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Biomedical subjects

M Zhang

Publications and source records attributed to M Zhang.

At least 469 records · Page 26Linked to original sources
PubMed1999

Capillary electrochromatography with novel stationary phases: II. Studies of the retention behavior of nucleosides and bases on capillaries packed with octadecyl-sulfonated-silica microparticles.

An octadecyl-sulfonated silica (ODSS) stationary phase specially designed for performing capillary electrochromatography (CEC) at relatively strong electroosmotic flow (EOF) proved useful for the separations of some nucleosides and bases. The ODSS stationary phase is composed of a hydrophilic, negatively charged sublayer to which a nonpolar top layer containing octadecyl ligands is covalently attached. The charged sublayer contains sulfonic acid groups which ensure a relatively strong EOF. Due to the presence of permanently charged sulfonic acid groups in the sublayer, the hydrophilic nature of the sublayer and the hydrophobic character of the top octadecyl layer, retention and selectivity of charged and relatively polar nucleosides and bases on the ODSS stationary phase are based on electrostatic interaction, hydrophilic interaction, and reversed-phase mechanisms. This yielded for the ODSS stationary phase a unique selectivity towards the nucleosides and bases, thus allowing their rapid separation. To gain insight into the chromatographic behavior of nucleosides and bases on the ODSS stationary phase, the results were compared to those obtained on an octadecyl-silica (ODS) capillary under otherwise the same elution conditions. Due to the difference in the nature of the organic layers on the surface of the ODSS and ODS stationary phases, the elution order on both stationary phases differed significantly, and the ODSS capillary proved more suitable for the separation of the nucleosides and bases than the ODS capillary.

Base Pairing↗
PubMed1999

Enhancement of phosphorylation and transcriptional activity of the glucocorticoid receptor in human synovial fibroblasts by nimesulide, a preferential cyclooxygenase 2 inhibitor.

OBJECTIVE: To examine the effect of 2 nonsteroidal antiinflammatory drugs (NSAIDs), nimesulide (NIM), a preferential cyclooxygenase 2 (COX-2) inhibitor, and naproxen (NAP), on the functional parameters and transcriptional activity of the glucocorticoid receptor (GR) system in cultured human synovial fibroblasts (HSF). METHODS: HSF were incubated with NIM (0.3, 3, and 30 microg/ml), NAP (15, 30, and 90 microg/ml), and dexamethasone (DEX; 0.01, 0.1, and 1 microM) on a time- and dose-dependent basis. The numbers of GR binding sites per cell were determined by radioligand receptor assay. Total cellular, cytoplasmic, or nuclear GR protein was measured by Western analysis using a specific anti-human GR antibody. Phosphorylation of GR was determined by specific immunoprecipitation of protein extracts from 32P-orthophosphate-labeled HSF. Mitogen-activated protein kinase p44/42 (MAPK) phosphorylation was followed by Western analysis using a specific anti-phosphoMAPK antibody. Levels of activated nuclear GR capable of binding specifically to a 32P-labeled oligonucleotide harboring the glucocorticoid/hormone response element (GRE) were evaluated by gel electrophoretic mobility shift analysis. The effects of NIM and DEX on transcriptional activation of the mouse mammary tumor virus (MMTV) promoter was determined by transfecting HSF with MMTV-luciferase (reporter gene) constructs. RESULTS: NIM had no effect on the number of GR binding sites, in contrast to NAP and DEX. NIM and NAP did not influence cellular GR protein levels or nucleocytoplasmic shuttling, although DEX lowered GR messenger RNA and protein levels after 48 hours. NIM, but not NAP, markedly increased MAPK phosphorylation (suggesting an increase in MAPK cascade activity), GR phosphorylation, GR binding to GRE, and transcriptional activation of MMTV promoter through the GRE site in the promoter. CONCLUSION: This study is the first to report that the antiinflammatory effects of NIM, an NSAID, may be partly related to its activation of the GR system.

Blotting, Western↗
PubMed1999

Functional magnetic resonance imaging evidence for task-specific activation of developmentally abnormal visual association cortex.

Functional magnetic resonance imaging was performed on a 36-year-old woman with muscular dystrophy, intractable epilepsy, and bilateral temporo-occipital lissencephaly. We observed islands of task-specific activation in lissencephalic cortex homologous to visual association regions activated in normal subjects on the same visual confrontation naming task. This result suggests lissencephalic cortex may develop specific functional connections with other brain regions.

