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41.
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A Chen LF Sheu YS Ho YF Lin WY Chou JY Wang WH Lee 《American journal of kidney diseases》1998,31(3):443-452
The administration of glucocorticoids has been reported to exacerbate proteinuria in a few patients with glomerulonephritis. This effect has not been well recognized, and the pathogenetic mechanism responsible for this phenomenon remains to be clarified. In this study, we observed that a high daily oral dose (0.5 mg/kg body weight) of dexamethasone was capable of inducing overt proteinuria in mice, beginning on day 5 and persisting for a 19-day duration. One fourth of mice also intermittently presented with slight hematuria beginning on day 12. Renal lesions in the dexamethasone-treated mice, which were killed on day 23, were characterized by mild mesangial expansion, segmental or global hyalinosis/sclerosis in deep cortical glomeruli, and focal tubular changes. No glomerular inflammatory cell infiltration or proliferative lesion was noted in any of the mice. Ultrastructural features of glomeruli included mesangial widening characterized by either an increase of mesangial matrix, dilated mesangial channels filled with slightly electron-dense material or mesangial lysis-like appearance showing intracytoplasmic microcysts filled with electron-lucent material, and evidence to support injury of endothelial cells, erythrocytes, and podocytes. An immunofluorescence study revealed enhanced glomerular deposition of IgG, IgA, IgM, and fibrinogen (P < 0.001, compared with normal control mice), but no glomerular C3 deposition was identified in any of the dexamethasone-treated mice. Charge analysis showed no impairment in anionic property of glomerular tufts in the dexamethasone-treated mice. In addition, the dexamethasone-induced proteinuria was greatly attenuated by treatment with a low molecular weight heparin, although it was not reduced by an angiotensin-converting enzyme inhibitor. Data from these experiments suggest that a large dose of glucocorticoids is potentially nephrotoxic. Alteration of a size-dependent permeability may predominantly contribute to the dexamethasone-induced proteinuria. However, the effect of glomerular hyperfiltration may be only partially involved in the pathogenesis of this dexamethasone-induced glomerulopathy in mice. 相似文献
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E-K Park EJ Lee S-H Lee KH Koo JY Sung EH Hwang JH Park C-W Kim K-C Jeong B-K Park Y-N Kim 《British journal of pharmacology》2010,160(5):1212-1223
Background and purpose:
Lipid rafts and caveolae are membrane microdomains with important roles in cell survival signalling involving the Akt pathway. Cholesterol is important for the structure and function of these microdomains. The ginsenoside Rh2 exhibits anti-tumour activity. Because Rh2 is structurally similar to cholesterol, we investigated the possibility that Rh2 exerted its anti-tumour effect by modulating rafts and caveolae.Experimental approach:
A431 cells (human epidermoid carcinoma cell line) were treated with Rh2 and the effects on cell apoptosis, raft localization and Akt activation measured. We also examined the effects of over-expression of Akt and active-Akt on Rh2-induced cell death.Key results:
Rh2 induced apoptosis concentration- and time-dependently. Rh2 reduced the levels of rafts and caveolae in the plasma membrane and increased their internalization. Furthermore, Akt activity was decreased and consequently, Akt-dependent phosphorylation of Bad, a pro-survival protein, was decreased whereas the pro-apoptotic proteins, Bim and Bax, were increased upon Rh2 treatment. Unlike microdomain internalization induce by cholesterol depletion, Rh2-mediated internalization of rafts and caveolae was not reversed by cholesterol addition. Also, cholesterol addition did not restore Akt activation or rescue cells from Rh2-induced cell death. Rh2-induced cell death was attenuated in MDA-MB-231 cells over-expressing either wild-type or dominant-active Akt.Conclusions and implications:
Rh2 induced internalization of rafts and caveolae, leading to Akt inactivation, and ultimately apoptosis. Because elevated levels of membrane rafts and caveolae, and Akt activation have been correlated with cancer development, internalization of these microdomains by Rh2 could potentially be used as an anti-cancer therapy. 相似文献45.
