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Biomedical subjects

H Wang

Publications and source records attributed to H Wang.

At least 1,711 records · Page 95Linked to original sources
PubMed1997

[The infrared spectra of alkyl hydrogen styrylphosphonates and their complexes with metals].

The infrared spectra in the range of 4000 approximately 650cm(-1) for alkyl hydrogen styrylphosphonates (HA (SP)), 2-ethylhexyl hydrogen 2-ethylhexylphosphonate and di-2-ethylhexyl hydrogen phosphate and their complexes with metals were recorded. The tested HA (SP) included n-octyl, 2-ethylhexyl, 1-methylheptyl and sec-alkyl (C11-13) hydrogen styrylphos- phonates. The metals studied were Fe ( III ), Cr ( III ), In ( III ), Nd ( III ), Cu ( II ), Co ( II ), Ni ( II ), Ca( II ) and Mg( II ). In the spectra of these organophosphorus compounds adsorption at approximately 1450cm(-1) is present only in HA (SP). The Spectra of HA (SP) show the broad absorption of hydrogen bonded OH at approximately 2200 and 2600cm(-1) ( vOH ). For each of the organophosphorus monoacids upon complexation with the metals excepting Ca and Mg, the vOH disappears and the v(P=O) shifts to a lower frequency , wthereas in the cases of Ca and Mg the OH, P=O and P--O-- absorption bands all become broader.

English Abstract↗
PubMed1997

The effect of cisapride in patients with reflux esophagitis: an ambulatory esophageal manometry/pH-metry study.

OBJECTIVES: The mechanisms responsible for the efficacy of cisapride in gastroesophageal reflux disease remain unclear. The current study was designed to test the hypothesis that cisapride decreases esophageal acid exposure by augmenting esophageal motility and improving acid clearance. METHODS: Eighteen patients with reflux esophagitis underwent combined 24-h ambulatory esophageal manometry/pH-metry at baseline and then again after 2 wk of cisapride therapy (10 mg q.i.d.). RESULTS: Esophageal acid exposure was significantly decreased during cisapride therapy (total percentage of time pH was < 4: 8.3 +/- 2.0% at baseline vs 3.8 +/- 0.6% on cisapride). This was not associated with significant changes in contraction amplitude or duration, peristaltic velocity, or the proportion of peristaltic contractions. The number of reflux episodes per hour was unchanged by cisapride therapy; however, cisapride significantly decreased the number of prolonged duration reflux episodes as well as the duration of the longest reflux episode. Although the relative proportion of peristaltic versus nonperistaltic contractions occurring during reflux episodes was unchanged by cisapride therapy, there was a significant increase in the mean number of contractions per minute (both peristaltic and nonperistaltic combined) occurring during reflux episodes. CONCLUSIONS: These data suggest that cisapride decreases esophageal acid exposure by improving esophageal clearance and that this occurs because of an increase in the number of esophageal contractions rather than by augmenting contraction amplitude or duration or the proportion of peristaltic sequences.

Adult↗
PubMed1997

Consecutive maintenance of human solitary and hereditary colorectal polyps in SCID mice.

Recently, the sequential changes from adenoma to adenocarcinoma have been well studied in human colorectal carcinogenesis. To study the precise clonal changes from colorectal polyps to cancer, we have established an experimental system to maintain human colorectal polyps in severe combined immunodeficient (SCID) mice that have been improved by the selective inbreeding of C.B17-scid/scid homozygous male and female showing undetectable serum IgG and IgM (< 1 microgram/ml). Two of two solitary polyps from two nonhereditary colon polyp patients, four of five colon polyps from two Peutz-Jeghers' syndrome patients and one polypoid lesion from a familial polyposis coli (FAP) patient grew very slowly but steadily, at approximately one-tenth the rate of their malignant form, (i.e., adenocarcinoma), in the improved SCID mice and were maintained for a long period (more than 2 years), over several mouse generations. However, two polyps from FAP and Peutz-Jeghers' syndrome patients could not be transplanted further because of microinfection at the transplanted site due to incomplete sterilization of original human tumors prior to surgical operation (endoscopic polypectomy). Transplanted colon polyps had a semitransparent, soft and sticky appearance, with cells containing large amounts of mucin. Malignant transformation of human colon polyp to adenocarcinoma has not been observed during the maintenance period (about 2 years) in SCID mice. In the consecutively maintained human colon polyps, however, K-ras mutations were detected at codon 12, while these mutations were not found in their original polyps in the patients.

