脑梗死患者颅内血管狭窄的危险因素分析

目的分析脑梗死患者颅内血管狭窄的危险因素。方法对186例脑梗死患者行经颅多普勒超声检查,检测血尿酸和血脂包括总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、甘油三酯。结果血管狭窄组患者总胆固醇(5.04±1.23 mmol/L)和低密度脂蛋白胆固醇水平(2.99±1.01 mmol/L)均显著高于无狭窄组患者(分别为4.60±1.12 mmol/L和2.59±0.69 mmol/L,P<0.05);Pearson相关分析表明,颅内血管峡窄与高血压史(r=0.206,P=0.005)、糖尿病史(r=0.238,P=0.001)、总胆固醇(r=0.181,P=0.016)、低密度脂蛋白胆固醇(r=0.227,P=0.003)及尿酸(r=0.132,P=0.016)相关;Logistic回归分析表明,高血压、糖尿病、低密度脂蛋白胆固醇、尿酸进入回归方程,它们对颅内血管狭窄的OR值分别为2.345、2.554、1.764和1.006(P<0.05)。结论除高血压和糖尿病外,尿酸和低密度脂蛋白胆固醇亦是脑梗死患者颅内血管狭窄形成的独立危险因素。     

树鼩高密度脂蛋白亚类及其载脂蛋白构成与抗动脉粥样硬化的关系

树鼩HDL_3和HDL_2共占血浆总脂蛋白的90%以上,是转运血浆胆固醇的主要脂蛋白,其HDL_2中载脂蛋白构成独特,琼脂糖电泳显示为β脂蛋白,可能在转运脂质中起特殊作用。喂高胆固醇饲料后,血浆HDL_3及HDL_2浓度明显增加,HDL_2中的apo E比例也显著增加,高酪蛋白饲料则能抑制高胆固醇对HDL的作用,并使HDL_3中出现一新的MW22.4kD蛋白成分。这些改变有利于HDL加快转运胆固醇至肝脏分解代谢。     

氟化物对大鼠脂代谢的影响

给５４积Ｗｉｓｔａｒ雄性大鼠自由饮用染氟水，浓度分别为０．６（对照组），１００和２００ｍｇ／Ｌ，于染氟后第２，４，６周分批处死，测血清和肝组织的胆固醇，甘油三酯含量。结果显示，染氟第６周，染氟组大鼠血清胆固含量显著增高，肝组织胆固醇含量显著降低。２００ｍｇ／Ｌ摄氟组大鼠血清甘油三酯含量在第４周显著降低，肝组织甘油三酯含量在第６周显著降低。提示，氟可影响大鼠脂代谢，引起高胆固醇血症。     

Cholesterol metabolism and non-cholesterol sterols in patients with ileal pouch anastomosis

Background: Previous studies suggest only minor changes in bile acid metabolism after panproctocolectomy with ileal pouch construction.Aims/Methods: To investigate these changes further, we studied cholesterol absorption and serum, biliary and fecal non-cholesterol sterols and lipids in 12 ileal pouch patients and 10 controls.Results: In patients, cholesterol absorption was markedly reduced and was associated with low serum total and LDL cholesterol and LDL triglyceride levels, but surprisingly, cholesterol synthesis, as indicated by sterol-balance data or serum cholesterol precursor levels, was within low normal limits. The high proportions of serum plant sterol to cholesterol, particularly that of campesterol, were not related to cholesterol absorption, but were attributable to a markedly reduced biliary cholesterol secretion. Interestingly, in these patients the fractional absorption of campesterol was normal, whereas that of sitosterol, like cholesterol, was reduced and was positively related to the intestinal influx of cholesterol. The patients' serum cholestanol proportion was normal, but the proportion of the cholestanol formed during intestinal passage was significantly reduced (17.9% vs 65.2% in controls).Conclusions: Thus ileal pouch patients are characterized by sterol malabsorption, lowered serum total and LDL-cholesterol levels, but unexpectedly without any increase in cholesterol synthesis. The lack of high serum cholestanol, shown earlier frequently in unoperated patients with ulcerative colitis, may indicate reversible cholestasis, a finding deserving further exploration.     