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We defined erythropoietin (EPO) resistance by the ratio of the weekly EPO dose to hematocrit (Hct), yielding a continuously distributed variable (EPO/Hct). EPO resistance is usually attributed to iron or vitamin deficiency, hyperparathyroidism, aluminum toxicity, or inflammation. Activation of the acute-phase response, assessed by the level of the acute-phase C-reactive protein (CRP), correlates strongly with hypoalbuminemia and mortality in both hemodialysis (HD) and peritoneal dialysis (PD) patients. In this cross-sectional study of 92 HD and 36 PD patients, we examined the contribution of parathyroid hormone (PTH) levels, iron indices, aluminum levels, nutritional parameters (normalized protein catabolic rate [PCRn]), dialysis adequacy (Kt/V), and CRP to EPO/Hct. Albumin level serves as a measure of both nutrition and inflammation and was used as another independent variable. Serum albumin level (deltaR2 = 0.129; P < 0.001) and age (deltaR2 = 0.040; P = 0.040) were the best predictors of EPO/Hct in HD patients, and serum albumin (deltaR2 = 0.205; P = 0.002) and ferritin levels (deltaR2 = 0.132; P = 0.015) in PD patients. When albumin was excluded from the analysis, the best predictors of EPO/Hct were CRP (deltaR2 = 0.105; P = 0.003) and ferritin levels (deltaR2 = 0.051; P = 0.023) in HD patients and CRP level (deltaR2 = 0.141; P = 0.024) in PD patients. When both albumin and CRP were excluded from analysis in HD patients, low transferrin levels predicted high EPO/Hct (deltaR2 = 0.070; P = 0.011). EPO/Hct was independent of PTH and aluminum levels, PCRn, and Kt/V. High EPO/Hct occurred in the context of high ferritin and low transferrin levels, the pattern expected in the acute-phase response, not in iron deficiency. In well-dialyzed patients who were iron replete, the acute-phase response was the most important predictor of EPO resistance. 相似文献
48.
NTRODUCTIONSinceMuto[1]reportedthatTNFαandIL1wererelatedtofulminanthepatitis,thestudiesontherelationshipbetweencytokinesa... 相似文献
49.
张家港市位于苏南水网地区,全市85余万人口,面积998 km2,人口密度高达860人·km-2.全市工商经济和服务行业发达,外来流动人口达6000人·d-1,外来常住人口达10万人·a-1,而且本地人口流动量大,经对该市塘桥镇8000人调查,30%以上人口每天至少有一次不在家内用餐.农村人口以前普遍饮用河塘水及浅井水,其中饮用4 m~6 m深的井水者近40万人. 相似文献
50.
冠心病合并2型糖尿病患者血脂检测 总被引:1,自引:0,他引:1
目的:观察冠心病(CHD)合并2型糖尿病患者血脂水平的变化,并探讨CHD合并2型糖尿病的危险性与脂质代谢紊乱间的相关性.方法:检测CHD组患者29(男18,女11)例,年龄40~70(平均55.2)岁;CHD合并2型糖尿病组[CHD伴非胰岛素依赖型糖尿病(NIDDM)]患者22(男12,女10)例,年龄41~70(平均56.5)岁;正常对照组[健康献血员31(男17,女14)例,年龄38~50(平均43.5)岁]的血脂水平.结果:CHD伴NIDDM组患者总胆固醇(TC),三酰甘油(TG),低密度脂蛋白胆固醇(LDLC)和载脂蛋白B(ApoB)水平明显高于CHD组患者[TC:(5.87±1.02)mmol/Lvs(4.10±1.13)mmol/L;TG:(2.10±1.05)mmol/Lvs(1.13±0.85)mmol/L;LDLC:(4.23±0.97)mmol/Lvs(2.97±0.90)mmol/L;ApoB:(0.90±0.18)mmol/Lvs(0.58±0.19)mmol/L,均P<0.01],但CHD伴NIDDM组患者高密度脂蛋白胆固醇(HDLC),载脂蛋白A1(ApoA1)水平明显低于CHD组患者[HDLC(0.71±0.12)mmol/Lvs(0.94±0.16)mmol/L,ApoA1:(0.73±0.19)mmol/Lvs(1.03±0.20)mmol/L,均P<0.01].结论:CHD合并2型糖尿病患者在脂质代谢紊乱方面存在更多致CHD的危险因素,应重视这类患者的血脂检测并及时纠正脂质代谢紊乱,以降低CHD的危险性. 相似文献