Adenomatous Polyposis Coli↗
PubMed1997

The critical role of p38 MAP kinase in T cell HIV-1 replication.

BACKGROUND: Replication of HIV-1 in human T lymphocytes requires the activation of host cellular proteins. This study identifies p38 mitogen-activated protein kinase (MAPK) as one such kinase necessary for HIV-1 replication in T cells. MATERIALS AND METHODS: Primary human T lymphocytes were infected with the LAI strain of HIV-1 and Jurkat cells were infected with the RF strain of HIV-1. HIV replication was measured by reverse transcriptase activity. Cellular expression of endogenous p38 MAPK protein was analyzed using immunoprecipitation. Blockade of p38 MAPK expression was achieved using antisense oligonucleotides to p38 MAPK and the guanylhydrazone compound CNI-1493, an inhibitor of p38 MAPK activation. RESULTS: HIV-1 infection of both primary human T lymphocytes and a T cell line rapidly activated the cellular p38 MAPK pathway, which remained activated for the duration of the culture. Addition of phosphothioated antisense oligonucleotides to p38 MAPK specifically inhibited viral replication. Blockade of p38 MAPK activation by addition of CNI-1493 also inhibited HIV-1 viral replication of primary T lymphocytes in a dose- and time-dependent manner. Stimulation of p38 MAPK activation did not occur with the addition of heat-inactivated virus, suggesting that viral internalization, and not just membrane binding, is necessary for p38 MAPK activation. CONCLUSIONS: These results indicate that activation of the p38 MAPK cascade is critical for HIV-1 replication in primary T lymphocytes, and that blockade of this signal transduction pathway may be a novel therapeutic approach to the treatment of HIV-1 infection.

Blotting, Western↗
PubMed1997

An investigation of attitudes, beliefs and behaviour of leprosy patients, family members and PHC workers towards multidrug therapy in Yangzhou and Dongtai Districts of China.

To improve the operational efficiency of multidrug therapy (MDT) implementation in rural areas, an investigation into the attitudes, beliefs and behaviour of leprosy patients and their family members as well as primary health care (PHC) workers towards MDT was carried out in Yangzhou and Dongtai Districts of China. A sample of 370 leprosy patients, 594 family members and 730 PHC workers was interviewed or investigated individually using questionnaires. The results showed that: 1, the presently used MDT is acceptable to a wide range of patients although a small number of patients have various problems in their treatment; 2, the patients' habit in daily drug administration, their awareness of the risk of default and confidence in MDT have a positive influence in increasing drug compliance; and 3, the supervision and encouragement of family members to patients' treatment which is associated with their knowledge on MDT is also beneficial to patients' drug compliance. However, only half of the PHC workers had a basic knowledge of MDT and a desire to participate in MDT implementation, a finding which clearly calls for urgent attention and improvement. In order to ensure the effective implementation of MDT, there is a need to educate leprosy patients and their family members as well as PHC workers to establish the patients' correct awareness of MDT, obtain the family support and motivate the PHC workers.

Adult↗
PubMed1997

Macrophage-induced nitric oxide and prostanoid dependent relaxation of arterial smooth muscles.

