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Biomedical subjects

C Han

Publications and source records attributed to C Han.

At least 73 records · Page 4Linked to original sources
PubMed1999

[Inhibitory effects of tea polyphenols and tea pigments on liver precancerous lesions in rats].

A liver precancerous model in rats was established with diethylnitorsamine(DEN) injected intraperitoneally as initiator and promoted by partial hepatectomy and injection of CCl4. The model was used to study the chemopreventive effect of tea polyphenols and tea pigments. A water solution of 0.1% tea polyphenols or tea pigments was given to Wistar rats as drinking water during the 56-day experiment period. A stable and sensitive early marker of liver cancer--GST-Pi positive foci or nodule was measured by a immunohistochemical method. Both tea polyphenols and tea pigments decreased the density and area of the GST-Pi foci. The expression of GST-Pi mRNA in chemical induced precancerous liver tissue was measured by Northern Blotting technique, and the expression of GST-Pi isoenzyme in liver tissue was detected by Western Blotting method. The results showed that both tea polyphenols and tea pigments effectively reduced the GST-Pi expression at both transcription and translation level. It is concluded that the inhibition of tea polyphenols and tea pigments on GST-Pi overexpression induced by chemical carinogen may be one of the mechanisms of their inhibition on the occurrence and progression of liver precancerous lesions in rats.

Animals↗
PubMed1999

Identification and characterization of immunoreactive calcitonin gene-related peptide from lymphocytes of the rat.

There is accumulating evidence that the immune system can produce neuropeptides. In the light of these facts, we obtained direct evidences to prove that T lymphocytes also synthesize and secrete calcitonin gene-related peptide (CGRP), a neuropeptide localized within primary sensory nerves. By using CGRP specific RIA, CGRP-like immunoreactivity (LI) was found in the extracts of rat lymphocytes from thymus and mesenteric lymph node. The intracellular concentration of lymphocyte-derived CGRP-LI of rat thymus and mesenteric lymph node was 745+/-39 and 447+/-33 fg/10(6) cells, respectively. CGRP-LI in lymphocytes was shown to co-elute with synthetic rat CGRP and sensory neuron-derived CGRP by reverse-phase HPLC. In addition, the CGRP-LI located in the T lymphocytes was also shown by immunocytochemical method examined by electron microscopy. The CGRP mRNA detected by RT-PCR was also present in these lymphocytes and was also identified to be the same one in sensory neurons. These data suggest that CGRP is synthesized and secreted in T lymphocytes of both thymus and lymph node in the rat, and this is identified to be the same one in neuronal tissue. Lymphocyte-derived CGRP may act in an autocrine/paracrine mode and play an important role in certain physiological and pathophysiological conditions.

Animals↗
PubMed1999

Blockade of nitric oxide synthase potentiates the suppression of vasodilators by norepinephrine in the hepatic artery.

We have previously shown that nitric oxide (NO) and adenosine suppress vasoconstriction induced by norepinephrine infusion and sympathetic nerve stimulation in the hepatic artery and superior mesenteric artery. NO is involved in the control of basal vascular tone in the superior mesenteric artery but not the hepatic artery. The vasodilation induced by adenosine is inhibited by NO in the superior mesenteric artery but not in the hepatic artery. Based on these known interactions of catecholamines, adenosine, and NO, the objective of this study was to test the hypothesis that NO modulates the interaction between vasoconstrictors and vasodilators in the hepatic artery. We examined the ability of norepinephrine to suppress adenosine-mediated vasodilation and the role of NO in this interaction. Hepatic arterial blood flow and pressure were monitored in pentobarbital-anesthetized cats. The maximum hepatic arterial vasoconstrictor response to norepinephrine infusion was potentiated by blockade of NO production using Nomega-nitro-L-arginine methyl ester (L-NAME), and the potentiation was reversed by L-arginine. The maximum dilator response to adenosine was only slightly suppressed (14.0+/-5.8%, P < 0.05) by norepinephrine infusion; however, after the NO blockade, the suppression by norepinephrine of the vasodilation induced by adenosine was substantially potentiated (45.2+/-9.1%, P < 0.05). Similar results were obtained for isoproterenol-induced vasodilation. We conclude that the interaction between these vasodilators and norepinephrine was modulated by NO which inhibited the vasoconstriction and the suppression of vasodilators caused by norepinephrine and that in the absence of NO production, norepinephrine-induced constriction and the ability to antagonize dilation is substantially potentiated.

