Search PubMed⌕ Search

Biomedical subjects

C Tang

Publications and source records attributed to C Tang.

At least 127 records · Page 7Linked to original sources
PubMed1997

Hypothalamic galanin gene expression and peptide levels in relation to circulating insulin: possible role in energy balance.

The peptide galanin (GAL) exists in dense concentrations within the medial hypothalamus and is synthesized in a population of neurons within the paraventricular nucleus (PVN). This peptide has been linked to energy homeostasis through its behavioral, metabolic and endocrine actions, including pancreatic insulin secretion. This investigation examined whether circulating insulin, in turn, has impact on hypothalamic GAL production, GAL mRNA and peptide concentrations in the hypothalamus. Streptozotocin (STZ)-induced diabetic rats, compared to control subjects, were tested with or without insulin replacement. After STZ treatment, the rats exhibited hyperglycemia, increased food and water intake, and decreased weight gain compared to controls. These changes were reversed by daily, subcutaneous injections of insulin. Measurements of GAL mRNA, via solution hybridization/nuclease protection assay, revealed a 6-fold elevation after STZ treatment compared to controls, accompanied by a similar rise in GAL peptide levels. This increase in GAL message and peptide was reversible by insulin and was detected in a mediodorsal hypothalamic (MDH) dissection which contains the PVN. It was not seen in a dissection of the mediobasal hypothalamus that includes the GAL-synthesizing neurons of the arcuate nucleus. Measurements of GAL in discrete hypothalamic nuclei of STZ diabetic rats showed a 100% increase in peptide concentrations (p < 0.05) in the PVN that was insulin responsive. Other hypothalamic areas examined failed to exhibit any change in peptide. These findings are consistent with other evidence indicating an inverse association, between circulating insulin and GAL message or peptide in the PVN, that may have physiological relevance in the control of energy balance.

Animals↗
PubMed1997

[Protein kinase C involved in the protecttve effect of anoxic preconditioning on vascular smooth muscle cells].

It has been known that anoxic preconditioning (APC) has protective effects not only on cardiomyocyte, but also on vasculature. However, the effects of APC on vascular smooth muscle cells (VSMC) is unknown. On the model of anoxia/reoxygenation (A/R) injury of rabbit VSMC, the effect of APC was observed. It was found that APC could increase the survival rate of VSMC after A/R injury, lower the leakage of lactate dehydrogenase (LDH) and protein from cells, and attenuate peroxidation injury and calcium overload of VSMC. The results also showed that PMA, an activator of protein kinase C (PKC), could mimic, but H7 or polymyxin B (inhibitors of PKC) could abolish the above protective effect of APC. It is suggested that the protective effect of APC on VSMC during A/R injury might be due to the activation of PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

[The effect of NO-like relaxing factor on vascular reactivity in tourniquet shock rat].

This work was done on rat tourniquet shock (ToS) model. It was found that reactivity of isolated perfused aortic ring to noradrenaline decreased, while cGMP content of the aortic tissue increased. These changes could be potentiated by perfusion with L-arginine (NO-precursor). On the other side, when the aortic ring was perfused with L-NNA (NO-synthesis inhibitor) or methylene blue (soluble cGMPase inhibitor), the changes could be attenuated. The effect of these drugs are independent of the presence of vascular endothelium. The results suggest that non-endothelium-derived NO-like relaxing factor may be one of the factors causing low vascular reactivity of the ToS animals.

Animals↗
PubMed1997

[The effect of endurance training and exhaustive exercise on metallothionein in rats].

To understand physiological role of metallothionein (MT) during exercise, MT levels in liver, brain, heart, lung, blood vessel, skeletal muscle and serum were observed in rats. The results showed that the levels of MT were decreased by 13-34% in lung, liver, heart and skeletal muscle of rats trained by swimming for 10 weeks and were increased by 21%-75% in skeletal muscle, heart, brain, lung and liver of rats after exhaustive swimming respectively, compared with normal control rats. (P < 0.05 and P < 0.01). But the levels of MT in blood vessel and serum were not changed in two groups of rats by swimming for 10 weeks and acute exhaustive swimming (P > 0.05). It is suggested that the different changes of MT levels under physical training and acute exhaustive exercise may be of importance in protection against oxygen free radicals.