We have studied mechanisms of vasodilation induced by supernatant fluid of rat macrophages (Mø), using an arterial bioassay preparation. The cells emigrated by an intraperitoneal injection of thioglycollate were isolated and cultured for 12 h in RPMI 1640 medium with and without 2.0 mM L-arginine. More than 98% of the isolated cells clearly demonstrated Wright's esterase staining and phagocytosis of acetylated low-density lipoprotein. The bioassay preparation was made of dog isolated femoral arteries with and without the endothelium. The supernatant of macrophages cultured in the L-arginine-free RPMI 1640 caused a significant reduction of the precontraction in the bioassay rings, being approximately 51.6-66.7% of sodium nitroprusside (SNP) induced maximum vasodilation in each ring. The supernatant of macrophages cultured in the RPMI 1640 containing 2.0 mM L-arginine produced a significantly smaller relaxation (approximately 32.3-33.3%). The Mø-induced vasodilation was significantly inhibited by the coculture of the macrophages with 1 microM dexamethasone, 10 microM cycloheximide, 50 microM N omega-nitro-L-arginine methyl ester (L-NAME), 10 microM indomethacin, or 10 microM aspirin. The L-NAME-induced inhibition was significantly reversed by an additional treatment with 100 microM L-arginine. The coculture with both L-NAME and indomethacin caused a reduction of the Mø-induced vasodilation (approximately 12.5-13.4%) similar to reductions produced by dexamethasone (approximately 10.8-12.1%) and cycloheximide (approximately 11.4-12.4%). Coculture with 10 micrograms/mL bacterial lipopolysaccharide caused a slight facilitation of the Mø-induced vasodilation (approximately 78.2-79.6%). These findings suggest that supernatant fluid of rat exuded macrophages cultured with low concentrations of L-arginine causes an endogenous nitric oxide (NO) and vasodilative prostaglandin dependent relaxation of arterial smooth muscles.

Animals↗
PubMed1997

Prevention of stroke with perindopril treatment in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: To determine the protective effects of perindopril treatment in the prevention of stroke and the relation between preventive effects and the histopathology of the brain and kidneys in male stroke-prone spontaneously hypertensive rats (SHRSP). DESIGN: Prospective animal study. INTERVENTIONS: Beginning at 6 weeks of age, SHRSP were treated with either distilled water (control) or perindopril for different periods (8, 12 or 24 weeks) and at different dosages (1 or 4 mg/kg per day). OUTCOME MEASURES: Regular determination of systolic blood pressure, heart rate and body weight until death; at necropsy, macroscopic and microscopic examinations of the brain and kidneys. RESULTS: Control SHRSP developed severe hypertension (up to 250 mm Hg) by 11 weeks of age and died of stroke within 14 weeks of age. Treatment with perindopril (4 mg/kg per day for 8 or 12 weeks or either 1 or 4 mg/kg per day for 24 weeks) attenuated the blood pressure rise and prevented stroke. In untreated SHRSP, the last blood pressure measurement before the first stroke sign was significantly higher than in SHRSP of the same age treated with perindopril. Withdrawal of the treatment resulted in a rise in blood pressure in all the treatment groups, to approximately 260 mm Hg within 4 weeks. Most of the rats treated for 8 or 12 weeks died within 10 weeks after withdrawal of treatment, whereas those treated for 24 weeks survived up to 43 weeks of age. Treatment also prevented damage to the brain and kidneys and reduced the severity of lesions in the brain and kidneys after treatment withdrawal. CONCLUSION: Treatment of SHRSP with perindopril prevents stroke through the suppression of blood pressure rise and prevention of tissue damage in the brain and the kidneys. Longer treatment decreased the rate of mortality due to stroke after the withdrawal of treatment as well as the severity of lesions in the brain and kidneys.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

The selective recognition of antibody IgY for digestive system cancers.

Biological methods for cancer therapies are very important. A small and efficient target carrier is the key component for anti-cancer drugs. In our laboratory, the antibody IgY was extracted from egg yolk of a SPF hen. The SPF hen was immunized with an antigene of P110 protein which was purified from human stomach cancer MGC-803 cells. Results indicated that the antibody IgY can specifically recognize gastrointestinal system cancers. It may become an important carrier for antitumorigenic drugs.

Adenocarcinoma↗
PubMed1997

Kinetic analysis of furosine and pentosidine in CAPD patients.

Advanced glycation end products (AGEs) have been noted in the peritoneal tissue of continuous ambulatory peritoneal dialysis (CAPD) patients, and this may cause an increase in membrane permeability. In vivo and in vitro kinetic analysis was carried out on furosine and pentosidine, early and late glycation products. Plasma furosine and pentosidine were measured by HPLC in patients with renal dysfunction with or without diabetes mellitus (DM) and dialysate pentosidine and furosine in CAPD patients. Only those dialysis patients without residual renal function were used in this study. Plasma furosine was remarkably high in DM, hemodialysis (HD), and CAPD patients. Plasma pentosidine appeared to depend on renal function and was not influenced by diabetic condition. Plasma pentosidine was significantly higher in CAPD than HD patients. A weak positive correlation was noted between dialysate and plasma furosine and pentosidine, indicating the main source of furosine and pentosidine in PD effluent to be plasma. Serial dialysate sampling showed furosine and pentosidine to increase linearly. Mean dialysate/plasma (D/P) of furosine and pentosidine were 0.043 and 0.012, respectively. Protein-bound product size and in situ formation of furosine in the peritoneal cavity would be the reason for these differences in D/P. In situ formation of early glycation products in the peritoneal cavity may be concluded to take place in CAPD patients, and high plasma pentosidine may lead to its accumulation in tissue, resulting, possibly, in pathological change.

