameters up to eightfold greater than normal, and they degenerated by day 20. These findings provide the first evidence for a role of ankyrinB in the nervous system and support an interaction between 440-kD ankyrinB and L1 that is essential for maintenance of premyelinated axons in vivo.

Animals↗

PubMed1998

Serotonergic hyperinnervation of the frontal cortex in an animal model of depression, the bulbectomized rat.

We studied the influence of olfactory bulbectomy in rats on three different parameters of serotonin (5-HT) presynapses, 5-HT transporter density, tryptophan hydroxylase apoenzyme concentration, and the levels of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) in various brain regions. Compared with sham-operated controls, the Bmax values of [3H]paroxetine binding, the apoenzyme concentration of tryptophan hydroxylase and the level of 5-HIAA, and, therefore, the 5-HIAA/5-HT ratio were significantly and selectively increased in the frontal cortex of bulbectomized rats, measured 12 weeks after surgery. The most likely explanation of the concomitant increase in levels of all three markers of 5-HT presynapses in the frontal cortex is an increased density of 5-HT innervation in this remote projection field of the raphe nuclei. It is suggested that the bulbectomy-associated axotomy of 5-HT fibers projecting to the bulb stimulates collateral sprouting and synaptogenesis, especially in the frontal cortex. The resulting 5-HT hyperinnervation must be expected to alter global neuronal activity in this region and to impair the balance of information flow between this and other brain regions, resulting in a multitude of secondary behavioral and neurochemical changes. The frontocortical abnormalities observed by brain imaging studies in the brains of depressed patients may also be explained by a selective 5-HT hyperinnervation of this brain region.

Animals↗

PubMed1998

Expression of beta1,4-galactosyltransferase in the development of mouse brain.

Beta1,4-galactosyltransferase (GalTase, EC 2.4.1.38) transfers galactose to the terminal N-acetylglucosamine of complex-type N-glycans, which have great importance for cell-cell interactions during fertilization and early embryogenesis. In this study, the activity of beta1,4-galactosyltransferase in mouse brain during development was measured with the method of reverse HPLC using a fluorescence-labeled biantenary sugar chain, GlcNAcbeta1-2Manalpha1-6(GlcNAcbeta1-2Manalpha1- 3) Manbeta1-4GlcNAcbeta1-4GlcNAc-PA. The level of messenger RNA of this enzyme during the development of mouse brain was also investigated with Northern blot analysis. The results showed that: (1)beta1,4-galactosyltransferase showed similar branch specificity and kinetics for the biantenary substrate during development; (2) GalTase activity in fetal mouse brain was four times higher than that in adult mouse brain and decreased gradually in the course of development; (3) messenger RNA level was highest in fetal mouse and decreased dramatically after birth. However, the contents of mRNA were not parallel to the enzyme activity.

Animals↗

PubMed1998

The C-truncated delta-opioid receptor underwent agonist-dependent activation and desensitization.

The agonist-dependent activation and desensitization of a recombinant analog of delta-opioid receptor lacking the carboxyl-terminal (C-terminal) 31 residue peptide segment were discussed. The cDNA of the C-truncated delta-opioid receptor was created by polymerase chain reaction (PCR), stably expressed in Chinese hamster ovary cells and characterized by binding assay and function assay. Agonist [D-Pen2, D-Pen5]-enkephalin (DPDPE) stimulated the specific [35S]GTPgammaS binding to membrane fragments of cells expressing the C-truncated and the wild-type delta-opioid receptors in different levels dose-dependently. EC50 values of DPDPE on truncated and wild-types in stimulation were very similar. Agonist-dependent desensitization, which could be blocked by protein kinase inhibitor staurosporine (Stau), was observed after pretreating truncated receptors with 1 microM DPDPE for 10 min, the same as wild-types. The results reveal that the C-terminal of the delta-opioid receptor is not involved in controlling the G-protein activation and phosphorylation-related functional desensitization.

Animals↗

PubMed1998

Role of stress-activated mitogen-activated protein kinase (p38) in beta 2-integrin-dependent neutrophil adhesion and the adhesion-dependent oxidative burst.

