PubMed Health⌕ Search

Biomedical subjects

W Wan

Publications and source records attributed to W Wan.

At least 19 recordsLinked to original sources
PubMed2001

[In vitro culture of modified neonatal pig islets].

A cell-isolation-and-cell-culture-in-vitro method which can produce a mass of new-born pig islet-like clusters was introduced. The new-born pig pancreas were incubated in V-type collagenase (0.5-1.0 mg.ml-1) for 8-12 minutes, and then cultured in vitro for 7 days before large amount of highly purified porcine islets were produced. The neonatal pig islets had good insulin secretion and normal sub-cell structure. The results suggest that the neonatal pig islets are probably a fine donor source for clinical xenotransplantation of islets.

Animals↗
PubMed2001

[Effect of pentoxifylline on promoter activity of human alpha 1(I) procollagen gene].

OBJECTIVE: To study the effect of pentoxifylline (PTX) on promoter activity of human alpha 1(I) procollagen (COL1A1) gene and the influence of PTX on the promoter activity induced by insulin-like growth factor 1 and insulin. METHODS: The constructs of pCOLH2.5 containing -2483 approximately +42bp of the procollagen gene and chloramphenicol acetyltransferase (CAT) as reporter gene were transiently transfected into human skin fibroblasts. The cells were subsequently treated with PTX or IGF-1 or insulin, or PTX plus IGF-1 or insulin. The CAT activity was assessed 24h after PTX and the cytokines added. RESULTS: PTX of 0.4 mmol/L, 2 mmol/L, and 10 mmol/L decreased the CAT activity of pCOLH 2.5 to 82%+/-9%, 58%+/-8%, and 32%+/-13% of the control level, respectively. IGF-1 and insulin increased the activity of the construct. PTX could inhibit the CAT activity of pCOLH2.5 induced by IGF-1 and insulin. CONCLUSIONS: These studies indicate that PTX downregulates the promoter activity of the human COL1A1 gene, while IGF-1 and insulin upregulates it. PTX can inhibit the promoter activity induced by IGF-1 and insulin.

Collagen↗
PubMed2001

[Bispecific McAb mediated multiple tumor cytotoxicity in gastric cancer].

OBJECTIVE: McAb against CD3 and McAb against TNP were combined into bispecific McAb by chemical methods. With this bispecific McAb, human peripheral blood lymphocytes (PBLS) were introduced to in vitro and in vivo cytotoxic test of any tumor cells by different TNP-McAb against gastric cancer. METHODS: The activity of bispecific McAb prepared by chemical method, was detected by enzyme-linked immunosorbent assay (ELISA). The bispecific McAb was identified by bridge ELISA. Ouchterlony test and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Cytotoxic test of tumor cells in vitro and tumor growth inhibition test in vivo were performed for the bispecific McAb function. RESULTS: Anti-CD3 and Anti-TNP McAbs were successfully combined into bispecific McAb which could conjugate any TNP-McAb against gastric cancer and induce PBLS to cytotoxic test of gastric cancer cells in vitro and in vivo. CONCLUSION: The bispecific McAb may very will be useful in the immuno-biotherapy of tumors.

Animals↗
PubMed2001

[Modulation of the activity of human alpha1 (I) procollagen gene promoter by basic fibroblast growth factor (bFGF)].

OBJECTIVE: To investigate the modulating effect of bFGF on the proliferation of human cutaneous fibroblasts and on the activity of human alpha1 (I) procollagen gene promoter. METHODS: Human cutaneous fibroblasts were cultured and subcultured by tissue block culture technique. The influence of different concentrations of bFGF on the proliferation of fibroblasts was determined by ELISA method with BrdU incorporated into fibroblast DNA. Three plasmids containing various lengths of 5prime prime or minute flank sequences of human alpha1 (I) procollagen gene and CAT as reporter gene were constructed and transfected into the fibroblasts by FuGENE transfection reagent. The quantitative expression of the fibroblast CAT was determined by ELISA after treatment with bFGF. RESULTS: After 24 hours of treatment of the fibroblasts by serial concentrations (0.25 ng/ml similar 64.00 ng/ml) of bFGF in DMEM containing 2% (v/v) or 10% (v/v) FCS, the BrdU incorporation into DNA was determined. The proliferating rate of the fibroblasts differed significantly from each other in all the groups (P < 0.05). After the fibroblasts were transfected with the three plasmids and treated thereafter by 4 ng/ml and 16 ng/ml of bFGF for 24 hours, the relative CAT expression values were determined. It indicated that the expression value was evidently different between bFGF processing and control groups (P < 0.05). CONCLUSION: bFGF might inhibit the proliferation of human cutaneous fibroblasts and exert negative regulating effect on the human alpha1 (I) procollagen gene promoter sequence in dose -- dependent pattern.

