Changes of serum high sensitive C-reactive protein in patients with acute cerebral infarction

BACKGROUND： Serum high sensitive C-reactive protein （hs-CRP）, which regards as a high sensitive mark of systemic inflammatory response syndrome, can provide a lot of valuable information for the treatment and prognosis of cerebrovascular disease. OBJECTIVE： To observe the differences of blood glucose, lipid, homocysteine and previous disease history among patients with acute cerebral infarction at various levels of hs-CRP and compare changes of hs-CRP of patients with various degrees of neurologic impairment. DESIGN： Contrast observation. SETTING： Department of Neurology, Shenzhou Hospital, Shenyang Medical College. PARTICIPANTS： A total of 102 patients with acute cerebral infarction were selected from Department of Neurology, Shenzhou Hospital of Shenyang Medical College from February 2005 to September 2006, including 55 males and 47 females aged from 55 to 86 years. All accepted patients met the diagnostic criteria of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were diagnosed with CT or MRI examination. All patients provided the confirmed consent. Based on clinical criteria of neurologic impairment established by the Fourth National Cerebrovascular Disease Academic Meeting, patients were randomly divided into mild group （0 - 15 points, n =46）, moderate group （16 - 30 points, n =38） and severe group （31 - 45 points, n =18）. In addition, based on hs-CRP level within 72 hours, patients were divided into normal group （hs-CRP ≤3 mg/L, n =53） and increasing group （hs-CRP 〉 3 mg/L, n =-49）. METHODS： ① 2 mL venous blood was selected from hospitalized patients in the next morning to separate serum. Quantitative measurement of hs-CRP was dealt with Latex Enhnced Turbidimetric Immunoassay （LETIA）. ②Fasting venous blood was colleted from hospitalized patients in the next morning to measure numeration of white blood cells, fibrinogen, blood glucose, total cholesterol （TC）, triacylglycerol （TG）, high density lipoprotein cholesterol （HDL-C）, low density lipoprotein cholesterol （LDL-C） and homocysteine. ③Measurement data were compared with t test or analysis of variance. MAIN OUTCOME MEASURES： ①Comparisons of serum biochemical indexes among patients with various levels of hs-CRP; ②comparisons of risk factors among patients with various levels of hs-CRP; ③comparisons of levels of hs-CRP among patients with various degrees of clinical neurologic impairment. RESULTS： A total of 102 patients were involved in the final analysis. ①Plasma fibrinogen and numeration of leucocytes were more in the increasing group than those in the normal group （t =4.39, 3.54, P 〈 0.01）; while, there were no significant differences of blood glucose, TC, TG, HDL-C, LDL-C and homocysteine between the two groups （P 〉 0.05）. ② Percentage of patients with hypertension and diabetes mellitus （DM） was higher in the increasing group than the normal group （ Х^2=3.98, 4.23, P 〈 0.05）; while, percentage of patients with smoking in the increasing group was not significantly different from that of patients in the normal group （P 〉 0.05）. ③Level of hs-CRP of patients with severe neurologic impairment was higher than that of patients with moderate neurologic impairment （t =2.273, P 〈 0.05）; that of patients with moderate neurologic impairment was higher than that of patients with mild neurologic impairment （t =2.586, P 〈 0.05）; that of patients with severe neurologic impairment was obviously higher than that of patients with mild neurologic impairment （t = 4.913, P 〈 0.01）. CONCLUSION： ① With the increase of hs-CRP, plasma fibrinogen and numeration of leucocytes of patients with acute cerebral infarction is increased, especially, they are increased remarkably among patients who have history of diabetes mellitus and hypertension. ②Increase of level of hs-CRP can be regarded as one of marks to evaluate severity of acute stroke.

