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Biomedical subjects

Q Tang

Publications and source records attributed to Q Tang.

At least 91 records · Page 5Linked to original sources
PubMed1994

Identification of functional cysteine residues in human galactosyltransferase.

The functions of the five cysteine residues in human galactosyltransferase were investigated using site-directed mutagenesis to determine the location of the disulfide bond as well as the role of the sulfhydryl groups. The enzyme remains active when three of its cysteine residues at positions 171, 264 and 340 are mutated to serine separately. However, enzymatic activity is lost when either cysteine-129 or cysteine-245 is replaced with serine. The loss of GT activity suggests that these two cysteine residues form a disulfide bond. The three active mutated enzymes were studied kinetically. The kinetic constants of the enzymes with cysteine-171 or cysteine-264 replaced with serine are not significantly different from those of GT that does not have these substitutions. When cysteine-340 was mutated, however, the kinetic constant for UDP-galactose increased about 30 fold, while that for N-acetylglucosamine and Mn2+ remained unchanged. In addition, sulfhydryl inhibition studies reveal that cysteine-340 is the only cysteine residue that reacts with the sulfhydryl reagents. These results indicate that cysteine-340 may be involved in the binding of UDP-galactose.

Cysteine↗
PubMed1994

Prevention by acetylsalicylic acid of liver cirrhosis and carcinogenesis as well as generations of 8-hydroxydeoxyguanosine and thiobarbituric acid-reactive substances caused by a choline-deficient, L-amino acid-defined diet in rats.

Effects of acetylsalicylic acid (ASA) (aspirin) on the pathogenesis of fatty liver, cirrhosis and hepatocarcinogenesis caused by a choline-deficient L-amino acid-defined (CDAA) diet were examined in male Fischer 344 rats fed a CDAA diet supplemented with 0, 0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrations of > 0.2% prevented the development of both cirrhosis and preneoplastic and neoplastic nodules, but without any directly associated prevention of fatty changes. ASA also prevented hepatocyte proliferation and the generation of thiobarbituric acid-reactive substances and 8-hydroxydeoxyguanosine caused by feeding the CDAA diet, analyzed, respectively, after 1, 12 and 12 weeks. The results clearly indicate that the anti-inflammatory drug ASA, which is not a lipotropic factor, can prevent the pathogenesis of cirrhosis and hepatocarcinogenesis caused by a CDAA diet, which is possibly partly associated with the prevention of reactive oxygen species production.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Herpes simplex virus glycoproteins E and I facilitate cell-to-cell spread in vivo and across junctions of cultured cells.

Herpes simplex virus (HSV) glycoproteins E and I (gE and gI) can act as a receptor for the Fc domain of immunoglobulin G (IgG). To examine the role of HSV IgG Fc receptor in viral pathogenesis, rabbits and mice were infected by the corneal route with HSV gE- or gI- mutants. Wild-type HSV-1 produced large dendritic lesions in the corneal epithelium and subsequent stromal disease leading to viral encephalitis, whereas gE- and gI- mutant viruses produced microscopic punctate or small dendritic lesions in the epithelium and no corneal disease or encephalitis. These differences were not related to the ability of the gE-gI oligomer to bind IgG because the differences were observed before the appearance of anti-HSV IgG and in mice, in which IgG binds to the Fc receptor poorly or not at all. Mutant viruses produced small plaques on monolayers of normal human fibroblasts and epithelial cells. Replication of gE- and gI- mutant viruses in human fibroblasts were normal, and the rates of entry of mutant and wild-type viruses into fibroblasts were similar; however, spread of gE- and gI- mutant viruses from cell to cell was significantly slower than that of wild-type HSV-1. In experiments in which fibroblast monolayers were infected with low multiplicities of virus and multiple rounds of infection occurred, the presence of neutralizing antibodies in the culture medium caused the yields of mutant viruses to drop dramatically, whereas there was a lesser effect on the production of wild-type HSV. It appears that cell-to-cell transmission of wild-type HSV-1 occurs by at least two mechanisms: (i) release of virus from cells and entry of extracellular virus into a neighboring cell and (ii) transfer of virus across cell junctions in a manner resistant to neutralizing antibodies. Our results suggest that gE- and gI- mutants are defective in the latter mechanism of spread, suggesting the possibility that the gE-gI complex facilitates virus transfer across cell junctions, a mode of spread which may predominate in some tissues. It is ironic that the gE-gI complex, usually considered an IgG Fc receptor, may, through its ability to mediate cell-to-cell spread, actually protect HSV from IgG in a manner different than previously thought.