Cell Division↗
PubMed2000

[Localization and characterization of partial immunodominant antigen epitopes of Trichinella spiralis].

OBJECTIVE: To screen and characterize immunodominant antigen epitopes on the soluble antigens of Trichinella spiralis (T.s.). METHODS: 15 monoclonal antibodies (McAbs) against T.s. muscle larva(ML) soluble antigens were obtained by using hybridoma technique. The reactivity of monoclonal and polyclonal antibodies were tested by ELISA, Western blotting and indirect immunofluorescence assay(IFA). RESULTS: The Western blotting result showed that of the 15 McAbs, 6 could bind to the T.s. ML antigens displaying molecular weights of 40-70 kDa. Polyclonal sera could react with more than 10 bands having molecular weights of 20-200 kDa. Among the 6 McAbs, 4 could recognize epitopes on the cuticle surface and the other two could recognize epitopes on both the cuticle surface and the stichosome. CONCLUSION: The antigen epitopes of T.s. recognized by 6 McAbs had been characterized.

Animals↗
PubMed1999

Identification and characterization of the mouse MutS homolog 5: Msh5.

We have identified and characterized the complete cDNA and gene for the mouse MutS homolog 5 (Msh5), as a step toward understanding the molecular genetic mechanisms involved in the biological function of this new MutS homologous protein in mammals. The Msh5 cDNA contains a 2502-bp open reading frame (ORF) that encodes an 833-amino acid protein with a predicted molecular weight of 92.6 kDa, which shares 89.8% amino acid sequence identity with the human hMSH5 protein. Northern blot analysis demonstrated the presence of a Msh5 mRNA approximately 2.9-kb in length, most abundantly expressed in mouse testis. Yeast two-hybrid analysis indicated that the mouse Msh5 protein positively interacted with the human hMSH4 protein-suggesting that Msh5 shares common functional properties with its human counterpart. Sequence and structural analyses show that the mouse gene Msh5 spans approximately 18 kb and contains 24 exons that range in length from 36 bp for exon 7 to 392 bp for exon 1. Structural comparison with the human hMSH5 gene revealed that all of the Msh5 internal exons, but not introns, are conserved in length with the human hMSH5. The Msh5 gene is located on mouse Chromosome (Chr) 17 in a location that is syntenic to the region of human Chr 6 harboring the hMSH5 gene. The identification and characterization of Msh5 will facilitate studies of the potential functional roles of this new member of the MutS family.

Adenosine Triphosphatases↗
PubMed1999

Isolation of a mutant of Kluyveromyces sp. Y-85 resistant to catabolite repression.

The production of inulinase in Kluyveromyces sp. Y-85 is repressed by the carbon catabolites. To screen for derepression mutants, the strain of Kluyveromyces sp. Y-85 was treated with the mutagenic agent, ethyl methane sulfonate (EMS). Initially, mutants resistant to catabolite repression by 2-deoxy-D-glucose were isolated. One such mutant, Kluyveromyces sp. Y-85 K6, was found to exhibit stable, 2-fold higher expression of inulinase than the wild-type in glucose-containing medium, indicating that it is a promising strain for industrial production.

Journal Article↗
PubMed1998

Activation of midline thalamic nuclei by antipsychotic drugs.

The thalamus has been proposed as a site which may be involved in the production of the syndrome of schizophrenia and the response of schizophrenic symptoms to treatment. These studies test whether, consistent with this hypothesis, the activation of thalamic nuclei is a shared property of neuroleptic antipsychotic drugs. Rats were given single doses of the typical high and low potency neuroleptics haloperidol (1 mg/kg) and chlorpromazine (20 mg/kg), the atypical neuroleptics thiroridazine (20 mg/kg) and clozapine (20 mg/kg), the specific dopamine antagonist raclopride (3 mg/kg), the mixed dopamine/serotonin antagonist risperidone (3 mg/kg) or drug-free vehicle. Increased expression of Fos-like protein was utilized as a marker of cellular activation. All drugs tested, including typical and atypical antipsychotic agents, led to similar effects on the midline thalamic paraventricular, centromedian and rhomboid nuclei and the nucleus reuniens. These results suggest that midline thalamic nuclei may participate in neural circuits mediating some of the shared effects of antipsychotic drugs.

