Biomedical subjects

H Tian

Publications and source records attributed to H Tian.

At least 127 records · Page 7Linked to original sources

PubMed1995

Acidic fibroblast growth factor reduces rat skeletal muscle damage caused by ischemia and reperfusion.

Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad-spectrum mitogenic and non-mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aFGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatase (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of extra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future.

Adenosine Triphosphatases↗

PubMed1995

[Epidemiology of adult diabetes mellitus in a population of Capital Iron and Steel Company in Beijing].

To prevent the development of DM in susceptible individuals, 29859 subjects, aged from 30 to 64 years, from 32 units of the Company were studied by using WHO protocal and diagnostic criteria. The results showed that the average prevalence of DM and IGT was 3.63% and 4.19% respectively, standardized by census 1990 in Beijing, and it was increased with age. No sex difference in the prevalence of DM was found, but the prevalence of IGT was higher in females (5.55%) than in males. The obesity, overweight, positive DM family history and giant baby history, as well as high daily intake of protein were closely related to the prevalence of the disease. Smoking was in effective.

Adult↗

PubMed1995

[Changes of fructosamine content and their effects on platelet aggregation of glycosylated modification of low density lipoprotein in vitro].

The changes of fructosamine (FA) in low density lipoprotein (LDL) incubated in different durations and concentrations of glucose, electrophoretic mobility of different degrees of glycosylated modification of LDL, and the effects on platelet aggregation by glycosylated LDL were observed. The results revealed that FA content increased in LDL incubated with glucose and induced glycosylated modification of LDL, and FA content in LDL correlated to the duration of LDL incubated with glucose and also correlated to different concentrations of glucose. There was a positive correlation between electrophoretic mobility and FA content in LDL. The higher of FA content in LDL the higher of platelet aggregation. This study indicated that FA content in LDL reflected the degree of glycosylated modification of LDL, in which the physical, chemical and biological properties were changed.

Fructosamine↗

PubMed1995

[Determination of sterigmatocystin in cancerous tissues, blood and urine in patients with liver and stomach cancer].

Sterigmatocystin (ST) was determined with modified Southern-Western blot and indirect competitive enzyme-linked immunosorbent assay (IC-ELISA) for 28 specimens of cancerous tissues, 13 of blood and 20 of urine in 14 patients with liver and stomach cancer. Results showed DNA-ST adduct was detected in 14 specimens of cancerous tissues and/or pericancerous tissues. ST values were higher in four of 13 patients (65-113 micrograms/kg), as compared only in one of 14 healthy persons (68 micrograms/kg). And, ST values all were very low in urine, with a maximum of 13 micrograms/kg.

DNA Adducts↗

PubMed1995

Ischemia and reperfusion reduce the endogenous basic fibroblast growth factor (bF GF) in rat skeletal muscles.

Polyclonal antibodies directed against human recombinant basic fibroblast growth factor (bFGF) were used in immunohistochemical studies to localize this growth factor in normal and wounded rat skeletal muscles. bFGF immunoreactivity was found mainly in the extracellular matrix, primarily in the endomysium, including the heparin-containing basal lamina and also in the capillary basal membrane of both normal and wounded muscles, however the signal intensity was much stronger in normal muscles. After 4-hour ischemia, about 40% of skeletal muscle fibers lost their bFGF immunoreactivity. Muscles which experienced 4-hour ischemia and 24 reperfusion had only a weaker bFGF immunoreactivity. The pathological results supported the concept of destroyed cell connection and fiber necrosis in ischemia and reperfused muscles. The mechanisms involved in this reduced concentration of bFGF in wounded muscles included oxygen radical activation, inflammatory response and reduced secretion of endogenous bFGF. These results were only partially compatible with the established mitogenic role of this protein and suggested that a reduction of endogenous FGF may partly contribute to a delay in wound healing.

Animals↗

PubMed1995

[Effects of SL-probiotic preparation on the body weight and phagocytosis of white mice].

Effects of SL-probiotic preparation on the body weight and the phagocytic functions in white mice were studied. Bioassay of its toxicity showed SL-P was non-toxic. Body weight of the treated mice increased significantly as compared with that of controls 10 days after treatment with SL-probiotic preparation. Phagocytic activity, acid phosphatase activity, lysozyme activity of the peritoneal macrophages of the tested mice were enhanced significantly as compared with those of normal controls. The same results were obtained with respect to serum lysozyme activity. These observations showed that SL-probiotic preparation could activate macrophage function in mice and hence enhancement of non-specific immunity.

