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Biomedical subjects

S Q Yang

Publications and source records attributed to S Q Yang.

At least 55 records · Page 3Linked to original sources
PubMed1994

Tumor necrosis factor-alpha induces c-jun during the regenerative response to liver injury.

After liver injury, remaining hepatocytes proliferate to regenerate the liver. Although the precise mechanisms that initiate and localize regeneration are unknown, local induction of c-jun is a critical, early step in the response. Treatment of rats with antibodies to tumor necrosis factor-alpha (TNF-alpha), a mediator of liver injury, inhibits regenerative induction of jun nuclear kinase activity and nuclear c-jun expression and alters the DNA binding activity of the c-jun transcription factor, AP-1, in liver. Pretreatment with anti-TNF antibodies does not affect pulmonary or renal c-jun expression or AP-1 binding activity post-partial hepatectomy. In primary hepatocyte cultures, TNF-alpha directly promotes the proliferative actions of mitogens, supporting in vivo evidence that it sensitizes hepatocytes to mitogens. Thus local release of TNF may act in a paracrine fashion to initiate regeneration in the injured liver by promoting induction of critical growth-related genes, such as c-jun.

Animals↗
PubMed1994

[The clinical significance of detection of anti-BCG-A60 antibody by ELISA in diagnosis of tuberculosis].

In order to find out the clinical significance of detection of BCG-A60 antibody by ELISA in diagnosis of tuberculosis, 734 cases of non-tuberculosis patients and 560 cases of tuberculosis has been examined. The result of A60-ELISA test for IgG as diagnosilic criteria of tuberculosis, sensitivity is 84.5%, specificity is 89.3%, It shows satisfactory effect, so it can be used as an helpful method in clinical diagnosis of tuberculosis. IgG, IgA and IgM are measured at same time, and find that a combined use of the IgG and IgM ELISA studies considerably increases the significance of the test.

Antibodies, Bacterial↗
PubMed1994

Regenerative changes in C/EBP alpha and C/EBP beta expression modulate binding to the C/EBP site in the c-fos promoter.

CCAAT/enhancer binding proteins are a family of basic zipper DNA binding proteins that regulate transcription of several liver-specific genes and certain growth-related genes. Growth-related variations in the nuclear expression of one or more of the CCAAT/enhancer binding proteins may regulate the transition from the nonproliferative, differentiated phenotype of adult liver to the proliferative phenotype of regenerating liver. To evaluate this possibility, we used Northern- and Western-blot analyses to profile the expression of selected CCAAT/enhancer binding proteins in regenerating liver. Variations in CCAAT/enhancer binding protein expression were then correlated with changes in binding to the CCAAT/enhancer binding protein site of the c-fos promoter. Expression of both CCAAT/enhancer binding protein alpha and CCAAT/enhancer binding protein beta increases after partial hepatectomy. Steady-state levels of CCAAT/enhancer binding protein alpha mRNA increase 30% within an hour of partial hepatectomy (p < 0.05). This is followed by a transient increase in nuclear levels of CCAAT/enhancer binding protein alpha protein at 3 hr after partial hepatectomy (p = 0.08). In contrast, increases in CCAAT/enhancer binding protein beta mRNA and protein are more sustained. Levels of CCAAT/enhancer binding protein beta mRNA increase 400% to 500% within an hour of partial hepatectomy and remain increased throughout most of the prereplicative period (p < 0.01). Nuclear levels of CCAAT/enhancer binding protein beta protein are 200% to 300% greater than prehepatectomy levels at 3 hr (p < 0.001) to 6 hr (p < 0.05) and do not approach basal levels until 24 hr after partial hepatectomy. Gel mobility shift assays of nuclear extracts from regenerating livers indicate that these increases in nuclear protein expression are associated with increased DNA binding of CCAAT/enhancer binding protein alpha-beta heterodimers and beta-beta homodimers. These results demonstrate growth-related variations in the expression and DNA binding of both CCAAT/enhancer binding protein alpha and beta during liver regeneration and support the theory that altered CCAAT/enhancer binding protein DNA binding may contribute to regeneration-associated changes in liver cell phenotype.

Animals↗
PubMed1993

Blockage of clonidine-induced platelet aggregation in rabbits by procainamide.

