50岁以下冠心病患者冠脉病变特点及其危险因素的研究

目的：分析探讨50岁以下冠心病患者的冠状动脉（冠脉）病变特点及危险因素。方法：将生活于北京地区的128例50岁以下因冠心病或怀疑冠心病而行冠脉造影的患者，根据造影结果分为冠心病组（70例）和非冠心病组（58例），除分析其冠脉病变特点外，并将其危险因素对照分析。结果：前降支受累率最高，为78．6％。男性多支病变多于女性（P＜0．05）。冠心病家族史在两组间有显著差异（P＜0．05）。载脂蛋白A1（apoA1)、总胆固醇与高密度脂蛋白比值（TC／HDL）及载脂蛋白A1与载脂蛋白B比值（apoA1/apoB)在两组间均有显著差异（P＜0．05）。结论：冠脉病变男性重于女性，冠心病家族史是重要危险因素。apoA1和TC／HDL及apoA1/apoB对预测冠心病有一定意义。     

血浆apoB100水平升高不宜作为家族性混合型高脂血症与家族性高胆固醇血症鉴别诊断的指标

目的 探讨家族性混合型高脂血症与家族性高胆固醇血症血浆载脂蛋白A1（apoA1)、载脂蛋白B100（apoB100)水平的异同。方法 病例－对照／家系设计,家族性混合型高脂血症家系15个（93人）;家族性高胆固醇血症家系11个（94人）;对照家系12个（67人）。比较家系间及家系内受累组与未受累组血浆apoA1与apoB100水平。结果 两种高脂血症家系间及两种家系内受累组间血浆apoA1与apoB100水平未见统计学显著性差异;与对照家系相比,两种高脂血症家系血浆apoB100水平均显著升高（P＜0．01）,同时,家系内受累组血浆apoB100水平显著高于未受累组（P＜0．01）。结论 两种高脂血症家系受累组血浆apoB100水平均显著升高,故血浆apoB100水平升高不宜作为家族性混合型高脂血症与家族性高胆固醇血症鉴别诊断的指标。     

急性冠脉综合征患者血脂6项指标联合检测的临床意义

目的：探讨急性冠脉综合征(ACS)患者血脂6项指标的变化和临床意义。方法：比较59例ACS患者与47例健康对照组血浆血脂6项指标：总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)和载脂蛋白B(ApoB)、载脂蛋白A1(apoA1)的水平。结果：ACS组TC、TG、L...     

ApoB/apoA1 is an effective predictor of coronary heart disease risk in overweight and obesity

We investigated the relationship of apoB/apoA1 ratio and coronary heart disease (CHD) in persons who were overweight or obese.The subjects were divided by the body mass indexes (BMI) into the normal weight group (n=397,BMI<24 kg/m 2) and the overweight group (n=400,BMI>24 kg/m 2).Our results showed that the overweight group had higher blood pressure [(130.15±19.01) mmHg vs (123.66±18.70) mmHg] and higher levels of blood sugar [(7.09±2.89) mmol/L vs (6.21±2.59) mmol/L],triglyceride [(1.93±1.19) mmol/L vs (1....     

脑梗死伴颅内动脉粥样硬化性狭窄的影响因素分析

目的 探讨脑梗死伴颅内动脉粥样硬化性狭窄的影响因素。 方法 选取脑梗死住院患者 464 例,根据头颅 MRA 和 颈部 CEMRA 结果分为单纯颅内动脉狭窄（ICAS）组 199 例、单纯颅外动脉狭窄（ECAS）组 47 例、颅内合并颅外动脉狭窄（IECAS）组 113 例和无颅内颅外动脉狭窄（NCAS）组 105 例;其中 ICAS 组颅内动脉狭窄率≥50% 135 例、＜50% 64 例。测定与比较以上 4 组患 者间血清 TG、TC、LDL-C、HDL-C、载脂蛋白 B（apoB）、载脂蛋白 A1（apoA1）、尿酸（UA）和同型半胱氨酸（Hcy）等指标的差异,采用 单因素分析和多因素 logistic 回归分析脑梗死伴颅内动脉粥样硬化性狭窄的影响因素。 结果 以上 4 组患者平均年龄,高血压、糖尿 病患病情况,TC、LDL-C 水平,apoA1、apoB、apoB/apoA 方面比较,差异均有统计学意义（均 P＜0.05）。颅内外动脉狭窄分布显示,颅 外血管病变以颈内动脉颅外段和椎动脉颅外段为主,颅内动脉病变以大脑中动脉和颈内动脉颅内段为主。多支颅内动脉狭窄患者的 apoB 水平明显高于单支颅内动脉狭窄患者（P＜0.05）。apoB（OR=8.821）、apoB/apoA1（OR=10.149）和吸烟（OR=2.093）是脑梗死伴 颅内动脉粥样硬化性狭窄的影响因素。 结论 apoB、apoB/apoA1 是颅内动脉粥样硬化性狭窄的独立危险因素,可能成为今后临床 上筛查与治疗高危人群的靶点。     

