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Biomedical subjects

C Tang

Publications and source records attributed to C Tang.

At least 91 records · Page 5Linked to original sources
PubMed1998

Randomized trial of the effect of supplementation on the cognitive function of older people with subnormal cobalamin levels.

BACKGROUND: Low serum cobalamin levels are often found in apparently normal older subjects. A major worry of leaving cobalamin deficiency untreated is that it may lead to subtle deterioration in cognitive function. OBJECTIVES: To investigate the effect of supplementation on the cognitive function of older people with cobalamin deficiency by a randomized trial. METHODS: Fifty Chinese subjects more than 60 years old with serum cobalamin level < 120 pmol/l were randomized into supplement and control groups. Fasting serum methylmalonic acid levels (MMA) were measured. A battery of neuropsychological tests was administered. The supplement group received intramuscular cyanocobalamin injections, while the control group received no intervention. They were followed up at around 4 months. RESULTS: 78% of the subjects had raised MMA, indicating metabolic cobalamin deficiency. Supplemented subjects improved in performance IQ, but the amount of improvement was not significantly more than that of control subjects. Moreover, the supplement group fared worse than the control group at follow-up in some motor function scores. Three out of seven demented subjects had improvement in Mini-Mental State Examination scores, but there was no consistent improvement in other neuropsychological scores. CONCLUSIONS: This study suggested that cobalamin deficiency did not invariably cause cognitive impairment in older people. There remain the possibilities that cobalamin deficiency causes cognitive impairment or exacerbates coexisting dementia in some older people.

Aged↗
PubMed1998

Differential regulation of allergen-specific T(H2)- but not T(H1)-type responses by alveolar macrophages in atopic asthma.

BACKGROUND AND OBJECTIVE: Previous studies have suggested that quantitative differences in TH2-type cytokine responses in the airways are of particular importance in the pathogenesis of asthma. In this study we investigated whether alveolar macrophages (AMs) and peripheral blood monocytes (PMNs) are able to significantly influence the profiles of allergen-induced TH1 (IFN-gamma) and TH2 (IL-4 and IL-5) cytokine production by CD4+ T cells in atopic asthmatic subjects versus atopic nonasthmatic subjects and nonatopic normal subjects. METHODS: Peripheral blood CD4+ T cells were cultured alone or cocultured with either PMNs or AMs with allergen stimulation in the 3 groups. RESULTS: Although allergen stimulation did not change TH1 or TH2 cytokine responses in cultures of CD4+ T cells alone, the addition of PMNs to the cultures induced a significant increase in production of IL-4, IL-5, and IFN-gamma (P < .01 or P < .001) in atopic asthmatic subjects and atopic nonasthmatic subjects. However, PMNs induced a significant increase for IFN-gamma (P < .05) only in normal subjects. AMs from atopic asthmatic subjects significantly enhanced production of all 3 cytokines (P < .01 or P < .001), whereas the AMs from atopic nonasthmatic subjects significantly increased only production of IL-4 (P < .01) and IFN-gamma (P < .05) but not IL-5. Furthermore, IL-4 (P = .066) and IL-5 (P < .01) production in allergen-stimulated AM-CD4+ cell cocultures was higher in atopic asthmatic subjects but significantly lower in atopic nonasthmatic subjects (P < .05) as compared with the PMN-cocultures. For IFN-gamma, no difference was found between the AM and PMN cocultures in either atopic group. Allergen-stimulated IL-5 production in coculture with both AMs and PMNs inversely correlated with both baseline FEV1 percent predicted and PD20 methacholine in atopic asthmatic subjects (P < .05, P < .01, or P < .001). CONCLUSION: These data suggest that AMs from atopic asthmatic subjects but not atopic nonasthmatic subjects, play a significant role in airway pathogenic immunity through enhancing TH2-type cytokine production.

Adolescent↗
PubMed1998

Role of the Ped gene and apoptosis genes in control of preimplantation development.