Procainamide was capable of blocking the alpha 2-adrenergic receptor agonist clonidine-induced platelet aggregation, giving an antagonistic index, pA2, of 5.0 +/- 0.6 and half antagonistic concentration, A2, of 10.4 mumol.L-1. Clonidine showed half efficacy concentrations (EC50) of 44, 82, 182, 485, and 662 nmol.L-1, and affinity parameter (pD2) of 7.4, 7.1, 6.7, 6.3, and 6.2 respectively when different concentrations of procainamide were used as blocking reagent. The results indicated that the mechanism of inhibitory effect of procainamide on clonidine-induced platelet aggregation was to competitively antagonize activating alpha 2-receptors and others of clonidine on platelet membrane.

Animals↗
PubMed1993

Long-term ethanol consumption alters the hepatic response to the regenerative effects of tumor necrosis factor-alpha.

The pathogenesis of chronic alcoholic liver disease is uncertain, but it may reflect an impaired wound healing response to ethanol-induced liver injury. Cell-to-cell communication such as that mediated by the cytokine tumor necrosis factor is necessary for successful liver regeneration and complete recovery from liver injury. Hence disruption of intercellular regenerative signaling may contribute to the pathogenesis of chronic alcoholic liver disease. To test this hypothesis, the cytokine and regenerative responses triggered by partial hepatectomy were compared in ethanol-fed rats and isocalorically maintained, pair-fed controls. To further clarify the effect of ethanol on tumor necrosis factor-modulated regenerative effects, we evaluated some of the rats in each feeding group after pretreatment with antibodies to tumor necrosis factor. As expected, ethanol inhibited DNA synthesis and liver cell proliferation after partial hepatectomy. Ethanol-associated inhibition of liver regeneration occurred despite apparently similar serum concentrations of the tumor necrosis factor-inducible cytokine interleukin-6. Treatment with antibodies to tumor necrosis factor 1 hr before partial hepatectomy inhibited post-partial hepatectomy induction of interleukin-6 and liver regeneration in ethanol-fed and pair-fed rats. However, serum interleukin-6 was reduced more in ethanol-fed rats than in control rats (93% vs. 66%; p < 0.05). Antibodies to tumor necrosis factor also inhibited hepatic DNA synthesis more in ethanol-fed rats than in controls (85% vs. 50%; p < 0.05). In ethanol-fed rats, the increased effect of tumor necrosis factor antibody on post-partial hepatectomy DNA synthesis suggests heightened sensitivity of hepatocytes to tumor necrosis factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Ethanol-associated alterations in the kinetics of putrescine uptake and metabolism by the regenerating liver.

Biosynthesis of the polyamines, putrescine, spermidine, and spermine is required for DNA synthesis and liver regeneration after partial hepatectomy. We have previously reported that chronic ethanol consumption impairs polyamine synthesis and significantly retards liver regeneration after partial hepatectomy. In those studies, supplementation with putrescine restored hepatic DNA synthesis in ethanol-fed rats but exerted no effect in pair-fed controls. These differences in the response to putrescine treatment may have resulted from ethanol-associated differences in hepatic uptake, release, or metabolism of putrescine. To resolve these issues and define more completely how putrescine treatment affects DNA synthesis, we now assess the kinetics of putrescine uptake and metabolism after intraperitoneal or intravenous injection of radiolabeled putrescine (1.2 mmol/kg, specific activity 1 microCi/mmol) into rats fed 36% ethanol diets or isocaloric, nonethanol diets for 6 weeks prior to partial hepatectomy. After putrescine treatment, hepatic putrescine concentrations were greater in ethanol-fed rats than controls. Differences in post-treatment hepatic putrescine levels between ethanol and pair-fed groups could not be explained by differences in the rates of hepatic putrescine uptake or excretion into bile; residual de novo synthesis of putrescine from ornithine or metabolism of hepatic putrescine to its polyamine products, spermidine and spermine. Indeed, supplemental putrescine was not appreciably converted to spermidine or spermine in either ethanol or control rats. Hence, these latter polyamines are unlikely to be responsible for the treatment-associated improvement in DNA synthesis that has been noted in ethanol-fed rats. This suggests that putrescine itself acts to restore hepatic DNA synthesis in ethanol-fed rats.