Sphingosine kinase 1 dependent protein kinase C-δ activation plays an important role in acute liver failure in mice

AIM: To investigate the role of protein kinase C(PKC)-δ activation in the pathogenesis of acute liver failure(ALF) in a well-characterized mouse model of D-galactosamine(D-Gal N)/lipopolysaccharide(LPS)-induced ALF.METHODS: BALB/c mice were randomly assigned to five groups, and ALF was induced in mice by intraperitoneal injection of D-Ga IN(600 mg/kg) and LPS(10 μg/kg). Kaplan-Meier method was used for survival analysis. Serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) levels at different time points within one week were determined using a multiparameteric analyzer. Serum levels of high-mobility group box 1(HMGB1), tumor necrosis factor(TNF)-α, interleukin(IL)-1β, IL-6, and IL-10 as well as nuclear factor(NF)-κB activity were determined by enzyme-linked immunosorbent assay. Hepatic morphological changes at 36 h after ALF induction were assessed by hematoxylin and eosin staining. Expression of PKC-δ in liver tissue and peripheral blood mononuclear cells(PBMCs) was analyzed by Western blot.RESULTS: The expression and activation of PKC-δ were up-regulated in liver tissue and PBMCs of mice with D-Gal N/LPS-induced ALF. Inhibition of PKC-δ activation with rottlerin significantly increased the survival rates and decreased serum ALT/AST levels at 6, 12 and 24 h compared with the control group(P < 0.001). Rottlerin treatment also significantly decreased serum levels of HMGB1 at 6, 12, and 24 h, TNF-α, IL-6 and IL-1 β at 12 h compared with the control group(P < 0.01). The inflammatory cell infiltration and necrosis in liver tissue were also decreased in the rottlerin treatment group. Furthermore, sphingosine kinase 1(Sph K1) dependent PKC-δ activation played an important role in promoting NF-κB activation and inflammatory cytokine production in ALF.CONCLUSION: Sph K1 dependent PKC-δ activation plays an important role in promoting NF-κB activation and inflammatory response in ALF, and inhibition of PKC-δ activation might be a potential therapeutic strategy for this disease.

七氟烷对缺血再灌注后大鼠肺组织PKC-α表达的影响

目的建立在体大鼠肺缺血再灌注(IR)损伤模型,观察七氟烷对肺组织蛋白激酶C-α(PKC-α)表达的影响,探讨缺血再灌注后肺损伤和七氟烷肺保护的可能机制。方法96只雄性Wistar大鼠,参照改良的Eppinger方法建立在体大鼠肺缺血再灌注损伤模型。共分4组,每组24只大鼠:对照组(C组),开胸游离左肺门,未行阻断;IR组,阻断肺门45min后再灌注;sev-C组,吸入1MAC七氟烷,游离肺门不阻断;sev-IR组,吸入七氟烷后阻断左肺门45min再灌注。每组包括3个时点:缺血45min、再灌注60min、再灌注120min,每时点6只大鼠,另外再灌注120min时各组另取6只大鼠行支气管灌洗。记录各时点平均动脉压(MAP)、动脉氧分压(PaO2),测定湿干重比值(W/D)、肺通透指数(LPI)、肺组织胞质和胞膜PKC-α含量。结果IR和sev-IR组再灌注后W/D、LPI均上升(P<0.05),sev-IR组W/D、LPI升高的程度低于IR组(P<0.05);IR组再灌注60min、120min肺组织PKC-α在细胞膜表达增加(P<0.05),细胞质的表达减少(P<0.05)。sev-IR组PKC-α在细胞膜表达增加、胞质减少的程度都低于IR组(P<0.05)。结论肺缺血再灌注后血管通透性增加,PKC-α移位和激活参与介导再灌注后肺组织损伤,七氟烷预处理能抑制PKC-α移位和激活,对再灌注后肺组织具有一定的保护作用。

