糖尿病患者Apo－Al、Apo－B测定及其临床意义

本文对６０例糖尿病患者及６２例正常人的血清载脂蛋白（Ａｐｏ）－Ａｌ，Ａｐｏ－Ｂ高密度脂蛋白（ＨＤＬ）和低密度脂蛋白（ＬＤＬ）水平进行了测定，结果显示：（１）糖尿病患者Ａｐｏ－Ａｌ水平和Ａｐｏ－Ｂ水平均明显高于正常人（Ｐ＜０．０１）。（２）住院治疗前，糖尿病患者血清ＨＤＬ水平明显低于正常人（Ｐ＜０．０１）。（３）住院治疗期间糖尿病患者血清ＨＤＬ水平显著增高（Ｐ＜０．０１），而ＬＤＬ水平无明显改变（Ｐ＞０．０５）。     

The future of proteomics in the study of alcoholism

This article represents the proceedings of a workshop at the 2003 annual meeting of the Research Society on Alcoholism in Fort Lauderdale, FL. The workshop organizers/chairpersons were Chinnaswamy Kasinathan and Paul Manowitz. The presentations were (1) Introduction to the field of proteomics, by Kent Vrana; (2) Use of proteomics in the identification of urinary biomarkers for alcohol intake, by Chinnaswamy Kasinathan, Paul Thomas, and Paul Manowitz; (3) Proteomics screening illuminates ethanol-mediated induction of HDL proteins in macaques, by Kent Vrana, Randy Gooch, Travis Worst, Stephen Walker, Aaron Xu, Peter Pierre, Heather Green, and Kathleen Grant; and (4) Proteomics applied to the study of the liver, by Laura Beretta.     

Familial homozygous hypobetalipoproteinemia

An apparently new form of abetalipoproteinemia, homozygous hypobetalipoproteinemia, was studied in progeny of a mating of two parents each heterozygous for familial hypobetalipoproteinemia, which was characterized by three-generation vertical transmission on both maternal and paternal sides of the family. The two children, with an apparent homozygous form of hypobetalipoproteinemia, had, in addition to abetalipoproteinemia, acanthocytosis, intestinal etpithelial and hepatic steatosis and steatorrhea. No low desity lipoprotein (LDL) was detected by immunodiffusion with antisera to LDL or apoLDL. The defects in apolipoproteins in these two children were the same as those reported in children with abetalipoproteinemia inherited as an autosomal recessive trait. The genetic defect of hypobetalipoproteinemia, when homozygous, can lead to all of the known clinical and biochemical features of abetalipoproteinemia.     

Effect of simvastatin on high density lipoprotein subfractions and apolipoproteins in Type IIa hypercholesterolemia

Summary Changes in plasma concentrations of high density lipoproteins (HDL) and triglycerides may partly explain the ability of cholesterol-lowering drugs to decrease the incidence of coronary heart disease. We measured the response of fasting plasma lipids, lipoproteins, and apolipoproteins in 46 subjects with Type IIa hypercholesterolemia treated with simvastatin for 3 months. The initial dose of simvastatin (10 mg/day) was subsequently increased up to 40 mg/day if the plasma cholesterol concentration had not fallen below 5.2 mmol/l. Plasma concentrations of HDL cholesterol and of the apolipoproteins AI and AII were increased by simvastatin. The increase in HDL cholesterol (9%) was due to increases in both subfractions (HDL₂ 17%; HDL₃ 7%), changes that would be consistent with a beneficial effect on cardiovascular risk. Simvastatin decreased plasma triglyceride concentrations by 25%. Plasma total cholesterol concentrations fell by 35% after 3 months of treatment; this fall was proportional to the initial concentration and was due almost entirely to a 45% fall in low density lipoprotein cholesterol. In contrast, plasma concentrations of lipoprotein Lp(a) were not affected by simvastatin.     