Animals↗
PubMed1997

[Effect of L-arg and LNNA on contractile-relaxant response and cGMP level of thoracic aorta with endothelial injury in rat].

In this study, we have observed the effect of L-arginine(L-arg) and omega N-nitro-L-arginine (LNNA) on the contractile-relaxation response and the cGMP level in arterial strip using the model of rat thoracic aorta with endothelial injury and neointimal formation. Organ chamber experiment and radioimmunoassay showed that, the 3rd day after endothelial injury of the rat thoracic aorta, their endothelium-dependent relaxtion response caused by L-arg, as well as endothelium dependent contractile response caused by LNNA were impaired seriously, basic cGMP reduced obviously, and the change of cGMP caused by L-Arg and LNNA was impaired markedly. On the 10th day after injury a pronounced recovery was noticed, and 21st day, the situation was further improved, but could not restore completely. The results indicate that the production of EDRF in the rat thoracic aorta after endothelial injury may be impaired seriously, and could not recover completely for a longer time.

Animals↗
PubMed1997

Changes of plasma tPA and PAI activities in patients with diabetic retinopathy.

PURPOSE: To investigate the relationship between the diabetic retinopathy (DR) and the activity of plasma tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI). METHODS: tPA and PAI activities were measured by chromatogenous substrate assay in plasma samples obtained from patients with and without diabetic retinopathy (n = 42). Retinopathy was determined by stereoscopic color fundus photographs graded according to a modification of Chinese National Fundus Disease Academic Meeting. And 21 sex-age matched normal people were as controls. This study was in a masked fashion. RESULTS: 1. tPA activity was lower and PAI activity was higher in all of diabetic patients than those in controls (P < 0.001); 2. tPA activity was lower and PAI activity was higher in proliferative DR (PDR) subgroup than those in non-DR (NDR) and background-DR (BDR) subgroups (P < 0.01, respectively); 3. there was no significant difference between BDR and NDR subgroups (P > 0.05); and 4. the results also suggested that the severity of DR and duration of diabetes were correlated negatively with the activity of tPA but positively with that of PAI (r = -0.564, -0.416, 0.671, 0.442; P < 0.01, respectively). CONCLUSIONS: Reduced plasma tPA activity and enhanced PAI activity in diabetic patients, probably is one of the causes for thromboembolic diseases and are related to the severity of DR and duration of diabetes. Therefore, the change and imbalance between activities of plasma tPA and PAI might play a role in developing and progression of DR.

Adolescent↗
PubMed1997

IL-5 production by bronchoalveolar lavage and peripheral blood mononuclear cells in asthma and atopy.

There is increasing evidence to suggest a key role for interleukin-5 (IL-5) in the regulation of airway eosinophilia in asthma. We compared the capacity for IL-5 production in atopic asthmatic, nonatopic asthmatic, atopic nonasthmatic and normal subjects, and evaluated the usefulness of peripheral blood cells for reflecting airway cell reactivity. Bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBMC) from 12 atopic and 10 nonatopic asthmatics (without inhaled steroid therapy), 9 atopic nonasthmatics, and 10 normal controls were cultured with or without house dust mite (HDM, 10 microg x mL-1) stimulation. CD4+ T-cell activation, IL-5 and interferon-gamma (IFN-gamma) production in the cultures were assessed. Both for BAL and PBMC samples, atopic and nonatopic asthmatic subjects showed comparable spontaneous production of IL-5, which was significantly higher than that either for atopic nonasthmatics or normal controls (p<0.05 or p<0.01). There was a significant correlation between the percentage of eosinophils in BAL and spontaneous production of IL-5 by BAL cells in both asthmatic groups (p<0.05 or p<0.01). Both these parameters were also associated with asthmatic airway narrowing as denoted by a negative relationship with baseline forced expiratory volume in one second (FEV1) as percentage predicted (p<0.05 and p<0.01, respectively). In contrast, IFN-gamma production by unstimulated BAL cells from normal controls was higher than that for BAL cell cultures of nonatopic asthmatic subjects (p<0.05). Following HDM stimulation, both atopic groups had comparable positive responses in terms of CD4+ T-cell activation, but there was relatively greater IL-5 production in asthmatic PBMC (p<0.05) and, in particular, BAL cell cultures (p<0.01). These findings suggest that elevated IL-5 production is a common feature of BAL cells and PBMC in atopic and nonatopic asthma. In addition, atopic asthmatics show greater IL-5 production in response to specific allergen compared with atopic nonasthmatics, an effect most marked in BAL cells compared to PBMC. Hence, peripheral blood mononuclear cells can reflect cytokine immunoreactivity of airway cells, but lack local cellular interactions, which limits their usage in asthma research.