PURPOSE: The properties of the mouse Ped gene and the genes that mediate apoptosis in mediating preimplantation embryonic survival were reviewed. METHODS: Preimplantation mouse oocytes and embryos were evaluated microscopically and biochemically for rate of development, degree of fragmentation, and gene expression to correlate these characteristics with embryo mortality, Biochemical assays included PCR for DNA analysis, RT-PCR for mRNA analysis, immuno-PCR for protein analysis, and TUNEL assay for assessment of apoptosis. RESULTS: Using the mouse as a model system we have identified a gene that controls the rate of development, the Ped gene. The Ped gene product is a class Ib major histocompatibility complex protein called the Qa-2 antigen. Research to understand the molecular mechanisms of Ped gene action and to identify the human homologue of the Ped gene is under way. We have also shown using the mouse model, that fragmented embryos show the morphological and biochemical characteristics of apoptosis. Genes in the two major gene families that regulate apoptosis, the caspase and Bcl-2 families, are expressed in mouse oocytes and preimplantation embryos. CONCLUSIONS: Preimplantation embryonic survival depends on two major morphological parameters: rate of development and degree of fragmentation. A fast rate of development and a low degree of fragmentation lead to a better chance of producing live offspring. Both rate of development and degree of fragmentation are genetically controlled, the former by the Ped gene and the latter most likely by genes that mediate apoptosis. It seems probable that regulation of apoptosis will prove to be a major mechanism that mediates oocyte and preimplantation embryonic survival.

Animals↗
PubMed1998

Industrial hygiene aspects of a sampling survey at a bleached-kraft pulp mill in British Columbia.

To validate exposure estimates used to investigate correlations between exposure and cancer risk, 1678 personal measurements were collected for 46 job titles during 73 day shifts at a bleached-kraft pulp mill. Measurements included shift-long average and short-term exposures to carbon monoxide, chlorine dioxide (ClO2), and hydrogen sulfide; and shift-long average exposures to calcium oxide and wood dust (WD). Overall results indicate low levels of exposure with a few noteworthy exceptions. Although ClO2 was the exclusive bleaching agent, 77 area samples indicated that chlorine (Cl2), not ClO2 was present in all areas apart from the chemical preparation area (chem-prep) and during a pulp spill. The highest shift-long exposures to Cl2 were measured in the chip yard and are attributed to uncontrolled stack emissions. Finally, WD samples collected from several laborers significantly exceeded regulatory limits, with the highest exposures measured in the steam and recovery area. For short-term exposures to ClO2 in chem-prep, 12 of 17 data-logging electro-chemical sensor sample results showed at least one peak that exceeded the short-term exposure limit of 0.3 ppm. The use of data-logging equipment quantified short-term exposures that previously had been characterized only anecdotally. The peaks were correlated with tasks and upset conditions and, given their transient nature, these exceedances could not have been detected using shift-long average-based sampling devices. Since the respiratory effects of significant short-term exposures to irritant gases such as Cl2 and ClO2 are well-documented, data-logging instruments are necessary to characterize exposures in the pulp and paper industry.

Air Pollutants, Occupational↗
PubMed1998

The mysterious case of persistent malocclusion.

We report an unusual case of malocclusion following a history of apparently blunt trauma. No maxillary or mandibular fractures were identified. The malocclusion persisted for several days. Finally computed tomography was performed, which revealed a foreign body in the infratemporal fossa. A 4-cm pencil was extracted from the patient's right temporomandibular joint.

Adolescent↗
PubMed1998

Role of endothelin in thrombolysis in rat abdominal aorta.

The endothelium of blood vessels is of great importance in maintaining blood fluidity and modulating thrombogenesis. Endothelin (ET) participates in thrombogenesis and its role in the pathogenesis of heart diseases such as acute myocardinal infarction has been proved, but little is known about the effect of ET on thrombolysis. Using a model of thrombosis in rat abdominal aorta induced by direct current-ferric trichloride, we found that the plasma ET level was 3.7 times the baseline after lysing the thrombus with urokinase (250,000 U/kg) while 5 micrograms/kg of exogenous ET prolonged the time of thrombolysis to 115% of baseline control. Plasma ET level was six times the baseline level. Incubation of a rat aortic strip in vitro with taurine (20 mmol/L) had no effect on baseline ET release, but taurine prohibited the stimulation of thrombin and A23187 of ET release in a dose-dependent way. Plasma ET decreased between 17 and 40% after injection of taurine, which also decreased by 45% the time of lysis of thrombus. From the above data it might be concluded that ET inhibits thrombolysis and that the abnormally increasing plasma ET can be attenuated by taurine, which is beneficial to thrombolysis.

Animals↗
PubMed1998

Expression of somatostatin receptors in human pancreatic tumor.