Adenosine↗
PubMed1999

Relationship between the clinical features and the viral antigen in the extremity blood of the patients with hemorrhagic fever with renal syndrome.

The direct immunogold silver staining (D-IGSS) method was used to detect the viral antigen in the extremity blood of 67 cases of hemorrhagic fever with renal syndrome. The positive rate of viral antigen was the highest during the fever, hypotension and oligouria phrase; and the rate dropped gradually during the polyuria and convalescent phase. It is suggested that clinical staging was positively related with the percentage of the viral antigen positive cells (P < 0.001). It is concluded that the positive rate was related to the extent of the injuries by direct viral attack and immune reaction. The D-IGSS was proved to be fast, simple, economical, with high sensitivity and specificity.

Adolescent↗
PubMed1999

The nucleotide sequence of a chinese isolate of wheat yellow mosaic virus and its comparison with a Japanese isolate. Brief report.

The nucleotide sequences of wheat yellow mosaic virus isolated in China were determined and compared with a Japanese isolate of the same virus. Results showed that the viral genome had 7629 nucleotides for RNA1 and 3639 nucleotides for RNA2, which shared 97. 1% and 94.6% of identities to the RNAs of Japanese isolate. The single open reading frames in RNA1 and RNA2 encoded polyproteins with 2407 amino acids and 903 amino acids respectively, from which ten proteins may be produced by autolytic cleavage processing as the Japanese isolate. Since the sequence of WYMV RNA1 showed identity of less than 70% with that of WSSMV, it is further confirmed that WYMV is a distinct species within Bymovirus.

Base Sequence↗
PubMed1999

Lifetime tobacco, alcohol and other substance use in adolescent Minnesota twins: univariate and multivariate behavioral genetic analyses.

AIMS: We sought to estimate the contribution of genetic and environmental factors to adolescent tobacco, alcohol and other substance use. DESIGN, SETTING AND PARTICIPANTS: The sample consisted of 327 monozygotic and 174 like-sex dizygotic twin pairs born in Minnesota and aged 17-18 years at time of assessment. Biometrical methods were used to estimate the contribution of additive genetic, shared and non-shared environmental factors to adolescent substance use. MEASUREMENTS: As part of a day-long psychological assessment, adolescent twins completed a computerized substance use interview to determine whether they had ever used tobacco, alcohol or other illicit drugs. FINDINGS: The heritability for the liabilities to tobacco, alcohol and other drug use was estimated to be 59%, 60% and 33% among males, and 11%, 10% and 11% among females. However, the gender difference was not statistically significant. Estimates of shared environmental effect were substantial and insignificantly higher among females (71%, 68% and 36%, respectively) than among males (18%, 23% and 23%, respectively). The covariation among the three substance use phenotypes could be accounted for by a common underlying substance use factor. Estimates of the contributions of genetic, shared environmental and non-shared environmental factors to variance in this factor were 23% 63% and 14%, respectively. CONCLUSIONS: These findings add to the growing behavioral genetic literature indicating that adolescent initiation of substance use, a powerful predictor of adult substance use diagnosis, is influenced primarily by environmental rather than genetic factors.

Adolescent↗
PubMed1999

Role of the sarcoplasmic reticulum in the modulation of rat cardiac action potential by stretch.

