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Biomedical subjects

Y Zeng

Publications and source records attributed to Y Zeng.

At least 217 records · Page 12Linked to original sources
PubMed1993

Involvement of nitric oxide in the blastogenic response deficiency in splenocytes from spontaneously hypertensive rats.

It has been shown that spontaneously hypertensive rats (SHR) exhibit some abnormalities in their immune system. These include a reduced delayed hypersensitivity response, a reduction in the number of rosette-forming cells and a decreased lymphocyte blastogenic response. In this study, we further investigated the blastogenic responses of splenocytes, thymocytes, and T-enriched lymphocytes from SHR. In SHR splenocytes, the blastogenic responses to concanavalin A (Con A), phytohemagglutinin (PHA), interleukin-2 (IL-2), and phorbol 12,13-dibutyrate (PDB) plus ionomycin were significantly reduced compared with those from Wistar-Kyoto rats (WKY). In SHR thymocytes and T-enriched lymphocytes, the blastogenic responses to these activators were the same as in WKY rats. The IL-2 production by SHR splenocytes was similar to that of WKY. To elucidate the possible mechanism responsible for the blastogenic defects in SHR splenocytes, the involvement of the nitric oxide (NO) synthetic pathway was studied. The inhibition of NO synthesis by NG-monomethyl-L-arginine (L-NMMA) corrected the defect in SHR splenocytes. L-NMMA had no effect on the splenocytes, thymocytes, or macrophage-depleted splenocytes from WKY or on thymocytes or macrophage-depleted splenocytes from SHR. The removal of macrophages from SHR splenocytes also corrected the blastogenic defect in these cells. Furthermore, the NO synthesis in Con A stimulated SHR splenocyte culture medium was statistically significantly higher than that in WKY. These results suggested that overproduction of nitric oxide by SHR macrophages may be responsible for the SHR splenocyte blastogenic defect.

Animals↗
PubMed1992

Long-term survival of xenogeneic pancreatic islet grafts induced by CTLA4lg.

Antigen-specific T cell activation depends on T cell receptor-ligand interaction and costimulatory signals generated when accessory molecules bind to their ligands, such as CD28 to the B7 (also called BB1) molecule. A soluble fusion protein of human CTLA-4 (a protein homologous to CD28) and the immunoglobulin (lg) G1 Fc region (CTLA4lg) binds to human and murine B7 with high avidity and blocks T cell activation in vitro. CTLA4lg therapy blocked human pancreatic islet rejection in mice by directly affecting T cell recognition of B7+ antigen-presenting cells. In addition, CTLA4lg induced long-term, donor-specific tolerance, which may have applications to human organ transplantation.

Abatacept↗
PubMed1992

Evidence that the hamster tunicamycin resistance gene encodes UDP-GlcNAc:dolichol phosphate N-acetylglucosamine-1-phosphate transferase.

A cDNA clone isolated from Chinese hamster ovary cells conferred elevated GlcNAc-1-P-transferase (GPT) activity and resistance to tunicamycin in transfected cells (Zhu, X., and Lehrman, M. A. (1990) J. Biol. Chem. 265, 14250-14255). It had been assumed that this cDNA, termed TRG for tunicamycin resistance gene, encoded GPT enzyme. However, other functions were not ruled out. Thus, by one of several mechanisms, the TRG protein could have instead functioned by activation of the transfected host's endogenous GPT enzyme. To analyze the biochemical function of the TRG protein, hamster TRG cDNA was stably expressed at high levels in Chinese hamster ovary cells. In addition, several antipeptide polyclonal antibodies directed against the predicted TRG protein were obtained. With these tools in hand, experiments were performed to test the hypothesis that the TRG encodes GPT enzyme, as well as to rule out other possible functions for the TRG protein. These experiments included examination of the effects of solubilization of membranes on TRG-dependent GPT activity, the apparent binding of tunicamycin to the TRG protein, and the immunoadsorption of GPT activity with TRG protein-specific antibodies. From these results, we conclude that the hamster TRG most likely encodes GPT enzyme.