Adult↗
PubMed1997

Tumor necrosis factor is a brain damaging cytokine in cerebral ischemia.

Two contrasting roles, one beneficial and the injurious, have been proposed for tumor necrosis factor (TNF) in the pathogenesis of cerebral ischemia. Reported here are results obtained in a standard model of permanent focal cortical ischemia in rats, in which the volume of cerebral infarction is measured after permanent occlusion of the middle cerebral artery. Administration of neutralizing anti-rat TNF antibodies (P114) into the brain cortex significantly reduced ischemic brain damage (85% reduced infarct volume as compared with preimmune-treated controls). Similar results were achieved by systemic administration of CNI-1493, a recently described tetravalent guanylhydrazone compound, which effectively inhibited endogenous brain TNF synthesis and conferred significant protection against the development of cerebral infarction (80% reduced infarct volume as compared with vehicle controls treated 1 h postischemia with 10 mg/kg). P114 anti-TNF and CNI-1493 were each cerebroprotective when given within a clinically relevant time window for up to 2 h after the onset of ischemia. These findings establish an important, pathophysiological role of TNF in mediating the progression of ischemic brain damage, and suggest that inhibiting TNF with CNI-1493 may be beneficial in the future treatment of stroke.

Animals↗
PubMed1997

Identification of an HMG-like protein involved in regulation of Na+/H+ exchanger expression.

In this study we characterized regulation of the Na+/H+ exchanger promoter in several tissue types. A conserved poly (dA:dT) region was important in regulation of the promoter. Nuclear extracts from rat myocardium and from mouse proximal tubule cells protected the poly (dA:dT) region of the NHE1 promoter. A protein from nuclear extracts also bound to the poly (dA:dT) element in gel mobility shift binding assays. The binding was specific and was removed by mutations in the poly (dA:dT) region. Characterization of the binding to the poly (dA:dT) region in gel mobility shift assays showed that it was reduced by high concentrations of the divalent cations Mg++ and Mn++. The inhibition by divalent cations was reduced by decreasing the pH of the binding assay. N-terminal sequencing of the poly (dA:dT) binding protein showed that it was a member of the HMG (high mobility group) family of nuclear proteins which are important in cell growth and proliferation. The results are the first direct detection of a protein that regulates the NHE1 promoter.

3T3 Cells↗
PubMed1997

Research on the mechanism of endothelin inflammatory effects on human mesangial cells.

OBJECTIVE: To investigate the mechanism of endothelin (ET) inflammatory effects on human mesangial cells (HMC). METHODS: The following experiments were performed on cultured HMC after ET-1 stimulation: (1) the expression of tumor necrosis factor-alpha (TNF alpha), interleukin-1 beta (IL-1 beta), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelin-1 (ET-1) itself messenger ribonucleic acid (mRNA) was determined by Northern Blot analysis; (2) the TNF alpha concentration was tested with radioimmunoassay; the IL-1 activity was assayed by the enhancement of thymocyte proliferation in response to mitogen; the surface expression of ICAM-1 and VCAM-1 was measured with cell enzyme linked immunoadsorbent assay (ELISA) analysis. RESULTS: ET-1 (10(-7) mol/L) induced the following changes on HMC: (1) up-regulation of the expression of TNF alpha mRNA and protein; (2) up-regulation of the expression of ICAM-1 and VCAM-1 mRNA and protein; (3) up-regulation of the expression of ET-1 itself mRNA. However, the expression of IL-1 mRNA and protein was not changed. CONCLUSIONS: ET-1 can stimulate HMC to produce TNF alpha, ICAM-1 and VCAM-1, and thereby induce inflammatory effects. ET-1 can also stimulate HMC to up-regulate the expression of ET-1 itself, so as to amplify inflammatory effects. So, ET-1 is actually an inflammatory mediator and may play an important role in the pathogenesis of glomerulonephritis.