Alcoholism↗
PubMed1992

Hepatitis B virus p25 precore protein accumulates in Xenopus oocytes as an untranslocated phosphoprotein with an uncleaved signal peptide.

We have analyzed the translocation of hepatitis B virus (HBV) precore (PC) proteins by using Xenopus oocytes injected with a synthetic PC mRNA. The PC region is a 29-amino-acid sequence that precedes the 21.5-kDa HBV capsid or core (C) protein (p21.5) and directs the secretion of core-related proteins. The first 19 PC amino acids provide a signal peptide that is cleaved with the resultant translocation of a 22.5-kDa species (p22.5), in which the last 10 PC residues precede the complete p21.5 C polypeptide. Most p22.5 is matured to 16-20 kDa species by carboxyl-terminal proteolytic cleavage prior to secretion. Here we show that some four unexpected PC proteins of 24 to 25 kDa are produced in addition to the secretion products described above. Protease protection and membrane cosedimentation experiments reveal that all PC proteins behave as expected for proteins that are translocated into the lumen of the endoplasmic reticulum except for the single largest PC protein (p25), which is not translocated. Like p21.5, p25 is a phosphoprotein that localizes to the oocyte cytosol and nucleus, and protease digestion studies suggest that the two molecules have similar two-domain structures. Radiosequencing of immobilized p25 demonstrates that it contains the intact PC signal peptide and represents the unprocessed translation product of the entire PC/C locus. Thus, while many HBV PC protein molecules are correctly targeted to intracellular membranes and translocated, a significant fraction of these molecules can evade translocation and processing.

Amino Acid Sequence↗
PubMed1992

Characterization of hepatitis B virus capsid particle assembly in Xenopus oocytes.

Little is known about the assembly of the 28-nm nucleocapsid or core particle of hepatitis B virus. Here we show that this assembly process can be reconstituted in Xenopus oocytes injected with a synthetic mRNA encoding the hepatitis B virus capsid protein (p21.5). Injected oocytes produce both a nonparticulate p21.5 species (free p21.5) and capsid particles. We describe rapid and simple methods for fractionating these species on a small scale either with step gradients of 10 to 60% (wt/vol) sucrose or by centrifugation to pellet the particles, and we characterize the oocyte core particles. Free p21.5 exhibits chemical and physical properties distinctly different from those of particles. Free p21.5 is partially cleaved by proteinase K, whereas core particles are almost completely resistant to cleavage. This suggests that the carboxyl-terminal protamine region, the main target for proteases within p21.5, is exposed in free p21.5 but faces the interior of the p21.5 core particle. Finally, pulse-chase experiments demonstrated that free p21.5 can be chased almost quantitatively into core particles, establishing that free p21.5 is fully competent to form particles and represents an assembly intermediate on the pathway for core particle formation. However, core particle assembly appears very dependent on p21.5 concentration and is rapidly compromised if the p21.5 concentration is lowered. The advantages of oocytes for studying assembly are discussed.

Animals↗
PubMed1992

Antibodies to tumor necrosis factor-alpha inhibit liver regeneration after partial hepatectomy.

Certain cytokines that are produced in liver may act as growth factors to facilitate wound healing and, hence, may influence liver regeneration. However, this hypothesis has not been directly tested. To determine whether the cytokine response evoked by partial hepatectomy (PH) modulates the process of liver regeneration, adult male rats were injected intraperitoneally with either goat polyclonal antibodies to rat tumor necrosis factor (TNF; 15 micrograms/g body wt) or an equal amount of goat anti-rat immunoglobulin G 1 h before PH. Animals were killed at 12, 24, 48, or 72 h post-PH, 1 h after injection with [3H]thymidine. Serum TNF levels were measured with the L929 cytotoxicity assay, titers of antibody to TNF were determined by enzyme-linked immunoabsorbent assay, and interleukin-6 (IL-6) concentrations were measured by B9 cell bioassay. Liver regeneration was assessed by [3H]thymidine incorporation into hepatic DNA and by immunohistochemical evidence of proliferating cell nuclear antigen (PCNA) expression. Antibodies to TNF were detected in treated rats but not in controls. Titers were highest at 12 h and progressively fell. Although TNF was never detected in serum, treatment with anti-TNF pre-PH significantly inhibited increases in serum IL-6 concentration post-PH. Anti-TNF pretreatment also inhibited [3H]thymidine incorporation into DNA, as well as expression of PCNA by both hepatocytes and liver nonparenchymal cells. These data indicate that TNF positively modulates liver regeneration after PH.