Bacterial LPS elicits both rapid activation of the stress-activated MAP kinase p38 in polymorphonuclear leukocytes (PMN) and rapid adhesion of the PMN to ligands for the leukocyte integrin CD11b/CD18. The functional correlation between these two events was examined. The time course for tyrosine phosphorylation of p38 in PMN in response to 10 ng/ml LPS in 1% normal human serum was consistent with participation in signaling for leukocyte integrin-dependent adhesion, with transient phosphorylation peaking at 10 to 20 min. The concentration dependence of p38 phosphorylation also resembled that for PMN adhesion, with <1 ng/ml LPS eliciting a response. Phosphorylation was inhibited by mAb 60b against CD14, but not by mAb 26ic, a nonblocking anti-CD14. The function of p38 in integrin-dependent adhesion and the adhesion-dependent oxidative burst was tested using a specific inhibitor of p38, SB203580. SB203580 inhibited adhesion by diminishing the initial rate of adherence in response to both LPS and TNF, with a half-maximal concentration in the range of 0.1 to 0.6 microM. It did not, however, block adhesion in response to formyl peptide or PMA. The p38 inhibitor also blocked the adhesion-dependent oxidative burst with a half-maximal concentration similar to that for adhesion. Timed delivery of the compound during the lag phase preceding H2O2 production suggested that p38 kinase activity was required throughout the lag but not after the oxidase was assembled. These results suggest that p38 functions in PMN to signal leukocyte integrin-dependent adhesion and the subsequent massive production of reactive oxygen intermediates.

CD18 Antigens↗

PubMed1998

Mutations uncover a role for two magnesium ions in the catalytic mechanism of adenylyl cyclase.

The recent determination of the crystal structure of adenylyl cyclase has elucidated many structural features that determine the regulatory properties of the enzyme. In addition, the characterization of adenylyl cyclase by mutagenic techniques and the identification of the binding site for P-site inhibitors have led to modeling studies that describe the ATP-binding site. Despite these advances, the catalytic mechanism of adenylyl cyclase remains uncertain, especially with respect to the role that magnesium ions may play in this process. We have identified four mutant mammalian adenylyl cyclases defective in their metal dependence, allowing us to further characterize the function of metal ions in the catalytic mechanism of this enzyme. The wild-type adenylyl cyclase shows a biphasic Mg2+ dose-response curve in which the high-affinity component displays cooperativity (Hill coefficient of 1.4). Two mutations (C441R and Y442H) reduce the affinity of the adenylyl cyclase for Mg2+ dramatically without affecting the binding of MgATP, suggesting that there is a metal requirement in addition to the ATP-bound Mg2+. The results of this study thus demonstrate multiple metal requirements of adenylyl cyclase and support the existence of a Mg2+ ion essential for catalysis and distinct from the ATP-bound ion. We propose that adenylyl cyclase employs a catalytic mechanism analogous to that of DNA polymerase, in which two key magnesium ions facilitate the nucleophilic attack of the 3'-hydroxyl group and the subsequent elimination of pyrophosphate.

Adenosine Triphosphate↗

PubMed1998

Characterization of a silencer element in the human aromatase gene.

Aromatase, a cytochrome P450, catalyzes three consecutive hydroxylation reactions converting C19 androgens to aromatic C18 estrogens. The control of human aromatase expression is complex in that several promoters drive aromatase expression in a tissue-specific manner. Promoters I.3 and II are situated within the 700-bp region immediately upstream of exon II of the human aromatase gene, and these promoters have been shown to drive aromatase expression in breast tumors. This paper reports the characterization of a negative regulatory element that is situated between promoters I.3 and II and down regulates the action of these promoters. This negative regulatory element is thought to be a silencer element (S1) because it acts in an orientation- and promoter-independent manner. The position of S1 (5'-CCAAGGTCAGAAATGCTGCAATTCAAGCCA-3') was mapped by DNase I footprinting and DNA deletion analyses. The region contains three pairs of inverted repeats, as indicated by an underline, probably explaining why S1 functions in both orientations. Chloramphenicol acetyltransferase functional analyses indicated that the transcriptional activity of promoter I.3 was suppressed two- to three-fold by S1. Mutations of two inverted repeat segments (i.e., TTC and CC) in S1 destroyed its silencing action and modified the protein binding patterns in DNA mobility shift analysis. UV cross-linking experiments with 32P-labeled bromodeoxyuridine-substituted S1 as the probe and nuclear extracts from MCF-7 breast cancer cells and skin fibroblasts revealed that four major nuclear proteins, with molecular masses of approximately 150, 45, 30, and 25 kDa, bound to this element. Interestingly, two smaller proteins could be competed by an unlabeled fragment which contains promoter I.3. In addition, mutation of S1 at the region CC destroyed the ability to compete with the wild-type S1 for the binding of 30- and 25-kDa proteins. These results led us to propose that S1 down regulates the action of promoter I.3, and the 30- and 25-kDa proteins present in the nuclear extract of MCF-7 cells and skin fibroblasts are involved in the silencer action.