Animals↗
PubMed1994

trans-dominant interference of type 5 adenovirus E1a mutants in cell transformation.

Two type 5 adenovirus (Ad5) early region 1a (E1a) mutants, H5in104 and H5dl105, were impaired in viral replication and cell transformation. In addition, these mutants trans dominantly inhibited the frequency with which H5sub309, a phenotypically wild-type mutant, and H5dl520, a high-frequency transformation mutant, transformed CREF cells. Inhibition of transformation varied in proportion to the input ratio of mutant to coinfecting virus. It was found that H5in104, but not H5dl105, could not complement Ad5 E1b mutants that failed to synthesize 19- or 55-kDa E1b product. H5dl105 yielded 10-fold less virus than the wild-type did in 293 cells, which constitutively express E1a and E1b products; similar low yields were also observed with H5in104 and H5dl105 in another E1a- and E1b-expressing transformed cell line, KB16. Marker rescue and DNA sequence analyses, however, indicated that the phenotypes of H5in104 and H5dl105 were the result of their respective E1a mutations. The data presented are the first to demonstrate that mutants of animal viruses can effect dominant interference with the viral function(s) that produce cell transformation.

Adenoviridae↗
PubMed1994

cDNA cloning of c33-c antigen gene derived from NS3 region of Chinese HCV genome, expression in Escherichia coli and development of HCV EIA second-generation diagnostic kit.

A cDNA fragment of about 860 bp corresponding to the c33-c gene in the non-structural region 3 (NS3) of HCV genome was obtained from one plasma derived from a Chinese HCV carrier who came from Tai' an of Shandong Province, China by the application of reverse transcription (RT) and polymerase chain reaction (PCR) techniques. After the sequence of the cDNA fragment was determined and compared with the equivalent region of the HCV-I (HCV-US) and HCV-II (HCV-BK) genomes, the nucleotide/amino acid sequence homologies were found to be 79.2%/91.3%/ and 91.3%/93.9%, respectively. The prokaryotic expression vector pBV220 was employed for the overproduction of c33-c native recombinant protein in E. coli cells. The expression products were detected by enzyme-linked immunosorbent assay (ELISA) and Western blotting with antisera of chronic hepatitis C patients, and a molecular weight 31 kD of c33-c viral protein was shown to account for 14% of the total cellular soluble proteins. This product was extracted from the bacterial lysate by lysozyme, Triton X-100 and urea treatment, and purified through ion exchange chromatography. The purified c33-c protein combined with a branch peptide MAP-C-19 representing immunodominant epitopes on the nucleocapsid region of HCV genome was used to develop a Chinese HCV EIA 2nd-generation diagnostic kit for the detection of anti-HCV antibodies. Its specificity, sensitivity and reproducibility were all in keeping with the indexes of the national standard for the quality control of the HCV diagnostic kit. The agreement rate between our kit and Abbott company's HCV EIA second-generation diagnostic kit was 99.33%, and the identified rate of positive anti-HCV of our kit was 2% more than that of the Abbott company's kit.

Amino Acid Sequence↗
PubMed1993

Effects of oxidative stress induced by redox-enzyme modulation on the progression stage of rat hepatocarcinogenesis.