Adult↗
PubMed1999

MPTP-Induced pallidal lesions in rhesus monkeys.

Dopamine neurons in the substantia nigra of the midbrain are the primary neuronal population affected by 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP) toxicity, which produces the pathological and behavioral features of Parkinson's disease in nonhuman primates and man. We have identified another injury site in magnetic resonance imaging (MRI) brain scans in 13 of 37 rhesus monkeys taken 10-12 months after administration of this neurotoxin via the right carotid artery. Focal lesions, ranging in volume from 6.75 to 60 mm3 in the rostral globus pallidus region, were seen on the right side of the brain in these 13 animals in addition to the midbrain effects. While no significant differences were seen between globus pallidus lesioned and nonlesioned animals in the severity of MPTP-induced parkinsonian symptoms, the response to levodopa was muted in pallidal-lesioned animals. To confirm the role of neurotoxicity in producing the lesions, brain scans from an additional 12 monkeys were evaluated during the acute period following exposure to either MPTP (n = 6) or saline (n = 6). Focal lesions in the rostral globus pallidus were seen as early as 2-4 h following a carotid artery infusion in two of six MPTP recipients, but no evidence of injury was seen in saline recipients. The globus pallidus includes important components of the neural circuitry regulating motor functions. The present results indicate that in addition to midbrain dopamine neurons, a focal region of the rostral globus pallidus is selectively vulnerable to MPTP toxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1999

Dexamethasone-induced hypertrophy in rat neonatal cardiac myocytes involves an elevated L-type Ca(2+)current.

The mechanism responsible for dexamethasone-induced hypertrophy in infants has not been defined. In this study, we have investigated the role of L-type Ca(2+)currents in the development of dexamethasone-induced hypertrophy in rat neonatal cardiac myocytes. Using cytoplasmic membrane capacitance measurements, we have shown that the size of the cells treated with dexamethasone were larger than those of the control cells. In addition, treating the cells with 1 microM dexamethasone for 48 h increased L-type Ca(2+)current density significantly, without affecting the voltage-dependent activation and steady state inactivation of the current. The increase in current density was associated with an elevation of the mRNA transcript encoding the L-type Ca(2+)channel subunit alpha(1)C. Dexamethasone treatment also resulted in an increase in the peak amplitude of the intracellular Ca(2+)transient measured by fura-2/epifluorescence. Finally, we have demonstrated that the hypertrophic effect of dexamethasone, characterized by the ratio of protein content per cell, was blocked by the L-type specific antagonist, nifedipine. In conclusion, an elevation of L-type Ca(2+)current is involved in the process of dexamethasone-induced cardiac myocyte hypertrophy in neonatal rats.

Animals↗
PubMed1999

The effects of La(III) on the peroxidation of membrane lipids in wheat seedling leaves under osmotic stress.

The physiological effects of the rare earth ion La3+ on the peroxidation of membrane lipids in wheat (Triticum aestivum L.) seedling leaves under osmotic stress were determined. With the passage of time under osmotic stress, the inhibition ability of lanthanum ions to the relative membrane permeability and concentration of malondialdehyde, superoxide radicals, and hydrogen peroxide caused by osmotic stress increased substantially, but no changes were noted in ferrous and relative water content. It indicated that lanthanum ions could not retain the water content because of osmotic stress. However, La3+ appears to decrease the production of *OH by reducing the content of O2*- and H2O2 of Haber-Weiss and Fenton reactions, which efficiently alleviated peroxidation of membrane lipids under osmotic stress and, to some degree, protected the membrane from injury of free radicals. Thus, La3+ increased the tolerance ability of plant to osmotic stress, which could assure the function of membrane normal temporally after stressed.

Hydrogen Peroxide↗
PubMed1999

Tumor necrosis factor expression in arterial walls of diabetic rats.

Immunohistochemistry was used to detect tumor necrosis factor (TNF-alpha) expression in arterial wall of diabetic rats. It was found that endothelial cells were swollen and markedly proliferative in these vessels and accordingly TNF-alpha showed strong positive immunohistochemical reaction in endothelial cells or extracellular intimal matrix of such vessels, which might be caused by the expression and release of TNF-alpha from monocytes and arterial wall cells stimulated by AGEs. These findings suggested that increased TNF-alpha expression might be associated with vascular damage and remodeling in diabetes.

Animals↗
PubMed1999

CGRP immunohistochemistry in wound healing and dentin bridge formation following rat molar pulpotomy.