We have investigated the role of sarcoplasmic reticulum (SR) in the modulation on rat action potentials by stretch. The action potentials were recorded intracellularly from rat atrial myocytes in an isolated atrial preparation with small, physiological stretch produced by pressure (1-3 mmHg) inside the atria. The SR function was inhibited by pharmacological interventions, either with ryanodine (100 nmol L-1), thapsigargin (10 nmol L-1) or caffeine (1 mmol L-1). The duration of action potentials was increased by stretch from 1 to 3 mmHg. The repolarization indices APD30% (P < 0.05), APD60% (P < 0.01), and APD90% (P < 0.01) were all increased significantly (n=10). Ryanodine, thapsigargin, and caffeine inhibited this prolongation, or even reversed the effect with repolarization indices APD30% (P < 0.05) and APD60% (P < 0.05) which decreased in stretch with thapsigargin treatment. As a conclusion, we suggest that the SR and the intracellular calcium balance play an important role in the modulation of the shape of the rat atrial action potential during stretch.

Action Potentials↗
PubMed1999

Intracellular acidosis modulates the stretch-induced changes in E-C coupling of the rat atrium.

By inducing a small reduction of the intracellular pH (0.18 units) with 20 mmol L-1 propionate we demonstrated that acidification changed the responses of isolated rat atria to stretch. Stretch (increase of the intra-atrial pressure) in normal pH increased the Ca2+ transients' amplitude (Indo-1 fluorescence) from 0.26 +/- 0.09 in 1 mmHg to 0.36 +/- 0.13 in 4 mmHg (P < 0.05, n=6), without affecting the diastolic [Ca2+]i level (n.s. n=6). The changes in Ca2+ balance during stretch were accompanied by a biphasic increase in the contraction force. Five minutes of continuous stretch increased the action potential duration (APD90%, P < 0.01, n=13) and decreased the APD15% (P < 0.001, n=13). During acidosis, the stretch-induced increase of the Ca2+ transient amplitude (0.4 +/- 0. 13 vs. 0.3 +/- 0.08, P < 0.05, n=6) was accompanied by the increase of the diastolic [Ca2+]i (1.16 +/- 0.07, P < 0.05, n=6) compared with non-acidotic control (1.06 +/- 0.06, n=6). Acidic intracellular pH also inhibited the stretch-induced changes in the action potentials (n=10) and slowed down the development of the contractile force during stretch. The results showed that acidosis modulates the mechanotransduction. It does this by interfering with the intracellular Ca2+ balance, inhibiting the Ca2+ extrusion mechanisms and reducing the Ca2+-buffering power of the cells. The physiological and pathological processes associated with stretch are therefore modulated by intracellular pH owing to its concerted effects on intracellular Ca2+ handling caused by a competitive inhibition of various Ca2+-binding molecules.

Acidosis↗
PubMed1999

Role of nitric oxide and prostaglandins in the potentiating effects of calcitonin gene-related peptide on lipopolysaccharide-induced interleukin-6 release from mouse peritoneal macrophages.

Previous data from our laboratory have shown that calcitonin gene-related peptide (CGRP) has a potentiating effect on lipopolysaccharide-(LPS) induced interleukin-6 (IL-6) release from mouse macrophages. However, the mechanism of this effect was not clear. Since the nitric oxide (NO) and prostaglandins (PGs) induced by LPS might modulate IL-6 release, we examined whether NO and PGs were also involved in the potentiating effect of rat CGRP (rCGRP) on LPS-induced IL-6 release from mouse macrophages. The IL-6 level in the medium was measured by enzyme-linked immunosorbent assay. Accumulation of NO was assessed by measuring the presence of nitrite by the Greiss reaction. PGI2 was assessed by measuring the formation of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) by radioimmunoassay. The results showed that the potentiating effect of rCGRP (0.1 nm) on LPS-induced IL-6 release was significantly inhibited by either 100 micrometers NG-monomethyl-L-arginine acetate (L-NMMA; an inhibitor of NO synthase) or 10 micrometers indomethacin (an inhibitor of cyclo-oxygenase). The LPS-induced NO and PGI2 production from these cells was increased significantly by rCGRP at 0.01-10 nm in a concentration-dependent manner, which was blocked by L-NMMA and indomethacin. These results suggest that rCGRP enhances the NO production elicited by LPS and subsequently increases the PGs production which is involved in the potentiating effect of rCGRP on LPS-induced IL-6 release from the peritoneal macrophages in the mouse.