Effects of oxidative stress induced by redox-enzyme modulation on the progression stage of hepatocarcinogenesis were examined by monitoring both hepatocyte injury and hepatocellular carcinoma development in F344 rats bearing preneoplastic liver nodules induced by the Cayama-Farber procedure. Redox-enzyme modulation, which included increased cytochrome P450 reductase activity induced by phenobarbital-Na (100 mg/kg, i.p. for 3 days), inhibition of DT-diaphorase by dicumarol (25 mg/kg, i.p.), depletion of glutathione by phorone (200 mg/kg, i.p.), supplementation with the Fe(III) sodium salt of EDTA (50 mg/kg, i.p.) and redox-cycling activation by menadione (50 mg/kg, i.g.), exerted no prominent hepatocyte injury within nodules but did cause slight injury in the surrounding hepatocytes in nodule-bearing rats. The same treatments induced severe hepatocyte injury in non-treated normal rats. Redox-enzyme modulation performed every other week for 33 weeks significantly reduced the number of hepatocellular carcinomas developing in nodule-bearing rats. These results indicate that preneoplastic nodules are resistant to the oxidative stress induction caused by redox-enzyme modulation treatment and that, despite toxic effects in surrounding hepatocytes, no progression pressure is exerted. Indeed, the treatment rather demonstrates an inhibitory effect of the evolution of the nodules into hepatocellular carcinomas.

Alanine Transaminase↗
PubMed1993

Inhibitory effects of inhibitors of arachidonic acid metabolism on the evolution of rat liver preneoplastic foci into nodules and hepatocellular carcinomas with or without phenobarbital exposure.

Effects of inhibitors of arachidonic acid (AA) metabolism on the evolution of preneoplastic foci into nodules and of nodules into hepatocellular carcinomas were examined in F344 male rat livers with or without phenobarbital (PB) exposure. p-Bromophenacyl bromide (BPB), acetylsalicylic acid (ASA), and quercetin (QU) were used as inhibitors of phospholipase A2, cyclooxygenase and lipoxygenase, respectively. Preneoplastic liver foci were induced by initiation with N-nitrosodiethylamine (200 mg/kg, i.p.) followed by selection using the procedure of Cayama et al. For the nodule experiment, starting 1 week after completion of the selection procedure, animals bearing foci were given diets containing 0.05% PB plus 0.75, 1, or 1.5% of one of the inhibitors, 0.05% PB alone, or 0.75, 1 or 1.5% of inhibitor alone, or basal diet for 9 weeks. For the carcinoma experiment, 3 weeks after completion of the selection procedure, animals bearing nodules were given the same diets mentioned above for 29 weeks. BPB, ASA and QU either with or without PB accelerated the remodeling of preneoplastic foci, significantly decreasing the numbers of persistent nodules and hyperplastic nodules. ASA either with or without PB significantly decreased the number of hepatocellular carcinomas per rat. BPB and QU, however, significantly decreased the numbers of hepatocellular carcinomas with but not without PB. The results suggested an involvement of AA metabolism in the process of evolution of preneoplastic foci into nodules and hepatocellular carcinomas in rat liver with or without PB exposure.

Acetophenones↗
PubMed1993

IL-8 gene expression in cultures of human corneal epithelial cells and keratocytes.

