Biomedical subjects

B Zhao

Publications and source records attributed to B Zhao.

At least 163 records · Page 9Linked to original sources

PubMed1997

Effects of gamma interferon and nitric oxide on the interaction of Mycobacterium avium subsp. paratuberculosis with bovine monocytes.

In this study, we examined the effects of recombinant bovine gamma interferon (rIFN-gamma) and nitric oxide (NO) on the interaction of M. avium subsp. paratuberculosis with bovine monocytes. Monocytes pretreated with rIFN-gamma exhibited slightly increased phagocytosis of M. avium subsp. paratuberculosis and modest inhibition of the intracellular growth of this microorganism. The number of viable intracellular bacilli decreased earlier in rIFN-gamma-pretreated monocytes than in control monocytes. After infection with M. avium subsp. paratuberculosis, NO was not constitutively released, but NO release from infected monocytes was induced by treatment with rIFN-gamma or with rIFN-gamma and lipopolysaccharide (LPS). Release of nitric oxide was inhibited by addition of N(G)-monomethyl-L-arginine; however, inhibition of nitric oxide did not alter the pattern of intracellular survival of M. avium subsp. paratuberculosis in rIFN-gamma-treated bovine monocytes. Although chemically generated nitric oxide killed M. avium subsp. paratuberculosis in a cell-free system in vitro, the amount of nitric oxide required was far greater than that released from infected monocytes stimulated with rIFN-gamma and LPS. Our data suggest that rIFN-gamma activates M. avium subsp. paratuberculosis-infected bovine monocytes to release nitric oxide but only modestly increases antimycobacterial activity of monocytes against this organism. This may be due, in part, to the fact that the amount of nitric oxide produced by rIFN-gamma-activated bovine monocytes is insufficient to kill intracellular M. avium subsp. paratuberculosis bacilli in vitro.

Animals↗

PubMed1997

[Facial proportions of the young with the beautiful faces of Sichuan descent].

In this study, eighteen indexes of facial proportions were established in 72 youngsters with beautiful faces of Sichuan descent, who haven't been done operation on and orthodontics in our country. The results indicated that there were not most sexual difference of the facial proportions between male and female in most indexes, and also were not national difference of facial proportions between Chinese and Japanese. It also showed some progresses in clinical practice.

Adolescent↗

PubMed1997

Path test reactions to the Chinese Standard Screening Allergens in 1,135 patients investigated for allergic contact dermatitis.

BACKGROUND: The patch test has become the standard method of investigating patients with allergic contact dermatitis. Many countries have developed standard screening allergens to make patch testing more efficient. A series of the Chinese Standard Screening Allergens were studied and modified. OBJECTIVE: This study investigated the frequency of contact allergies in suspected allergic contact dermatitis and tested the practicality of the Chinese Standard Screening Patch Test Allergens. METHODS: A total of 1,135 patients suspected of having allergic contact dermatitis were patch tested. Three hundred twelve (27.5%) were men, and their age ranged from 2 to 75 years old (mean age, 34.3 years), 823 (72.5%) were women, and their age ranged from 2 to 76 years old (mean age, 33.0 years). Nanjing Medical University supplied the Chinese Standard Screening Allergens and Finn-Chamber. All patients were patch tested according to the Chinese Standard Screening Patch Test Allergens with Finn-Chamber the protocol as established by the International Contact Dermatitis Research Group (ICDRG). RESULTS: From the 1,135 patients suspected to have allergic contact dermatitis, 650 (57.3%) had at least one positive reaction. Nineteen (95%) of the Chinese Standard Screening Patch Test Allergens had positive reactions higher than 1%. Of 485 patients with negative reaction to the Standard Allergens, 106 patients were tested with other suspected contactants according to history. Thirty-nine (36.8%) had positive reactions to the contactants they provided. The total positive rate therefore increased by 3.4%. CONCLUSIONS: Our study results indicate that the Chinese Standard Screening Patch Test Allergens are suitable for use in routine clinic in China.

Adolescent↗

PubMed1997

Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells.