Adult↗
PubMed1997

Atrial diagnostics in a tiered therapy implantable defibrillator.

Dual chamber sensing has been proposed in implantable defibrillators as an additional diagnostic modality for enhanced differentiation of ventricular and supraventricular tachycardias. A patient with different rates of wide QRS complex tachycardias is described in whom a tiered therapy implantable defibrillator with atrial sensing capability was implanted. Atrial diagnostic data in this patient enabled definitive diagnosis of his ventricular tachycardias and guided management decisions of his arrhythmia.

Defibrillators, Implantable↗
PubMed1997

Inhibition of platelet-derived growth factor-mediated signal transduction and tumor growth by N-[4-(trifluoromethyl)-phenyl]5-methylisoxazole-4-carboxamide.

Many reports have cited coexpression of platelet-derived growth factor (PDGF) and its receptors by tumor cells or cells supporting tumor growth, suggesting both autocrine and paracrine mechanisms for PDGF-mediated tumor growth. We found that a small organic molecule, N-[4-(trifluoromethyl)phenyl] 5-methylisoxazole-4-carboxamide (SU101, leflunomide), inhibited PDGF-mediated signaling events, including receptor tyrosine phosphorylation, DNA synthesis, cell cycle progression, and cell proliferation. SU101 inhibited PDGF-stimulated tyrosine phosphorylation of PDGF receptor (PDGFR) beta in C6 (rat glioma) and NIH3T3 cells engineered to overexpress human PDGFRbeta (3T3-PDGFRbeta). SU101 blocked both PDGF- and epidermal growth factor (EGF)-stimulated DNA synthesis. Previously, this compound was shown to inhibit pyrimidine biosynthesis by interfering with the enzymatic activity of dihydroorotate dehydrogenase. In the current study, EGF-stimulated DNA synthesis was restored by the addition of saturating quantities of uridine, whereas PDGF-induced DNA synthesis was not, suggesting that the compound demonstrated some selectivity for the PDGFR pathway that was independent of pyrimidine biosynthesis. Selectivity was further demonstrated by the ability of the compound to block the entry of PDGF-stimulated cells into the S phase of the cell cycle, without affecting cell cycle progression of EGF-stimulated cells. In cell growth assays, SU101 selectively inhibited the growth of PDGFRbeta-expressing cell lines more efficiently than it inhibited the growth of PDGFRbeta-negative cell lines. SU101 inhibited the s.c., i.p., and intracerebral growth of a panel of cell lines including cells from glioma, ovarian, and prostate origin. In contrast, SU101 failed to inhibit the in vitro or s.c. growth of A431 and KB tumor cells, both of which express EGF receptor but not PDGFRbeta. SU101 also inhibited the growth of D1B and L1210 (murine leukemia) cells in syngeneic immunocompetent mice, without causing adverse effects on the immune response of the animals. In an i.p. model of tumor growth in syngeneic immunocompetent mice, SU101 prevented tumor growth and induced long-term survivors in animals implanted with 7TD1 (murine B-cell hybridoma) tumor cells. Because PDGFRbeta was detected on most of the tumor cell lines in which in vivo growth was inhibited by SU101, these data suggest that SU101 is an effective inhibitor of PDGF-driven tumor growth in vivo.