The aim of the present study was to investigate the neuropeptide CGRP in order to determine the effect on dentin bridge formation during the healing process after pulpotomy. First maxillary molars in 56-day-old Wistar rats (n=60) were used. The rats were killed for a neurohistopathological examination at 1, 3, 7, 14, and 28 days postoperatively. Neuronal changes in the residual pulp were studied using CGRP immunohistochemistry. By 1-3 days postoperatively, the CGRP-IR nerve fibers with abnormal beaded or knob-like structures were found to be more swollen than in the control and the leakage of a CGRP-IR-positive substance from the involved end of the nerve fibers was seen. At 7 days postoperatively, a vast number of newly sprouted CGRP-IR nerve fibers appeared in the residual pulp and some of them terminated in the differentiating odontoblast layer and the initial matrix layer of the dentin bridge. By 14-28 days, the nerve density had become progressively lower in the residual pulp. Regenerated axons also terminated in the odontoblast layer and the fibrous matrix layer of the calcified dentin bridge. These findings suggest that such sensory neuropeptides as CGRP may, therefore, play a role in dentin bridge formation in the rat molar.

Animals↗
PubMed1999

Effect of six steroidal saponins isolated from anemarrhenae rhizoma on platelet aggregation and hemolysis in human blood.

Six steroidal saponins were isolated from Anemarrhena asphodeloides Bunge (Liliaceae), a traditional chinese medicine, and named anemarrhenasaponin I (An-I), anemarrhenasaponin Ia (An-Ia), timosaponin B-I (TB-I), timosaponin B-II (TB-II), timosaponin B-III (TB-III), and timosaponin A-III (TA-III). The effects of these six compounds on platelet aggregation and hemolysis in human blood were studied. All these compounds provoked remarkable inhibiting effect on platelet aggregation, and activated partial thromboplastin times (APTT) are sensitive to the presence of these six compounds. Using an in vitro system, APTT was delayed with the increment of the concentrations of these six compounds. In these six compounds, only timosaponin A-III appeared a strong effect on hemolysis, and anemarrhenasaponin Ia had a slight effect on hemolysis, other had no effect on hemolysis. These results suggested that these steroidal saponins isolated from Anemarrhena asphodeloides Bunge (Liliaceae) might be used as a novel antithrombotic therapeutic agents in post-myocardial infarction.

Antithrombins↗
PubMed1999

Regulation of transforming growth factor-beta1 gene expression and cell proliferation in human hepatocellular carcinoma cells (PLC/PRF/5) by tamoxifen.

Hepatocellular carcinoma (HCC) is a common, potentially lethal tumor in human patients. Because the serum levels of transforming growth factor-beta1 (TGF-beta1) correlate with outcome in patients with HCC and because TGFbeta1 mRNA expression is increased in HCC tissues, it raises the possibility that TGF-beta1 may be of importance in the development, growth, and metastases of HCC. Tamoxifen has been used for the treatment of human HCC. However, clinical trials have produced conflicting results. To further delineate whether tamoxifen may be of benefit in altering the course of HCC, we documented the effects of 4-hydroxytamoxifen and 17beta-estradiol on TGF-beta1 mRNA and protein levels and cell proliferation in a human HCC cell line. PLC/PRF/5 cells were treated with carrier (controls), 4-hydroxytamoxifen, 17beta-estradiol, or TGF-beta1. 4-Hydroxytamoxifen and 17beta-estradiol decreased TGF-beta1 mRNA and protein levels in a time- and dose-dependent manner. TGF-beta1 significantly inhibited PLC/PRF/5 cell proliferation, whereas both 4-hydroxytamoxifen and 17beta-estradiol stimulated PLC/PRF/5 cell proliferation. The stimulatory effects of 4-hydroxytamoxifen on PLC/PRF/5 cell proliferation raise concerns regarding its use in the treatment of HCC in human patients and suggest that 4-hydroxytamoxifen may have no beneficial effects in some patients with HCC.

Carcinoma, Hepatocellular↗
PubMed1999

Effects of acute ethanol exposure on polyamine and gamma-aminobutyric acid metabolism in the regenerating liver.