Animals↗
PubMed1992

Suppression of human nasopharyngeal carcinoma cell growth in nude mice by the wild-type p53 gene.

Wild-type and mutant human p53 genes were transfected into the nasopharyngeal carcinoma (NPC) cell line CNE-3. Tumorigenicity in nude mice showed that the tumor resulting from the cells transfected with the wild-type p53 gene grew more slowly and was smaller than that from the cells transfected with mutant p53 gene and that from control CNE-3 cells. In contrast, the tumor from the cells transfected with the mutant p53 gene grew faster than that produced by cells transfected with the wild-type p53 gene and that produced by control CNE-3 cells. The results demonstrate that the wild-type p53 gene could inhibit the NPC cell growth in nude mice and the mutant p53 gene could enhance the NPC cell growth in nude mice. The p53 gene may also play an important role in the pathogenesis of NPC.

Animals↗
PubMed1992

Detection of intrahepatic human islets following combined liver-islet allotransplantation.

This article describes the localization of intact insulin-containing intrahepatic islets after combined liver-islet allotransplantation. The patient was a 36-year-old woman who underwent upper abdominal exenteration for neuroendocrine carcinoma; 289,000 islets were transplanted via portal vein infusion immediately after complete revascularization of the liver. Immunosuppression was with low-dose FK-506. OKT3 and steroids were used to treat one rejection episode 2 weeks after transplantation, but the patient subsequently developed multiple infections and died 109 days after transplantation. At autopsy, the transplanted liver did not show any sign of rejection and well-preserved islets were present in portal triads sampled from the anterior inferior edge of the right lobe. Immunohistochemical labeling confirmed the presence of insulin-containing cells. This finding indicated that human islets can survive after intrahepatic allotransplantation, despite positive cross-match with no HLA antigen match, suggesting that upper abdominal exenteration and liver transplantation may constitute a protective factor for the survival of allogeneic human islets.

Adult↗
PubMed1992

The status quo, regional differences, and trend of the Chinese family structure.

"Based on the 10% machine aggregate data of the fourth census of 1990 and the 1% computer sampling data, this article attempts to analyze the status quo and regional differences of China's family structure and their relationships with the level of social and economic development, and the trend of the Chinese family structure since the 1980s."

Asia↗
PubMed1992

Some problems of future demographic processes in China.

"In this paper, which is based on a projection model of rural-urban population dynamics established by the authors, we make use of the investigative data of the one percent national population sample of 1987 and analog calculations on almost 200 demographic parameters to clarify the problematic relations between some key issues in China's future demographic processes. We advance a number of suggestions for the reference of policy-makers and planners."

Asia↗
PubMed1992

Cloning and expression of midecamycin 4"-acylase gene in spiramycin producing strains.

A recombinant plasmid p66B containing the midecamycin 4"-acylase gene was obtained by cloning this gene into plasmid vetor pIJ680 from the primary clone pCN6C5, presumably harboring the midecamycin biosynthetic gene. The expression of the midecamycin 4"-acylase gene (p66B) in spiramycin producing strains resulted mainly in the production of 4"-isovalerylspiramycin. Another positive clone pCN10F5 was discovered from the genomic library of S. mycarofacians 1748 by probing with p66B DNA BamHI-BamHI 2.3kb fragment. A BamHI-BamHI 8.0kb homologous region on pCN10F5 was determined by Southern hybridization and was subcloned into plasmids pWHM3 and pIJ680. Recombinant plasmids pWF5 and p6F5 with molecular size about 15.2kb and 13.3kb, respectively, were obtained. Transformation of spiramycin producing strains with these plasmids resulted in the production of two major components. Based on their physicochemical properties and spectral evidences, component I was identified as 4"-propionylspiramycin III, and component II as 4"-propionylspiramycin II. Southern hybridization confirmed that the BamHI-BamHI 8.0kb fragment was cloned in the spiramycin producing strain. Only pCN10F5 clone was identified from the genomic library of S. mycarofaciens 1748 when the 4"-isovaleryltransferase gene of carbomycin producing strain S. thermotolerans was used as a probe in colony hybridization. It suggests that there is a difference between the 4"-acyltransferase genes in the pCN6C5 and pCN10F5 clones.

