RBP4/TNF-α在冠心病患者血浆中的表达情况及与冠脉病变程度的相关性研究

目的 探讨视黄醇结合蛋白4(RBP4)和肿瘤坏死因子-α(TNF-α)水平与冠心病、冠脉病变程度的关系以及冠心病患者血浆RBP4和TNF-α 两者之间的相关性.方法 选择2015年12月—2017年2月至该院就诊并诊断为冠心病的90例患者临床资料.根据临床特点及结合冠脉造影的结果 分为:稳定型心绞痛(SAP)组28例、不稳定型心绞痛(UAP)组30例、急性心梗(AMI)组32例,另选该院体检健康者30例作为对照组;根据冠脉造影结果再将UAP组和AMI组患者分为单支病变组19例,双支病变组21例,三支病变组22例.采用酶联免疫吸附试验法(ELISA)检测各组患者血浆RBP4、TNF-α 的水平,分析冠心病不同类型及冠脉病变不同程度患者血浆中RBP4、TNF-α 变化趋势及两者之间的相关性,并采用SPSS17.0统计软件对所得数据进行分析.结果RBP4及TNF-α 水平在AMI、UAP、SAP及对照组四组间存在明显差异(P<0.05);RBP4与TNF-α 血浆水平在双支病变组与单支病变组及三支病变组与双支病变组相比呈现升高趋势,但三组血浆RBP4水平差异无统计学意义(P>0.05)、TNF-α 水平存在明显差异(P<0.05);冠心病患者血浆RBP4与TNF-α 血浆水平呈正相关(r=0.906,P<0.001).结论 RBP4及TNF-α 可视为冠心病的重要危险因素,可反映冠心病及冠脉病变的严重程度.冠心病患者血浆RBP4与TNF-α 水平相关,提示RBP4可能通过调节炎性反应,参与冠心病的发生、发展.     

冠心病患者炎性因子的变化及其与血清视黄醇结合蛋白4水平的相关性研究

目的探讨冠心病患者血清高敏C反应蛋白(hs-CRP)、白细胞介素-6(IL-6)、MCP-1与视黄醇结合蛋白4(RBP4)的相关性。方法分别收集健康组、动脉粥样硬化组、CHD组患者,检测其空腹血清RBP4、hs-CRP、IL-6、MCP-1水平。结果与健康组相比,AS组、CHD组患者血清RBP4、hs-CRP、IL-6、MCP-1含量明显升高(P<0.05或P<0.01);相关性分析显示AS组、CHD组患者血清RBP4与炎性因子hs-CRP、IL-6、MCP-1呈正相关。结论 RBP4参与了动脉粥样硬化的炎性反应过程,其可能通过多种途径直接或间接地参与冠心病的发生发展。     

冠心病患者视黄醇结合蛋白4及丝氨酸蛋白酶抑制剂水平分析

目的通过观察人体视黄醇结合蛋白4(RBP4)水平以及人体内脏脂肪特异性丝氨酸蛋白酶抑制剂(vaspin)的变化对冠心病患者的影响,探讨其临床意义。方法收集来自2013年5月至9月在山西省心血管病医院住院患者188例,其中病例组(冠状动脉造影示血管管腔直径狭窄≥50%)100例,对照组(除外冠心病诊断的患者)88例,采用酶联免疫吸附法测定血清RBP4、vaspin浓度。结果 1病例组与对照组在是否吸烟(χ2=7.477,P=0.006)、体质量指数(t=3.550、P=0.001)、C反应蛋白(t=2.61、P=0.013)、网膜素-1(t=2.718、P=0.008)、RBP4(t=2.581、P=0.012)、vaspin(t=2.416、P=0.018)、球状脂连蛋白(t=2.976、P=0.004)、总胆固醇(t=5.161、P=0.001)、低密度脂蛋白胆固醇(LDL-C)(t=3.437、P=0.001)差异有统计学意义;2相关分析显示,冠心病组中,RBP4与C反应蛋白(r=0.501、P=0.001)、总胆固醇(r=0.308,P=0.049)、LDL-C(r=0.399,P=0.008)呈正相关关系,与球状脂连蛋白(r=-0.314,P=0.049)呈负相关关系;vaspin与C反应蛋白(r=-0.426、P=0.004)、总胆固醇(r=-0.366、P=0.016)、LDL-C(r=-0.465,P=0.001)呈负相关关系,与球状脂连蛋白(r=0.364、P=0.009)呈正相关关系;RBP4与vaspin呈负相关(r=-0.512、P=0.001)。3经多因素逐步Logistic多元回归分析,采用逐步回归筛选变量,显示C反应蛋白、RBP4、LDL-C为冠心病的危险因素,血清vaspin球状脂连蛋白低水平为冠心病相关的危险因素。结论1RBP4为冠心病的危险因素;2血清低vaspin水平为冠心病的危险因素,可能是反映严重冠状动脉狭窄的新的血清标记物。     