Analysis of Variance↗
PubMed1999

The chemopreventive effects of tea on human oral precancerous mucosa lesions.

A double-blind intervention trial was conducted in patients with oral mucosa leukoplakia using a mixed tea product developed by the authors. Fifty-nine oral mucosa leukoplakia patients, diagnosed by established clinical and pathological criteria, were randomly divided into a treated group (3 g mixed tea oral administration and topical treatment) and a control group (placebo and glycerin treatment). After the 6-month trial, the size of oral lesion was decreased in 37.9% of the 29 treated patients and increased in 3.4%; whereas the oral lesion was decreased in 10.0% of the 30 control patients and increased in 6.7%. At the same time, the incidence of micronucleated exfoliated oral mucosa cells in the treated group (5. 4 per 1000 cells) was lower than that in the control group (11.3 per 1000 cells)(P < 0.01); whereas it was 1.4 per 1000 cells in 20 healthy subjects. The micronuclei and chromosome aberration rate in the peripheral blood lymphocytes showed the same results. In pathological examination, there were significant differences (P < 0. 05) in the number and total volume of the silver-stained Nucleolar Organizer Regions (AgNOR) and the proliferating index of Proliferation Cell Nuclear Antigen (PCNA) in oral mucosa cell nuclei between the treated group and the control group which indicates that cell proliferation was decreased in the treated patients. The overall results provide some direct evidence on the protective effects of tea on oral cancer.

Adult↗
PubMed1999

The effect of tea consumption on oxidative stress in smokers and nonsmokers.

While the anticarcinogenic effects of tea in animal models have been reported by several groups, human epidemiological studies examining tea consumption and cancer prevention have produced equivocal results. The beneficial properties of tea to human health may be related to the antioxidant properties of tea components. However, little evidence has been provided that tea consumption can either increase the antioxidant capacity or decrease oxidative stress in humans. In the present study, the effects of tea treatment (green tea) on biomarkers of oxidative stress were investigated in smokers and nonsmokers in two volunteer study groups (one in China and the other in United States). Green tea consumption in both study groups decreased oxidative DNA damage (8-OHdG in white blood cells and urine), lipid peroxidation (MDA in urine), and free radical generation (2, 3-DHBA in urine) in smokers. Nonsmokers (US study group) also exhibited a decrease in overall oxidative stress.

3,4-Methylenedioxyamphetamine↗
PubMed1999

Shear stress-induced nitric oxide antagonizes adenosine effects on intestinal metabolism.

The influence of nitric oxide (NO) on adenosine-induced metabolic effects was studied in the intestine. Blood flow supplied an in situ- isolated segment of small intestine in anesthetized cats via the superior mesenteric artery (SMA) and was controlled by a vascular circuit. The SMA and portal samples were taken for analysis of oxygen and lactate. Adenosine (0.4 mg. kg-1. min-1, intra-SMA) reduced oxygen consumption by 25.1 +/- 2.9 from 73.1 +/- 10.8 micromol. min-1. 100 g-1 and increased lactate production by 13.3 +/- 3.0 from 12.8 +/- 4.6 micromol. min-1. 100 g tissue-1 during constant-flow (CF, decreased shear stress) but not during constant-pressure (CP, increased shear stress) perfusion. Blockade of NO synthase using Nomega-nitro-L-arginine methyl ester did not affect the metabolic effects of adenosine during CF but eliminated the differences seen between CP and CF perfusion. A NO donor, 3-morpholinosydnonimine, attenuated the metabolic effects of adenosine during CF perfusion. The results suggested that shear-induced NO antagonized metabolic effects of adenosine but that the inhibition of vascular effects by NO was not shear dependent since it occurred in both CP and CF perfusion.

Adenosine↗
PubMed1999

Blood flow-dependent prostaglandin f(2alpha) regulates intestinal glucose uptake from the blood.

