不同孕期D-二聚体浓度分析

目的 :探讨产前孕妇血浆D 二聚体水平。方法 :排除D 二聚体增高的相关性疾病 ,将孕妇分成早、中、晚孕三组 ,并设非孕育龄妇女对照组 ,用免疫比浊法对检测对象进行D 二聚体水平分析。结果 :对照组D 二聚体为 0 .2 3 μg/ml± 0 .0 8μg/ml;早、中、晚孕组分别为0 .3 3 μg/ml± 0 .0 9μg/ml、0 .76μg/ml± 0 .2 4μg/ml、1.5 1μg/ml± 1.0 7μg/ml。孕妇各组比较差异显著 (P <0 .0 1) ,与对照组比较 ,D 二聚体均有明显增高 (P <0 .0 1)。结论 :产前孕妇D 二聚体水平普遍高于健康妇女 3～ 4倍。在进行DIC或静脉血栓临床诊断时 ,不能套用健康人正常参考范围 ,否则会造成临床诊断的错误。必须注意对纤维蛋白原 >5 g/L ,D 二聚体正常或略高于正常 ,或显著高于正常的产前孕妇进行动态观察 ,防止DIC发生     

Serum gastrin concentrations in children with primary gastroesophageal reflux and gastroesophageal reflux secondary to cow's milk allergy

PurposeThe assessment of the serum gastrin concentrations and the role of enterohormone in children with primary acid gastroesophageal reflux (GER) and GER secondary to cow's milk allergy (CMA).Materials/Methods138 children were diagnosed with pathological acid GER on the basis of pH-metric examination. 76 (28.8%) patients had primary GER and 62 (23.5%) patients had GER secondary to CMA.Serum gastrin concentration (fasting and postprandial) was assessed before treatment and 1 and 2 years after initiation of the therapy.ResultsThe children with primary GER had the fasting gastrin concentration 69.46 ± 11.87 μU/ml before treatment, 77.86 ± 26.35 μU/ml after 1 year and 83.78 ± 25.21 μU/ml after 2 years of treatment. The children with GER secondary to CMA had gastrin concentrations 89.61 ± 26.75, 73.17 ± 19.49 and 73.90 ± 20.31 μU/ml respectively. The mean postprandial gastrin concentration after treatment was higher than before treatment in children with both primary and secondary GER. The primary GER group had postprandial gastrin concentration 96.07 ± 33.51 μU/ml before treatment and 116.06 ± 33.95 μU/ml and 118.48 ± 33.96 μU/ml after 1st and 2nd year of therapy respectively. The secondary GER group had postprandial gastrin concentration 85.33 ± 14.12 μU/ml before treatment and 106.55 ± 24.51 μU/ml and 110.36 ± 24.67 μU/ml after 1st and 2nd year of therapy respectively.ConclusionsThe mean fasting serum gastrin concentrations in patients with primary and secondary GER were similar and mean postprandial concentrations were higher than fasting concentrations in both study groups.     

Pharmacokinetics of degradation products of fibrin and fibrinogen during alteplase therapy of acute myocardial infarction

Pharmacokinetics of fibrin degradation products (FbDP), D-dimers, fibrinogen degradation products (FgDP) and total degradation products (TDP) in plasma were investigated using ELISA methods in 12 patients undergoing therapy with alteplase (100 mg/3 h) for acute myocardial infarction. Peak concentrations of all degradation products occurred significantly later (1.6–2.5 h) than peak alteplase levels (2 min). Peak D-dimer concentrations (mean 2.6 μg/ml) were significantly lower than those of FbDP (7.1 μg/ml) or FgDP (7.8 μg/ml). However, the half-life of D-dimers (mean 13.3 h) was more than 4.5-fold longer than that of FbDP (2.9 h) or FgDP (2.8 h) (p<0.001). Consequently, areas under the plasma concentration-time curve (AUC) of D-dimers were comparable with those of FbDP or FgDP The ratios AUC(FbDP)/AUC(FgDP) and AUC(D-dimers)/AUC(FgDP) are proposed as new indices of fibrin specificity. Their values in this study (geometric mean, 95% CI) were 1.15 (0.60–2.20) and 1.30 (0.52–3.24) respectively. It is concluded that cross-linking may prolong the half-life of fibrin degradation products, and that complete time profiles of fibrin- and fibrinogen degradation products in plasma, rather than single point measurements, are essential for reliable quantification of fibrin specificity.     