Animals↗
PubMed1998

[Effects of dibutyl phthalate on the proliferation and apoptosis of leukemic cells].

This study was designed to investigate the effects of dibutyl phthalate (DBP) on the proliferation and apoptosis of leukemic cells. The results showed that DBP suppressed the proliferation of HL-60 and K562 leukemic cells in a dose-dependent and time-dependent manner. Inducing HL-60 and K562 leukemic cells to die via apoptosis were confirmed by that the percentage of the apoptotic cells in morphology and of the DNA fragmentation increased significantly and that typical ladders of apoptosis were shown by gel electrophoresis when HL-60 and K562 cells were exposed to the DBP. Also, K562 leukemic cells was less susceptible to the DBP than HL-60 cells. These results indicate that DBP can inhibit the proliferation of HL-60 and K562 leukemic cells and induced them to die via apoptosis.

Antineoplastic Agents↗
PubMed1996

Growth hormone (GH) and a GH antagonist promote GH receptor dimerization and internalization.

It has previously been shown that a human growth hormone (hGH) analog, hGH-G120R, acts as a GH antagonist (Chen, W. Y., Wight, D. C. , Wagner, T. E., and Kopchick, J. J. (1990) Proc. Natl. Acad. Sci. U. S. A. 87, 5061-5065; Chen, W. Y., White, M. E., Wagner, T. E., and Kopchick, J. J. (1991) Endocrinology 129, 1402-1408; Chen, W. Y., Chen, N-Y., Yun, J., Wang, X. Z., Wagner, T. E., and Kopchick, J. J. (1994) J. Biol. Chem. 269, 15892-15897). In this study, we report the ability of hGH and hGH-G120R to be internalized by GH receptor expressing cells. Additionally, results of chemical cross-linking experiments revealed that both native hGH and hGH-G120R form complexes similar in size to that expected for hGH when bound to recombinant hGH-binding protein (bp). The molecular mass of the complex was determined to be approximately 280 kDa which is consistent with multiple receptors interacting with the ligand. The predominant radiolabeled band detected was a complex of approximately 140 kDa which probably represents one GH molecule bound to one GH receptor. The cross-linked complexes were not detected in the presence of excess unlabeled hGH or hGH-G120R and were not observed in cells which do not express detectable levels of GH receptors. Also, GH induced tyrosine phosphorylation of a complex of proteins of approximately 95 kDa in these cells whereas hGH-G120R did not. Thus, we have separated the hGH or hGH-G120R/GHR binding and internalization capabilities from the ability to stimulate tyrosine phosphorylation of intracellular proteins.

Animals↗
PubMed1996

The thalamus as a site of action of antipsychotic drugs.

OBJECTIVE: Because recent data suggest that there are abnormalities of the thalamus in schizophrenia, the authors tested the effects of antipsychotic drugs on thalamic sites. METHOD: Nine rats were given acute doses of the typical neuroleptic haloperidol (N = 3), the atypical neuroleptic clozapine (N = 3), or a drug-free vehicle (N = 3). Cellular activation was assessed by using immunohistochemistry to determine expression of the immediate response gene c-fos. RESULTS: Both antipsychotic drugs induced increased Fos immunoreactivity, suggesting increased activity in cells of the midline nuclei of the thalamus. CONCLUSIONS: The shared clinical effects of antipsychotic drugs may be mediated in part through actions on the thalamus.

Animals↗
PubMed1996

Dispositional optimism and coping with academic examinations.

Correlations between scores on dispositional optimism and four categories of coping strategies for academic examinations for a group of 248 Hong Kong undergraduates were .25 for Self-encouragement and -.20 for Cognitive Avoidance. These results lend partial support to the association of adaptive coping and optimism, measured by the Life Orientation Test.

Achievement↗
PubMed1995

Acute administration of typical and atypical antipsychotic drugs induces distinctive patterns of Fos expression in the rat forebrain.