Aromatase↗

PubMed1998

Cap43, a novel gene specifically induced by Ni2+ compounds.

To better understand the molecular mechanism(s) involved in the essentiality, toxicity, and/or carcinogenicity of nickel compounds, a mRNA differential display technique was used to identify gene(s) that were specifically induced by these carcinogens. Differential expression of several genes was observed in human lung A549 cells exposed to nickel subsulfide. One gene, Cap43, which expressed a 3.0-kb mRNA encoding a Mr 43,000 protein, was found to be induced within 4-6 h by either Ni3S2 or NiCl2 in A549 cells and attained a level as high as 30-fold within 24-36 h of treatment. Twelve other tested metal compounds failed to induce Cap43 expression, leading to the conclusion that, with regard to metals, the induction of this gene was nickel-specific. Oxidative stress that is often caused by metals and heat shock did not induce Cap43 further, suggesting a specific nature in the signaling pathway involved in Cap43 induction. Activation of signaling pathways with vanadate did not induce Cap43 nor did trifluoperazine block its induction by nickel; however, okadaic acid, a serine/threonine phosphatase inhibitor, induced Cap43 to a greater extent than any nickel compound tested. Homocysteine did not induce Cap43 in a number of cell lines, with the exception of human endothelial cells. The Cap43 gene was found to be induced by nickel not only in all tested human and rodent cell lines in vitro but also in several rat organs after oral exposure to NiCl2. We have found that the primary signal for Cap43 induction was an elevation of free intracellular Ca2+ caused by Ni2+ exposure because Cap43 was induced by calcium ionophores and its induction was attenuated by bis-(O-aminophenyl)-ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl)-ester, a chelator of intracellular Ca2+. We found that the Cap43 gene was evolutionarily conserved and similarly regulated in humans, mice, and rats. Recent studies have shown that Cap43 is expressed at lower levels in colon cancer. Further studies of Cap43 regulation by Ca2+ should enhance our understanding of the role of Cap43 in cell function and cancer pathogenesis.

Amino Acid Sequence↗

PubMed1998

Genetic selection of mammalian adenylyl cyclases insensitive to stimulation by Gsalpha.

We describe the development of a genetic system allowing for the isolation of mutant mammalian adenylyl cyclases defective in their responses to G protein subunits, thus allowing for the identification of structural elements within the cyclase that are responsible for the recognition of these regulators. Expression of mammalian type V adenylyl cyclase in a cyclase-deleted yeast strain can conditionally complement the lethal phenotype of this strain. Type V adenylyl cyclase-expressing yeast grow only when the cyclase is activated by coexpression of Gsalpha or addition of forskolin to the medium; however, growth arrest is observed in the presence of both activators or under basal conditions. Utilizing this genetic system, we have isolated 25 adenylyl cyclase mutants defective in their response to Gsalpha. Sequence analysis and biochemical characterization of these mutants have identified residues in both cytoplasmic domains of the cyclase that are involved in the specific binding of and regulation by Gsalpha.

Adenylyl Cyclases↗

PubMed1998

Single- and multiple-dose pharmacokinetic comparison of a sustained-release tablet and conventional tablets of naproxen in healthy volunteers.

The pharmacokinetics of a new sustained-release tablet of naproxen (500 mg once daily) were compared with a conventional tablet (250 mg twice daily) after single- or multiple-dose oral administration in healthy volunteers using an open, randomized two-way crossover experimental design. Naproxen was well absorbed from the sustained-release tablet (approximately 97%) compared with the conventional tablet. Pharmacokinetic data showed that the sustained-release formulation reached significantly delayed mean peak plasma levels (Cmax) in both single- and multiple-dose studies and lower Cmax in a single-dose study than the conventional formulation. However, there were no statistically significant differences in other pharmacokinetic parameters, including area under the concentration-time curve (AUC), elimination half-life (t1/2), and elimination rate constant (Ke), in either single- or multiple-dose studies between the two treatments. In addition, there were no significant differences between formulations in Cmax, minimum plasma concentration (Cmin), and fluctuation index in the multiple-dose study.

Adult↗