Acid Phosphatase↗

PubMed1994

Immune dysregulation in TGF-beta 1-deficient mice.

Approximately 2 wk after birth, mice having a TGF-beta 1 null mutation (TGF-beta 1(-/-)) exhibit a progressive wasting syndrome and death. Associated with this phenotype is a multifocal infiltration of lymphocytes and macrophages into target organs, especially the heart, lungs, and salivary glands. To explore the consequences of TGF-beta 1 deficiency on the immune system, lymphocyte phenotype and function were analyzed. Initially, lymphoid organ architecture seemed to be normal and, as symptoms developed, the thymus decreased in size, whereas lymph nodes were enlarged. Phenotypically, the TGF-beta 1(-/-) lymphoid cells seemed to be more differentiated in the thymus and activated in the lymph nodes, but remarkably unaffected in the spleen. Moreover, TGF-beta 1(-/-) spleen and lymph nodes displayed enhanced numbers of proliferating cells, as measured by proliferating cell nuclear Ag and/or cyclin-dependent kinase levels. Consistent with this hyperproliferative response, constitutive levels of IL-2 mRNA were elevated in the thymus and both IL-2 and IL-2R mRNA were increased in the lymph nodes. In contrast with the activation profile of TGF-beta 1(-/-) lymphoid cells in vivo, mitogen challenge of these cells in vitro revealed suppressed proliferation that was associated with a defect in inducible IL-2 mRNA expression and IL-2 secretion. Moreover, the addition of rIL-2 restored the deficient mitogen-induced proliferation. The mechanism leading to T cell anergy remains unclear; however, these data confirm the essential role for TGF-beta 1 in maintaining normal immune function.

Animals↗

PubMed1994

Synthetic fibronectin peptides interrupt inflammatory cell infiltration in transforming growth factor beta 1 knockout mice.

Pronounced mononuclear leukocyte (MNL) infiltration occurs in multiple organs of mice homozygous for a transforming growth factor beta 1 (TGF-beta 1) loss-of-function gene mutation [TGF-beta 1 (-/-)], followed by cachexia and eventually death. Consistent with the increased leukocyte adhesion and tissue infiltration, MNLs isolated from spleen, thymus, and peripheral blood of symptomatic TGF-beta 1 (-/-) mice, as compared to littermate controls, exhibited increased adhesion to extracellular matrix proteins and to endothelial cells in vitro. Incubation of TGF-beta 1 (-/-) MNLs with selected synthetic peptides corresponding to cell- and heparin-binding sequences of fibronectin (FN) significantly attenuated adhesion of these cells not only to FN but also to endothelial cells in vitro. Based on these observations, mice were treated with the FN peptides in an attempt to rescue them from tissue inflammation and cardiopulmonary failure. Daily injections of a combination of four synthetic FN peptides that interact with beta 1-integrins and/or cell surface proteoglycans blocked the massive infiltration of MNLs into the heart and lungs of TGF-beta 1 (-/-) mice. Peptide treatment initiated on day 8, coincident with the first evidence of increased leukocyte-endothelial cell interactions, not only blocked tissue infiltration but also moderated the lethal wasting syndrome.

Amino Acid Sequence↗

PubMed1994

Effect of postexposure vaccination in a chimpanzee model of hepatitis A virus infection.

Passive transfer of antibodies to hepatitis A virus (HAV) in immune globulin (IG) effectively prevents hepatitis A when given after exposure, but does not provide lasting protection from infection. Hepatitis A vaccines have been shown to generate quickly levels of antibody equivalent to those found after IG administration. The effect of hepatitis A vaccine in preventing infection following fecal-oral exposure was evaluated in a chimpanzee model of HAV infection. Two animals were vaccinated 1 and 3 days, respectively following inoculation and two inoculated animals served as unprotected controls. Of the two immunized animals, one had no evidence of HAV infection, while the other had an attenuated infection with no evidence of virus shedding. These results suggest that while postexposure hepatitis A vaccination may be infection permissive, it attenuates disease expression and prevents virus shedding.

Alanine Transaminase↗

PubMed1994

[The role tumor necrosis factor in multiple organ dysfunction caused by bowel ischemia and reperfusion].