PURPOSE: To determine if human corneal keratocytes and epithelial cells synthesize and release IL-8 after stimulation with selected proinflammatory cytokines. METHODS: Human corneal keratocytes and epithelial cells were isolated from human corneal buttons and grown independently in vitro. Epithelial cell cultures stained positive in immunofluorescent tests with antibody specific for keratin (AE1/AE3), whereas keratocyte cultures were unreactive. Both cell types reacted with anti-vimentin antibody. Cultures of the two cell types were treated with various concentrations of human recombinant interleukin-1 alpha or TNF-alpha. Culture supernatants were then assayed at timed intervals by enzyme-linked immunosorbent assay for IL-8 content. Cytokine mRNA levels in cell lysates were monitored by Northern blot analysis. RESULTS: Exposure of corneal keratocytes and epithelial cells to either interleukin-1 alpha or TNF-alpha stimulated IL-8 mRNA synthesis and IL-8 production in a dose-response fashion. It was also found that TNF-alpha stimulated the synthesis of comparable amounts of IL-8 in both cell types. However, when IL-8 synthesis between the two cell types was compared after interleukin-1 alpha stimulation it was found that keratocytes synthesized 33 times more IL-8 than did epithelial cells. CONCLUSIONS: The results establish that pro-inflammatory cytokines can induce IL-8 synthesis in both human corneal epithelial cells and human corneal keratocytes. They also suggest that interleukin-1 alpha may play a more active role in amplifying inflammatory responses in the stroma than in the epithelial layer of the cornea.

Blotting, Northern↗
PubMed1993

Parkinsonism induced with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in cats: behavioral, biochemical and pathological studies.

Intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in four cats produced akinesia, bradykinesia, crouched posture, feeding difficulty, and so on, lasting for two weeks. Madopar therapy ameliorated these motor impairments. Reduction of the concentration of dopamine and its metabolites was determined in the substantia nigra and putamen by high performance liquid chromatography (HPLC). Depletion of noradrenaline, serotonin and their metabolites was also seen. Loss of nerve cells and proliferation of glial cells in the substantia nigra were observed under the light microscope. The results indicate that MPTP-induced Parkinsonism in the cat provides an animal model that can be used for basic and therapeutic research on Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

[Analysis of estrogen receptors in normal bone and bone tumor tissues].

Thirteen human normal bone and fifteen bone tumor tissues were assayed for estrogen receptor (ER) by Dextran-coated Charcoal method (Scatchard plot). The results showed that the concentrations of ER in normal bone tissues (15.12 +/- 14.68 fmol/mg pro) were higher than that of bone malignant tumors (8.04 +/- 6.71 fmol/mg pro) P < 0.05). The binding dissociation constants (Kd) of ER in bone tumors (18.46 +/- 27.10 x 10(-11) mol/L) was lower than those in normal ones (39.91 +/- 20.13 x 10(-11) mol/L) (P < 0.025). The percentages for positive score of ER in normal and tumor ones (23.1%, 26.7%) were not significantly different (P > 0.05). Our study indicated that the variations of concentration and affinity of ER in bone related to the tumor incidence. That cytosol ER content was decreased in malignant bone tumors whereas that of affinity increase suggests an impairment or change of an intact receptor mechanism in this tissues.

Adolescent↗
PubMed1991

Induction of 8-hydroxydeoxyguanosine but not initiation of carcinogenesis by redox enzyme modulations with or without menadione in rat liver.

Inducibility of oxidative stress in rat liver in vivo by menadione-associated redox cycling activation under redox enzyme modulating conditions was examined by monitoring hepatocyte injury and 8-hydroxydeoxyguanosine (8-OHdG) levels of liver DNA. In addition, the treatment-associated liver tumor initiating activity was assessed in terms of development of gamma-glutamyl-transpeptidase (GGT)- and glutathione S-transferase placental form (GST-P)-positive foci and hyperplastic nodules. With or without following menadione treatment (50 mg/kg, i.g.), redox enzyme modulations of increased cytochrome P450 reductase activity induced by phenobarbital (PB)-Na (100 mg/kg, i.p. for 5 days), inhibition of DT-diaphorase by dicumarol (25 mg/kg, i.p.) and depletion of glutathione by phorone (200 mg/kg, i.p.), with or without further supplement of iron EDTA-Na-Fe(III) (70 mg/kg, i.p.), caused both substantial hepatocyte necrosis and 8-OHdG production in Fischer 344 male rats. Subsequent feeding with a 0.05% PB diet for 64 weeks resulted in slightly increased development of GGT-positive foci but not GST-P positive lesions or hyperplastic nodules, suggesting a lack of tumor-initiating activity of the oxidative DNA damage associated with redox enzyme modulations with or without menadione.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1990

[Prevention and treatment of emphysema in the guinea pig with ligustrazine].