Somatostatin (SST) and its analogues are candidates for use as endocrine agents in the treatment of pancreatic neoplasm. To determine whether the status of SST receptors in the human pancreatic tumors differs from that in the tumor-free pancreata of the human and whether pancreatic adenocarcinoma expresses the same subgroup of SST receptors as found in gastrinomas, this study visualized and characterized SST receptors in human control pancreata (n = 10) as well as pancreatic cancers (n = 12) and gastrinomas (n = 8) with storage phosphor autoradiography. Both pancreatic adenocarcinoma and gastrinoma expressed specific SST receptors. The binding capacity (Bmax, 35.4 +/- 7.6 fmol/mg protein) and the affinity (Kd, 0.32 +/- 0.27 nM) of SST receptors in gastrinomas were significantly higher than in pancreatic cancers (Bmax, 15 +/- 2.5 fmol/mg protein; Kd, 2.16 +/- 0.4 nM). No specific SST receptors were detected in the human control pancreata. Octreotide showed similarly high potencies of inhibition of 125I-SST-28 binding as SST-28 in gastrinomas. Unlike gastrinomas, little competitive binding of 125I-SST-28 was found with octreotide in pancreatic cancers. In conclusion, compared with the control pancreas, an up-regulation of SST receptors was present in both pancreatic cancer and gastrinoma. The subgroup of SST receptors in pancreatic cancers differs from that in gastrinomas.

Adenocarcinoma↗
PubMed1998

Phosphorylation of beta-adrenergic receptor leads to its redistribution in rat heart during sepsis.

The role of receptor phosphorylation on the redistribution of beta-adrenergic receptors (beta-ARs) in rat hearts during different phases of sepsis was investigated. Sepsis was induced by cecal ligation and puncture (CLP). Changes in the distribution of beta-ARs in the sarcolemmal and light vesicle fractions were studied using (-)-[4,6-propyl-3H]dihydroalprenolol ([3H]DHA). Phosphorylation of beta-ARs was studied by perfusing hearts with [32P]H3PO4 followed by identification of the phosphorylated beta-ARs with immunoprecipitation using anti-beta 1-AR antibody. The results show that septic rat hearts exhibit an initial hypercardiodynamic (9 h after CLP; early sepsis) and a subsequent hypocardiodynamic (18 h after CLP; late sepsis) state. [3H]DHA binding studies show that, during early sepsis, the maximum binding capacity (Bmax) was increased by 26% in sarcolemma but was decreased by 30% in light vesicles, whereas, during late sepsis, the Bmax was decreased by 39% in sarcolemma but increased by 31% in light vesicles. These data indicate that beta-ARs in the rat heart were externalized from light vesicles to sarcolemma during early sepsis but were internalized from surface membranes to intracellular sites during late sepsis. The immunoprecipitation studies reveal that the externalization of beta-ARs during early sepsis was coupled with a concomitant decrease (-28.5 to -30.6%, P < 0.01) in the receptor phosphorylation, whereas the internalization of beta-ARs during late sepsis was accompanied by a simultaneous increase (30.3 to 33.8%, P < 0.01) in the receptor phosphorylation. Because the phosphorylation/dephosphorylation of beta 1-ARs regulate their functional coupling and may reflect their subcellular distribution, it is suggested that the increase in receptor phosphorylation seen in late sepsis leads to the receptor internalization observed in late sepsis; similarly, externalization of (dephosphorylated) receptors in early sepsis may give rise to the apparent decrease in sarcolemmal receptor phosphorylation observed during this interval.

Adenosine Triphosphate↗
PubMed1998

Alveolar macrophages from atopic asthmatics, but not atopic nonasthmatics, enhance interleukin-5 production by CD4+ T cells.

Recent studies have demonstrated that different antigen-presenting cell (APC)-related factors in the microenvironment of a T cell may determine its profile and quantity of cytokine expression and production. We have therefore examined the effects of alveolar macrophages and peripheral blood monocytes on interleukin (IL)-5 production by peripheral blood CD4+ T cells from atopic people with asthma (AA), atopic people without asthma (AN), and nonatopic normal subjects (N). In response to allergen stimulation, IL-5 production was significantly enhanced by the addition of monocytes to CD4+ cell cultures in AA and AN patients (p < 0.05 and 0.01, respectively), but not in N subjects. In mitogen-stimulated CD4+ cell plus monocyte cocultures, there was a small increase in IL-5 production in all three groups (p < 0.05 for AN). In contrast, the addition of alveolar macrophages to parallel cultures significantly amplified IL-5 production only in AA patients (p < 0.05 or 0.01). Furthermore, IL-5 production by CD4+ cells in alveolar macrophage cocultures, stimulated by allergen or mitogen, was higher than that in monocyte cocultures in AA patients (p < 0.05). Conversely, in AN and N subjects, the IL-5 values for alveolar macrophage cocultures were lower than those for peripheral blood monocytes. In blocking studies, antibodies against IL-1alpha, IL-1beta, IL-6, or tumor necrosis factor-alpha differentially suppressed macrophage-enhanced IL-5 production (p < 0.05 for IL-1beta and IL-6) and expression of the activation marker CD25 (p < 0.05 for IL-1alpha and IL-6) by allergen-stimulated CD4+ cells in AA patients. These observations suggest that alveolar macrophages influence the quantity of IL-5 production by T cells in the airways and, as a consequence, the development of asthma in atopic individuals.