Impact of non-di-(2-ethylhexyl)phthalate cardiopulmonary bypass tubes on inflammatory cytokines and coagulation-fibrinolysis systems during cardiopulmonary bypass

Di-(2-ethylhexyl)phthalate (DEHP), an excellent plasticizer for poly(vinyl chloride) (PVC), is a known endocrine-disrupting chemical. This study was designed to investigate whether a new non-DEHP bilayer tube reduced the release of DEHP, suppressed inflammatory cytokines, and altered coagulation-fibrinolysis systems. Sixteen patients undergoing coronary artery bypass grafting (CABG) were randomly assigned to the non-DEHP bilayer group (group B, n = 8), or the noncoated PVC group (group N, n = 8). The level of DEHP in the blood was measured before and after cardiopulmonary bypass (CPB). The levels of interleukin-6 (IL-6), D-dimer, and thrombin-antithrombin complex (TAT) were also measured at six points during and after CPB. DEHP was significantly lower in group B (472 ± 141 ng/ml) after CPB compared with group N (2094 ± 1046 ng/ml). The IL-6 level was significantly lower in group B (151 ± 131 pg/ml) than group N (206 ± 224 pg/ml) 180 min after protamine administration. The D-dimer level was significantly lower in group B 60 min after protamine administration (6.2 ± 2.4 μg/ml in group B vs 10.4 ± 4.5 μg/ml in group N) and 180 min after protamine administration (4.4 ± 0.7 μg/ml in group B vs 7.3 ± 2.7 μg/ml in group N). Group B had a tendency toward reduced postoperative bleeding compared with group N at any time. The bilayer tube was superior to the noncoated tube in terms of the inhibition of DEHP release, inflammatory cytokines, and the fibrinolysis system.     

<Emphasis Type="SmallCaps">D</Emphasis>-dimer concentrations in dogs with kidney disease with or without protein-losing nephropathy

Limited information is currently available regarding the range of D-dimer concentrations in dogs with kidney disease (KD). The objective of the present cross-sectional study was to investigate the concentration of D-dimers in dogs with KD irrelevant of the underlying cause or the time course of the KD and the potential association of D-dimers elevation with serum creatinine concentration, concurrent protein-losing nephropathy (PLN) or the age of the animals. D-dimers were measured by a semi-quantitative plasma latex agglutination assay in 31 healthy dogs (group A) and in 30 dogs with KD (group B), without evidence of concurrent extra-renal disease that may precipitate hypercoagulation. Significantly higher median D-dimer concentrations (p?=?0.0133) and a higher prevalence of increased D-dimers (≥250 μg/L) (p?=?0.011) were documented in dogs with KD as compared to healthy dogs, and the increased D-dimers were not associated with the serum creatinine concentration, the coexistent PLN or the age of the dogs. In conclusion, the detection of increased D-dimers in the context of impaired kidney function should be cautiously interpreted in the dog and should not be invariably assumed to imply the presence of a state of hypercoagulability.     

一氧化氮合酶2抑制剂对大鼠心肌梗死后左心室形态及心功能的影响

目的：观察选择性一氧化氮合酶2（NOS2）抑制剂S-甲基硫脲（SMT）对心肌梗死（MI）后左心室形态学和血流动力学指标的影响，探讨NOS2在MI后心功能障碍形成过程中的作用。方法： 于大鼠冠状动脉结扎前30 min给予SMT灌胃，6周后测定左心室形态学和血流动力学指标、心肌NOS2表达量、血浆NO2-/NO3-水平、心肌纤维化程度。结果： MI后6周，心脏非梗死区NOS2表达量、血浆NO2-/NO3-水平、中心静脉压和左室舒张末压高于对照组。使用SMT可降低血浆NO2-/NO3-水平［(26.6±6.1） μmol/L vs （50.1±10.4） μmol/L, P＜0.01］，减少心肌梗死范围（36.0%±7.2% vs 42.6%±8.6%, P＜0.05），减轻心室扩张［LVD，（6.6±0.3） mm vs （7.2±0.3） mm, P＜0.01］，减小心肌细胞直径［(15.1±1.6） μm vs （16.9±2.3） μm, P＜0.05］，减轻心肌纤维化［CVF，4.1%±1.1% vs 5.7%±1.2%, P＜0.01］，降低中心静脉压［（0.9±0.3） mmHg vs （1.5±0.5） mmHg, P＜0.01］和左室舒张末压［（8.1±2.4） mmHg vs（13.4±3.1） mmHg, P＜0.01］，提高存活率（72.4% vs 39.3%, P＜0.05）。结论： 大鼠MI后，NOS2可能起促进心功能障碍形成的作用。抑制NOS2可以减轻心室重构，改善心功能。     