This study demonstrated that ligustrazine possesses inhibitory effect obviously on elastic enzyme in vitro, and it can be used to prevent and treat emphysema instead of serum. Using light microscope and electron microscope, the authors observed morphological indexes and analyzed the indexes with stereology and statistics in lung tissues of guinea pigs. The results showed that there was no obvious difference between the ligustrazine administration group and the saline control group as pathological changes were not found in the ligustrazine administration group under microscope. The shapes of elastic proteins were the same under electron microscope observation. Aerosol inhalational method induced emphysema model of elastic enzyme in guinea pig could be improved with ligustrazine treatment.

Animals↗
PubMed1987

Catecholamine induced cardiac hypertrophy.

Cardiac hypertrophy was induced in adult female Wistar rats by daily subcutaneous injections of isoproterenol (0.3 mg/kg body weight). Heart weight increased 39% after eight days of treatment. Left ventricular pressure development (positive dP/dt) in hearts four days after hypertrophy induction was significantly increased, while negative dP/dt remained unchanged. RNA polymerase activity in isolated myocyte and nonmyocyte nuclei was stimulated 29 and 23%, respectively 24 h after a single isoproterenol injection. In the myocyte fraction, RNA polymerase activation progressively increased up to four days of treatment and then returned to control values after eight days. In the nonmyocyte nuclear subset, RNA polymerase activity showed no further stimulation and gradually returned to control values after eight days of treatment. Chromatin template function was substantially stimulated in the early stage (one to four days) of hypertrophy in both myocyte and nonmyocyte fractions. Titration of chromatin against a fixed amount of RNA polymerase (5 micrograms) in the presence of rifampicin and heparin showed that less chromatin from hypertrophied hearts was required to saturate the enzyme. These results indicate that both myocyte and nonmyocte chromatin from hypertrophied hearts can support greater enzyme binding than normal chromatin. The alkaline sucrose density centrifugation profile of DNA in myocyte and nonmyocyte chromatin from day 4 hypertrophied hearts was less fragmented. These observations suggest that during the early phase of isoproterenol-induced cardiac hypertrophy, enhanced RNA polymerase activity and chromatin template function play a coordinated role in RNA synthesis. The increased template activity could be due to alterations in chromatin composition which was indicated by the change in their enzyme binding capacity and DNA fragmentation profile.

Animals↗
PubMed1985

Myocyte and nonmyocyte RNA polymerase activity and chromatin template function.

Myocardial and nonmyocardial cell nuclei were isolated from ventricles of adult male Wistar rats by means of sucrose density centrifugation. RNA polymerase activity in myocyte nuclei was approximately 80-90% higher than in nonmyocytes. Total myocyte chromatin template activity using Escherichia coli RNA polymerase was linear and about onefold greater than the nonmyocyte fraction over a fivefold range of chromatin concentrations. Preincubation time required for RNA polymerase to form a stable binding complex with chromatin was at least 40 min for myocyte and 30 min for nonmyocyte nuclear subsets. Titration of chromatin against a fixed amount of RNA polymerase (5 micrograms) showed that 5 micrograms of myocyte chromatin (as DNA) and 8 micrograms of nonmyocyte chromatin (as DNA), respectively, were required to saturate the enzyme. These results indicate that myocyte chromatin can support greater enzyme binding than can nonmyocyte chromatin. The distribution of DNA fragments from isolated myocyte and nonmyocyte nuclei were similar when alkaline sucrose density centrifugation was used. Chromatin prepared from these nuclear subsets showed no difference in degree of DNA fragmentation. These observations indicate that compared with nonmuscle cells, myocytes from adult rat hearts have higher RNA polymerase activity, greater overall chromatin template function, and higher binding capacity for RNA polymerase. Collectively, these data suggest that adult cardiac muscle cells should have a larger potential for RNA synthesis than nonmuscle cells.