Adult↗
PubMed1998

[Activation of CD4 T lymphocyte and release of interleukin-5 in airway from patients with atopic asthmatics].

OBJECTIVE: To evaluate the action of CD4T cell and release of interleukin-5 in airway from patients with atopic asthma by the allergen-specific stimulation. METHODS: Twelve atopic asthmatics (AA), 9 atopic non-asthmatics (AN), and 10 normal controls(N) underwent whole-lung inhalation challenge with house dust mite allergen (HDM) extract. The Levels of CD4CD25T lymphocytes, eosinophils(EOS), interleukin-5 (IL-5) and eosinophil cationic protein (ECP) in bronchoalveolar lavage (BAL) and peripheral blood mononuclear cells (PBMC) were investigated with and without HDM challenge. RESULTS: AA differed from AN in having late airway reactions (LAR) after HDM inhalation (P < 0.01), which was correlated with an percentage of BAL eosinophils, CD4CD25T cell IL-5 production and ECP release. CONCLUSION: These findings suggest that the activation of CD4T lymphocytes is correlated with both asthmatic and atopic status. The allergen-specific stimulation is believed to play a major role in CD4 T cell activation in atopic asthma. IL-5 is selective cytokine for EOS activation and modulating local eosinophil recruitment and activation in airway.

Adult↗
PubMed1998

[CD4+ T cell activation and IL-5 production in atopic and nonatopic asthmatics].

OBJECTIVE: To understand the reasons and roles of CD4+ T cell activation and IL-5 production in atopic and asthmatic patients. METHOD: Bronchoalveolar lavage(BAL) cells and peripheral blood mononuclear cells (PBMC) from 12 atopic and 10 nonatopic asthmatics, 9 atopic nonasthmatics, and 10 normal controls were cultured with or without house dust mite(HDM), CD4+ T cell activation, and IL-5 production were assessed. RESULT: The percentage of CD4+, CD25+ in unstimulated PBMC cultures were not significantly different in the four groups, but it increased following HDM stimulation in both PBMC and BAL cultures in two atopic groups(P < 0.01). The percentage of CD4+, CD25+ in unstimulated BAL cell culture increased in two asthmatic groups (P < 0.05, P < 0.01). The levels of spontaneous IL-5 released from both BALF cells and PBMC in two asthmatic groups were higher than those in AN and N (P < 0.05, P < 0.01). A significant elevation in IL-5 release following HDM stimulation in PBMC and BALF cells was observed in the both asthmatic and atopic groups; but the value in AA was higher than that in NAA, and it was also higher in BALF cells than in PBMC. CONCLUSION: The allergen stimulation is important reasons for CD4+ T cell activation and IL-5 production in atopics. CD4+ T cell activation and IL-5 production are common feature in atopic and nonatopic asthma, it correlates with both asthmatic and atopic status.

Adult↗
PubMed1998

Induction of sensitivity to doxorubicin and etoposide by transfection of MCF-7 breast cancer cells with heregulin beta-2.

HER2 (erbB-2) proto-oncogene amplification and/or overexpression correlate with poor prognosis in many malignancies. The precise biological role of this oncogenic signaling pathway (which also involves the HER4 gene) in breast cancer is unclear. One property conferred by this oncogene relates to response to drug therapy. Clinical studies support an association between HER2 overexpression and resistance to alkylating agents (cisplatinum and cyclophosphamide). Data from the Cancer and Leukemia Group B 8869/8541 study indicate enhanced dose responsiveness to doxorubicin (Adriamycin) in patients who overexpress the HER2 receptor. Heregulin beta-2, a naturally occurring ligand that activates the HER2 receptor by inducing its heterodimerization with the HER4 receptor, has recently been cloned. The ability of this ligand to phosphorylate the HER2 receptor exogenously allows us to study the effect of HER2 activation on cancer cell behavior. To study the relationship between chemotherapy response and activation of HER2, MCF-7 cells expressing biologically active heregulin were assessed for response to doxorubicin and etoposide, both of which are topoisomerase IIalpha (topo IIalpha) inhibitors. Several clones show markedly increased sensitivity to these drugs. In addition, the same wild-type MCF-7 cells transfected with heregulin beta-2 under the control of an inducible promoter also show this dose-response relationship to doxorubicin after the expression of heregulin beta-2 is activated by zinc. The modulation of topo IIalpha was studied in the cell lines transfected with heregulin. topo IIalpha mRNA and protein (total protein and enzymatic decatenating activity) were found to be up-regulated in heregulin beta-2-transfected cells. Moreover, topo IIalpha promoter activity was also modestly increased in heregulin beta-2-transfected cells. Because up-regulation of topo IIalpha in vitro and in clinical specimens is associated with increased response to doxorubicin (presumptively by an increase in drug substrate), this may be the mechanism of the increased sensitivity to doxorubicin seen in heregulin beta-2-transfected cells. This implies that activation of HER2 or one of the other members of the receptor family may increase sensitivity to doxorubicin by up-regulation of topo IIalpha. This finding suggests the use of receptor/ligand expression to direct patient-specific therapeutic choices (e.g., doxorubicin versus alkylator-based regimens) and the use of biological agents (such as heregulin) in combination with certain chemotherapeutic agents to enhance response to treatment in breast cancer patients.

