纤维蛋白胶存在的问题与相应的解决方法

分析了纤维蛋白胶存在的问题,如蛋白胶不同供体来源、成份来源、应用的简易性与有效性、止血功效局限、机械强度与纤溶抑制剂的选择等,并提出相应的解决方案.     

大黄Zhe虫丸对难治性肾病综合征抗凝血酶Ⅲ、纤溶酶原、血小板聚集率的影响

目的 探讨大黄Zhe虫丸对难治性肾病综合征（RNS）高凝状态（HCS）的治疗作用。方法 将68例RNS随机分为实验组和对照组,实验组服用大黄Zhe虫丸,实验对照组用潘生丁。观察患者血中抗凝血酶Ⅲ（AT-Ⅲ）、纤溶酶原（PLG）、血小板聚集率（PAgT)的变化。结果 实验组治疗后患者血中AT－Ⅲ、PLC极显著回升（P＝0．000;P＝0．000）,PAgT极显著降低（P＝0．000）。实验组显著优于对照组。结论 大黄Zhe虫丸是治疗RNS－HCS的有效药物。     

大黄 虫丸对难治性肾病综合征抗凝血酶Ⅲ、纤溶酶原、血小板聚集率的影响

目的 探讨大黄 虫丸对难治性肾病综合征(RNS)高凝状态(HCS)的治疗作用。方法将68例RNS随机分为实验组和实验对照组,实验组服用大黄 虫丸,实验对照组服用潘生丁。观察患者血中抗凝血酶Ⅲ(AT-Ⅲ)、纤溶酶原(PLG)、血小板聚集率(PAgT)的变化。结果 实验组治疗后患者血中AT-Ⅲ、PLG极显著回升(P=0.000;P=0.000),PAgT极显著降低(P=0.000)。实验组显著优于对照组。结论 大黄 虫丸是治疗RNS-HCS的有效药物。     

纤维蛋白溶解系统的动力学模型与数值模拟

为了探讨蛋白C对凝血酶激活的纤维蛋白抑制剂(thrombin activatable fribrinolysis inhibitor,TAFI)的作用的影响,近而更深一步弄清楚血凝块形成初期TAFI对纤维蛋白溶解的调节机理,根据生物试验建立了一个关于蛋白C和TAFI的凝血动力学模型.通过对模型的动力学分析和数值模拟得到:凝血酶激活的纤维蛋白抑制剂刺激因素必须大于一个阈值纤溶系统才能发挥作用;当TAFI少量缺乏时,对血液凝固的影响不是太大;只有当TAFI的缺乏达到一定程度时,才会导致疾病的发生;但当TAFI过量时对系统的影响很大;系统对TAFI的需求随着蛋白C的增加而增加.     

大黄虫丸对难治性肾病综合征抗凝血酶Ⅲ、纤溶酶原、血小板聚集率的影响

目的探讨大黄虫丸对难治性肾病综合征 (RNS)高凝状态 (HCS)的治疗作用。方法将68例RNS随机分为实验组和实验对照组 ,实验组服用大黄虫丸 ,实验对照组服用潘生丁。观察患者血中抗凝血酶Ⅲ(AT-Ⅲ )、纤溶酶原 (PLG)、血小板聚集率 (PAgT)的变化。结果实验组治疗后患者血中AT -Ⅲ、PLG极显著回升 (P=0 .000 ;P=0 .000) ,PAgT极显著降低 (P=0 .000)。实验组显著优于对照组。结论大黄虫丸是治疗RNS -HCS的有效药物。     

口服阿司匹林对冠心病人血小板活性和聚集率的影响

本文观察了冠心病人口服阿司匹林（aspirin,ASP）前后血小板膜表面GMP-140（GMP-140）和血小板聚集率的变化,旨在探讨ASP对冠心病患者血小板活性和聚集率的影响,为临床预防和治疗冠心病提供理论依据。     

阿斯匹林对冠心病患者血小板活性和聚集的影响

对冠心病患者服用阿斯匹林（ＡＳＡ）前后的血小板α－颗粒膜蛋白１４０（ＧＭＰ－１４０）水平和血小板聚集进行了测定。结果显示：冠心病患者治疗前血小板ＧＭＰ－１４０水平和聚集率显著高于正常人（Ｐ〈０．００１）,使用阿斯匹林（ＡＳＡ）治疗后两种指标明显下降（Ｐ〈０．００１）,达到正常人水平（Ｐ〉０．０５）,提示ＡＳＡ能直接降低ＧＭＰ－１４０水平,抑制血小板活化和聚集,有效地防止冠状血管的进一步损害。     

2型糖尿病患者血浆D-二聚体和血小板聚集率的临床分析

糖尿病2型(T 2DM)是常见病和多发病,常伴发动脉粥样硬化和微血管病变,凝血和纤溶活性异常是其原因之一.D-二聚体(D-D)是直接反映凝血酶和纤溶酶生成的指标,血小板聚集率(PAgT)是反映血小板聚集功能的指标.本文检测分析T 2DM患者D-D和PAgT的变化.     