血浆载脂蛋白水平及apoB/apoA1与急性冠脉综合征的相关性研究

目的探讨血浆载脂蛋白A1,B(apoA1,B)水平及apoB/apoA1比值与急性冠综合征(ACS)的相关性。方法入选我院经冠脉造影检查的119例可疑冠心病患者,其中不稳定型心绞痛组(UA组)54例,急性心肌梗死组(AMI组)33例,冠脉造影阴性者设为对照组32例。分别测定血浆总胆固醇(TC)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)及apoA1、apoB,计算apoB/apoA1比值,比较各组各项测定指标及apoB/apoA1的水平变化,并进行多因素logistic回归分析。结果 UA组与AMI组apoA1分别为(1.10±0.12)mmol/L,(1.07±0.14)mmol/L,与对照组(1.19±0.17)mmol/L相比显著偏低(P均<0.01);UA组与AMI组apoB分别为(1.00±0.14)mmol/L,(1.10±0.13)mmol/L,与对照组(0.92±0.14)mmol/L相比显著偏高(P<0.05,P<0.01);UA组与AMI组的apoB/apoA1分别为0.91±0.19,0.97±0.18,与对照组(0.79±0.18)相比显著偏高(P<0.05,P<0.01)。多因素logistic回归分析示apoB/apoA1(OR=4.462,95%CI2.153～9.255,P<0.001)及apoB(OR=2.764,95%CI1.174～6.511,P<0.001)与ACS显著相关。结论 apoB与apoB/apoA1均是ACS的独立危险因素,而apoB/apoA1是ACS最显著的独立危险因素。     

Urine acidification has no effect on peroxisome proliferator-activated receptor (PPAR) signaling or epidermal growth factor (EGF) expression in rat urinary bladder urothelium

We previously reported prevention of urolithiasis and associated rat urinary bladder tumors by urine acidification (via diet acidification) in male rats treated with the dual peroxisome proliferator-activated receptor (PPAR)alpha/gamma agonist muraglitazar. Because urine acidification could potentially alter PPAR signaling and/or cellular proliferation in urothelium, we evaluated urothelial cell PPARalpha, PPARdelta, PPARgamma, and epidermal growth factor receptor (EGFR) expression, PPAR signaling, and urothelial cell proliferation in rats fed either a normal or an acidified diet for 5, 18, or 33 days. A subset of rats in the 18-day study also received 63 mg/kg of the PPARgamma agonist pioglitazone daily for the final 3 days to directly assess the effects of diet acidification on responsiveness to PPARgamma agonism. Urothelial cell PPARalpha and gamma expression and signaling were evaluated in the 18- and 33-day studies by immunohistochemical assessment of PPAR protein (33-day study only) and quantitative real-time polymerase chain reaction (qRT-PCR) measurement of PPAR-regulated gene expression. In the 5-day study, EGFR expression and phosphorylation status were evaluated by immunohistochemical staining and egfr and akt2 mRNA levels were assessed by qRT-PCR. Diet acidification did not alter PPARalpha, delta, or gamma mRNA or protein expression, PPARalpha- or gamma-regulated gene expression, total or phosphorylated EGFR protein, egfr or akt2 gene expression, or proliferation in urothelium. Moreover, diet acidification had no effect on pioglitazone-induced changes in urothelial PPARgamma-regulated gene expression. These results support the contention that urine acidification does not prevent PPARgamma agonist-induced bladder tumors by altering PPARalpha, gamma, or EGFR expression or PPAR signaling in rat bladder urothelium.     

TG、HDL-C、ApoA1在老年人2型糖尿病合并急性脑梗塞中的表达

目的探讨TG、HDL-C、apoAl与老年人2型糖尿病合并急性脑梗塞的关系。方法对我科2005年1月-2009年12月收治的老年人2型糖尿病急性脑梗死40例为发病组。健康体检人员40例为对照组,进行血清总胆固醇（CHOL）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白A1、B（apoAl、apoB）、空腹及餐后2小时血糖（GLU）检查。结果发病组TG水平均显著高于对照组（P〈0．01）,HDL-C、apoAl水平显著低于对照组（P〈0．05）。结论高,IG、低HDL-C及apoAl水平是脑梗塞的独立危险因素。剩留血管风险应得到高度重视。     

The role of phospholipid transfer protein in lipoprotein‐mediated neutralization of the procoagulant effect of anionic liposomes

Summary. Background: Serum has the ability to neutralize the procoagulant properties of anionic liposomes, with transfer of phospholipids (PLs) to both high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) particles. Phospholipid transfer protein (PLTP) mediates transfer of PLs between HDL and other lipoproteins and conversion of HDL into larger and smaller particles. Objectives: To examine the role of PLTP in the neutralization of procoagulant liposomes. Methods: Procoagulant liposomes were incubated with different lipoproteins in the presence or absence of PLTP, and then tested for their ability to stimulate thrombin formation. Results and Conclusions: In the absence of added PLTP, the lipoprotein‐enriched fraction, total HDL, HDL₃ and very high‐density lipoprotein (VHDL) were all able to neutralize the procoagulant properties of the liposomes. In these samples, endogenous PLTP was present, as judged by Western blotting. In contrast, no PLTP was present in LDL, HDL₂ and lipoprotein‐deficient serum, all of which displayed no ability to neutralize the procoagulant liposomes. The phospholipid (PL) transfer activity was dependent on both enzyme (PLTP) and PL acceptor (lipoproteins). After treatment of the VHDL fraction with antiserum against PLTP, the neutralization of procoagulant activity was reduced, but could be regained by the addition of active PLTP. The neutralizing activity was dependent on a catalytically active form of PLTP, and addition of a low activity form of PLTP had no effect. In conclusion, PLTP was found to mediate transfer of anionic PLs to HDL and LDL, thereby neutralizing the effect of procoagulant liposomes, resulting in a reduction of procoagulant activity.