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Biomedical subjects

Z Ni

Publications and source records attributed to Z Ni.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effect of antioxidant therapy on blood pressure and NO synthase expression in hypertensive rats.

Earlier studies have demonstrated evidence for increased reactive oxygen species, enhanced NO synthase (NOS) expression, and elevated NO production in spontaneously hypertensive rats (SHR). Given the negative-feedback regulation of NOS by NO, we hypothesized that enhanced NO inactivation by ROS may contribute to compensatory upregulation of NOS in SHR. The present study was designed to test this hypothesis. Eight-week-old male SHR and Wistar-Kyoto rats were treated for 3 weeks with either a placebo or the potent antioxidant, lazaroid (desmethyltirilazad, 10 mg. kg(-1). d(-1), by gastric gavage). Tail arterial blood pressure, urinary excretion of NO metabolites (ie, nitrate and nitrite), and immunodetectable NOS isotype proteins in the vascular, renal, cardiac, and cerebral tissues were measured. The placebo-treated SHR group showed a marked elevation of blood pressure and a significant upregulation of aorta, kidney, and cardiac tissue endothelial and inducible NOS (eNOS and iNOS, respectively) proteins and of brain and renal tissue neuronal NOS. Lazaroid therapy ameliorated hypertension and mitigated the upregulation of eNOS and iNOS in vascular, renal, and cardiac tissues but had limited effect on the expression of renal and brain neuronal NOS. In contrast, lazaroid therapy had no effect on blood pressure, urinary nitrate and nitrite excretion, or tissue NOS isotype expressions in the Wistar-Kyoto group. These findings support the role of oxidative stress in the genesis and/or maintenance of hypertension and compensatory upregulation of the expression of eNOS and iNOS in SHR.

Animals↗
PubMed2000

Changes in the firing pattern of globus pallidus neurons after the degeneration of nigrostriatal pathway are mediated by the subthalamic nucleus in the rat.

Changes in the neuronal activity of globus pallidus (GP) have been shown in animal models of parkinsonism. In order to study the implication of the subthalamic nucleus (STN) in these changes, the effects of STN lesions alone or in combination with 6-hydroxydopamine (6-OHDA) -induced damage to the substantia nigra compacta (SNc) were examined in rats using electrophysiological recordings of GP cells. In normal rats, the firing rate was 22.1+/-1.4 spikes/s. The pattern was regular in 45%, irregular in 49% and bursty in 6% of the cases. In rats with STN lesions, the firing rate of GP units (20.15+/-1.25 spikes/s) did not differ from that of normal rats and only regular (46%) and irregular (54%) cells were found; a bursty pattern was not observed. 6-OHDA lesions of the SNc induced no change in the firing rate of GP neurons (21.5+/-1.4 spikes/s, P>0.05) but a significant decrease in the percentage of regular cells (27%, P<0.001), a significant increase in burst cells (21%, P<0.001) with no change in the percentage of irregular units (52%) were observed. In rats with combined SNc and STN lesions, the firing pattern did not change from that of normal rats. The present results show that STN lesions induced the disappearance of bursts in normal rats and normalization of firing pattern in the GP units of rats with 6-OHDA lesions suggesting that the STN plays an important role in the modulation of the pattern of activity of GP neurons which may account for the therapeutic effect of STN lesions in Parkinson's disease.

Animals↗
PubMed2000

[The prevention of primary liver cancer by selenium in high risk populations].

