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Biomedical subjects

C Han

Publications and source records attributed to C Han.

At least 127 records · Page 7Linked to original sources

Serologic association between human papillomavirus type 16 infection and esophageal cancer in Shaanxi Province, China.

BACKGROUND: The existence of large geographic variations in the prevalence of esophageal cancer in some countries, such as China, indicates that environmental risk factors may be important in the development of this disease. Some studies have implicated genital-mucosal strains of human papillomaviruses (HPVs) in the etiology of this cancer. PURPOSE: We conducted a case-control study in Shaanxi Province, China, an area with a population at high risk for esophageal cancer, to assess the association of this disease with infection by HPV type 16 (HPV16), the most common cancer-associated genital-mucosal HPV type. METHODS: Ninety individuals with esophageal cancer and 121 cancer-free control subjects were identified among the patients in two hospitals in Xi'an, Shaanxi Province. The control subjects were matched to the case patients on the basis of age and sex. Blood specimens were drawn from all study subjects, and serum was isolated by routine methods. The presence of HPV16 antibodies in serum samples was determined by use of an enzyme-linked immunosorbent assay (ELISA) that used baculovirus-derived HPV16 virus-like particles as the antigen. A similar ELISA that used bovine papillomavirus type 1 (BPV1) virus-like particles as the antigen controlled for the specificity of HPV16 seroreactivity. Data from the HPV16 and the BPV1 assays were normalized with respect to results obtained in each assay with a control serum of known HPV16 seroreactivity. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to examine the association between HPV16 seroreactivity and esophageal cancer. Reported P values are two-sided. RESULTS: The mean seroreactivity to HPV16 virus-like particles was significantly higher for the cancer patients than for the control subjects (mean value +/- standard deviation = 0.85 +/- 0.22 versus 0.74 +/- 0.18; P<.0001). When the cancer patients and control subjects were compared by sex and age groups, the differences in mean seroreactivity remained statistically significant. The difference in mean seroreactivity to BPV1 virus-like particles between cancer patients and control subjects was not statistically significant (0.81 +/- 0.28 versus 0.88 +/- 0.32; P = .12); this result was not altered when sex and age groups were compared. By use of a cutoff point for HPV16 seropositivity that was established in studies of cervical neoplasia, 24% of the cancer patients were seropositive compared with 7% of the control subjects, yielding a sex- and age-adjusted OR of 4.5 (95% CI = 1.8-11.9). In general, the OR for esophageal cancer increased with increasing HPV16 seroreactivity. CONCLUSIONS AND IMPLICATIONS: HPV16 infection may be a risk factor for esophageal cancer. Further studies of the association between HPV16 infection and the incidence of esophageal cancer are needed.

Antibodies, Viral↗

Quantification of mRNAs for three alpha 1-adrenoceptor subtypes in rat aorta by solution hybridization.

We used solution hybridization to quantify mRNAs for alpha 1A-, alpha 1B-and alpha 1D-adrenoceptor(AR) in rat aortae. The results showed that the mRNA for alpha 1A-, alpha 1B- and alpha 1D-AR was 0.28 +/- 0.03 fmol, 0.35 +/- 0.03 fmol and 0.82 +/- 0.09 fmol, respectively, in 40 micrograms total RNA extracted from rat aorta. The dominant expression of alpha 1D-AR further support the recent findings that alpha 1D-AR is a major functional receptor subtype of AR in rat aorta.

Animals↗

Endogenous inotropic factor-induced endothelium-dependent relaxation of vascular smooth muscle.

1. Possible contractile or relaxation effects of an endogenous inotropic factor (EIF) isolated and purified from porcine heart left ventricle were examined in rat isolated aortic ring preparations. 2. EIF induced a dose-dependent relaxation of the rat isolated aortic ring preparation pre-contracted with 0.4 microM phenylephrine (PE); 200 microliters (in 5 ml bath) of EIF caused relaxation of aortic rings by as much as 67.4 +/- 4.5%. In another set of experiments, in the presence of 100 microliters EIF, the PE concentration-response contractile curve shifted to the right, the maximal contractile force was reduced by as much as 32.8% and the EC50 of PE increased from 0.2 to 0.3 microM. 3. The relaxation effect of EIF was demonstrated to be endothelium-dependent. Additional experiments demonstrated that EIF-induced relaxation in an isolated aortic ring could be inhibited by 2 microM NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, suggesting the involvement of nitric oxide in EIF-induced relaxation of the muscle. 4. Atropine (0.2 microM) or indomethacin (10 microM) had no significant effect on EIF-induced relaxation. 5. These data suggest that EIF, a novel endogenous inotrope from porcine myocardium, also acts as an endothelium-dependent vasodilator substance mediating relaxation in the rat isolated aorta mainly by release of nitric oxide. The possibility of EIF acting through muscarinic receptor and the involvement of prostacyclin were excluded.