3T3 Cells↗
PubMed1997

[The protective effect of captopril on the ischemic myocardium in dogs through coronary sinus retroperfusion].

The protective effect of coronary sinus retroperfusion of Captopril on the ischemic myocardium was observed in dogs with acute myocardial infarction (AMI). The results showed that the infarction size and the level of coronary sinus plasma endothelin (ET) and manodialdenyde (MDA) were smaller and lower when Captopril was administered by coronary sinus retroperfusion than that by systemic intravenous injection. These results suggest that (1) Captopril can be distributed adequately in the local ischemic myocardial zones when administered by coronary sinus retroperfusion in the presence of coronary artery occlusion, (2) Captopril can more effectively protect ischemic myocardium by inhibition of the ET release and against the oxygen free radicals in ischemic myocardial area when used by coronary sinus retroperfusion.

Animals↗
PubMed1997

[Effects of subretinal fluid containing proteins with different molecular weights on the proliferative vitreoretinopathy].

The stimulating effects of subretinal fluid (SRF) containing different molecular weight proteins which were isolated by fast performance liquid chromatography (FPLC) and ultrafiltration on the proliferative vitreoretinopathy (PVR) were investigated. The results showed that (1) the PVR was induced by 10-30 kD proteins injecting vitreously, and the forming duration of PVR was about two weeks; (2) the location of inducing PVR was mainly on medullary ray area in the rabbit eye; (3) In the SRF there were growth factors which were mainly those proteins with molecular weight between 10 kD and 30 kD.

Adult↗
PubMed1996

The stalk region of the Escherichia coli ATP synthase. Tyrosine 205 of the gamma subunit is in the interface between the F1 and F0 parts and can interact with both the epsilon and c oligomer.

The soluble portion of the Escherichia coli F1F0 ATP synthase (ECF1) and E. coli F1F0 ATP synthase (ECF1F0) have been isolated from a novel mutant gammaY205C. ECF1 isolated from this mutant had an ATPase activity 3.5-fold higher than that of wild-type enzyme and could be activated further by maleimide modification of the introduced cysteine. This effect was not seen in ECF1F0. The mutation partly disrupts the F1 to F0 interaction, as indicated by a reduced efficiency of proton pumping. ECF1 containing the mutation gammaY205C was bound to the membrane-bound portion of the E. coli F1F0 ATP synthase (ECF0) isolated from mutants cA39C, cQ42C, cP43C, and cD44C to reconstitute hybrid enzymes. Cu2+ treatment or reaction with 5,5'-dithio-bis(2-nitro-benzoic acid) induced disulfide bond formation between the Cys at gamma position 205 and a Cys residue at positions 42, 43, or 44 in the c subunit but not at position 39. Using Cu2+ treatment, this covalent cross-linking was obtained in yields as high as 95% in the hybrid ECF1 gammaY205C/cQ42C and in ECF1F0 isolated from the double mutant of the same composition. The covalent linkage of the gamma to a c subunit had little effect on ATPase activity. However, ATP hydrolysis-linked proton translocation was lost, by modification of both gamma Cys-205 and c Cys-42 by bulky reagents such as 5,5'-dithio-bis (2-nitro-benzoic acid) or benzophenone-4-maleimide. In both ECF1 and ECF1F0 containing a Cys at gamma 205 and a Cys in the epsilon subunit (at position 38 or 43), cross-linking of the gamma to the epsilon subunit was induced in high yield by Cu2+. No cross-linking was observed in hybrid enzymes in which the Cys was at position 10, 65, or 108 of the epsilon subunit. Cross-linking of gamma to epsilon had only a minimal effect on ATP hydrolysis. The reactivity of the Cys at gamma 205 showed a nucleotide dependence of reactivity to maleimides in both ECF1 and ECF1F0, which was lost in ECF1 when the epsilon subunit was removed. Our results show that there is close interaction of the gamma and epsilon subunits for the full-length of the stalk region in ECF1F0. We argue that this interaction controls the coupling between nucleotide binding sites and the proton channel in ECF1F0.