The purpose of this study was to document induction of apoptosis by vitamin E succinate (VES; RRR-alpha-tocopheryl succinate) in human breast cancer cells in culture and to characterize potential c-jun involvement. VES at 18.8 microM (10 micrograms/mL) induced DNA synthesis arrest, reduced total cell numbers, and induced apoptosis in estrogen receptor-positive and estrogen-responsive MCF-7 human breast cancer cells. VES at 10 micrograms/mL induced apoptosis in greater than 60% of cells within 3 d of treatment. Apoptosis was documented by detection of fragmented or condensed nuclei in 4',6-diamindino-2-phenylindole-stained cells, detection of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeled DNA, and DNA laddering. Analyses of mRNA and protein levels of candidate molecules involved in apoptosis showed that MCF-7 cells treated with VES exhibited elevated and persistent expression of c-jun. MCF-7 cells stably transfected with a dominant-negative interfering mutant c-jun, TAM-67, and expressing high levels of mutant jun exhibited approximately 50% blockage of VES-mediated apoptosis. In addition to increased c-jun expression after VES treatment, VES-treated MCF-7 cells exhibited elevated activator protein-1 (AP-1) binding activity. Comparisons of AP-1 binding factors by super-shift analyses with jun-specific antibodies in cells sensitive to VES-induced apoptosis (empty-vector control 7-1 cells) and cells resistant to VES-induced apoptosis (TAM-67-containing TAM-9 cells) showed that the sensitive cells expressed c-jun and jun D and the resistant cells TAM-67 AP-1 binding proteins after VES treatment. These studies suggested that c-jun may be involved in the apoptotic process initiated by VES treatment of human MCF-7 breast cancer cells.

Apoptosis↗

PubMed1997

Determinants of plasma platelet-activating factor acetylhydrolase: heritability and relationship to plasma lipoproteins.

Plasma platelet-activating factor acetylhydrolase (PAF-AH) is the enzyme that inactivates PAF (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine). We determined the relative contributions of genetic and environmental factors to variation in plasma PAF-AH activity in 240 individuals from 60 nuclear families. Regression of mean-offspring PAF-AH activity on the mid-parent value indicated that 62% of the variation in plasma PAF-AH activity was heritable. Spousal values were weakly negatively correlated, indicating that familial aggregation of PAF-AH activity is due to genetic rather than to environmental factors. Among normolipidemic individuals, plasma PAF-AH activity was strongly correlated with the plasma concentration of low density lipoprotein cholesterol (LDL-C), and treatment with lovastatin resulted in proportional decreases in plasma PAF-AH activity and LDL-C concentrations. To further elucidate the relationship between PAF-AH and plasma concentrations of LDL, plasma PAF-AH activity was measured in families with well-defined, monogenic disorders of LDL metabolism. Plasma PAF-AH activity cosegregated with plasma LDL-C concentrations in familial hypercholesterolemia, but not in familial hypobetalipoproteinemia. We speculate that the rate of removal of LDL from the circulation may determine the clearance rate of PAF-AH, thereby modulating the activity of PAF-AH in blood.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1997

[Impact of nitric oxide on endothelin gene expression in intrapulmonary arteries of chronic hypoxic rats].

OBJECTIVE: To investigate the impact of nitric oxide on endothelin-1 (ET-1) mRNA expression in pulmonary artery endothelial cells and pulmonary artery smooth muscle cells of chronic hypoxic rats. METHODS: In situ hybridization was performed on lung sections from 40 chronic hypoxic rats treated either with L-Arginine (L-Arg) or N omega-nitro-L-arginine methyl ester (L-NAME) by using cRNA probe for ET-1. RESULTS: Most intrapulmonary arteries had 1%-50% of the endothelial cells expressing ET-1 mRNA in both one-week and two-week hypoxic rats (75% +/- 3% and 71% +/- 6%, respectively), which was significantly inhibited by L-Arg but augmented by L-NAME administration. Most pulmonary artery smooth muscle cells showed no ET-1 mRNA signals in both one-week and two-week hypoxic rats (85% +/- 6% and 98% +/- 2%, respectively). However, L-NAME increased ET-1 mRNA expression in pulmonary artery smooth muscle cells of hypoxic rats. CONCLUSION: Nitric oxide inhibited ET gene expression in both pulmonary artery endothelial cells and smooth muscle cells of rats exposed to chronic hypoxia.