Animals↗

Rapid nitric oxide- and prostaglandin-dependent release of calcitonin gene-related peptide (CGRP) triggered by endotoxin in rat mesenteric arterial bed.

1. Our objective was to determine whether endotoxin (ETX) could directly trigger the release of calcitonin gene-related peptide (CGRP) from perivascular sensory nerves in the isolated mesenteric arterial bed (MAB) of the rat and to determine whether nitric oxide (NO) and prostaglandins (PGs) are involved. 2. ETX caused time- and concentration-dependent release of CGRP, and as much as a 17 fold increase in CGRP levels in the perfusate at 10-15 min after the administration of ETX (50 micrograms ml-1). 3. CGRP-like immunoreactivity in the perfusate was shown to co-elute with synthetic rat CGRP by reverse-phase h.p.l.c. 4. Pretreatment of MAB with capsaicin or ruthenium red inhibited ETX-induced CGRP release by 90% and 71%, respectively. ETX-evoked CGRP release was decreased by 84% during Ca2(+)-free perfusion. 5. The release of CGRP evoked by ETX was enhanced by L-arginine by 43% and inhibited by N omega-nitro-L-arginine (L-NOARG) and methylene blue by 37% and 38%, respectively. L-Arginine reversed the effect of L-NOARG. 6. Indomethacin and ibuprofen also inhibited the ETX-induced CGRP release by 34% and 44%, respectively. No additive inhibition could be found when L-NOARG and indomethacin were concomitantly incubated. 7. The data suggest that ETX triggers the release of CGRP from capsaicin-sensitive sensory nerves innervating blood vessels. The ETX-induced CGRP release is dependent on extracellular Ca2+ influx and involves a ruthenium red-sensitive mechanism. Both NO and PGs appear to be involved in the ETX-induced release of CGRP in the rat mesenteric arterial bed.

Animals↗

Modulation of myocardial alpha 1- but not beta-adrenoceptors after 90-day tail-suspension.

We have previously demonstrated that prolonged simulated microgravity (tail-suspension) leads to cardiac alterations with increased resting heart rate, myocardial degradation changes and attenuated myocardial contractility. The present study investigated the potential role of adrenoceptor mechanisms underlying them. Changes of myocardial alpha 1-adrenoceptor (alpha 1-AR) and beta 1-adrenoceptor (beta-AR) in 90-day tail-suspended rats was investigated by the method of radioligand binding assay and application of Scatchard's method. The results showed significantly decreased quantity of specific binding of 125I-BE[2-beta-(4-hydroxy-3-[125I]indophenyl)-ethylaminomethyltetralone] to alpha 1-AR present in membrane derived from ventricular myocardium of the suspended animals, despite the affinity of the alpha 1-AR to 125I-Be was unchanged. But neither the quantity nor the affinity of beta-AR binding to 125I-Pindolol was significantly altered. In addition, the spontaneously beating rate of isolated right atria from tail-suspended animals showed little change in sensitivity and reactivity to the stimulations of graded phenylephrine (alpha-agonist, measured in the presence of beta-antagonist propranolol) and isoproterenol (beta-agonist), compared with the control rats. There were also no obvious differences of the effects of the isoproterenol on the contractility of isolated left ventricular papillary muscles between the two groups. Since myocardial alpha 1-AR mediated-effects include production of cardiac hypertrophy and enhancement of myocardial glucose uptake and glycolysis, the down-regulation of the alpha 1-AR may be a contributor to the cardiac cellular accumulation and the myocardial degradation changes as found in our tail-suspended rats. The data from this study also suggest that the myocardial beta-adrenoceptors are not affected by the prolonged tail-suspension.

Adrenergic alpha-Agonists↗

[Reconstruction of TMJ condyle cartilage defects with autogenous free periosteal grafts].

How to reconstruct the damaged articular cartilage has been one of the main subjects in treatment of articular disease for a long time. In this experimental study, fullthickness cartilage defects of 4 mm x 5 mm in size were created in rabbit's TMJ condyle cartiage on the left sides. The autogenous free periosteum were transplanted to the defects by using biological gelatin. Postoperatively, the animals were killed at intervals of 1, 2, 4, 8, 12 and 16 weeks. The regenerative cartilage in the defects were examined by gross appearance and histology. The result showed that mesenchymal cells in the cambium layer of periostum can transform into chondroblasts under the mechanical stress.