OBJECTIVE: To study the preventive effects of selenium on primary liver cancer. METHODS: After screening of blood samples in 18,000 males from 20 to 65 years-old in Qidong, Jiangsu province (a high risk area for liver cancer), 2,065 cases of HBsAg positive, AFP negative and normal liver function (normal ALT values) were found. The subjects were randomly divided into two groups, based on their residence areas; 1,112 subjects (experimental group) received one tablet of sodium selenite (0.5 mg Se) every day and 953 subjects (control group) received one placebo tablet every day. RESULTS: During three years of intervention and follow up, the blood selenium concentration and glutathione peroxidase activity of the subjects in the experimental group were increased and had significant difference as compared with those of the control group (P < 0.01). At the same time, the prevalence rate of micronucleus cells in peripheral blood lymphocytes in the experimental group was significantly lower than that of the control group (P < 0.01), and the incidence of new liver cancer in the experimental group (3 057.55/10(6), 34 cases out of 1,112 subjects) was significantly lower than the control group (5 981.11/10(6); 57 cases out of 953 subjects) (P < 0.01). CONCLUSION: The results confirms that selenium supplementation in general populations lived in high risk is effective in the prevention of liver cancer and the using of selenium tablets is simple and feasible.

Adult↗
PubMed2000

[Cloning and expression of Shiga-like toxin type II variant B gene of E. coli].

A structure sequence and a DNA fragment including the signal peptide sequence and structure sequence of Shiga-like toxin II variant B subunit gene were amplified from E. coli strain O138 by PCR. After digested with restriction endonuclease EcoRI and BamHI, the two genes were orientally inserted into the polycloning site of expression vector pYA3334 (asd+) respectively. Recombinant plasmids pB0 and pB1 were constructed and amplified in E. coli X6212 (asd-). pB0 and pB1 were then introduced into avirulent Salmonella typhimurium vaccine strain X4550 (asd-) by serial transformation through intermediate strain X3730 (asd-) to construct recombinant SLT-IIvB strain. Results of nucleotide sequencing of the cloned fragments in pB0 and pB1 revealed that they were in correct ORF of SLT-IIvB. The results of SDS-PAGE and Western-blot showed that 7.6 kD protein of SLT-IIvB antigen was expressed at pretty high level in recombinant strain X4550(pB0). The results of mice immunization indicated X4550(pB0) could initiate the host to produce specific antibodies to SLT-IIvB and LPS-O antigen of X4550. So the recombinant strain X4550 (pB0) is worth considering as a candidate vaccine strain against porcine edema disease and Salmonella typhimurium infections.

Animals↗
PubMed1999

Nitric oxide synthase isotype expression in salt-sensitive and salt-resistant Dahl rats.

Previous studies have suggested that salt-sensitive hypertension in humans and experimental animals may in part be due to dysregulation of the L-arginine/nitric oxide system. This study was conducted to determine the endothelial, inducible, and neuronal nitric oxide synthase expressions in the kidney, heart, aorta, and brain of salt-sensitive and salt-resistant Dahl rats. We studied salt-sensitive and salt-resistant Dahl rats maintained on high- (8%) and regular- (0.2%) salt diets for 3 weeks. Blood pressure was modestly elevated in both Dahl salt-sensitive and salt-resistant rats consuming regular diet and severely increased in sensitive but not resistant rats consuming the high-salt diet. The Dahl salt-sensitive animals showed a significant reduction in kidney, heart, and aorta inducible nitric oxide synthase protein abundance on the regular diet, with further reductions on the high-salt diet. In addition, the high-salt diet markedly downregulated endothelial nitric oxide synthase expression in the kidney and aorta but not in the heart of the Dahl salt-sensitive animals. The rise in blood pressure in the Dahl salt-sensitive rats on the high-salt diet was accompanied by a significant elevation of brain neuronal nitric oxide synthase protein. In contrast, salt-resistant animals showed no change in heart, kidney, and aorta endothelial or brain neuronal nitric oxide synthase and considerably less intense changes in inducible isotype than that seen in the salt-sensitive group in response to the high-salt diet. In conclusion, the study revealed a marked downregulation of inducible nitric oxide synthase in the Dahl salt-sensitive rats on the regular diet, with further reductions on the high-salt diet. Furthermore, Dahl salt-sensitive rats consuming the high-salt diet showed significant reductions of kidney and aorta endothelial nitric oxide synthase and an upregulation of brain neuronal nitric oxide synthase expression.