Antibiotics, Antineoplastic↗
PubMed1997

Regional cerebral blood flow during the Wisconsin Card Sort Test in schizotypal personality disorder.

Regional cerebral blood flow (rCBF) was measured by single photon emission computed tomography in 10 patients with schizotypal personality disorder (SPD) and nine age- and sex-matched normal volunteers. Subjects performed both the Wisconsin Card Sort Test (WCST) and a control task, the Symbol Matching Test (SMT). Four-way analyses of variance were performed to assess relative rCBF of the prefrontal cortex and of the medial temporal region. Normal volunteers showed more marked activation in the precentral gyrus, while SPD patients showed greater activation in the middle frontal gyrus. Relative flow in the left prefrontal cortex was correlated with better WCST performance in normal volunteers. SPD patients, however, showed no such correlations in the left prefrontal cortex, but demonstrated correlations of good and bad performance with CBF in the right middle and inferior frontal gyrus, respectively. Thus, at least some SPD patients demonstrate abnormal patterns of prefrontal activation, perhaps as a compensation for dysfunction in other regions.

Adult↗
PubMed1997

Epidermal growth factor and betacellulin mediate signal transduction through co-expressed ErbB2 and ErbB3 receptors.

Interleukin-3 (IL-3)-dependent murine 32D cells do not detectably express epidermal growth factor receptors (EGFRs) and do not proliferate in response to EGF, heregulin (HRG) or other known EGF-like ligands. Here, we report that EGF specifically binds to and can be crosslinked to 32D transfectants co-expressing ErbB2 and ErbB3 (32D.E2/E3), but not to transfectants expressing either ErbB2 or ErbB3 individually. [125I]EGF-crosslinked species detected in 32D. E2/E3 cells were displaced by HRG and betacellulin (BTC) but not by other EGF-like ligands that were analyzed. EGF, BTC and HRG also induced receptor tyrosine phosphorylation, activation of downstream signaling molecules and proliferation of 32D.E2/E3 cells. 32D transfectants were also generated which expressed an ErbB3-EGFR chimera alone (32D.E3-E1) or in combination with ErbB2 (32D. E2/E3-E1). While HRG stimulation of 32D.E3-E1 cells resulted in DNA synthesis and receptor phosphorylation, EGF and BTC were inactive. However, EGF and BTC were as effective as HRG in mediating signaling when ErbB2 was co-expressed with the chimera in the 32D.E2/E3-E1 transfectant. These results provide evidence that ErbB2/ErbB3 binding sites for EGF and BTC are formed by a previously undescribed mechanism that requires co-expression of two distinct receptors. Additional data utilizing MDA MB134 human breast carcinoma cells, which naturally express ErbB2 and ErbB3 in the absence of EGFRs, supported the results obtained employing 32D cells and suggest that EGF and BTC may contribute to the progression of carcinomas that co-express ErbB2 and ErbB3.

Animals↗
PubMed1997

Structures of the tyrosine kinase domain of fibroblast growth factor receptor in complex with inhibitors.

A new class of protein tyrosine kinase inhibitors was identified that is based on an oxindole core (indolinones). Two compounds from this class inhibited the kinase activity of fibroblast growth factor receptor 1 (FGFR1) and showed differential specificity toward other receptor tyrosine kinases. Crystal structures of the tyrosine kinase domain of FGFR1 in complex with the two compounds were determined. The oxindole occupies the site in which the adenine of adenosine triphosphate binds, whereas the moieties that extend from the oxindole contact residues in the hinge region between the two kinase lobes. The more specific inhibitor of FGFR1 induces a conformational change in the nucleotide-binding loop. This structural information will facilitate the design of new inhibitors for use in the treatment of cancer and other diseases in which cell signaling by tyrosine kinases plays a crucial role in disease pathogenesis.

3T3 Cells↗