Acyltransferases↗
PubMed1992

[Isolation and characterization of mutactimycin-producing mutant].

Natural non-antibiotic producing Streptomyces sp. 1254 was mutagenized by UV irradiation and two active mutants were isolated. Mutant 113 produced novel anthracycline compounds designated mutactimycins. Mutactimycin A was active against the bacteriophage of Bac. subtilis and some viruses in tissue culture. The mutant 2-6 synthesized a basic water-soluble antimicrobial antibiotic. Chemical analysis of the whole cell hydrolysate and the morphological characterization showed that the strain 1254 and its mutant 2-6 were of chemotype I, belonging to the genus of Streptomyces, and the mutant 113 was of chemotype IV without mycolic acid. Co-synthesis test of strain 1254 and a blocked mutant of strain 113 gave the active compounds identical with mutactimycins. Using the actI gene as a probe, the Southern hybridization revealed homology between the actinorhodin polyketide biosynthase gene and the total DNA of the strain 1254. Based on these data it was deduced that Streptomyces sp. 1254 should have a biosynthesis pathway for mutactimycin, but some of its genes might fail in expression and mutagenesis would make the silent gene(s) active.

Antibiotics, Antineoplastic↗
PubMed1992

Islet cell allotransplantation in diabetic patients. Histologic findings in four adults simultaneously receiving kidney or liver transplants.

Refined methods of islet cell purification have led to unprecedented success of islet cell allotransplantation via portal vein infusion in diabetic patients, resulting in marked reduction of exogenous insulin requirements and recently even insulin independence. The authors report the histologic findings of islet cell allografts in the liver of four patients who had undergone combined kidney-islet or liver-islet transplantation. Islet cell clusters were detected in subcapsular location at the edge of portal triads. The early post-transplant period was characterized by patchy mixed portal infiltrates. Only minimal inflammation but decreased islet cell granulation was observed in one patient 6 months after transplantation. As histologic detection of transplanted islet cells becomes available, additional parameters for evaluation of graft survival might be defined by morphologic assessment.

Adult↗
PubMed1992

[Studies on the beta-D-fucosidase from Aspergillus phoenicis].

Although beta-D-fucosidase (beta-D-fucoside fucohydrolase, EC 3.2.1.38) has been isolated from various sources, the identity of this enzyme is still not settled. We have purified a specific beta-D-fucosidase in electrophoretically homogeneous form crude extracts of Aspergillus phoenicis by polyethyleneglycol 6000-phosphate buffer aqueous two-phase separation, and successive chromatography on DEAE-Sephadex A-50, hydroxyapatite and Sephadex G-100 columns. The molecular weight of the enzyme was estimated to be 57000 by SDS-polyacrylamide gel electrophoresis and 50000 to 60000 by gel filtration on Sephadex G-100. The enzyme showed optimum coside were 2.4mmol/L, and 1.28 mumol min-1 the pH range 5.5-6.5 and below 35 degrees C. The Km and the Vmax values for pNP-beta-D-fucoside were 2.4mmol/L, and 1.28 mumol.min-1.mg-1 respectively. The enzyme was strongly inhibited by sulfhydryl group reagents, PCMB-NEM and iodoacetate. It was also inhibited by EDC, DEP and NBS. Thus, -SH, -COOH groups, histidyl and tryptophyl residues were essential for enzyme activity. The purified beta-D-fucosidase showed high specificity toward p-nitrophenyl beta-D-fucoside. The enzyme was inhibited by D-fucose and D-fucono-gamma-lactone, but not by D-galactose, D-galactono-gamma-lactone, D-glucose or D-glucono-gamma-lactone; the latter compounds are specific inhibitors of beta-D-galactosidase and beta-D-glucosidase respectively. Thus, this enzyme is the most strictly specific beta-D-fucosidase when compared with those previously reported.

Aspergillus↗