卡托普利对家兔急性心肌梗塞早期血小板活化及纤溶活性的影响

本研究观察了家兔急性心肌梗塞（ＡＭＩ）早期血浆血小板α－颗粒膜蛋白（ＧＭＰ－１４０）、血栓素Ｂ２（ＴＸＢ２）、组织型纤溶酶酶原激活剂（Ｔ－ＰＡ）及其抑制物（ＰＡＩ－１）水平的变化及卡托利干预的ＰＡ活性显著降低；相关分析表明，血浆ＧＭＰ－１４０浓度与ＰＡＩ－１活性显著正相关。卡托普利干预后，血浆ＧＭＰ－１４０浓度、ＴＹＸＢ２浓度、Ｔ－ＰＡ浓度、ｔ－ＰＡ含量、ＰＡＩ－１活性均明显降低，而ｔ－ＰＡ活性显     

不同类型冠心病患者凝血和纤溶状态分析

冠心病（CHD）患者存在凝血和纤维蛋白溶解失衡,主要表现为凝血功能增强及纤维蛋白溶解降低,从而导致冠状动脉内血栓形成。本文检测血浆纤维蛋白原（Fg）、D-二聚体（D-D）、血小板最大聚集率（PAGM）和血小板平均体积（MPV）,旨在为不同类型对冠心病分析和临床治疗提供参考依据。     

Effect of Obesity and Roux-En-Y Gastric Surgery on Omeprazole Pharmacokinetics

IntroductionThe prevalence of obesity is increasing globally. The principal aim was to evaluate whether gastric bypass surgery modifies the bioavailability and pharmacokinetic (PK) parameters of omeprazole.MethodsControlled, open-label, bioavailability clinical trial in patients undergoing Roux-en-Y gastric bypass (RYGB). Healthy patients with obesity (body mass index >35) were included and assessed for omeprazole PKs before and after RYGB (1 and 6 months). PK sampling was done at baseline and several times up to 12 h after drug dosing. Pre- and post-surgery parameters were compared using paired ANOVA or Wilcoxon tests, and control versus cases using ANOVA or Mann-Whitney tests. Given the post-surgery change in body weight, parameters were corrected by dose/body weight.ResultsFourteen case and 24 control subjects were recruited; 92% were women (N = 35/38). In patients who underwent RYGB, maximum plasma concentration (C_max) was significantly reduced at 1 and 6 months after surgery compared with presurgery values (p = 0.001). Regarding the AUC, the values are lower at 1 and 6 months after surgery than at baseline (p < 0.001). The drug clearance was also increased in the first month after surgery. No differences were found between patients 6 months after surgery and controls. C_max and AUC corrected by dose/body weight were significantly different between the baseline surgery subjects and controls.Discusion/ConclusionsOmeprazole bioavailability is reduced in patients with obesity at 1 and 6 months after RYGB. However, omeprazole PK parameters 6 months after RYGB are similar to control subjects, and thus no dose correction is required after RYGB for a given indication.     

奥美拉唑与西咪替丁治疗应激性胃溃疡的疗效观察

观察奥美拉唑与西咪替丁治疗应激性胃溃疡的临床效果及对患者生活质量的影响。方法 选择2016年1月~2018年1月我院收治的64例应激性胃溃疡患者,随机分为观察组和对照组,各32例。对照组患者应用西咪替丁治疗,观察组应用奥美拉唑治疗。比较两组患者的临床疗效、止血时间、胃泌素水平、生活质量评分及不良反应发生率。结果 观察组患者总有效率为96.88%,高于对照组的78.13%,差异有统计学意义（P＜0.05）;治疗后,观察组患者胃泌素水平低于对照组[（95.24±2.36）pg/ml vs （112.48±2.26）pg/ml] ,差异有统计学意义（P＜0.05）;观察组患者止血时间短于对照组,且生活质量评分高于对照组,差异有统计学意义（P＜0.05）;观察组患者不良反应发生率为3.13%,低于对照组的18.75%,差异有统计学意义（P＜0.05）。结论 对应激性胃溃疡患者实施奥美拉唑的效果较西咪替丁更佳,且更有助于提升患者日常生活质量。     