视黄醇结合蛋白4与冠心病的关系

目的研究视黄醇结合蛋白4(RPB4)与冠心病(CHD)之间的关系。方法研究对象78例,分为两组:正常对照组和冠心病组。测定血浆RPB4水平,采集有关数据。结果冠心病组血浆RPB4水平明显高于正常对照组[(44.72±16.98),(39.60±12.10),P<0.05]。相关分析显示血浆RBP4与腰围、腰臀比、BMI、TC、ln(TG)、FINS、FCP、ln(HOMA-IR)呈正相关。多元逐步回归分析,ln(TG)是血浆RBP4独立相关因素。结论血浆RBP4在冠心病的发病过程中起一定作用。     

视黄醇结合蛋白 4和 C反应蛋白血清水平与绝经后乳腺癌发生转移的相关性

目的 回顾性分析视黄醇结合蛋白4(RBP4)和C反应蛋白(CRP)血清水平与绝经后乳腺癌发生转移的相关性.方法 收集蚌埠医学院第二附属医院2016年11月至2020年6月资料完整的绝经后乳腺癌156例,其中74例无转移为对照组,82例已经转移为观察组.抽取血液样本,采用酶联免疫吸附法(ELISA)检测RBP4及CRP浓度.结果 logistic回归分析提示激素受体阴性、Her-2阴性、Ki67≥14％、高RBP4、高CRP是绝经后乳腺癌发生转移的危险因素(P<0.05).观察组病人血清RBP4和CRP水平高于对照组[(38.68±6.39)μg/mL比(35.09±4.95)μg/mL;(6.42±3.60)mg/L比(4.67±2.72)mg/L](P<0.05).发生内脏转移病人血清RBP4及CRP水平高于发生骨转移病人.ROC曲线下面积分析显示,RBP4联合CRP检测可提高诊断的特异性和敏感性.结论 血清RBP4和CRP与绝经后乳腺癌发生转移有明显相关性.RBP4与CRP对于诊断乳腺癌发生转移具有预测与评估价值.     

视黄醇结合蛋白4遗传多态性与2型糖尿病的关系

视黄醇结合蛋白（retinol binding protein,RBP）属于视黄醇运载蛋白,其血清水平常作为临床营养状况、肝肾疾病的早期诊断和疗效的评价指标。最新研究发现：视黄醇结合蛋白4（RBP4）为一种新的脂肪源性信使,参与了胰岛素抵抗和2型糖尿病的发生。这一发现使得RBP4开始倍受关注。本文主要介绍视RBP4的结构、遗传多态性及其与2型糖尿病之间的最新研究进展。     

早期应用氟伐他汀治疗冠心病80例

冠心病是指冠状动脉粥样硬化使血管腔狭窄／阻塞或／和因冠状动脉功能性改变（痉挛）导致心肌缺血缺氧或坏死而引起的心脏病,统称为冠状动脉性心脏病Ⅲ。冠心病可造成严重的心血管事件,死亡率高,早期应用他汀类药物治疗冠心病可减少心血管事件发生,提高生存率。     

冠心病的预防

危险因素的早期检测和危险分层是冠心病预防的重点,现已明确与心血管疾病有关的8个主要危险因素为：高血压、吸烟、饮酒、缺乏身体活动、水果和蔬菜摄入不足、肥胖、高胆固醇血症和糖尿病。但回顾分析发现约1／3冠心病患者并不具备“经典”危险因素,因而非“经典”危险因素的筛查具有重要意义。近年来大量研究提示高同型半胱氨酸血症与冠心病发生相关,进一步研究发现血液中同型半胱氨酸浓度每增加5mmol／L．其患冠心病的风险增加近20％。提示高同型半胱氨酸血症可能是冠心病一项独立危险因素;另外,有研究刚提示。     

冠心病患者冠状动脉病变与左心室舒张功能的相关性分析

<正>冠心病是常见的心内科疾病,是由于冠状动脉发生粥样硬化致心肌缺氧、缺血而引发的心脏病,心力衰竭是其重要并发症之一。近年来的一些临床研究证实~([1-3]),冠心病患者发生左心室收缩功能降低之前,就已经出现舒张功能异常。但目前临床对冠心病患者冠状动脉病变严重程度与机体左心舒张功能下降程度之间的关联性研究还不多。本研究旨在通过分析不同冠状动脉病变程度的冠心病不稳定型心绞痛患者左心室舒张功能的状况,进     

糖调节受损对冠状动脉粥样硬化影响

目的探讨糖调节受损对冠心病患者冠状动脉病变的影响。方法收集2007年12月至2009年12月在景德镇市第一人民医院行冠状动脉造影确诊为冠心病的患者共204例,分成糖尿病组（68例）、糖调节受损组（76例）及血糖正常组（60例）,分析三组之间冠状动脉病变情况。结果 204例冠心病患者中,33.3%合并糖尿病,37.3%有糖调节异常,29.4%血糖正常,三组间的基线水平差别;糖调节受损组及糖尿病组较血糖正常组更容易发生多支血管病变（1.89±0.71VS2.07±0.79VS1.59±0.81,P〈0.05）,且糖调节受损与糖尿病组之间差异无明显统计学意义。结论糖调节受损和糖尿病具有同等危害冠状动脉的作用,较血糖正常者更容易发生多支冠状动脉病变。餐后2h血糖、HbA1c增高是急性冠脉综合征的危险因素,而HDL-C起着保护作用,提示冠心病合并糖调节受损患者需早期防治。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.