Animals↗

[Relationship between expression of P21ras and cellular DNA in pleomorphic adenoma of lacrimal gland].

BACKGROUND: The pleomorphic adenoma is the most frequent tumor of the human lacrimal gland comprising about 50% of the epithelial tumors of this organ. Although being benign, local recurrences can occur when the first removal was incomplete and malignant transformation is also not in frequent. It is well known that many sorts of cellular oncogene products are involved in the initiation, promotion and progression of the human neoplasm. Our purpose was to know whether there is abnormal expression of P21ras in pleomorphic adenoma. METHODS: We have undertaken a study of the expression of P21ras in 5 normal tissues and 32 pleomorphic adenoma of lacrimal gland by immunohistochemical means using the monoclone antibody F-132-62 and the nuclear DNA content in the tumor was assayed by image analysis technique. RESULTS: Normal tissues of lacrimal gland were negative, 12 tumors were stained positively with the antibody. The DNA content of 14 cases of tumor was increased. Their DNA ploidy distribution pattern showed two or several peaks. Good correlation has been found between the expression of P21ras and DNA ploidy distribution pattern, the DNA ploidy distribution pattern of tumor which expressed p21ras showed mainly two or several peaks. P< 0.05. CONCLUSIONS: The result of our studies may suggest that there are increased expression of p21ras in pleomorphic adenoma and the expression of p21ras is related to the promotion and progression of pleomorphic adenoma of lacrimal gland.

Adenoma, Pleomorphic↗

[Protection of dl-(15R)-15 methyl-PGE2 methyl ester (PG6E) on experimental ulcers in rats].

The effects of dl-(15R)-15 methyl-PGE2 methyl ester (PG6E), in experimental ulcers induced by absolute alcohol, HCl, indomethacin, pyloric ligation and chronic acetic acid in rats were studied. PG6E at doses 10-80 micrograms.kg-1 was shown to have significant protective effect. PG6E (30-60 micrograms.kg-1) was also found to reduce markedly the acid secretion, pepsin activity, DNA content of the juice collected from pylorus ligated stomach of rats and increase markedly the content of gastric mucosa hexosamine in mice given PG6E (30-60 micrograms.kg-1 po for 3 d). At doses of 40-80 micrograms.kg-1, PG6E was able to have no significant effect on gastric emptying time in rats and gastrointestinal tract movement in mice. It appears that PG6E was shown to inhibit the aggressive factors and increase the protective factors of gastric mucosa. This may hopefully become a new antiulcer agent.

Animals↗

Alterations of alpha1-adrenoceptor subtypes in the hearts of thyroxine-treated rats.

Alterations in the cardiac alpha1-adrenoceptor and its subtypes in thyroxine-treated rats were studied by means of radioligand binding assays, measurement of contractile response and reverse transcription-polymerase chain reaction (RT-PCR). The results showed that in thyroxine-treated rats the cardiac alpha1-adrenoceptor density (Bmax) was reduced from 51.6 +/- 6.0 fmol/mg in control to 40.9 +/- 3.7 fmol/mg (P<0.01); and the percentage of high affinity sites for 5-methyl-urapidil decreased from 23.3 +/- 2.0% in control to 10.8 +/- 2.0% in thyroxine-treated rats (P<0.05). The data indicated that the high-affinity sites for 5-methyl-urapidil (alpha1A-adrenoceptor) were reduced (from 12.0 to 4.4 fmol/mg), but the low-affinity sites for 5-methyl-urapidil (alpha1B- plus alpha1D-adrenoceptor) were not changed (from 39.6 to 36.5 fmol/mg). RT-PCR showed that steady-state levels of mRNA for alpha1A- and alpha1B-adrenoceptors were decreased, while that for alpha1D-adrenoceptor was raised in thyroxine-treated rats. In the isolated electrically driven left atria the phenylephrine-induced maximal contractions were reduced from 258 +/- 17 mg in control to 188 +/- 24 mg in thyroxine-treated rats (P<0.05). The pA2 values of 5-methyl-urapidil were reduced from 8.89 +/- 0.36 in control to the hyperthyroidism of 7.87 +/- 0.43 in thyroxine-treated rats (P<0.05). Chlorethylclonidine preincubation shifted concentration-response curves for phenylephrine to the right and reduced the maximal response to a lesser extent in thyroxine-treated rats than in control rats. Thus we concluded that the total number of cardiac alpha1-adrenoceptors is reduced in thyroxine-treated rats. The change is subtype selective, with alpha1A- and alpha1B-adrenoceptors being reduced in number and alpha1D-adrenoceptor being increased.