Fos expression in the rat brain was investigated by immunohistochemistry after i.p. administration of single doses of a wide range of typical neuroleptic antipsychotic drugs (including the potent dopamine D2 antagonist haloperidol and the mixed monoamine antagonist chlorpromazine) and atypical antipsychotic drugs (including the weak dopamine D2 antagonists clozapine and thioridazine, the relatively pure D2 antagonist raclopride and the mixed D2 and serotonin S2 antagonist risperidone). For comparison to the effects of the antipsychotic drugs and also because the unique clinical therapeutic effects of clozapine have been attributed to S2 blockade, the S2 antagonist ritanserin was also studied. The single shared effect of all antipsychotic drugs tested was the induction of significantly increased Fos immunoreactivity in the nucleus accumbens (NAc). Fos-positive neurons in the NAc were mostly localized in patches throughout its rostrocaudal extent. Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and lateral striatum. Fos-positive neurons in the striatum were distributed more lateral than medial and declined from rostral to caudal levels. Haloperidol, thioridazine and risperidone also markedly increased Fos expression in the lateral septum. Distinguishing it from the other neuroleptics, clozapine did not increase Fos expression in the lateral striatum, but induced a significant increase in Fos expression in the prefrontal cortex. Ritanserin did not induce Fos expression in any brain region examined, suggesting that S2 antagonism is not responsible for the effects of antipsychotic drugs observed here. Our results suggest that there are distinctive patterns of Fos expression in the forebrain induced by typical and atypical antipsychotic drugs. Notably, Fos expression in the NAc, as a shared property of all the antipsychotic drugs, may be related to the actions mediating the therapeutic effects of these drugs in the treatment of psychotic disorders. The density of Fos-positive neurons stimulated by antipsychotic drugs in the striatum appeared to be correlated with the relative severity of extrapyramidal side-effects produced by these drugs and may be related to the mechanisms mediating these effects.

Analysis of Variance↗
PubMed1994

Neural and biochemical mediators of endotoxin and stress-induced c-fos expression in the rat brain.

We and others have reported that c-fos protein is induced in the hypothalamus and brain stem of the rat following central and peripheral injections of endotoxin (lipopolysaccharide; LPS). We have now examined possible mechanisms through which LPS induces c-fos protein. The cyclooxygenase inhibitor indomethacin and the glutamate NMDA antagonist MK801 inhibited c-fos protein in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and the A1/A2 regions of the brain stem induced by IP or IV injections of LPS (40 micrograms). The H1 histamine antagonist diphenhydramine, but not the H2 histamine antagonist cimetidine, reduced the amount of c-fos labeling. MK801 also attenuated the effects of stress (foot shock) on c-fos protein; however, indomethacin had no effect on c-fos protein induced by stress. We next examined the importance of visceral afferent innervation on the response to LPS or stress. Subdiaphragmatic vagotomy completely blocked the induction of c-fos protein following IP injections of LPS; however, vagotomy had a minimal effect on c-fos protein induced in the PVN and SON following IV injections of LPS, but potentiated c-fos induction following foot shock. Thus, prostaglandin synthesis, glutamate release, histamine receptors, and visceral afferents represent functional biochemical and neural pathways through which endotoxin activates c-fos protein in specific autonomic and neuroendocrine regulatory nuclei. Activation of NMDA glutamate receptors may represent a final common pathway for the induction of c-fos protein in the brain induced by both endotoxin and stress.

Animals↗
PubMed1994

Interleukin-2-induced enhancement of an antigen-specific IgM plaque-forming cell response is mediated by the sympathetic nervous system.

Interleukin (IL)-2, a lymphokine produced by activated T-cells, stimulates T-cell proliferation and differentiation and potentiates B-cell production of antigen-specific immunoglobulins. IL-2 also increases hypothalamic norepinephrine turnover without affecting plasma corticosterone levels, which suggests that it selectively impacts on central sites that mediate sympathetic outflow to lymphoid organs. Because sympathetic stimulation during the early phases of an immunoglobulin (Ig)M plaque-forming cell (PFC) response to sheep red blood cells results in an increase in the subsequent number of antibody-forming cells, we assessed whether the enhancing effects of IL-2 on the PFC response are mediated by the sympathetic nervous system. The peak splenic IgM PFC response was increased in male Sprague-Dawley rats and BALB/c mice administered recombinant human IL-2 (50, 100 or 200 ng i.p.) in close temporal congruity with sheep red blood cell administration (i.e., 1 day before or immediately before immunization), compared with vehicle-treated controls. IL-2 administered at a later interval after immunization (i.e., 2 days) did not increase the number of antibody-forming cells. Intact sympathetic innervation of the spleen was required for the IL-2-induced immunoenhancement to occur because cutting the splenic nerve 10 days prior to IL-2 administration blocked the lymphokine's potentiation of the IgM PFC response. The immunostimulatory effects of IL-2 were also blocked in mice administered the beta adrenergic antagonist propranolol (5 mg/kg) immediately and 1 day after IL-2 administration. The alpha adrenergic antagonist phentolamine (5 mg/kg) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