奥美拉唑与西咪替丁治疗应激性胃溃疡患者的疗效评价

目的：评价奥美拉唑与西咪替丁治疗应激性胃溃疡患者的疗效。方法选取我院自2012年2月~2014年2月收治的86例应激性胃溃疡患者的临床资料进行回顾性分析。结果观察组临床总有效率93.02%(40/43)明显高于对照组74.42%(32/43),其差异具有统计学意义(x2=13.210,<0.05)。结论奥美拉唑治疗应激性胃溃疡患者疗效显著,且改善胃液PH值、血清胃激素水平。     

Effects of gastric acidity on food intake in rats

Intragastric infusion of hydrochloric acid lowered rats' intragastric pH, but failed to produce any increase or decrease in food intake. Conversely, infusions of base (aluminum and magnesium hydroxide) increased pH without altering food intake.     

硫糖铝混悬液联合洛赛克治疗上消化道出血的临床疗效分析

目的研究硫糖铝混悬液联合洛赛克治疗上消化道出血的临床疗效。方法收集上消化道出血患者193例,随机分成对照组（n=93）与观察组（n=100）。对照组予以洛赛克40mg静脉滴注,每日2次;观察组在对照组的基础上171服硫糖铝混悬液10mL,每日3次。结果观察组总有效率达90％,与对照组相比存在统计学差异（P〈0．05）。结论硫糖铝混悬液联合洛赛克治疗上？肖化道出血临床疗效好、副作用小,值得基层医院推广。     

香烟烟雾对小白鼠结肠粘膜表面结构的影响

本实验选昆明种小白鼠２４只，分为１０、１５、２０、２５ｍｉｎ四个熏烟实验组。实验结果表明，香烟全烟雾可引起结肠粘膜发生破损、糜烂、粘膜表面不光滑，结肠腺开口数目减少，开口面积减小，体重和摄食量减少等变化，这些变化均随每次熏烟时间的延长，实验天数的增加而加重     

Conjunctival Interleukin-13 Expression in Mucous Membrane Pemphigoid and Functional Effects of Interleukin-13 on Conjunctival Fibroblasts in Vitro