Comparative thrombolytic and immunogenic properties of staphylokinase and streptokinase

The comparative thrombolytic properties of natural (STAN) and recombinant (STAR) staphylokinase (STA) and of streptokinase were studied in hamsters with a pulmonary embolus consisting of a platelet-poor, platelet-rich (300000 platelets/μI), platelet-enriched (1500 000 platelets/ μl) or mechanically compressed human plasma clot. Intravenous infusion over 1 h in doses ranging between 0 and 0.50 mg/kg induced dose-dependent progressive clot lysis without systemic fibrinogen breakdown. The relative thrombolytic potencies, on a weight base, of the STA preparations versus streptokinase were comparable in the platelet-poor clot model (50% lysis requiring 13 μg/kg STA and 12 μg/kg streptokinase) and in the platelet-rich clot model (50% lysis with 28 μg/kg STA and with 32 μg/kg streptokinase), but 5-fold higher in the platelet-enriched clot model (50% lysis with 46 μg/kg STA and with 210 μ/kg streptokinase) and 2-fold higher in the mechanically compressed clot model (50% lysis with 36 μg/kg STA and with 71 μg/kg streptokinase).Dog plasma at baseline contained streptokinase-neutralising activity (neutralising 0.24±0.14 μg streptokinase per ml plasma in a human plasma-based clot lysis assay, mean ±SD) but apparently no STA-neutralising activity. Repeated administration of 40 μg/kg over 1 h of streptokinase at weekly intervals in 5 dogs, increased the streptokinase-neutralising titre to 1.1±0.98 μg/ml plasma after 2 weeks and to 2.9±2.5 μg/ml after 3 weeks (p=0.13 and 0.05 versus baseline, respectively), whereas the thrombolytic potency towards a ¹²⁵I-fibrin-labelled plasma clot inserted into an extracorporeal arteriovenous loop was reduced from 58±4% at baseline to 10±3% after 2 weeks and 4±1% after 3 weeks (p<0.001 vs baseline). Repeated weekly administration of an equipotent dose of STA (4 μg/kg) did not induce measurable STA-neutralising activity after 2 weeks and was associated with persistent, although somewhat reduced clot lysis (58 ± 4% lysis at baseline and 33±7% at 2 weeks, p=0.02). After 3 weeks however, STA-neutralising activity became detectable in plasma (0.34±0.30 μg/ml, p=0.07 vs baseline) and resistance to clot lysis became obvious (6±2% versus a baseline value of 58±4%, p<0.01).Thus, in the hamster model, STA has a thrombolytic potency towards platelet-poor and platelet-rich clots comparable to that of streptokinase, but it is relatively more efficient than streptokinase for the dissolution of platelet-enriched or retracted clots. Furthermore, STA might be less immunogenic than streptokinase as evidenced by less rapid induction of antibody formation and resistance to clot lysis upon repeated administration. Thrombolytic therapy of patients with acute myocardial infarction with STA thus might constitute a potential alternative to treatment with streptokinase, with a better efficacy towards platelet-rich arterial clots and possibly with reduced allergic side effects.     

The investigation for the relationship among serum leptin,erythrocyte membrane Ca2+-ATPase activity and hypertensive disorder complicating pregnancy