Intestinal glucose uptake (GUi) from blood increased when blood flow (BF) was increased. The increase in BF could elevate shear stress. Therefore, we hypothesize that shear stress-induced release of autacoids mediates the increase in GU(i). A surgically separated segment of small intestine was perfused in situ with the use of an arterial circuit in anesthetized cats. Arterial and portal blood samples were taken simultaneously for assessment of GU(i). Adenosine was used to elevate intestinal BF. The GU(i) increased by 45.0 +/- 18.3 from 25.3 +/- 3.8 micromol. min(-1). 100 g tissue(-1) when the BF increased about four times. It was not a direct effect of adenosine because GU(i) was not altered if the flow was held constant. This increase was blocked by a cyclooxygenase inhibitor, indomethacin, but not by nitric oxide synthase blocker N(G)-nitro-L-arginine methyl ester. Furthermore, prostaglandin F(2alpha) (PGF(2alpha)) but not PGE(2) or PGI(2) reversed the blockade of the increase in GU(i) after indomethacin during elevated blood flow, whereas they had no influence on basal uptake. The results suggest that shear stress-induced release of PGF(2alpha) mediated the increase in GU(i) when blood flow was elevated.

Animals↗
PubMed1999

Nitric oxide mediates hepatic arterial vascular escape from norepinephrine-induced constriction.

The involvement of nitric oxide (NO) in the vascular escape from norepinephrine (NE)-induced vasoconstriction was investigated in the hepatic arterial vasculature of anesthetized cats. The hepatic artery was perfused by free blood flow or pump-controlled constant-flow, and NE (0.15 and 0.3 microg x kg(-1) x min(-1), respectively) was infused through the portal vein. In the free-flow perfusion model, the NE-induced hepatic vasoconstriction recovered from the maximum point of the constriction, resulting in 36.6 +/- 5. 9% vascular escape. Blockade of NO formation with N(omega)-nitro-L-arginine methyl ester (L-NAME, 2.5 mg/kg ipv) potentiated NE-induced maximum vasoconstriction, and the potentiation was reversed by L-arginine (75 mg/kg ipv). Furthermore, NE-induced vasoconstriction became more stable after L-NAME, resulting in an inhibition of vascular escape (7.5 +/- 3.3%), and the inhibition was reversed by L-arginine (23.0 +/- 6.4%). Similar potentiation of NE-induced vasoconstriction and inhibition of hepatic vascular escape by L-NAME (40.4 +/- 4.3% control vs. 10.2 +/- 3.7% post-L-NAME escape) and the reversal by L-arginine were also observed in the constant-flow perfusion model. The data suggest that NO is the major endogenous mediator involved in the hepatic vascular escape from NE-induced vasoconstriction.

Animals↗
PubMed1999

Green tea and its major components ameliorate immune dysfunction in mice bearing Lewis lung carcinoma and treated with the carcinogen NNK.

The protective effects of tea and/or its components on dysfunction of immune functions during tumor growth and carcinogenesis in mice were studied using two experimental models: C57/BL6J mice transplanted with Lewis lung carcinoma (LLC) and Kunming mice treated with a single dose of 4-(methylnitrosamino-)-1-(3-pyridyl)-1-butanone (NNK). In C57/BL6J mice bearing LLC, the weight of the thymus decreased, the proportion of CD4(+)-positive T lymphocytes and the ratio of CD4+ to CD8+ decreased, luminol-enhanced chemiluminescence of white blood cells in peripheral blood stimulated by zymosan increased, and plaque-forming cells (PFC) decreased. However, in LLC-bearing mice given green tea as drinking water, all immune functions were improved, along with inhibition of tumor growth. In Kunming mice treated with NNK, during the four weeks of observation, their immunologic indicators, such as phagocytosis of macrophages in the abdominal cavity, luminol-enhanced chemiluminescence of white blood cells, plaque-forming cells, and delayed-type hypersensitivity, increased or decreased to various extents compared with normal controls. However, these changes were significantly prevented in the mice given green tea, mixed tea, or tea polyphenol as drinking water. In conclusion, tea and its components ameliorated immune dysfunction in mice bearing LLC or treated with the carcinogen NNK.