Animals↗

PubMed1996

Studies on protective mechanisms of four components of green tea polyphenols against lipid peroxidation in synaptosomes.

The comparison of the protective effects of four components of "green tea polyphenols' (GTP) - (-)-epigallocatechin gallate, EGCG; (-)-epicatechin gallate, ECG; (-)epigallocatechin, EGC; and (-)epicatechin, EC - against iron-induced lipid peroxidation in synaptosomes showed that: (1) the inhibitory effects of those compounds on TBA reactive materials from lipid peroxidation decreased in the order of EGCG > ECG > EGC > EC; (2) the scavenging effects of those compounds on lipid free radicals produced by lipid peroxidation could be classified as follows: ECG > EGCG > EC > EGC. Furthermore, we investigated the iron-chelating activity and the free radical scavenging activity of those compounds as their protective mechanisms against lipid peroxidation in synaptosomes. As for the iron-chelating activity, the ratio of EGC, EGCG, ECG or EC to iron(III) was 3:2, 2:1, 2:1 and 3:1, respectively. The hydroxyl radical (HO) scavenging activity of those compounds was investigated in a photolysis of the H2O2 system. It was found that their ability to scavenge hydroxyl radicals decreased in the order of ECG > EC > EGCG >> EGC. It was also found that they could scavenge lipid free radicals in the lecithin/lipoxidase system and their scavenging activity was classified as follows: ECG > EGCG >> EGC > EC. Moreover, we found that their antioxidant active positions were different from each other and the stability of the semiquinone free radicals produced by those compounds in NaOH solution decreased in the order of EGCG > ECG >> EC. The results indicated that the ability of those compounds to protect synaptosomes from the damage of lipid peroxidation initiated by Fe2+/Fe3+ was dependent not only on their iron-chelating activity and free-radical scavenging activity, but also on the stability of their semiquinone free radicals.

Animals↗

PubMed1996

Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation.

Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells. The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved. A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity. This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease.

Alzheimer Disease↗

PubMed1996

Preventive effect of Ginkgo biloba extract on apoptosis in rat cerebellar neuronal cells induced by hydroxyl radicals.

The ability of oxidative stress to induce apoptosis, and the effect of Ginkgo biloba extract (EGb761) on this induction were studied in primary cultured rat cerebellar neuronal cells. Cells were exposed to hydroxyl radicals by treating them with 20-50 microM hydrogen peroxide (H2O2) and 100 microM ferrous sulfate. Hydroxyl radical treatment fragmented the DNA in a manner typical of apoptosis cells, producing a ladder pattern of 200 base pair increments on 1% agarose gel electrophoresis. Pretreatment of cells with 100 micrograms/ml EGb reduced hydroxyl radical induced cells apoptosis (determined by flow cytometry) and DNA fragmentation. The results indicate that hydroxyl radicals induce apoptosis in rat cerebellar neuronal cells and this induction can be prevented by EGb.

Animals↗

PubMed1996

Human immunodeficiency virus protease ligand specificity conferred by residues outside of the active site cavity.

To gain greater understanding of the structural basis of human immunodeficiency virus (HIV) protease ligand specificity, we have crystallized and determined the structures of the HIV-1 protease (Val32Ile, Ile47Val, Val82Ile) triple mutant and simian immunodeficiency virus (SIV) protease in complex with SB203386, a tripeptide analogue inhibitor containing a C-terminal imidazole substituent as an amide bond isostere. SB203386 is a potent inhibitor of HIV-1 protease (Ki = 18 nM) but shows decreased inhibition of the HIV-1 protease (Val32Ile, Ile47Val, Val82Ile) triple mutant (Ki = 112 nM) and SIV protease (Ki = 960 nM). Although SB203386 binds in the active site cavity of the triple mutant in a similar fashion to its binding to the wild-type HIV-1 protease [Abdel-Meguid et al. (1994) Biochemistry 33, 11671], it binds to SIV protease in an unexpected mode showing two inhibitor molecules each binding to half of the active site. Comparison of these two structures and that of the wild-type HIV-1 protease bound to SB203386 reveals that HIV protease ligand specificity is imparted by residues outside of the catalytic pocket, which causes subtle changes in its shape. Furthermore, this work illustrates the importance of structural studies in order to understand the structure-activity relationship (SAR) between related enzymes.