Cells, Cultured↗
PubMed1997

Postoperative immunotherapy for patients with hepatocarcinoma using tumor-infiltrating lymphocytes.

OBJECTIVE: To explore a more effective immunotherapy for cancer by studying tumor-infiltrating lymphocytes (TIL) of patients with hepatocarcinoma. METHODS: TIL isolated from freshly resected tumors of 12 patients with hepatocarcinomas were activated, expanded and cultured in vitro by incubation with interleukin-2, and then infused to the patients. The TIL cytotoxicity and phenotype were determined by MTT and immunohistochemical ABC methods. RESULTS: The average weight and number of cells of the tumor tissues for culture of TIL were 4.8 g and 5.8 x 10(7) respectively, and the median expansion time was 31.8 days in vitro. The maximal expansion achieved 1000 fold, and the mean amplification rate was 198.5 fold. Lymphokine-activated killer cell culture supernatant could stimulate TIL growth. Ten of 12 patients received immunotherapy of TIL. The number of cells infused reached 4 x 10(8)-1.1 x 10(10). In 3 cases of our series, TIL infusions were done through a drug pump with a catheter embedded in the hepatic artery. Eight patients whose primary hepatic carcinomas were resected completely were followed up for 16 months with only one case (12.5%) having recurrence. The recurrence rates of them at 6 and 12 months after tumor resection were remarkably lower than those of the patients who did not receive TIL infusion (19.4% and 41.6%, respectively). One patient whose tumor was not able to be removed received TIL infusion twice and local alcohol injection several times. He has been alive for 9 months. CONCLUSIONS: TIL isolated from the tumors of patients with hepatocarcinoma can be activated and expanded in vitro. It demonstrated remarkably cytotoxic activity against tumor targets. TIL infusion is an effective immunotherapy for patients with hepatocarcinoma in reducing recurrence after operation.

Adult↗
PubMed1997

[Polymerase chain reaction in the detection of patients infected by Chlamydia trachomatis after treatment].

OBJECTIVE: To investigate the value of polymerase chain reaction (PCR) for follow-up patients infected by Chlamydia trachomatis. METHODS: Follow-up specimens were collected from 30 patients. Chlamydia trachomatis positive were detected by PCR and direct fluorescence assay test (DFA) in the 30 patients before therapy. 15 patients were treated with minocycline (100 mg twice daily) for 10 days, and 15 patients were treated with 1.0 g of azithromycine as a single oral dose. RESULTS: After 1-2 weeks of antimicrobial therapy, all patients had negative DFA for Chlamydia trachomatis, but 9 had positive Chlamydia trachomatis DNA as detected by PCR. CONCLUSIONS: The 9 specimens were not confirmed to livae viable organisms of Chlamydia trachomatis. The debris of nonviable Chlamydia trachomatis DNA was excluded from urinogenital tract at about one month.

Adult↗
PubMed1997

[The effects of ethinyl estradiol on glucose metabolism in postmenopausal women].

OBJECTIVE: To study the effects of ethinyl estradiol on glucose metabolism in postmenopausal women. METHODS: Postmenopausal women were randomized as nine cases (group A) receiving 0.025 mg ethinyl estradiol (EE) and ten cases (group B) receiving EE 0.05 mg for three months. The oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT) were performed before and after EE respectively. The levels of plasma glucose, insulin were measured and the area under curve (AUC) and insulin sensitivity indexes (SI) were calculated. RESULTS: Both two dosages of EE administration effectively decreased the levels of fasting plasma glucose and insulin and significantly reduced the AUC of insulin. SI was increased significantly. There were no significant differences in AUC of glucose before and after treatment in group A, but in group B the AUC of glucose significantly increased after treatment. CONCLUSIONS: EE may significantly reduce the levels of fasting plasma glucose and insulin concentrations and abate the insulin resistance in postmenopausal women; 0.05 mg EE possibly causes the deterioration in glucose tolerance, suggesting the use of 0.025 mg EE as an appropriate dosage.

Blood Glucose↗