To explore the role of tumor necrosis factor (TNF) in the pathogenesis of multiple organ dysfunction following bowel ischemia and reperfusion, 98 rats were subjected to occlusion of the superior mesenteric artery for 45 minutes. It was found that the plasma TNF level increased rapidly after release of the clamp, peaking to 27.59 +/- 11.13 ng/ml 2 hours after reperfusion. Its changes in quantity was directly related to endotoxin in the portal circulation. Furthermore, the results showed that pretreatment with monoclonal antibody to TNF-alpha could significantly lowered the plasma TNF content and notably improved the functions of various organs. This study demonstrated that release of TNF might result in systemic hypotension and remarkable damage to liver, kidneys and lungs, which contributed to the development of sepsis and multiple system organ failure following severe ischemia-reperfusion injury of the intestine.

Animals↗

PubMed1994

Contents of trace elements in the hair of aplastic anemia patients and their treatment based on an overall analysis of symptoms and signs.

The content of 12 trace elements in the hair of 20 aplastic anemia patients was determined and compared with that of normal subjects as control. The results showed that patients with deficiency of yin had a significant decrease in lithium, calcium, strontium, and chromium, those with deficiency of yang had a distinct decrease in zinc magnesium barium, strontium, calcium, and lithium, and those with deficiency of both yin and yang had a general decrease in all the 12 trace elements. Changes in trace element content in hair may serve as a guide to opening up new vistas in the treatment of aplastic anemia on the basis of an overall analysis of symptoms and signs.

Adolescent↗

PubMed1993

Normal T cell receptor-mediated signaling in T cell lines stably expressing HIV-1 envelope glycoproteins.

A series of T cell lines transfected to stably express HIV-1 envelope (env) glycoproteins were analyzed for viability and for T cell signaling. One transfectant was distinguished by its stable expression of gp120 and gp41, whereas the remainder of the T cell lines were similar to previously reported env-expressing T cells in synthesizing predominantly unprocessed env glycoprotein gp160. All of the transfectants were additionally constructed to express tat and rev proteins. None of these cell lines displayed growth abnormalities or spontaneous cell fusion, although the cell line synthesizing env gp120/gp41 could be induced to fuse and die when cocultured with a second cell expressing surface CD4. A cell line expressing only gp160 and the transfectant expressing gp160, gp120, and gp41 could be triggered normally via CD3-cross-linking as measured by protein tyrosine phosphorylation and by the induction of the CD69 activation marker. At levels of env protein expression sufficient to mediate syncytium formation and to kill cells, these HIV-1 env transfectants displayed no intrinsic T cell signaling abnormalities, suggesting that mechanisms other than a direct intracellular action of the tat or env proteins may be contributing to the deficit in Ag-specific T cell activation described subsequent to HIV infection in vivo and in vitro.

CD4-Positive T-Lymphocytes↗

PubMed1993

Lipid composition and fluidity of the human immunodeficiency virus envelope and host cell plasma membranes.

Previous studies have indicated that human immunodeficiency virus (HIV) is enclosed with a lipid envelope similar in composition to cell plasma membranes and to other viruses. Further, the fluidity, as measured by spin resonance spectroscopy, is low and the viral envelope is among the most highly ordered membranes analyzed. However, the relationship between viral envelope lipids and those of the host cell is not known. Here we demonstrate that the phospholipids within the envelopes of HIV-1RF and HIV-2-L are similar to each other but significantly different from their respective host cell surface membranes. Further, we demonstrate that the cholesterol-to-phospholipid molar ratio of the viral envelope is approximately 2.5 times that of the host cell surface membranes. Consistent with the elevated cholesterol-to-phospholipid molar ratio, the viral envelopes of HIV-1RF and HIV-2-L were shown to be 7.5% and 10.5% more ordered than the plasma membranes of their respective host cells. These data demonstrate that HIV-1 and HIV-2-L select specific lipid domains within the surface membrane of their host cells through which to emerge during viral maturation.

Animals↗

PubMed1993

Antibody response to nonstructural proteins of hepatitis A virus following infection.

The nonstructural proteins of hepatitis A virus (HAV), produced during active virus replication, are alternative antigens that could be used to differentiate disease from inactivated vaccine-induced antibodies. An assay based on immune precipitation of proteins translated from transcripts of the P2 region of viral cDNA was used to evaluate the development of antibodies after natural infection or vaccination. Antibodies against P2 proteins were found in all sera from clinical cases of hepatitis A following the acute phase. Chimpanzees vaccinated with inactivated or cell-adapted HAV had no detectable antibodies against P2 products, either before or after wild type virus challenge. A serosurvey of sera positive for total anti-HAV (HAVAB, Abbott Laboratories, North Chicago) suggested that some individuals had no detectable antibodies to the P2 antigen by immune precipitation. These results were attributed to the lower sensitivity of the immunoprecipitation assay, since antibodies to capsid proteins, as measured by immunoprecipitation, were also not detected in most of these sera.