Analysis of Variance↗
PubMed1999

Nitric oxide synthase expression in the course of lead-induced hypertension.

We recently showed elevated reactive oxygen species (ROS), reduced urinary excretion of NO metabolites (NOx), and increased NO sequestration as nitrotyrosine in various tissues in rats with lead-induced hypertension. This study was designed to discern whether the reduction in urinary NOx in lead-induced hypertension is, in part, due to depressed NO synthase (NOS) expression. Male Sprague-Dawley rats were randomly assigned to a lead-treated group (given lead acetate, 100 ppm, in drinking water and regular rat chow), a group given lead and vitamin E-fortified chow, or a normal control group given either regular food and water or vitamin E-fortified food for 12 weeks. Tail blood pressure, urinary NOx excretion, plasma malondialdehyde (MDA), and endothelial and inducible NOS (eNOS and iNOS) isotypes in the aorta and kidney were measured. The lead-treated group exhibited a rise in blood pressure and plasma MDA concentration, a fall in urinary NOx excretion, and a paradoxical rise in vascular and renal tissue eNOS and iNOS expression. Vitamin E supplementation ameliorated hypertension, lowered plasma MDA concentration, and raised urinary NOx excretion while significantly lowering vascular, but not renal, tissue eNOS and iNOS expression. Vitamin E supplementation had no effect on either blood pressure, plasma MDA, or NOS expression in the control group. The study also revealed significant inhibition of NOS enzymatic activity by lead in cell-free preparations. In conclusion, lead-induced hypertension in this model was associated with a compensatory upregulation of renal and vascular eNOS and iNOS expression. This is, in part, due to ROS-mediated NO inactivation, lead-associated inhibition of NOS activity, and perhaps stimulatory actions of increased shear stress associated with hypertension.

Animals↗
PubMed1999

[Likelihood ratio and ROC curve in evaluation of iron parameters for diagnosing iron deficiency].

OBJECTIVE: To evaluate the value of iron parameters in diagnosing iron deficiency (ID). METHODS: Cross-sectional study was performed for diagnostic tests. Ninety consecutive patients with anemia including iron deficiency anemia without chronic diseases (36 cases), chronic diseases (54) were divided into chronic diseases without ID(ACD) (23 cases) and chronic diseases with ID(CDID) (31) by bone marrow iron staining. The exclusion criteria included hemolytic anemia, deficiency of Vitamin B12 or folic acid, blood transfusion, taking iron preparations within one month and hematological malignancies. By using absence of bone marrow iron as gold standard of ID, we compared the diagnostic powers in the diagnosis of iron deficiency for sTfR, serum iron, total iron binding capacity, serum ferritin (SF), transferrin saturation and the presence of hypochromic red cells by analyzing the likelihood ratio, the area under ROC(AUCROC). RESULTS: AUCROC for sTfR in determining ID in groups IDA + CDID vs. ACD, IDA vs. ACD and CDID vs. ACD were 0.9 (95% CI: 0.82-0.98), 0.96(0.9-0.99) and 0.84 (0.72-0.96) respectively, AUCROC for SF in above groups 0.87 (95% CI: 0.77-0.87), 0.94(0.86-0.99) and 0.77(0.63-0.91) respectively. AUCROC for other iron parameters in determining iron deficiency in chronic diseases was lower than 70%. CONCLUSION: ROC and LR are useful tools for evaluating iron parameters in diagnosing iron deficiency. TfR is a best parameter in determining iron deficiency in chronic diseases than SF and other iron parameters.

Anemia, Iron-Deficiency↗
PubMed1999

Effect of Astragalin on matrix secretion and beta 1 integrin mRNA expression in human mesangial cells.