Recently, it has been suggested that ethanol-induced inhibition of liver regeneration results from decreases in hepatic putrescine levels and/or increases in hepatic gamma-aminobutyric acid (GABA)ergic activity. Because putrescine can be metabolized by diamine (DAO) and monoamine (MAO) oxidases to GABA, we documented the effects of acute ethanol exposure on hepatic MAO or DAO activity following partial hepatectomy (PHx) in rats. We also documented the effects of ethanol on GABA transaminase (GABA-T), the enzyme responsible for GABA metabolism in the liver, and tissue putrescine and GABA levels. Adult, male Sprague-Dawley rats (200-250 g) were treated with either ethanol (3 g/kg) or equal volumes of saline by gastric gavage 1 h prior to a 70% PHx or sham surgery. Rats were then sacrificed (n = 5-7/group) at various times (0-72 h) post-PHx. Enzymatic activity and putrescine/GABA levels were determined by standard isotopic techniques and high-performance liquid chromatography respectively. Hepatic DAO activities in ethanol-treated rats were transiently higher than in saline-treated controls (30% increases at 6 h, p < 0.05). Hepatic MAO and GABA-T activities in acute ethanol-treated rats were essentially identical to saline-treated controls. Although hepatic putrescine levels were similar in ethanol- and saline-treated rats, hepatic GABA levels were approximately three times higher in ethanol-treated rats at 12 and 24 h post-PHx (p < 0.0001). In conclusion, the results of this study indicate that acute ethanol exposure has a limited effect on the enzymatic conversion of putrescine to GABA following partial hepatectomy in the liver. The results also indicate that increased GABAergic inhibition rather than decreased putrescine stimulation is more likely to play a role in ethanol-induced inhibition of hepatic regeneration.

4-Aminobutyrate Transaminase↗
PubMed1999

Expression and role of heat-shock protein 65 (HSP65) in macrophages during Trypanosoma cruzi infection: involvement of HSP65 in prevention of apoptosis of macrophages.

The 65-kDa heat-shock protein (HSP65) is thought to play a role in host defense against infections with various microbial pathogens and in autoimmune inflammatory disorders. We investigated the biological function and expression mechanism of HSP65 in macrophages of mice infected with Trypanosoma cruzi. BALB/c mice, which are susceptible to T. cruzi, showed high levels of parasitemia, and 80% of these mice died within 42 days after the infection, whereas resistant C57BL/6 or DBA/2 mice showed low levels of transient parasitemia and all survived. HSP65 expression was correlated with resistance to T. cruzi infection; HSP65 was more strongly expressed in macrophages of resistant C57BL/6 and DBA/2 mice than in macrophages of susceptible BALB/c mice. Immunodeficient BALB/c-nu/nu (nude) and C.B-17 scid/scid (SCID) mice were shown to be highly susceptible to this infection, and they did not express detectable levels of HSP65, suggesting that T cells play essential roles in the expression of HSP65 as well as in protective immunity against the infection. CD4(+) T cells, but not CD8(+) T cells or gammadelta T cells, were the cell population responsible for the induction of HSP65 expression in macrophages. Furthermore, depletion of asialo GM-1(+) NK cells made resistant C57BL/6 mice more susceptible to the infection, and HSP65 expression in their macrophages was abolished. Semiquantitative reverse transcription PCR analyses showed that both interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) mRNA levels in CD4(+) T cells became low when resistant C57BL/6 mice were depleted of NK cells, suggesting that NK cells contribute to functional differentiation of CD4(+) T cells and thereby affect the induction of HSP65 expression. To determine the function of HSP65, macrophages were treated in vitro with antisense oligonucleotide for HSP65 prior to inducing HSP65 with IFN-gamma plus TNF-alpha or T. cruzi infection. This treatment did not affect the production of nitric oxide following activation, but the treated macrophages became susceptible to apoptosis. These results indicate that HSP65 plays a role in preventing the apoptosis of macrophages and thereby contributes to host resistance against T. cruzi infection.

Animals↗
PubMed1999

DNA immunization with Plasmodium falciparum serine repeat antigen: regulation of humoral immune response by coinoculation of cytokine expression plasmid.

We immunized mice with plasmid expressing the 47-kDa amino-terminal domain of the Plasmodium falciparum serine repeat antigen (SERA) using gene gun and investigated humoral immune response to SERA antigen. Significant SERA-specific IgG was observed in BALB/c mice after immunization three times with SERA expression plasmid. Furthermore, these levels were increased by the coinoculation of cytokine (IFN-gamma, IL-4, GM-CSF, or IL-12) expression plasmid. In respect to the SERA-specific Ig subclasses, coinoculation of IFN-gamma, GM-CSF, or IL-12 expression plasmid increased the levels of SERA-specific IgG2a, and these were much higher than that in mice immunized with SERA expression plasmid alone. In contrast to the SERA-specific IgG2a, coinoculation of any cytokine expression plasmid did not change the levels of SERA-specific IgG1. These results indicate that cytokine expression plasmid enhances and regulates humoral immune response elicited by SERA DNA immunization.