Objective: To study the significance of Leptin and the activity of erythrocyte membrane Ca2+-ATPase (EMCA) in the development of hypertensive disorder complicating pregnancy. Methods: Radioimmunoassay was used to test the level of serum Leptin,and the activity of EMCA was determined chemically in 38 pregnant women with hypertensive disorder complicating pregnancy and 36 normotensive pregnant women. Results: The level of serum Leptin in hypertensive disorder complicating pregnancy(gestational hypertension: 13.76 ± 3.46 ng/ml; preeclampsia:15.76 ± 5.47 ng/ml; eclampsia: 18.32 ± 6.38 ng/ml)was significantly higher than that in normotensive pregnant women (11.33 ± 2.93 ng/ml), respectively. The average EMCA activity of patients with hypertensive disorder complicating pregnancy (gestational hypertension: 1.65 ± 0.24 μmol· pi/mg·h; preeclampsia: 1.37 ± 0.19 μmol·pi/mg·h; eclampsia:1.12 ± 0.14 μ mol·pi/mg·h) was significantly lower than that of normotensive pregnant women(1.83 ±0.38 μ mol·pi/mg·h),respectively. There was a negative correlation between the level of serum Leptin and the activity of RMCA in hypertensive disorder complicating pregnancy (r = -0.63). Conclusion: Inhibition of EMCA activity of erythrocyte in hypertensive disorder complicating pregnancy may increase cytoplasmic free calcium, which contributes to the development of hypertensive disorder complicating pregnancy. The negative correlation between the level of serum Leptin and the activity of EMCA, also suggested that serum Leptin and the activity of EMCA may play a role in the development of hypertensive disorder complicating pregnancy.     

Measurement of aortic compliance from the transthoracic admittance plethysmogram in the living dog

An attempt was made to measure the compliance and elastic modulus of the thoracic aorta from simultaneous recordings of the transthoracic admittance plethysmogram and intra-aortic pressure in living dogs. Initially, the compliance values determined by this method were correlated with those measured from the volume-pressure relationships in three different silicone-rubber tubes; these two groups of values were consistent with each other within the error range of ±10%. The mean value of the compliance of the thoracic aortae in four normal dogs (13–15 kg) measured by this method was 0·00387±0·00100 ml/mmHg cm. The elastic modulus E and velocity v of the pulse wave were calculated from this value; E=2·71±0·79×10⁵ dN/m² and v=4·52±2·44 m/s. These data were compared with those reported previously by other investigators. Taking simplicity, safety and practicability into consideration, it was concluded that this method would only be useful in clinics for the rough estimation of the elastic properties of the thoracic aorta.     

Pharmacokinetics of multiple doses of ceftizoxime and their influence on fecal flora

The pharmacokinetics of ceftizoxime, a new β-lactam antibiotic, were studied in eight normal volunteers after single and multiple i.v. doses of 2×2 g daily for eight days. The mean maximum serum concentration after the first 20 min of infusion on the first day was 176.9 ± 32.9 μg/ml decreasing to 11.0 ± 4.1 μg/ml after 4 h and to 0.67 ± 0.2 μg/ml after 12 h. Mean 12 h urine recovery was 78.8 ± 9.0 %. The half-life of ceftizoxime was 136 ± 36 min. Volume of distribution was 22.9 ± 8.1 1/100 kg body weight, AUC_tot 208 ± 33 μg/ml · h, total body clearance 151 ± 33 ml/min, and renal clearance 110 ± 23 ml/min. No ceftizoxime accumulation was registered during the administration period. Computed multiple-dose values were in good agreement with the measured values, and the pharmacokinetic parameters on the first, fourth and eighth days showed no significant differences. During the study period, the fecal flora displayed a reduction of sensitive gram-negative aerobic bacteria, a slight increase in the amount of enterococci (10⁶ to 10⁸/g feces), and no change in the number ofBacteroides fragilis. Some resistant gram-negative strains increased during the administration period, but most of them could no longer be detected two weeks after administration. Tolerance of ceftizoxime was good in four volunteers. Four other volunteers had gastro-intestinal symptoms and mild fever reactions. One female volunteer was assumed to have an allergic drug reaction. Biochemical, hematological, virological and serological data showed no abnormalities in seven volunteers.     