Animals↗

Inhibition of oncogene expression by green tea and (-)-epigallocatechin gallate in mice.

The effects of tea drinking on the tobacco-specific nitrosamine 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone (NNK)-induced mouse lung oncogene expression and the effect of topical application of the tea polyphenol component (-)-epigallocatechin-3-gallate (EGCG) on 12-O-tedradecanoylphorbol-13-acetate (TPA)-induced mouse skin oncogene expression were investigated. In the first experiment, mice were treated with NNK (1.3 mg/kg body wt ip) once a day for three days and were given 2% tea in drinking water during the whole experimental period. After four or eight weeks, the lung tissue of the mice treated with NNK displayed a significantly high level of expression in c-myc, c-raf, and c-H-ras oncogenes, and they were all inhibited by tea drinking with inhibitory rates of 50%, 20%, and 50%, respectively. In the second experiment, a single application of 10 nmol of TPA to mouse skin led to a marked increase in the transcripts' level of ornithine decarboxylase (ODC) gene, protein kinase C (PKC) gene, and c-myc oncogene at four hours after TPA administration. Topical application of EGCG (1 or 5 mumol) one hour before the application of TPA inhibited all TPA-induced gene expression in a dose-dependent fashion. These results confirm the anticarcinogenic effects of tea and suggest that a possible mechanism is the effect of tea on carcinogen-induced oncogene expression.

Animals↗

Divergent human papillomavirus type 16 variants are serologically cross-reactive.

It is not known whether DNA sequence variants of human papillomavirus type 16 (HPV-16) are distinct serotypes. To examine this question, the reactivities of women's sera from Zaire (n = 97) and Denmark (n = 123) were compared in IgG-specific ELISAs based on virus-like particles (VLPs) composed of the L1 major capsid protein derived from an HPV-16 variant common in central Africa (Z-1194) or one common in northern Europe (114K). These L1s differ in seven amino acids. There was a strong correlation between reactivity in the two assays for both sets of sera (correlation coefficients, 0.73 and 0.85 for Zairian and Danish sera, respectively). In only 1 serum was there evidence for a specific reaction to one but not the other VLP variant. The results support the conclusion that the virions of strains Z-1194 and 114K are serologically cross-reactive.

Cross Reactions↗

Strategy for dose escalation using 3-dimensional conformal radiation therapy for lung cancer.

PURPOSE: Local failure is a major obstacle to the cure of locally advanced non-small-cell lung cancer. 3-Dimensional conformal radiation therapy (3-DCRT) selects optimal treatment parameters to increase dose to tumor and reduce normal tissue dose, potentially permitting dose escalation. There are several ongoing trials of dose escalation using 3-Dimensional conformal radiation therapy for non-small-cell lung cancer. We performed this analysis to determine if data derived from dose volume histograms could be used as the basis for designing the method of dose escalation in these trials. METHODS AND MATERIALS: Between 1990 and 1993, 31 patients were treated with 3-DCRT and had complete normal tissue dose volume histograms created as part of the planning process. The stage distribution was stage I/II 13%, stage IIIa in 45%, and stage IIIb in 42%. The median radiation dose to gross disease was 70.2 Gy (52.2-72 Gy). Elective mediastinal irradiation (50.4 Gy) was administered to 52% (16/31) of patients. RESULTS: The major toxicity encountered in this experience was pulmonary. Dose-volume-histogram data were used to analyze the predictors of toxicity and showed a correlation between risk of pulmonary toxicity and indices of dose to lung parenchyma. Grade 3 or higher pulmonary toxicity occurred in 38% (3/8) of pts with >30%of lung volume receiving > or =25 Gy, versus 4% (1/23) of pts. with < or = 30% lung receiving > or = 25 Gy (p=0.04). Grade 3 or higher pulmonary toxicity occurred in 29% (4/14) of patients with a predicted pulmonary normal tissue complication probability of 12% or higher versus 0% (0/17) in patients with a predicted probability of less than 12% (p=0.03). The single fatality occurred in a patient with a calculated pneumonitis probability of 85% and a high percent (49%) lung volume receiving >= 25 GY. CONCLUSION: This preliminary experience demonstrates a correlation between lung dose-volume-histogram data and the risk of severe pulmonary toxicity. This provides an opportunity to modify the method of radiation dose escalation. Dose-volume-histogram data can allow escalation according to the risk to the lung parenchyma (which is the major organ of concern) rather than escalation according to tumor dose levels. Because of teh major inter-patient variability of intrathoracic tumor bulk and anatomic distribution, this strategy is intuitively appropriate. This approach may facilitate completion of dose escalation studies and identification of maximum tolerable pulmonary dose levels.