Animals↗
PubMed1999

Comparative study of photophysical properties of isomeric tetrapyridyl- and tetra-(N-hexadecylpyridiniumyl) porphyrins.

Photophysical properties (absorption spectra, fluorescence spectra, lifetimes and quantum yields) were studied for the three isomers of tetrapyridylporphyrins (TPyPs) in CHCl3 and tetra-(N-hexadecylpyridiniumyl) porphyrins (TC16PyPs) in CHCl3, CH3OH and Triton X-100 micelle solution. While the ground-state and excited-state properties are very similar for the three isomers of neutral TPyP, significant differences exist among the isomers of amphiphilic TC16PyP. Amphiphilic porphyrins bearing hydrophilic pyridinium and hydrophobic long-chain alkyl groups are characterized by reduced fluorescence quantum yields, biexponential fluorescence decay, and appreciable aggregation in nonpolar solvents. The observed biexponential fluorescence decay of amphiphilic porphyrins can be interpreted in terms of mixing of the S1 and a close-lying CT state in which an electron is transferred from the porphyrin core to the electron-deficient pyridinium group.

Isomerism↗
PubMed1999

Lenacil degradation in the environment and its metabolism in the sugar beets.

14C-Lenacil photolysis and hydrolysis studies were conducted at 2 ppm in sterilized buffers at pH 5, 7, and 9 for up to 15 and 30 days, respectively. The degradation of (14)C-lenacil in three soils and in two sediments systems was monitored for up to 100 days. Residue level and metabolites were analyzed in sugar beets following the application of (14)C-lenacil at 4- and at 6-leaf stages at the rate of 204 g ai/ha and 321 g ai/ha, respectively. Lenacil was stable in the dark and at pH 5 and 7 under irradiation. At pH 9 under irradiation, the half-life (DT(50)) was 41 days. Lenacil DT(50) in three soils ranged from 81 to 150 days. The DT(50) in two sediments ranged from 32 to 105 days. In mature sugar beets, the total radioactive residue was 0.16 ppm in the tops and <0.03 ppm in the roots. The majority of lenacil metabolites identified were hydroxylated or oxidized products and their conjugates.

Carbon Radioisotopes↗
PubMed1999

Cloning and tissue expressional characterization of a full-length cDNA encoding human neuronal protein P17.3.

A full-length cDNA of 595 bp was isolated from a human fetal brain cDNA library. It contains an open reading frame encoding 153 amino acids, with an 18-bp 5'UTR and a 118-bp 3'UTR in which there is an atypical polyadenylation signal (ATTAAA). The calculated molecular weight of the deduced protein is 17.3 kU. The predicted isoelectric point is 4.89. On account of its high homology to mouse neuronal protein NP15.6 (81.2% identity), the deduced protein was named neuronal protein 17.3 (NP17.3). When its secondary structure was examined by the GGBSM program of PCGENE software, it was found that 32.6 and 15.0% of its amino acids are involved in forming alpha-helices and beta-sheets, respectively. Examined with the PESTFIND program, a typical PEST region found in rapidly degraded proteins was found between residue 48 and residue 68.

5' Untranslated Regions↗
PubMed1999

Solution structure of the extended neuronal nitric oxide synthase PDZ domain complexed with an associated peptide.

The PDZ domain of neuronal nitric oxide synthase (nNOS) functions as a scaffold for organizing the signal transduction complex of the enzyme. The NMR structure of a complex composed of the nNOS PDZ domain and an associated peptide suggests that a two-stranded beta-sheet C-terminal to the canonical PDZ domain may mediate its interaction with the PDZ domains of postsynaptic density-95 and alpha-syntrophin. The structure also provides the molecular basis of recognition of Asp-X-Val-COOH peptides by the nNOS PDZ domain. The role of the C-terminal extension in Asp-X-Val-COOH peptide binding is investigated. Additionally, NMR studies further show that the Asp-X-Val-COOH peptide and a C-terminal peptide from a novel cytosolic protein named CAPON bind to the same pocket of the nNOS PDZ domain.

Adaptor Proteins, Signal Transducing↗