Animals↗
PubMed1984

Development of isoproterenol-induced cardiac hypertrophy.

The development of cardiac hypertrophy was studied in adult female Wistar rats following daily subcutaneous injections of isoproterenol (ISO) (0.3 mg/kg body weight). A time course was established for the change in tissue mass, RNA and DNA content, as well as hydroxyproline content. Heart weight increased 44% after 8 days of treatment with a half time of 3.4 days. Ventricular RNA content was elevated 26% after 24 h of a single injection and reached a maximal level following 8 days of therapy. The half time for RNA accumulation was 2.0 days. The total content of hydroxyproline remained stable during the first 2 days of treatment but increased 46% after 4 days of therapy. Ventricular DNA content was unchanged during the early stage (1-4 days) of hypertrophic growth but increased to a new steady-state level 19% above the controls after 8 days of treatment. Intraventricular pressures and coronary flow measures were similar for control and experimental animals following 4 days of developed hypertrophy. However, dP/dt in the ISO-treated hearts was slightly but significantly (P less than 0.05) elevated. These data indicate that the adaptive response to ISO shows an early hypertrophic phase (1-4 days) characterized by a substantial increase in RNA content and cardiac mass in the absence of changes in DNA. However, prolonged stimulation (8-12 days) appears to represent a complex integration of both cellular hypertrophy and hyperplasia within the heart.

Animals↗
PubMed1984

Regression of isoproterenol-induced cardiac hypertrophy.

Cardiac hypertrophy was induced in adult female Wistar rats after 8 days of daily subcutaneous injections of isoproterenol (ISO). Regression from hypertrophy was studied following 1, 2, 4, 8, 12, and 20 days of ISO withdrawal. After 8 days of treatment cardiac mass increased 40%. Following ISO withdrawal, ventricular regression occurred during the first 8 days. After 12-20 days of recovery, a new steady-state heart weight to body weight ratio was established that was 12-13% above the controls. The half-time recovery for heart weight was 3.8 days. Ventricular RNA content was stimulated 76% after 8 days of ISO-induced hypertrophy. During regression RNA content decreased rapidly during the first 8 days with a half-time of 3.4 days. Following 20 days of recovery ventricular RNA was still 31% above the controls. However, myocyte RNA was stimulated 86% following 8 days of ISO treatment and returned to control level after 12 days of regression. Myocardial DNA was increased 23% in the hypertrophied hearts and did not change during the recovery period. Hydroxyproline was increased in the ISO-treated hearts and decreased only slightly during the recovery interval. These data indicate that ISO-induced hypertrophy was reversible while ventricular RNA content only partially recovered. Nevertheless, myocyte RNA showed a large stimulation that was completely reversible at least after 12 days of recovery.

Animals↗
PubMed1984

Protein synthesis in compensatory hypertrophy of rat plantaris.

Protein synthesis in rat plantaris muscle undergoing surgically induced hypertrophy was studied using a perfused hindquarter preparation. The tissue mass of the hypertrophied muscle increased 11, 33, 33, and 104% at 2, 5, 15, and 50 days postsurgery. Total tissue protein synthesis was unchanged during the early phase but was significantly elevated after 15 and 50 days of work overload. Myosin synthesis was also significantly elevated after 15 and 50 days of hypertrophic growth. Increases in muscle protein content (milligrams per muscle) for each protein fraction examined were temporally in step with the altered synthetic rates. The shift in muscle fibre-type profile from approximately 10% alkaline-labile fibres in the control muscle to about 25% alkaline-labile fibres in the hypertrophied muscle also followed a similar time course. These data suggest that during compensatory hypertrophy, enhanced protein synthesis may be the dominant mechanism for the massive accumulation of muscle protein. However, its contribution to muscle growth does not become evident until about 15 days after the initial growth stimulus.

Animals↗