冠心病患者高密度脂蛋白胆固醇与冠脉病变的相关性研究

目的探讨血浆高密度脂蛋白胆固醇(HDL-C)水平与冠脉病变的关系。方法选取153例行冠脉造影确诊的冠心病患者,并对冠脉病变程度进行分型,观察其与各项冠心病危险因素相关指标的关系。结果冠心病患者HDL-C比对照组明显降低,而总胆固醇(TC)、体重指数(BMI)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)比对照组明显增加,急性冠脉综合征组(ACS)患者比稳定型心绞痛组(ACS)HDL-C明显降低,TC明显增加P<0.001。HDL-C与冠脉病变类型、病变支数成负相关,TC与之成正相关。结论HDL-C与冠脉病变程度具有负相关关系。血HDL-C水平有可能成为一项有价值的、能预测冠心病事件的检查方法。     

SERUM LIPID AND APOLIPOPROTEIN A AND B LEVELS IN FAMILIAL HYPERCHOLESTEROLEMIA

Serum lipid and apolipoprotein A (apo A) and B (apo B) levels were studied in a family with familial hypercholesterolemia (FH), which comprised two heterozygous parents, five heterozygous children, one homozygote and one normal child. Lipid levels were compared with those of age- and sex-matched normal controls. All subjects with FH had total serum cholesterol and low density lipoprotein-cholesterol (LDL-C) levels greater than the 90th percentile value for the reference range. High density lipoprotein-cholesterol (HDL-C) levels were less than the corresponding 13th percentile in heterozygous subjects. The homozygous child had grossly elevated levels of LDL-C and apo B, and very low levels of HDL-C and apo A. The most powerful discriminating variable between normal, heterozygous and homozygous family members was the LDL-C/HDL-C ratio.     

A20基因在动脉粥样硬化损伤中对内皮细胞的保护作用

目的　探讨A2 0基因抑制氧化型低密度脂蛋白 (oxidizedlowdensitylipoprotein ,oxLDL)诱导内皮细胞凋亡及相关机制。方法　逆转录 聚合酶链反应检测A2 0基因在oxLDL诱导内皮细胞中的表达。DOTAP脂质体转染pCAGGSEHA2 0和pMAMneo于原代培养的脐静脉内皮细胞 ,经G4 18筛选 ,A2 0表达经免疫荧光鉴定。原位末端标记法、原位杂交检测转染前后oxLDL诱导内皮细胞凋亡情况及同型半胱氨酸蛋白酶 (caspase 3)的表达情况。结果　A2 0基因在oxLDL诱导内皮细胞中不表达。oxLDL诱导内皮细胞凋亡达 2 6 % ,A2 0基因能显著抑制oxLDL诱导的内皮细胞凋亡情况及caspase 3的表达。结论　A2 0基因在动脉粥样硬化的防治中可能有一定作用     

JCL roundtable: Lipids and inflammation in atherosclerosis

Clinical effort in lipidology focuses largely on mitigating effects of atherosclerosis, a pathologic process localized to the intimal layer of larger arteries. This JCL Roundtable brings together 3 leading researchers to discuss the current understanding of pathogenesis in atherosclerosis. We begin by recognizing that low density lipoprotein concentrations in arterial intima far exceed concentrations in other connective tissues, consistent with the response-to-retention hypothesis of atherogenesis. High density lipoproteins facilitate reverse cholesterol transport and also have antioxidant and anti-inflammatory roles. New evidence points to remnants of triglyceride-rich lipoproteins as promoters of atherogenesis, highlighted by deleterious effects of apolipoprotein C-III. The multifaceted role of inflammation is becoming clearer through discoveries related to leukocyte recruitment, efferocytosis, resolution of inflammation, and crystal formation. MicroRNAs represent a new, complex mode of gene regulation bearing on lipoprotein and inflammation biology. Progress in understanding atherosclerosis portends a future in which residual risk related to obesity, diabetes, and other factors will yield to new targeted therapies.