Amino Acid Sequence↗

PubMed1996

Expression of the D-MEF2 transcription in the Drosophila brain suggests a role in neuronal cell differentiation.

D-MEF2 is a MADS domain transcription factor expressed in the cardiac, somatic, and visceral muscle cell lineages in the Drosophila embryo. Genetic studies have demonstrated that D-mef2 gene function is required for the proper differentiation of all three of these muscle types. We show that D-MEF2 is also expressed in a limited number of other cells types during development, including Kenyon cells present in the mushroom bodies of the Drosophila brain. This finding suggests a role for D-mef2 in neuron differentiation. To investigate D-mef2 expression in muscle and Kenyon cells, we assayed 26 kb of D-mef2 5'-flanking and intragenic DNA for regulatory sequences controlling the expression of the gene. Our results show that separable enhancer sequences direct D-mef2 gene expression in the myogenic and neuronal cell lineages. The identification of these regulatory DNAs provides a starting point for the analysis of transcriptional regulators controlling the cell-specific expression of D-mef2 and a means to address the function of D-mef2 in Kenyon cell differentiation.

Animals↗

PubMed1996

Scavenging effect of Chinonin on NO and oxygen free radicals and its protective effect on the myocardium from the injury of ischemia-reperfusion.

The scavenging effect of Chinonin on NO and oxygen free radicals and its protective effect on myocardium from the ischemia-reperfusion injury was studied with electron spin resonance (ESR) and chemiluminescence techniques. Chinonin can effectively inhibit the oxidative activity of ONOO-, (the IC50 = 7 x 10 (-5) mmol/L) and scavenge oxygen free radicals generated from the reaction of xanthine and xanthine oxidase (the IC50 = 2/5 x 10(-4) mmol/l). It is difficult to find another antioxidant which can scavenge so effectively both ONOO- and oxygen free radicals simultaneously. In the system of ischemia-reperfusion injury of myocardium, Chinonin can, in parallel, scavenge the NO and oxygen free radicals generated from the ischemia-reperfused myocardium, and decrease the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart and therefore protect the heart from ischemia-reperfusion injury. The protective effect of 0.1 mmol/l Chinonin is similar to that of 1500 U/ml SOD and catalase.

Animals↗

PubMed1996

Influence of purified apoprotein E on platelet activation induced by serotonin.

Serotonin induces platelet activation. Purified apoprotein E of 300 micrograms/ml prevented morphological alterations of blood platelets stimulated with serotonin (5 microM). Lower concentrated apoprotein E showed no such clear effects. These findings suggest that apoprotein E may liter atherosclerosis by suppressing agonist-induced platelet activation.

Apolipoproteins E↗

PubMed1996

Different adhesion types and active sensitivity of platelet subpopulations.

Two different adhesion patterns of blood platelets with different sensitivity to adenosine were demonstrated by means of reflection contrast microscopy with consecutive image analysis and cell affinity chromatography. High-performance liquid chromatography revealed that thrombin-induced serotonin release of adenosine-sensitive platelets was lower than that of adenosine-resistant cells. Our results indicate platelet heterogeneity and suggest that the platelets with lower adenosine sensitivity may be actively involved in the early interaction between platelets and injured endothelium.

Adenosine↗

PubMed1996

Changes in glycerophospholipid profile in experimental nephrotic syndrome.