Animals↗
PubMed1992

Differential expression of guanine nucleotide-binding proteins enhances cAMP synthesis in regenerating rat liver.

Events leading to cAMP accumulation after partial hepatectomy (PH) and effects of cAMP on hormonal induction of DNA synthesis in hepatocytes were characterized. Hepatic cAMP peaked biphasically post-PH and paralleled changes in adenylyl cyclase activity. Fluctuations in cyclase activity were not explained by variations in glucagon receptor kinetics, but reflected altered G-protein expression. Membrane levels of the stimulatory G-protein, Gs alpha, increased early after PH and were sustained. Levels of the inhibitory G-protein, Gi2 alpha, increased more slowly, peaked later, and quickly fell. Levels of both G-proteins correlated poorly with levels of their mRNAs, suggesting posttranscriptional factors modify their membrane concentrations. When growth factor-induced DNA synthesis was compared in hepatocyte cultures grown with or without agents that increase intracellular cAMP, DNA synthesis was inhibited by sustained high levels of cAMP but was enhanced when high cAMP levels fell. In both regenerating liver and hepatocyte cultures, the expression of a "differentiated" hepatocyte gene, phosphoenolpyruvate carboxykinase, correlated with elevated cAMP levels. These data suggest that the differential expression of G-proteins integrates signals initiated by several growth factors so that the accumulation of cAMP is tightly regulated post-PH. The ensuing variations in cAMP levels modulate both growth and differentiated functions during liver regeneration.

Animals↗
PubMed1992

Chronic ethanol consumption disturbs G-protein expression and inhibits cyclic AMP-dependent signaling in regenerating rat liver.

Evidence suggests that ethanol desensitizes hepatocytes to the trophic effects of hormones. Cyclic AMP-dependent signals are important regulators of intermediary metabolism, cellular proliferation and differentiation, and modulate liver growth during hepatic regeneration. The events leading to cyclic AMP accumulation after partial hepatectomy were characterized in rats consistently fed ethanol-containing diets and compared with results in rats fed isocaloric amounts of nonethanol diet to determine whether altered cyclic AMP-dependent signal transduction contributes to ethanol-associated aberrations in hepatic growth regulation. Ethanol treatment significantly inhibited hepatic accumulation of cyclic AMP after partial hepatectomy. This was most likely the result of decreased synthesis of cyclic AMP because activation of adenylyl cyclase by agents acting through receptors (e.g., glucagon or isoproterenol), GTP-binding proteins (GTP-gamma-S) and directly on adenylyl cyclase (e.g., forskolin) was significantly inhibited in ethanol-fed rats. Both homologous and heterologous desensitization contributed to this effect. beta 1-Adrenergic receptors were relatively down-regulated 6 hr after partial hepatectomy in ethanol-fed rats, whereas glucagon receptor kinetics were similar in the two groups. Liver membrane expression of GTP-binding proteins differed markedly after partial hepatectomy in ethanol-fed and pair-fed rats. Ethanol significantly inhibited post-partial hepatectomy induction of the stimulatory G protein, Gs alpha but led to overexpression of the inhibitory, G(i)2 alpha, subunit. Steady-state messenger RNA levels of these G proteins were similar in ethanol-fed and pair-fed rats, suggesting that ethanol inhibits G protein expression posttranscriptionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1991

The protective role of zinc in the toxic action of coal dust upon mouse macrophages.

Macrophages from mice were cultured at 37 degrees C with 1640 medium containing 10% bovine serum. The macrophage suspension was made from 50 Swiss mice and was cultured in the following groups: control group; coal dust group (with added coal dust particles (10 micrograms/ml) smaller than 4 microns diameter); subdivided zinc-coal dust group (as coal dust group with zinc added in three different concentrations--namely, 10 ppm, 30 ppm, and 60 ppm). Cells were examined by light microscopy. Obvious differences were found in the rate of cell deaths between the coal dust group and the zinc-coal dust group after culture for 48 hours. The cell membranes were ruptured after culturing with coal dust, and the presence of zinc appeared in some degree to protect cell membranes from damage caused by the dust. Staining the cells with Gomori's modified method, showed that acid phosphatase particles in the zinc-coal dust group were more numerous than in the coal dust group. The results indicate that the trace element zinc may play an important part in protecting against the cytotoxic action of coal dust.