Adult↗

PubMed1993

Clinical and prognostic investigations on M2/t(8;21) acute nonlymphocytic leukemia.

Clinical and prognostic investigations were conducted in 46 cases of M2/t(8;21) leukemia and 29 cases of M2/NN patients. Results showed that most patients with M2/t(8;21) were young males with higher incidence of extramedullary infiltrations. Complete remission rate was higher but with earlier relapse. The prognosis of patients with M2/t(8;21) with loss of one sexual chromosome was poor.

Adult↗

PubMed1992

Participation of tyrosine phosphorylation in the cytopathic effect of human immunodeficiency virus-1.

Protein tyrosine phosphorylation is a common mechanism of signaling in pathways that regulate T cell receptor-mediated cell activation, cell proliferation, and the cell cycle. Because human immunodeficiency virus (HIV) is though to affect normal cell signaling, tyrosine phosphorylation may be associated with HIV cytopathicity. In both HIV-infected cells and transfected cells that stably express HIV envelope glycoproteins undergoing HIVgp41-induced cell fusion, a 30-kilodalton protein was phosphorylated on tyrosine with kinetics similar to those of syncytium formation and cell death. When tyrosine phosphorylation was inhibited by the protein tyrosine kinase inhibitor herbimycin A, envelope-mediated syncytium formation was coordinately reduced. These studies show that specific intracellular signals, which apparently participate in cytopathicity, are generated by HIV and suggest strategies by which the fusion process might be interrupted.

Benzoquinones↗

PubMed1992

Serological approaches to distinguish immune response to hepatitis A vaccine and natural infection.

Currently, the immune status of an individual exposed to hepatitis A virus (HAV) is determined by assays which measure antibodies against the capsid proteins. These assays indicate exposure to the viral capsid that could result from either infection or from vaccination. Recent data indicate that proteins from the non-structural genome region of the virus (P2 or P3), which are only produced during active virus replication, generate antibodies after clinical disease. A sub-genomic cDNA segment of HAV corresponding to the P2 region was used for in vitro transcription-translation followed by immune precipitation of the translated products under non-denaturing conditions. Serial serum specimens from experimentally infected chimpanzees and humans naturally infected with hepatitis A verified the development of antibodies to P2 proteins following infection. A serosurvey of individuals positive for antibodies to the HAV capsid (HAV AB assay, Abbott Laboratories) revealed that 50-60% of children and 16-32% of adults had no detectable antibodies to the P2 antigen by immune precipitation. These results may reflect subclinical infections resulting in a lower level of antibodies against the non-structural antigens or may represent a greater sensitivity of the competitive assay (HAV AB) used to detect capsid antibodies compared to the immunoprecipitation assay used to detect non-structural antigens.

Adult↗

PubMed1992

Signals delivered via the Qa-2 molecule can synergize with limiting anti-CD3-induced signals to cause T lymphocyte activation.

Qa-2 is a glycolipid anchored, MHC encoded class I molecule expressed at high levels on all murine peripheral T lymphocytes. Anti-Qa-2 antibodies have previously been found to stimulate T cells to proliferate in the presence of crosslinking antibody and PMA. We have examined the effect of anti-Qa-2 antibodies on T cells stimulated with a suboptimal concentration of immobilized anti-CD3. When anti-Qa-2 antibodies were co-immobilized with limiting anti-CD3, in the absence of PMA, a clear augmentation of T cell proliferation was seen. Interestingly, the co-stimulatory anti-Qa-2 antibodies could be directed against epitopes mapped to either the alpha 3 or the alpha 1/alpha 2 Qa-2 domains. As was the case with activation induced by soluble/crosslinked anti-Qa-2 antibodies plus PMA, CD8+ T cells were less able to be costimulated with anti-Qa-2 antibodies than CD4+ cells. Surprisingly, Ca2+ mobilization was only seen when two anti-Qa-2 antibodies reactive to separate structural domains were co-crosslinked on the surface of Indo-1 loaded T cells with a suboptimal concentration of anti-CD3. Collectively these results raise questions regarding the mechanism of Qa-2 mediated signaling and its potential role in T cell activation.

Animals↗