We investigated changes in the glycerophospholipids in kidney tissue and its various intracellular fractions in rats with nephrotic syndrome induced by puromycin aminonucleoside. The ethanolamine plasmalogen, 1-O-alk-1'-enyl-2-acyl-GPE (EP), was increased in kidney tissue obtained from the puromycin-treated animals. A similar increase was found in the mitochondria and endoplasmic reticulum (microsomes) of this tissue. These increases were not found in the liver. Since platelet-activating factor (PAF) is known to be produced in increased amounts in inflammatory disorders, it is suggested that the higher plasmalogen found in rat kidneys during experimental nephrotic syndrome might be derived from increased levels of this autacoid. The increase in PAF may also result in the elevation of plasma PAF-acetylhydrolase (AH) activity observed in these animals.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1996

Oxidized low density lipoprotein inhibits platelet plasma membrane Ca(2+)-ATPase.

Oxidized low density lipoprotein (LDL) has been shown to enhance platelet activation. Since platelet activation is accompanied by an increase in cytosolic calcium, the effects of oxidized LDL on plasma membrane Ca(2+)-ATPase, plasma membrane fluidity and cytoplasmic calcium were studied in human platelets and purified platelet plasma membranes. Our results demonstrate that oxidized LDL, but not native LDL, inhibits the activity of Ca(2+)-ATPase in purified platelet plasma membranes (P < 0.01). Addition of the free radical scavenger alpha-tocopherol had no effect on the ability of oxidized LDL to inhibit the Ca(2+)-ATPase. An increased cytoplasmic calcium level in whole platelets was induced by oxidized LDL (P < 0.01), indicating that the plasma membrane Ca(2+)-extrusion pump may also be inhibited in vivo by oxidized LDL, although other mechanisms for the increase in cytoplasmic calcium are possible. Since no change in membrane fluidity was observed in platelet plasma membranes exposed to oxidized or native LDL as estimated by steady state trimethylammonium diphenylhexatriene (TMA-DPH) anisotropy, oxidized LDL does not affect the Ca(2+)-ATPase by grossly changing the membrane environment. The present results suggest that exposure of platelets to oxidized LDL causes inhibition of the plasma membrane Ca(2+)-ATPase which contributes to the observed increase in cytoplasmic calcium and increased sensitivity to agonists.

Blood Platelets↗

PubMed1996

RRR-alpha-tocopheryl succinate enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II expression by human MDA-MB-435 breast cancer cells.

The proliferation of MDA-MB-435 human breast cancer cells was inhibited by RRR-alpha-tocopheryl succinate (vitamin E succinate, VES). Conditioned media (CM) from VES growth-inhibited cells contained potent antiproliferative activity, part of which is contributed by transforming growth factor-beta (TGF-beta) isoforms. Antibody neutralization analysis, employing TGF-beta isoform-specific antibody reagents, showed that TGF-beta 1, -beta 2, and -beta 3 were present in the CM from VES-treated cells. Culturing MDA-MB-435 cells with VES did not alter the levels of constitutively expressed 2.4-kb TGF-beta 1, 3.0- and 4.0-kb TGF-beta 2, or 1.2- and 3.5-kb TGF-beta 3 mRNA transcripts. Inhibition of DNA synthesis by MDA-MB-435 cells was increased by combinations of suboptimal levels of VES and purified TGF-beta 1. VES-treated MDA-MB-435 cells exhibited enhanced binding of radiolabeled TGF-beta 1, and Western immunoblotting analyses showed that VES treatment enhanced TGF-beta type II receptor protein expression. TGF-beta type I receptor protein levels were not modified by VES treatments. Although the mRNA transcript for the 5.5-kb TGF-beta type II receptor was upregulated after four hours of treatment with VES, this treatment did not modify the 6.5-kb TGF-beta type I or the 6.5-kb TGF-beta type II receptor mRNAs. Results demonstrate that biologically active TGF-beta 1, -beta 2, -beta 3 and levels of TGF-beta type II receptor expressed by human breast cancer cells are enhanced by VES treatment.

Blotting, Western↗

PubMed1996

Role of lipoproteins in platelet activation.

Native low density lipoprotein influences platelets principally in a time- and dose-dependent manner. Oxidized low density lipoprotein activates platelets and promotes platelet adhesion. Certain parts of high density lipoprotein may decrease the risk of platelet activation. The calcium signaling pathway, protein kinase C pathway, and cytotoxic effect are probably involved in the platelet activation process.

Calcium↗