可溶性HLA-G1与NK-92细胞表面ILT2及KIR2DL4受体相互作用的研究

 目的 探讨可溶性 HLA-G1（sHLA-G1）对人 NK-92 细胞杀伤活性的抑制与细胞表面免疫球蛋白样转录分子 2（ILT2）和杀伤细胞免疫球蛋白样受体 2DL4（KIR2DL4）受体的关系。 方法 ①通过原核表达技术获得 sHLA-G1 重组蛋白（重组蛋白），并采用蛋白质印迹法进行鉴定。②取 NK-92 细胞，加入终浓度 20 μg/ml 的重组蛋白分别培养 10、30 min，再分别加入抗 HLA-G1/G5、抗ILT2 和抗 KIR2DL4 抗体，采用流式细胞术检测各组 NK-92 细胞表面 sHLA-G1 和 ILT2、KIR2DL4 受体表达阳性率；以 NK-92 细胞单独培养作为对照组。③以人白血病 K562 细胞为靶细胞，以经不同方式处理的 NK-92 细胞为效应细胞，效靶比为5:1，共同培养 2 h，采用流式细胞术检测 NK-92 细胞对 K562 细胞的杀伤率。NK-92 细胞处理方式为单纯重组蛋白处理（分别加入终浓度为 0、10、20 μg/ml 的重组蛋白培养 30 min）和表面受体封闭 + 重组蛋白处理（分别加入抗 ILT2、抗 KIR2DL4、抗 LT2 + 抗 KIR2DL4 抗体培养 30 min，再分别加入终浓度为 0、10、20 μg/ml 的重组蛋白培养 30 min）。 结果 ①蛋白质印迹分析表明所获重组蛋白为带有组氨酸标签的特异蛋白。②NK-92 细胞与 20 μg/ml 重组蛋白共培养 30 min 后，sHLA-G1 表达阳性率明显高于而 ILT2、KIR2DL4 受体表达阳性率均明显低于对照组（均 P < 0.05）。③以终浓度 0、10、20 μg/ml 的重组蛋白处理的 NK-92 细胞对 K562 细胞的杀伤率分别为 39.79% ± 2.00%、27.79% ± 0.75%、21.36% ± 0.67%（两两比较，均 P < 0.01）；单独封闭 ILT2 受体，杀伤率分别为 23.09% ± 1.63%、21.13% ± 0.38%、18.42% ± 0.47%（两两比较，均 P < 0.01）；单独封闭 KIR2DL4 受体，杀伤率分别为 30.74% ± 0.44%、26.03% ± 0.38%、21.15% ± 0.35%（两两比较，均 P < 0.01）。 结论 sHLA-G1 通过与 NK-92 细胞表面 ILT2 和 KIR2DL4 受体直接结合而抑制 NK-92 细胞的杀伤活性。     

增强自噬减轻大鼠造影剂所致急性肾损伤的实验研究

目的 建立造影剂所致急性肾损伤(CI-AKI)大鼠模型,探讨自噬在CI-AKI中的作用及机制.方法 将18只雄性Sprague-Dawley大鼠随机分为对照组(Con组)、CI-AKI组和雷帕霉素+造影剂组(Rapa组).CI-AKI组腹腔注射超大剂量的碘海醇(12.25 g/kg I),Rapa组于碘海醇注射前1周连续腹腔注射雷帕霉素(5 mg/(kg·d)),Con组腹腔注射等剂量的生理盐水.注射后24 h观察大鼠血肌酐水平、肾组织病理、肾组织中LC3Ⅱ/Ⅰ和Beclin-1表达水平及过氧化氢酶(CAT)含量的变化.结果 与Con组比较,CI-AKI组大鼠血肌酐水平明显升高((239.93±27.00) μmol/L比(51.70±10.59)μmol/L,P＜0.05),肾小管重度损伤,肾组织中自噬相关蛋白LC3Ⅱ/Ⅰ和Beclin-1表达均增加(均P＜0.05),而CAT含量减少((14.86±0.32)U/mg比(18.72±1.46)U/mg),差异具有统计学意义(P＜0.05).与CI-AKI组比较,雷帕霉素预处理增加了肾组织中LC3Ⅱ/Ⅰ和Beclin-1的表达及CAT含量((17.62±1.86)U/mg比(14.86±0.32)U/mg,P＜0.05),减轻了造影剂所致的肾小管损伤,并降低了血肌酐水平((187.62±47.76) μmol/L比(239.93±27.00) μmol/L),差异具有统计学意义(P＜0.05).结论 造影剂可诱导自噬激活,增强自噬可减轻造影剂所致氧化应激损伤及肾损伤.     