Animals↗
PubMed1999

Tea preparations protect against DMBA-induced oral carcinogenesis in hamsters.

The preventive effects of green tea, tea pigments, and mixed tea (a composite of whole water extract of green tea, tea polyphenols, and tea pigments) on 7,12-dimethyl-benz[a]anthracene (DMBA)-induced oral carcinogenesis in golden Syrian hamsters were studied. The right buccal pouches of animals were topically treated with 0.5% DMBA three times per week for 15 weeks. Animals were killed separately after 6, 10, and 15 weeks of DMBA treatment. Oral tumors were counted and measured, and mean tumor burden was calculated. The incidence of preneoplastic lesions and micronucleated cells, the number and volume of silver-stained nucleolar organizer regions (AgNOR), the labeling index of proliferating cell nuclear antigen, and the level of epidermal growth factor receptor expression were studied. The results showed that oral administration of 1.5% green tea, 0.1% tea pigments, and 0.5% mixed tea as the sole source of drinking water for two weeks before initiation of the DMBA treatment and until the end of the experiment significantly reduced the mean tumor burden and the incidence of dysplasia and oral carcinoma (p < 0.01). The frequency of micronucleated cells, the number of AgNOR, the total volume of AgNORs, the labeling index of proliferating cell nuclear antigen, and the level of epidermal growth factor receptor expression in the oral mucosal cells were also significantly reduced (p < 0.01). These results clearly indicated that tea preparations could effectively inhibit DMBA-induced oral carcinogenesis in hamsters. Protection from DNA damage and suppression of cell proliferation could be important mechanisms of the anticarcinogenic effects of the tea preparations.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Alpha(1)-adrenoceptor subtypes mediating inotropic responses in rat heart.

We studied the distribution of alpha(1)-adrenoceptor subtypes by radioligand binding assays using (125)I-labeled 2-beta(4-hydroxyphenyl)-ethylaminomethyl)-tetralone (BE2254) and RNase protection assays, and determined the role of each subtype in mediating the inotropic response in rat heart. Chlorethylclonidine preincubation causes a approximately 72% decrease in the maximal binding capacity (B(max)). On the other hand, protection from phenoxybenzamine alkylation by 5-methyl-urapidil or BMY7378 decreased B(max) by 59 and 70%. By competitive inhibition, we have identified 19 to 28% and 30% high-affinity binding sites for the alpha(1A)- and alpha(1D)-selective antagonists in rat ventricles, with the alpha(1B)-adrenoceptor estimated as 45%. Consistent with the receptor-binding result, a similar distribution of mRNAs encoding alpha(1A), alpha(1B,) and alpha(1D) (22, 39, and 39%), based on RNase protection assays, was observed. In addition, we demonstrated that the noradrenaline response through alpha(1)-adrenoceptor was antagonisted by 5-methyl-urapidil, RS-17053, BMY7378, and WB4101 in contraction functional experiments. K(I) values for the above compounds were defined for all three alpha(1)-adrenoceptor subtypes expressed in the human embryonic kidney 293 cell stably, and were further compared with the corresponding pA(2) values. Interestingly, the correlation was significantly higher for alpha(1A) (r(2) = 0.73) and alpha(1B) (r(2) = 0.66) than alpha(1D) (r(2) = 0.35) in these experiments. Because the potential of alpha(1D) measured to be 21% based on protection from phenoxybenzamine-caused inhibition by BMY7378, the combined potential of alpha(1A) and alpha(1B) can be estimated as approximately 80%. Taken together, these results suggest that the three alpha(1)-adrenoceptor subtypes coexist in rat heart, with alpha(1A) and alpha(1B) playing a more prominent role in the positive inotropic response to noradrenaline.

Adrenergic alpha-Agonists↗