Adenylyl Imidodiphosphate↗
PubMed1996

Emergence of preferred structures in a simple model of protein folding.

Protein structures in nature often exhibit a high degree of regularity (for example, secondary structure and tertiary symmetries) that is absent from random compact conformations. With the use of a simple lattice model of protein folding, it was demonstrated that structural regularities are related to high "designability" and evolutionary stability. The designability of each compact structure is measured by the number of sequences that can design the structure-that is, sequences that possess the structure as their nondegenerate ground state. Compact structures differ markedly in terms of their designability; highly designable structures emerge with a number of associated sequences much larger than the average. These highly designable structures possess "proteinlike" secondary structure and even tertiary symmetries. In addition, they are thermodynamically more stable than other structures. These results suggest that protein structures are selected in nature because they are readily designed and stable against mutations, and that such a selection simultaneously leads to thermodynamic stability.

Amino Acid Sequence↗
PubMed1996

Flk-1 as a target for tumor growth inhibition.

A number of growth factor receptor tyrosine kinases have been implicated in angiogenesis, including epidermal growth factor receptor, fibroblast growth factor receptor, platelet-derived growth factor receptor, Flk-1/KDR, Flt-1, Tie-1, and Tek/Tie-2. Flk-1/KDR, a receptor for vascular endothelial growth factor (VEGF), is expressed exclusively in endothelial cells. Using dominant-negative methods, Flk-1 was shown to play a role in angiogenesis and the growth of a variety of tumor types. Because of this, a drug discovery effort was established to identify Flk-1 kinase inhibitors. For initial screening, an ELISA in, a 96-well format was used to measure VEGF-induced Flk-1 tyrosine phosphorylation in whole cells. Compounds that inhibited ligand-induced receptor autophosphorylation were confirmed by antiphosphotyrosine immunoblotting. Inhibition of VEGF-stimulated DNA synthesis in human endothelial cells was also assessed. Inhibitors were further evaluated for their effects on vessel formation using the chorioallantoic membrane assay. Using these methods, antiangiogenesis compounds that inhibit Flk-1 tyrosine kinase activity, endothelial cell mitogenesis, and blood vessel formation in the chorioallantoic membrane assay have been found.

3T3 Cells↗
PubMed1996

Amygdala activity at encoding correlated with long-term, free recall of emotional information.

Positron emission tomography of cerebral glucose metabolism in adult human subjects was used to investigate amygdaloid complex (AC) activity associated with the storage of long-term memory for emotionally arousing events. Subjects viewed two videos (one in each of two separate positron emission tomography sessions, separated by 3-7 days) consisting either of 12 emotionally arousing film clips ("E" film session) or of 12 relatively emotionally neutral film clips ("N" film session), and rated their emotional reaction to each film clip immediately after viewing it. Three weeks after the second session, memory for the videos was assessed in a free recall test. As expected, the subjects' average emotional reaction to the E films was higher than that for the N films. In addition, the subjects recalled significantly more E films than N films. Glucose metabolic rate of the right AC while viewing the E films was highly correlated with the number of E films recalled. AC activity was not significantly correlated with the number of N films recalled. The findings support the view derived from both animal and human investigations that the AC is selectively involved with the formation of enhanced long-term memory associated with emotionally arousing events.

Adult↗
PubMed1996

Characterization of the interface between gamma and epsilon subunits of Escherichia coli F1-ATPase.