丙型肝炎患者HCV-RNA载量与免疫球蛋白及补体表达水平的相关性

目的 探讨丙型肝炎患者HCV-RNA载量与免疫球蛋白及补体表达水平的相关性.方法 收集2014年6月至2016年5月西安市第九医院收治的丙型肝炎患者132例作为研究对象,对其进行HCV-RNA病毒载量检测,按照检测结果将其分为低载量、中载量以及高载量组,对各组进行免疫球蛋白IgA、IgG、IgM检测以及补体C3、C4检测,分析丙肝患者病毒载量与免疫球蛋白及补体水平的相关性.结果 丙型肝炎患者IgA、IgG、IgM表达量分别为[(3.95±0.72) g/L,(19.33±4.64) g/L及(2.93±0.50)g/L],高于健康对照组的表达量[(2.13 ±0.51) g/L,(11.25±2.63) g/L及(1.21±0.35) g/L],C3、C4表达量分别为[(0.82±0.19) g/L及(0.13±0.08)g/L],低于健康对照组[(1.20±0.31)g/L及(0.27±0.11)g/L],差异有统计学意义(P＜0.05).不同病毒载量患者免疫球蛋白及补体表达水平存在差异(P＜0.05).Pearson相关性分析结果显示,HCV-RNA病毒载量与血清免疫球蛋白表达水平呈正相关,与血清补体表达水平呈负相关(P＜0.05).结论 不同病毒载量丙型肝炎患者具有不同的免疫球蛋白及补体表达水平,应当尽量控制HCV-RNA病毒载量,从而减少免疫损伤.     

Cardiac effects of splanchnic and non-splanchnic blood volume redistribution during aortic occlusions in dogs

Translocation of blood from the lower body dilates the left ventricle during occlusion of the descending thoracic aorta and by increased activation of the Frank-Starling mechanism, stroke volume is maintained despite raised aortic blood pressure. The contributions from the splanchnic and non-splanchnic blood volumes to the left ventricular dilation were examined by ultrasonic measurements of myocardial chord length (MCL) in atropinized open-chest dogs. End-diastolic MCL rose by 2.5±0.9% during abdominal suprarenal aortic occlusion, draining blood from the non-splanchnic region, and by 7.4±1.7% during thoracic aortic occlusion draining blood from both splanchnic and non-splanchnic regions. Systolic left ventricular pressure rose by 16±3 mmHg and 76±12 mmHg, respectively. End-diastolic MCL rose by 6.0±1.2% during combined thoracic aortic and abdominal infrahepatic vena cava occlusion draining blood solely from the splanchnic region and further by 2.5±0.8% by blood drained from the non-splanchnic region after release of the vena cava occlusion. Similar results were obtained using a shunt permitting selective drainage first from the non-splanchnic region during thoracic aortic occlusion. Blood translocation from the non-splanchnic region maintains cardiac output during abdominal aortic occlusion. During occlusion of the thoracic aorta, drainage from the splanchnic region accounts for about 70% of the increase in end-diastolic MCL.     

超敏C反应蛋白,脂蛋白相关磷脂酶A2及D-二聚体与冠心病患者相关性研究的临床意义

目的 探讨冠心病患者的脂蛋白相关磷脂酶A2(1 ipoprotein associated phospholipase A2,LpPLA2)、超敏C反应蛋白(hypersensitive C reactive protein,hs-CRP)和D-二聚体的相关性情况,从而为临床提供更多的参考价值.方法 选择2014年1月至2016年1月期间在荷泽市立医院急诊就诊的150例冠心病患者作为观察组,并取同时期的130例健康志愿者作为对照组,对入组者的血清Lp-PLA2、hsCRP以及D-二聚体进行检测.同时对其低密度脂蛋白(low density lipoprotein,LDL)、肌钙蛋白(Cardian troponin I,TNI)、肌红蛋白(myoglobin,Myo)、肌酸激酶同工酶(creatine kinase isoenzyme,CK-MB)进行检测.结果 观察组患者的Lp-PLA2、hs-CRP以及D-二聚体水平分别是(43.62±13.23) g/L、5.09 mg/L、173.0 mg/L,明显高于对照组志愿者的(21.49±7.63) g/L、2.61 mg/L、68.0 mg/L,差异有统计学意义(P＜0.05).观察组的Lp-PLA2与LDL密切相关,并和冠脉病变的支数相关;D-二聚体和hs-CRP相关,同时和心功能等级相关.结论 Lp-PLA2主要和LDL等脂类代谢以及冠脉病变的程度密切相关,hs-CRP则是和D-二聚体水平以及心肌损伤标志物有密切关联,说明了炎症和血栓、心肌损伤有关.心功能降低容易导致D-二聚体水平升高从而诱发血栓.因此,对于冠心病患者,可以通过Lp-PLA2、hs-CRP以及D-二聚体水平指标来预测其预后情况.     