Interleukin-13 (IL-13) is the dominant effector cytokine of fibrosis in pulmonary and liver disease. Excessive conjunctival fibrosis in the immunobullous disease ocular mucous membrane pemphigoid (MMP) causes blindness; the pathogenesis of scarring in this disease is incompletely understood. To determine whether IL-13 is involved in conjunctival fibrosis in MMP, we studied the expression of IL-13 in ocular MMP patients before and after systemic immunosuppression and examined the effects of IL-13 on normal human conjunctival fibroblasts. We found high stromal cell expression of IL-13 in active ocular MMP by immunohistochemistry; 80% of these cells were CD3-positive T cells. Following immunosuppression, in clinically uninflamed, treated, ocular MMP patients, the number of IL-13 positive cells was significantly reduced, but this was still fourfold greater than in normal conjunctiva. IL-13 stimulated collagen lattice contraction and migration, and decreased production of mmp-3 and mmp-10 by human conjunctival fibroblasts. The addition of T cell culture supernatant to IL-13 synergistically augmented fibroblast migration. IL-13 also up-regulated surface expression of HLA-DR, CD80, CD40, and CD154 by conjunctival fibroblasts, suggesting a potential mechanism for fibroblast-T cell cross talk, via which fibroblasts may actively engage in perpetuating chronic inflammation and continued fibrosis. Together, these findings suggest that IL-13 is involved in conjunctival fibrosis in MMP, and that IL-13 has both profibrotic and pro-inflammatory effects on human conjunctival fibroblasts.Autoimmune conjunctivitis caused by ocular mucous membrane pemphigoid (MMP), also known as ocular cicatricial pemphigoid, is a blinding disease characterized by recurrent episodes of inflammation and aggressive conjunctival fibrosis. It is part of a spectrum of immunobullous disease associated with linear deposition of IgG and IgA autoantibodies directed against epithelial basement membrane zone proteins, which most commonly involves oral and ocular mucosa. In ocular mucosa, unlike oral mucosa, scarring is a clinical hallmark of the disease.¹ Although the mechanisms have not been clearly demonstrated, autoantibodies are thought to cause blistering by disrupting basement membrane adherence via activation of complement, neutrophils and pro-inflammatory cytokines.² In the eye, blisters are infrequently seen, and the disease manifests as chronic recurrent cicatricial conjunctivitis.The functional consequences of the inflammatory lesions that heal with scarring are most evident in the eye, where patients with severe conjunctival fibrosis become blind in 30% of cases.³ Developing effective anti-fibrotic agents would therefore have therapeutic potential, but is challenging because the cellular and molecular mechanisms of conjunctival scarring in MMP are incompletely understood. Given that conjunctival fibrosis can still progress, despite apparent clinical control of inflammation by conventional immunosuppressive therapy,^4,5 better understanding of the changes in treated tissue compared with actively inflamed tissue might assist and guide in the development of adjunctive local therapies to target conjunctival fibrosis.Interleukin-13 is a key profibrotic mediator that has been identified as the dominant effector cytokine of fibrosis in experimental models of skin, hepatic, and pulmonary fibrosis and airway remodeling in asthma.^6,7,8,9 It is produced by type 2 helper T cell (Th2) cells, mast cells, and basophils, and is a potent stimulator of eosinophil-, lymphocyte- and macrophage-rich inflammation, mucosal metaplasia, tissue fibrosis, and parenchymal remodeling.^10,11 Fibrosis associated with repetitive injury in chronic inflammatory disease is strongly linked with CD4⁺ Th2 responses involving interleukin (IL)-4, IL-5, IL-13, and IL-21.¹² As CD4⁺ and CD8⁺ T cells are the predominant cells in the conjunctival subepithelial infiltrate in ocular MMP,^13,14,15 it has been hypothesized that T cells play an important role in the pathogenesis of conjunctival fibrosis in MMP. As in most chronic immune-mediated fibroproliferative disorders,¹⁶ both Th1 (interferon [IFN]γ) and Th2 cytokines (IL-4, IL-5) are present in MMP lesions,^17,18,19,20 but it is not known whether the Th2 cytokine IL-13 plays a role in the autoimmune conjunctivitis and fibrosis observed in ocular MMP.IL-13 is unique in that it is not thought to exert any control over T cell function,¹⁰ so unlike IL-4, it does not appear to be important in the initial differentiation of CD4⁺T cells into Th2-type cells, but rather appears to be important in the effector phase of inflammation and repair, via its effects on monocytes/macrophages, dendritic cells, fibroblasts, and other inflammatory and stromal cells. IL-13 has been shown to exert direct pro-fibrotic effects on fibroblasts isolated from human lung and skin.^21,22,23,24 Fibroblasts isolated from different bodily sites exhibit different functional properties and site-specific gene expression,²⁵ so these effects cannot necessarily be extrapolated to fibroblasts from other tissues such as the conjunctiva. Although the effects of IL-13 on normal human conjunctival fibroblast proliferation, apoptosis, and matrix metalloproteinase expression have been reported,^26,27 its effects on other functional activities carried out by normal conjunctival fibroblasts have not been fully investigated.Fibrosis is an excessive repair response, where the replacement of normal parenchymal tissue by connective tissues is uncontrolled, and there is an imbalance between accumulation of extracellular matrix, and remodeling and collagen turnover. Fibrosis typically results from chronic inflammation due to a persistent irritant that damages tissues.^12,28 Inflammatory cells, including macrophages and Th2 lymphocytes, play important roles in the chronic inflammation resulting in fibrosis, by releasing cytokines, chemokines, and growth factors, and also through direct interaction with fibroblasts.^12,16,28 Rather than simply being structural cells, it is also recognized that fibroblasts play an active role in the persistence of inflammation by secreting cytokines and chemokines, recruiting and maintaining the survival of T cells and other inflammatory cells via both soluble factors, and by direct cross talk with lymphocytes via the CD40/CD154 pathway.^25,29 It has previously been shown that IFNγ up-regulates CD40 expression on human lung fibroblasts, and that IL-13 increases CD154 levels in human lung fibroblasts, but the effects of IL-13 on co-stimulatory molecule expression by human conjunctival fibroblasts has yet to be elucidated.In the present study, we sought to explore the potential role of IL-13 in ocular MMP, and its effects on conjunctival fibroblast-related profibrotic and pro-inflammatory activity.     

Effect of bradykinin on platelet aggregation

The effect of bradykinin on ADP-induced aggregation of blood platelets was investigated in rabbits. Bradykinin reduced the degree of aggregation; maximal inhibition of aggregation was observed with the use of bradykinin in a concentration of 10–100 ng/ml. Higher concentrations of bradykinin were less effective. An essential condition for inhibition was a period of preincubation of bradykinin with the platelets. Inhibition of aggregation by bradykinin also was observed on canine platelets.Group for the Study of Mechanisms of Thrombosis, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Sciences of the SSSR E. I. Chazov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 8, pp. 139–141, August, 1979.