The interaction faces of the gamma and epsilon subunits in the Escherichia coli F1-ATPase have been explored by a combination of cross-linking and chemical modification experiments using several mutant epsilon subunits as follows: epsilonS10C, epsilonH38C, epsilonT43C, epsilonS65C, epsilonS108C, and epsilonM138C, along with a mutant of the gamma subunit, gammaT106C. The replacement of Ser-10 by a Cys or Met-138 by a Cys reduced the inhibition of ECF1 by the epsilon subunit, while the mutation S65C increased this inhibitory effect. Modification of the Cys at position 10 with N-ethylmaleimide or fluoroscein maleimide further reduced the binding affinity of, and the maximal inhibition by, the epsilon subunit. Similar chemical modification of the Cys at position 43 of the epsilon subunit (in the mutant epsilonT43C) and a Cys at position 106 of the gamma subunit (gammaT106C) also affected the inhibition of ECF1 by the epsilon subunit. The various epsilon subunit mutants were reacted with TFPAM3, and the site(s) of cross-linking within the ECF1 complex was determined. Previous studies have shown cross-linking from the Cys at positions 10 and 38 with the gamma subunit and from a Cys at position 108 to an alpha subunit (Aggeler, R., Chicas-Cruz, K., Cai, S. X., Keana, J. F. W., and Capaldi, R. A. (1992) Biochemistry 31, 2956-2961; Aggeler, R., Weinreich, F., and Capaldi, R. A. (1995) Biochim. Biophys. Acta 1230, 62-68). Here, cross-linking was found from a Cys at position 43 to the gamma subunit and from the Cys at position 138 to a beta subunit. The site of cross-linking from Cys-10 of epsilon to the gamma subunit was localized by peptide mapping to a region of the gamma subunit between residues 222 and 242. Cross-linking from a Cys at position 38 and at position 43 was with the C-terminal part of the gamma subunit, between residues 202 and 286. ECF1 treated with trypsin at pH 7.0 still binds purified epsilon subunit, while enzyme treated with the protease at pH 8.0 does not. This identifies sites around residue 70 and/or between 202 and 212 of the gamma subunit as involved in epsilon subunit binding.

Amino Acid Sequence↗
PubMed1996

The significance of heregulin in breast cancer tumor progression and drug resistance.

The erbB-2 receptor plays an important role in the prognosis of breast cancer and is expressed at high levels in nearly 30% of tumors in breast cancer patients. While evidence accumulates to support the relationship between erbB-2 overexpression and poor overall survival in human breast cancer, understanding of the biological consequence(s) of erbB-2 overexpression remains elusive. The discovery of heregulin has allowed us to identify a number of related but distinct biological endpoints which appear responsive to signal transduction through the erbB-2/4 receptor. These endpoints of growth, invasiveness, and differentiation have clear implications for the emergence, maintenance, and/or control of malignancy, and represent established endpoints in the assessment of malignant progression in human breast cancer. Preliminary studies in vitro have shown that heregulin induces a biphasic growth effect on cells with erbB-2 overexpression. Interestingly, we observed that expression of heregulin correlates with a more aggressive/invasive, vimentin-positive phenotype in breast cancer cells lines. Therefore, we have postulated that heregulin is involved in breast cancer tumor progression. We have shown that heregulin induces in vitro chemoinvasion and chemotaxis of breast cancer cells as well as growth in an anchorage dependent and independent manner. Interestingly, a heregulin neutralizing antibody inhibits chemotaxis and results in cell growth inhibition and blockade of the invasive phenotype. Strikingly, genetically engineered cells which constitutively express heregulin demonstrate critical phenotypic changes that are associated with a more aggressive phenotype. Specifically, these cells are no longer dependent on estrogen for growth and are resistant to tamoxifen in vitro and in vivo, and moreover these cells metastasize to lymph nodes in athymic nude mice. These tumors appear to have lost bcl-2 expression as compared with the control tumors. In addition, presumably by activation/regulation of topoisomerase II, the heregulin-transfected cells become exquisitely sensitive to doxorubicin and VP-16. Clearly, mechanistic aspects of the erbB-2/4 and heregulin interaction need to be understood from a therapeutic standpoint which could provide additional insights into synergistic treatments for certain patients, or improve treatment regimens for a large number of women. The study of heregulin and its co-expression with erbB-2/4 receptor and the assessment of its involvement in the progression from the in situ stage of breast tumors to the invasive one will additionally increase the relevance of heregulin as a prognostic/diagnostic factor. We believe that our studies provide new insights into breast cancer diagnosis, prognosis, and treatment.

Breast Neoplasms↗