CHOP/GADD153在血管紧张素Ⅱ诱导心肌细胞凋亡中的表达及作用

目的： 离体观察CHOP/GADD 153蛋白表达变化与血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞凋亡的关系，并探讨CHOP/GADD 153反义寡核苷酸抗凋亡作用。方法: 对体外培养的乳鼠心肌细胞，单用AngⅡ刺激或预加不同浓度CHOP/GADD 153反义寡核苷酸干预后，再加入AngⅡ刺激。用MTT法检测细胞活力，乳酸脱氢酶(LDH)检测试剂盒测定培养上清液中LDH含量，Annexin V流式细胞仪检测细胞凋亡率，Western blotting法检测CHOP/GADD 153、Bcl-2及Bax表达变化。结果: AngⅡ组,心肌细胞CHOP/GADD 153表达(0.75±0.06)显著高于对照组(0.20±0.02)，P<0.01；心肌细胞活性(66.32±2.09)%显著低于对照组(100.00±0.00)%，P<0.05；培养上清液中LDH含量(79.36±5.69)U/L显著高于对照组(20.23±2.83)U/L；细胞凋亡率(16.62±2.09)%显著高于对照组(3.33±0.28)%，P<0.05；Bcl-2表达(0.44±0.05) 显著低于对照组(0.73±0.05),P<0.01；Bax表达(0.90±0.10) 显著高于对照组(0.69±0.08),P<0.01；Bax/Bcl-2比值(2.00±0.22)显著高于对照组 (0.93±0.09),P<0.01。预加CHOP/GADD153反义寡核苷酸干预，可显著逆转AngⅡ的以上作用，虽对Bax 蛋白表达无显著影响，但对照组Bax/Bcl-2的比值显著低于AngⅡ组 (P<0.01)，而错义寡核苷酸无此效应。脂质体组与对照组无显著差异。结论: CHOP/GADD153表达升高可能是AngⅡ诱导的心肌细胞凋亡机制之一，CHOP/GADD153反义寡核苷酸能抑制AngⅡ诱导的心肌细胞凋亡。     

尾加压素Ⅱ对大鼠胸主动脉球囊损伤后血管重塑的作用

目的： 探讨尾加压素Ⅱ(UII)在血管损伤后重塑过程中的作用。方法: 建立大鼠胸主动脉球囊拉伤模型，随机分为4组（n=5）,分别为假拉伤组、拉伤组、UII组（胸主动脉球囊拉伤并持续泵入UII 1.0 nmol·kg-1·h-1）和urantide组( 胸主动脉球囊拉伤并持续泵入urantide 10 nmol·kg-1·h-1)。于第21 d取胸主动脉，分别检测血管形态改变、UII表达、平滑肌细胞增殖和胶原表达。结果: ①术后第21 dUII组收缩压高于拉伤组［（140.0±10.0) mmHg vs (132.0±3.4) mmHg, P>0.05］,明显高于urantide 组［（140.0±10.0) mmHg vs (128.0±2.4) mmHg, P<0.05］。②胸主动脉球囊损伤后,损伤血管局部UII表达增强。③同拉伤组比, UII组进一步促进了内膜的增生,管腔面积狭窄率明显增加(0.13±0.05 vs 0.07±0.02, P<0.05);细胞增殖指数明显增加(0.74±0.16 vs 0.40±0.11,P<0.01);胶原表达也明显增加(以IOD计量,318±127 vs 78±26, P<0.01)。④同拉伤组比,urantide组管腔面积狭窄率没有减轻(0.09±0.03 vs 0.07±0.02, P>0.05);细胞增殖指数明显增加(0.73±0.15 vs 0.40±0.11, P<0.01);胶原表达增多但无统计学意义(以IOD计量,200±79 vs 78±26, P>0.05)。结论: 大鼠胸主动脉损伤后局部UII表达增强；外源性UII促进新生内膜平滑肌细胞增殖和胶原表达，加重了损伤血管的狭窄，提示UII参与了损伤后修复的过程；10 nmol·kg-1·h-1urantide不能抑制损伤后血管重塑的进程, 拮抗UII的机制尚有待进一步探讨。     