Adult↗

[Antiulcer effect of polycyclicamine compound HH01 on experimental gastric ulcer in rats].

HH01(1-methyl-3,4,5,6,9,10-hexahydro-7H-cyclopenta [j,k]-1,3-dioxolo [4,5-h]-pyrrolo[2,1-b] [3]-benzazepine) A and B in doses 30 mg.kg-1 and 60 mg.kg-1 were shown to protect gastric mucosa of rats from damage induced by absolute ethanol, cold-immersion stress and pylorus ligation. No effect was found in indomethacin model in mice. HH01 was found to decrease secretion of gastric juice and HCl in pylorus ligated rats. The content of DNA in gastric juice of animals treated with HH01 was lower than in control. The results suggest that HH01 is effective as an anti-ulcer agent, but its mechanism of action is yet unknown.

Animals↗

Specific inhibition of the contraction of the rat aorta by estradiol 17 beta.

Short-term exposure to estradiol 17 beta is known to inhibit the contraction of vascular smooth muscle preparations that is thought to be mediated by a [Ca++]-dependent mechanism. The purpose of this investigation was to examine the effect of prolonged exposure of vascular preparations to estradiol 17 beta to provide significant time for protein synthesis. We find that treatment of rat aortic rings with estradiol 17 beta (0.37-37 microM) for 15 to 180 min and subsequent removal of the estrogen by washing, attenuated the vasoconstrictor responses to phenylephrine and potassium chloride in a time-dependent manner. The maximum inhibitory effect took 120 min to develop. The inhibitory effect was endothelium independent and not blocked by the cyclooxygenase inhibitor, indomethacin, or by the endothelium derived relaxing factor inhibitor, Nw-nitro-L-arginine methyl ester. This effect was highly stereo-specific in that the 17 alpha isomer was significantly less potent than the 17 beta isomer of estradiol. Further, compared to other steroids, estradiol 17 beta was the most potent. The inhibitory effect of estradiol was blocked completely by pretreatment with the protein synthesis inhibitors, cycloheximide and puromycin, but not by actinomycin D. Electron microscopy showed an increase in ribosomal expression at the rough endoplasmic reticulum after incubation of the rat aorta with estradiol for 120 min. This indicates increased protein synthesis after exposure to estradiol 17 beta. We speculate that the time dependent inhibitory effect of estradiol 17 beta on vascular smooth muscle is related to protein synthesis at the translational level.

Animals↗

Calcitonin gene-related peptide release in endotoxicosis may be mediated by prostaglandins.

Three cyclo-oxygenase inhibitors (ibuprofen, indomethacin, and high dose aspirin) and two inhibitors of thromboxane biosynthesis (imidazole and low dose aspirin) were used to evaluate the role of prostaglandins and thromboxane in the release of calcitonin gene-related peptide (CGRP) during endotoxicosis. Endotoxin (lipopolysaccharide B from Salmonella Enteritidis, 5 mg/kg, intravenously) was administered to rats lightly anesthetized with ether during injection. After 3 h, endotoxin significantly elevated plasma CGRP levels by 3-fold. Ibuprofen (50 mg/kg, subcutaneously), indomethacin (10 mg/kg, subcutaneously) and high dose aspirin (100 mg/kg, intraperitoneally (i.p.)), but not imidazole (30 mg/kg, i.p.) or low dose aspirin (15 mg/kg, i.p.), significantly blocked endotoxin-induced CGRP elevations, suggesting that a prostaglandin, but not thromboxane, served as a mediator of CGRP release during endotoxicosis. Because endotoxin-induced production of prostaglandins is greatly diminished in endotoxin-tolerant rats (following multiple exposures to low dose endotoxin), we tested whether endotoxin-induced CGRP release also becomes diminished in tolerant rats. Accumulation of plasma CGRP was greatly diminished in endotoxin-tolerant rats exposed to endotoxin (5 mg/kg, intravenously), consistent with a mediator role for prostaglandins in the CGRP release during endotoxicosis.

Animals↗

[An experimental study on the effect of operation at one side of the temporomandibular joint on the opposite side].

Condylectomy and menisectomy were performed in left TMJ of 14 rabbits, of them, 7 were treated with periosteal interposition and 7 without. Sixteen weeks after operation, condylar cartilage of the right side were studied and compared with 7 normal rabbits by means of histology and histochemistry. The results show that an operation of high condylectomy and menisectomy with or without interposition on one side of TMJ will result in degenerative changes in the other side (non-operated side). The degenerative changes in the rabbits without any interposition are more serious than those with periosteal interposition.

Animals↗