Acid Phosphatase↗
PubMed1990

A computer program for selection of oligonucleotide primers for polymerase chain reactions.

We have designed a computer program which rapidly scans nucleic acid sequences to select all possible pairs of oligonucleotides suitable for use as primers to direct efficient DNA amplification by the polymerase chain reaction. This program is based on a set of rules which define in generic terms both the sequence composition of the primers and the amplified region of DNA. These rules (1) enhance primer-to-target sequence hybridization avidity at critical 3'-end extension initiation sites, (2) facilitate attainment of full length extension during the 72 degrees C phase, by minimizing generation of incomplete or nonspecific product and (3) limit primer losses occurring from primer-self or primer-primer homologies. Three examples of primer sets chosen by the program that correctly amplified the target regions starting from RNA are shown. This program should facilitate the rapid selection of effective and specific primers from long gene sequences while providing a flexible choice of various primers to focus study on particular regions of interest.

Algorithms↗
PubMed1990

Hemorrhagic fever with renal syndrome. Separation of human peripheral blood T and B cells and detection of viral antigen.

In this study, total blood lymphocytes were prepared from patients with hemorrhagic fever with renal syndrome (HFRS) by a density gradient on Ficoll-Hypaque. T and B cells were then purified by passing the total lymphocytes over a nylon wool column. The purities of total lymphocytes, T cells and B cells were 97.8 +/- 2.3%, 91.6 +/- 4.5% and 74.2 +/- 12.1%, respectively. Also, after modification of cell fixation and smear drying, the number of cells were increased and the time needed for slide preparation was shortened. Detection of viral antigen by immunofluorescence assay using monoclonal antibodies to Hantavirus (HTNV) showed that the total lymphocytes. T cells and B cells were infected by HTNV during the early stages of HFRS and no specific fluorescence was seen in the cells from the late diuretic phase to convalescent phase. The results suggest that virus replication in blood lymphocytes may partly contribute in the early stages to the impairment of cell immune response and in vivo spread of HTNV to its target sites.

Antigens, Viral↗
PubMed1990

Isolation of a strain of Hantaan virus from peritoneal exudate cells of a patient with hemorrhagic fever with renal syndrome.

A new strain of Hantaan virus (HTNV), GH716, was isolated from the peritoneal exudate cells (PEC) of a patient with severe hemorrhagic fever with renal syndrome (HFRS). The isolate was propagated in Vero E6 cells. At each passage the virus-infected cells were examined for HTNV with immunofluorescence technique using monoclonal antibodies (McAb) 25-1 and 84-1 against HTNV. From passage 5 on, fluorescent intensity tended to stabilize at (+++) and infectivity titer reached 10(5) TCID50/ml. Using 14 McAb to 76-118 and BI strains of HTNV, we found that strain GH716 was antigenically similar to strain 76-118 (Apodemus type) and different from strain R22 (Rattus type), suggesting that GH716 may fall into the Apodemus type of HTNV. This is the first isolation of an HTNV from human PEC collected on the tenth day of illness. The successful isolation of strain GH716 may provide an alternative source of obtaining HTNV during the later stages of HFRS.

Animals↗
PubMed1990

[Influences of 3,4,5-trihydroxystibene-3-beta-mono-D-glucoside on rabbits' platelet aggregation and thromboxane B2 production in vitro].

Platelet aggregation and thromboxane B2 (TXB2) production induced by arachidonic acid (AA) or Adenosine diphosphate (ADP) were studied by turbidimetry and radioimmunoassay in rabbits. 3,4,5-tri-hydroxystibene-3-beta-mono-D-glucoside (PD) 6.7-107.2 mumol/L inhibited platelet aggregation and the production of TXB2 as well. The inhibitions by PD were dose-dependent: 48-90% (AA-induced) and 43-69% (ADP-induced) for platelet aggregation; 50-87% (AA-induced) and 43-68% (ADP-induced) for TXB2. There were positive correlations between the inhibition of platelet aggregation and production of TXB2.

Animals↗