Serum biochemistry of ostrich (Striothio camelus) in Iran

Serum biochemistry (Striothio camelus), was determined in 75 clinically normal ostrich (42 females and 33 males, 39 under 2 years of age and 36 over 2 years). The following results were obtained: total protein 3.35±0.61 g/dl; prealbumin 0.1±0.01 g/dl; albumin 1.49±0.25 g/dl; α1 globulin 0.24±0.08 g/dl; α2 globulin 0.71±0.19 g/dl; β globulin 0.42±0.18 g/dl; γ globulin 0.63±0.21 g/dl; glucose 163±17 mg/dl; cholesterol 65±15 mg/dl; creatinin 0.26±0.05 mg/dl; triglyceride 151±56 mg/dl; urea 8.68±0.77 mg/dl; uric acid 11.87±3.56 mg/dl; aspartate amino transferase 357±95 U/l; alanin amino transferase activity 14.24±2.7 U/l; alkaline phosphatase 490±241 U/l; and lactate dehydrogenase 1124±31 0U/l.     

Serum interleukin – 4 and tumor necrosis factor alpha concentrations in children with primary acid gastroesophageal reflux and acid gastroesophageal reflux secondary to cow's milk allergy

AimThe possible role of serum interleukin 4 (IL-4) and tumor necrosis factor alpha (TNF- α) in pathogenesis of the reflux symptoms in children with primary acid gastroesophageal reflux (GER) and acid GER secondary to cow's milk allergy (CMA).Material and methodsOut of 264 children, 76 (28.8%) patients with primary GER and 62 (23.5%) patients with GER secondary to CMA (pH – monitoring) serum IL-4 and TNF- α concentrations were assessed before treatment, 1 and 2 years after the initiation of the periodically administered pharmacotherapy.ResultsChildren with primary GER had mean IL-4 concentrations 0.17 ± 0.06 pg/ml before treatment, 0.08 ± 0.07 pg/ ml after 1-year and 0.07 ± 0.06 pg/ml after 2-years of treatment. The mean IL-4 concentrations were 1.07 ± 0.24, 0.5 ± 0.22 and 0.44 ± 0.19 pg/ml respectively in children with GER secondary to CMA.The mean serum TNF- α concentrations was 3.62 ± 1.30 pg/ml before treatment, 2.16 ± 1,35 pg/ ml after 1 year and 1.65 ± 1.16 pg/ml after 2 years of treatment in children with primary GER. In group with GER secondary to CMA mean serum TNF- α concentrations were 4.95 ± 1.88, 2.53 ± 0.80 and 2.02 ± 0.78 pg/ml respectively. Statistical analysis of the concentration of both cytokines showed their differentiation between them and in the study groups.ConclusionsThe highest mean serum IL-4 and TNF-α concentrations were observed in children with GER secondary to CMA and in children in control group (with cow's milk allergy and/or other food allergy diagnosed – CMA/FA) before the treatment administration.     

Effect of heparin administration on fibrinogenolysis during thrombolytic therapy with tissue plasminogen activator for acute myocardial infarction

Heparin accelerates plasminogen activation by tissue type plasminogen activator (t-PA). Previous investigators have postulated that heparin administration during t-PA therapy might lead to enhanced fibrinogenolysis. In this paper, important coagulation parameters from a randomised trial of early versus delayed heparin administration, during t-PA therapy for acute myocardial infarction, were analysed. In contrast to the prediction, the late heparin group had significantly greater fibrinogen depletion (nadir fibrinogen 1.06±0.65 g/1 vs 1.46±0.61 g/l, p=0.0001) and higher fibrinogen degradation products (peak FBDP 675.9±785.3 μg/ml vs 299.7±543.5 μg/ml, p=0.0001). A possible mechanism for these findings is discussed. It has previously been demonstrated that heparin and FBDP are competitive activators of plasminogen activation by t-PA. It has also been shown that the stimulation of plasminogen activation by FBDP contributes substantially to fibrinogenolysis by t-PA. Thus, heparin may reduce fibrinogenolysis by interfering with the stimulation of plasminogen activation by FBDP.