OBJECTIVE: To investigate the effect of Astragalin on human renal mesangial cells. METHODS: Cultured human mesangial cells were treated with Astragalin and Astragalin serum in different concentrations in the presence or absence of PDGF-BB, the proliferation and type IV collagen secretion of mesangial cells were measured by MTT assay and ELISA, and expression of beta 1 integrin gene was estimated by reverse transcription-polymerase chain reaction (RT-PCR) method, suspectively. RESULTS: After 72 hours Astragalin or Astragalin serum treatment, the proliferation of mesangial cells induced by PDGF-BB was inhibited significantly in a dose-dependent manner compared with untreated controls (P < 0.05 and P < 0.01). After 24 hours of Astragalin or Astragalin serum treatment, the secretion of type IV collagen protein in presence of PDGF-BB was significantly decreased and beta 1 integrin mRNA level decreased significantly compared with untreated control (P < 0.05, P < 0.01). CONCLUSIONS: Astragalin inhibits cell proliferation and matrix over-synthesis which might be mediated, at least, partly by decrease of beta 1 integrin gene over-expression. The study suggested that Astragalin might play a role in preventing the progression of chronic renal diseases.

Antineoplastic Agents, Phytogenic↗
PubMed1999

[Expression and characteristics of laryngeal carcinoma-associated antigen].

OBJECTIVE: To study the characteristics of laryngeal carcinoma-associated antigen (LCAA) and its expression on laryngeal carcinoma tissue. METHODS: The binding of a cocktail monoclonal antibodies Lc9, Lc11, Lc12 to human laryngeal squamous-cell carcinoma, laryngeal precancerous lesions and normal laryngeal mucosa was examined by immunohistochemical method. LCAA isolated and purified by gel-filtration, and chromotography from 3 laryngeal squamous-cell carcinomas. The reactivity of the purified antigen was determined after treatment with trypsin, NaIO4, methanol and heating. RESULTS: The positive rate of LCAA expression in 90 cases of laryngeal carcinoma, 14 cases of precancerous lesions and in 10 cases of normal laryngeal mucosa was 97.7%, 50.0% and 0, respectively. LCAA was a glycoprotein, moderately heat stable. The purified antigen gave two bands of apparent molecular weights of 61,400 and 56,500 on SDS-PAGE and Western blot. CONCLUSION: The results provide a basis for immunoimaging diagnosis and targeting chemotherapy for laryngeal cancer.

Antigens, Neoplasm↗
PubMed1999

[On the problems of fitting linear regression models for hierarchically structured data in medical research].

There are a large number of the hierarchically structured data in the field of medical sciences, which have been analyzed usually by conventional linear regression models. The objective of this paper is to explore the problems and the relationship of parameter estimates of the three common linear regression models in fitting the hierarchically structured date, and the correction of the precision of parameter estimates. It is shown that the estimate of parameter and it's precision of linear regression models is related to the variation of independent variable between and within level 2 units, and the difference of residual estimates is associated with the difference of parameter estimates. The three common linear regression models are all inappropriate for the hierarchically structured data, but the standard error of the level 1 combined model can be corrected by variance inflation factor in conditions.

Analysis of Variance↗
PubMed1999

[Application of intraclass correlation coefficient to reliability assessment].

To evaluate the reliability of questionnaire and expound the simple method of calculating and testing the intraclass correlation coefficient (ICC), the authors gave an example of how to simply calculate and conduct the hypothesis testing of ICC by using the analysis table of variance. The results demonstrated a high test-retest reliability of the illustrative questionnaire. By using ANOVA table, the calculation and hypothesis testing of the ICC is easy to do. The method can be used in the analysis of quantitative data, and categorical data as well.

Aged↗
PubMed1999

[Studies on localization of laryngeal carcinoma associated antigen by immunoelectromicroscopy].