1981～2001年北京市职业人群血清总胆固醇水平的变动

分析1981年至2001年20年间北京市部分职业人群血清总胆固醇水平的变化。在力求做到血脂测定标准化的基础上，回顾性分析20年来北京市部分机关和企事业单位工作人员47434人次总胆固醇水平的变化，按年度、性别、年龄分组统计，结果发现，总胆固醇水平从1981年至1988年间上升幅度较大，年龄调整均值男性上升0．73mmol／L(28m/dL)，女性上升0．62mmol／L(24mg/dL)。至1990年已达最高值，2001年低于1991年，男、女年龄调整均值分别回落0．21mmol/L(8mg/dL)及0．23mmol/L(9mg/dL)。男女总胆固醇水平随年龄上升，从青年至老年，男性上升约20％，而女性升高达35％，上升趋势基本一致。不同年龄组间上升幅度有明显的男女差异，青年期男性大于女性，中年以后女性上升幅度增大，从40～49岁至50～59岁组男性平均上升3％．而女性上升达14％．60岁以后上升很少。所以总胆固醇水平在50岁以前男性高于女性，50岁以后女性高于男性。以1985年、1991年和2001年为例，无论男女，年龄标化的高胆固醇检出率[总胆固醇≥5．17mmol／L(200mg/dL)、≥5．69mmol/L(220mg/dL)及≥6．02mmol／L(240mg/dL)]1991年比1985年明显增高，而2001年与1991年相差不多且有所回落。目前北京市职业人群的总胆固醇年龄调整均值男性4．86mmol/L(188mg/dL)，女性4．78mmol/L(185mg/dL)，年龄标化高胆固醇检出率≥5．7mmol／L者约20％，≥6．2mmol/L者约10％。结果提示，北京市职业人群血清总胆固醇水平及年龄标化的高胆固醇检出率在80年代升幅较大．90年代不再升高且有所回落。     

The benign long term effect of cholesterol crystal synovial cysts

Summary Synovial effusions containing cholesterol crystals are uncommon. Most of the few reported cases have been found in patients with seropositive rheumatoid arthritis. In vitro studies, as well as an animal model, have suggested that cholesterol crystals could have a role in inflammation of the joints. In this report we present a case of seronegative arthritis, complicated by large carpal synovial cysts which contained numerous cholesterol crystals. The long-term presence of the cysts, without evidence of joint destruction, suggests that cholesterol crystal formation is probably a rare epiphenomenon, rather than a harbinger of inflammation.     

Effects of Statins on High-Density Lipoproteins: A Potential Contribution to Cardiovascular Benefit

PURPOSE: The objective was to systematically review clinical trial data on the effects of statins on high-density lipoproteins (HDL) and to examine the possibility that this provides cardiovascular benefits in addition to those derived from reductions in low-density lipoproteins (LDL). METHODS: The PubMed database was searched for publications describing clinical trials of atorvastatin, pravastatin, rosuvastatin, and simvastatin. On the basis of predefined criteria, 103 were selected for review. RESULTS: Compared with placebo, statins raise HDL, measured as HDL-cholesterol (HDL-C) and apolipoprotein A-I (apo A-I); these elevations are maintained in the long-term. In hypercholesterolemia, HDL-C is raised by approximately 4% to 10%. The percentage changes are greater in patients with low baseline levels, including those with the common combination of high triglycerides (TG) and low HDL-C. These effects do not appear to be dose-related although there is evidence that, with the exception of atorvastatin, the changes in HDL-C are proportional to reductions in apo B-containing lipoproteins. The most likely explanation is a reduced rate of cholesteryl ester transfer protein (CETP)-mediated flow of cholesterol from HDL. There is some evidence that the statin effects on HDL reduce progression of atherosclerosis and risk of cardiovascular disease independently of reductions in LDL. CONCLUSION: Statins cause modest increases in HDL-C and apo A-I probably mediated by reductions in CETP activity. It is plausible that such changes independently contribute to the cardiovascular benefits of the statin class but more studies are needed to further explore this possibility.     

TNF-α对HepG2细胞LXRα介导的胆固醇外流的影响及其分子机制

 目的:观察肿瘤坏死因子α（TNF-α）对肝X受体α（LXRα）启动子活性及其下游ATP结合盒转运蛋白（ABCA1和ABCG1）表达的影响,从而探讨TNF-α加速HepG2细胞内胆固醇积聚的分子机制。方法:构建LXRα基因的启动子表达载体,观察炎症因子TNF-α对LXRα启动子活性的影响,进一步将HepG2细胞分为对照组（control）、TNF-α组（20 μg/L）、高脂组（LDL,100 mg/L）及联合处理组（TNF-α 20 μg/L+ LDL 100 mg/L）。采用实时定量PCR和Western blotting检测LXRfα、ABCA1和 ABCG1的mRNA及蛋白的表达。［3H ］标记胆固醇,液体闪烁计数法检测胆固醇外流量。油红O染色和定量比色法分析细胞内胆固醇的含量。结果:成功构建LXRα启动子的萤火虫萤光素酶报告质粒,证明了该启动子有明显活性,TNF-α能明显抑制LXRα启动子的活性。进一步检测发现,和对照组相比,TNF-α下调了LXRα、ABCA1和ABCG1 mRNA与蛋白表达。高脂组胆固醇外流量增加,而TNF-α组胆固醇外流量明显降低。油红O染色显示,TNF-α使细胞内脂质染色明显增加。结论: TNF-α可通过抑制LXRα启动子活性从而抑制HepG2细胞内胆固醇外流导致肝细胞内脂质异常积聚。