OBJECTIVE: To study the localization of laryngeal carcinoma associated antigen (LCAA) in the carcinoma tissue. METHODS: Ninety cases of laryngeal carcinoma and 14 cases of laryngeal precancerous lesion and 10 cases of normal laryngeal mucosa were detected with three strains of monoclonal antibodies LC9, LC11, LC12 by immunochemistry. The positive sections of laryngeal carcinoma were observed under light microscope and electromicroscopy. RESULTS: The positive rates of LCAA were dramatically higher than that in normal epithelial and precancerous tissues (P < 0.01). The results showed that the mixed monoclonal antibody had tissue specificity. The MLC associated antigens only distributed in cell membranes and/or cytoplasm. No cell nucleus was stained. CONCLUSION: The LCAA is mainly located in cell membranous structure. This study may provide morphological basis for immunoimaging diagnosis and targeting chemotherapy by application of laryngeal carcinoma McAb.

Antigens, Neoplasm↗
PubMed1998

Egr-1 inhibits apoptosis during the UV response: correlation of cell survival with Egr-1 phosphorylation.

UV irradiation of normal or immortalized cells induces a rapid increase in the expression of several transcription factors and is thought to serve a protective function. The human fibrosarcoma cell line, HT1080 clone H4, expresses almost undetectable levels of Egr-1 and does not respond to UV-C irradiation by the induction of Egr-1. The H4 cells are hypersensitive to UV which induces apoptosis and reduces clonogenicity. The introduction of exogenous Egr-1 into H4 (H4E9 and H4E4 cell-lines) confers protection from UV damage as measured by a number of assays. In both NIH3T3 (with inducible Egr-1) and H4E9 (constitutive Egr-1) cells, UV irradiation gave enhanced transactivation of Egr-1 reporters that correlated with phosphorylated Egr-1. Studies using inhibitors indicated that protein kinase-C and tyrosine kinases are involved in the anti-apoptotic effects of Egr-1 after UV damage. This is the first description of a biological effect of phosphorylated Egr-1.

3T3 Cells↗
PubMed1998

Depressed renal and vascular nitric oxide synthase expression in cyclosporine-induced hypertension.

BACKGROUND: Introduction of cyclosporine (CsA) for clinical use has greatly enhanced the outcome of organ transplantation. However, CsA can cause nephrotoxicity and hypertension (HTN). This study was designed to test the hypothesis that CsA-induced HTN is related to depressed nitric oxide (NO) production. METHODS: Urinary excretion of NO metabolites (NOx) and endothelial and inducible NO synthase (eNOS and iNOS) proteins were determined in thoracic aortas and kidneys of CsA-treated (given CsA 18 mg/kg/day for 3 weeks) and placebo-treated rats. In addition, renal tissue eNOS and iNOS mRNA and aorta iNOS activity were measured. RESULTS: CsA administration resulted ina significant rise in arterial blood pressure (BP) coupled with a steady decline in urinary NOx excretion, suggesting depressed NO production. This was accompanied by a significant reduction in iNOS protein abundance in the kidney and thoracic aorta but no change in eNOS protein abundance. The fall in renal iNOS protein in CsA-treated rats was accompanied by a parallel decline in iNOS mRNA abundance and enzymatic activity. CONCLUSION: Administration of CsA for three weeks resulted in a significant rise in BP together with marked reductions in urinary NOx excretion, and renal and vascular iNOS expression. These observations suggest that CsA-induced HTN may be, in part, related to impaired NO production. If true, strategies designed to restore NO availability may mitigate HTN and other vascular complications of CsA therapy.

Animals↗
PubMed1998

Role of endothelin and nitric oxide imbalance in the pathogenesis of hypoxia-induced arterial hypertension.

BACKGROUND: We have recently demonstrated that prolonged hypobaric hypoxia can lead to a hematocrit-independent sustained arterial hypertension (HTN) in genetically normotensive Sprague-Dawley rats. The rise in blood pressure in the hypoxic animals was accompanied by a marked but transient increase in plasma endothelin level. In addition, hypoxia has been shown to decrease nitric oxide (NO) production by cultured endothelial cells. This study was designed to test the hypothesis that hypoxia-induced HTN may be mediated by increased endothelin and/or decreased NO production. METHODS: Blood pressure, plasma endothelin and urinary NO metabolites (NOx)were monitored in rats during a 24-hour exposure to hypobaric hypoxia (air pressure = 390 mm Hg). The results were compared with hypoxia (air pressure = 390 mm Hg). The results were compared with those obtained in animals maintained under normoxic condition (control group). To test the possible role of excess endothelin and depressed NO production, the studies were repeated using subgroups of animals treated with either an endothelin receptor ET-A/B blocker (L-754,142) or L-arginine. RESULTS: The untreated hypoxic group exhibited a threefold rise in plasma endothelin and a threefold fall in urinary NOx, prior to the onset of HTN. Endothelin receptor blockade led to a further fall in urinary NOx excretion and failed to mitigate HTN. In contrast, L-arginine supplementation improved the urinary NOx excretion and prevented HTN. Neither therapy affected the hypoxia-induced erythrocytosis. CONCLUSIONS: We conclude that hypoxia-induced HTN is associated with depressed NO production and can be mitigated by L-arginine supplementation.

Acetamides↗
PubMed1998

Downregulation of nitric oxide synthase in chronic renal insufficiency: role of excess PTH.

The available data on the effect of chronic renal failure (CRF) on nitric oxide (NO) metabolism are limited and contradictory. We studied rats with CRF 6 wk after a five-sixths nephrectomy and compared the results with those in the sham-operated controls, felodipine-treated CRF, and parathyroidectomized (CRF-PTX) animals. CRF was produced by surgical resection of the upper and lower thirds of the left kidney, followed by contralateral nephrectomy. We chose this model, as opposed to that produced by renal artery branch ligation, because the latter causes exuberant hypertension (HTN), which independently affects NO metabolism. The CRF group exhibited a mild HTN coupled with elevated basal platelet cytosolic Ca2+ concentration ([Ca2+]i), blunted hypotensive response to L-arginine, decreased hypertensive response to NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine, and normal hypotensive response to NO donor, sodium nitroprusside. This was associated with a significant reduction in urinary excretion of stable NO metabolites (NOX) and depressed NOS activity, as well as endothelial and inducible NO synthase (eNOS and iNOS, respectively) protein contents of thoracic aorta and the remnant kidney in the CRF animals. Calcium channel blockade and PTX lowered blood pressure, increased urinary NOX, and enhanced vascular NOS activity, as well as eNOS and iNOS protein expressions in the tested tissues. Thus CRF animals exhibited significant reductions in vascular NOS activity and eNOS and iNOS expressions. These abnormalities were reversed by calcium channel blockade and PTX, suggesting the possible causal role of CRF-induced dysregulation of [Ca2+]i.

Animals↗
PubMed1998

Decreased endothelial nitric oxide synthase in gastric mucosa of rats with chronic renal failure.

According to recent reports, chronic renal failure (CRF) increases the susceptibility of gastric mucosa to injury. Since nitric oxide plays a major role in gastric mucosal defense and injury, we investigated, in rats with CRF produced by five-sixths nephrectomy and in control rats, the expression of nitric oxide synthase(NOS) in the stomach and measured mucosal and submucosal gastric blood flow. In CRF rats, gastric mucosal blood flow was significantly reduced compared with control rats, whereas submucosal and serosal blood flow was significantly increased. CRF significantly decreased endothelial NOS (eNOS) mRNA abundance by 53% (P < 0.01) and reduced expression of eNOS protein by 42% (P < 0.01) compared with the controls. Enzyme activity of eNOS was significantly reduced in gastric mucosa of CRF rats (P < 0.05). These data are consistent with reduced gastric mucosal blood flow in CRF rats and can explain altered susceptibility of gastric mucosa to injury in CRF rats.

Animals↗