2型糖尿病患者高敏C-反应蛋白与糖尿病肾病的关系

目的:探讨2型糖尿病肾病(DN)不同时期血清高敏C-反应蛋白(hs-CRP)的浓度变化与DN的关系。方法:采用速率散射比浊法测定144例2型糖尿病患者和49名正常对照的血清hs-CRP水平。根据尿白蛋白排泄率(UAER)将2型糖尿病患者分为3组:正常蛋白尿组53例、微量白蛋白尿组57例和临床蛋白尿组34例。结果:(1)2型糖尿病组的血清hs-CRP值较对照组显著升高(U=1458.5,P<0.001);(2)hs-CRP值随UAER的增加而增加(H=74.068,P<0.001);(3)hs-CRP值与空腹血糖、血尿酸、纤维蛋白原成正相关(r=0.26、0.33、0.30,P均<0.001),与高密度脂蛋白呈负相关(r=-0.14,P<0.05)。结论:C-反应蛋白可能参与了2型糖尿病和糖尿病肾病的发生发展。

C-反应蛋白水平与脑梗死病情及预后的量化研究

目的探讨脑梗死患者血清C-应蛋白(C-reactive protein,CRP)水平与病情严重程度及反预后的量化关系。方法对病程为2周以内的90例脑梗死患者进行入院时和1周后血清C-应蛋白水反平测定。入院时C-应蛋白测定值为CRP11周后检测值为CRP2据入院时C-应蛋白测定值进行反,;根反分组。A组:CRP1≤2.00m g/L,B组:2.00m g/L<CR P1≤9.50m g/L,C组:CRP1>9.50m g/L。应用美国国立卫生研究院卒中量表(NIH SS)及Barthel指数(BI)记分法,对入院时90例患者(NIH SS1及BI1)和随访的58例患者(NIH SS2及BI2)进行神经功能缺损程度评分。结果入院时血清C-应蛋白水平与发病时反及治疗后3个月随访时的神经功能缺损严重程度呈显著相关(P≤0.001),且这种相关性存在量化关系:CRP1≤2.00m g/L时,N IH SS1中位数为5.00分,BI2中位数为100.00分;2.00m g/L<CRP1≤9.50m g/L,NIH SS1中位数为7.00分,BI2中位数为85.00分;CR P1>9.50m g/L时,N IH SS1中位数为13.00分,BI2中位数为47.50分。入院时血清C-应蛋白水平与相应的神经功能缺损程度及治疗后3个月恢复期水平反之间差异具有显著意义(P<0.05或P<0.001)。血清CRP2水平与入院时及治疗后3个月时的神经功能缺损程度间差异无显著性意义(P>0.05)。

代谢综合征与超敏C-反应蛋白

代谢综合征（metabolic svndrome，MS）是多系统代谢异常集聚的病理状态，是由于胰岛素抵抗（insulin resistance，IR）引起的一系列生理和代谢紊乱，其中以肥胖、高血压、血糖和血脂异常四项最为突出，曾被称为死亡四重奏。MS及其各个组分的发病机制十分复杂，尚未充分了解，目前很多证据表明炎症在肥胖、IR等多种MS组分的发生发展中起作用。随着近十几年来研究的进展，人们越来越多地认识到C-反应蛋白（C—reactive protein，CRP）在心血管领域强有力的预测因子的角色，且随着检测手段的进步，采用更敏感的方法检测到的CRP，

颅脑损伤患者血清C-反应蛋白的变化与意义

颅脑损伤是一种急性发生的脑组织损伤，成为严重危害生命健康的疾病。C－反应蛋白（C—reactive protein．CRP）是人体重要的急性期反应蛋白，是一种非特异性炎性因子．正常人体内含量甚微，当机体出现创伤、感染、心肌缺血或其他炎性反应会使血液CRP明显升高。

C-反应蛋白与心血管疾病的相关研究进展

长期以来，C-反应蛋白（C-reactive protein，CRP）被视为炎症、感染和组织损伤急性期反应物。自20世纪90年代末以来．人们发现CRP增高可强烈预测未来冠状动脉事件。越来越多的证据表明，炎症过程在动脉粥样硬化及其并发症的发生发展中起着重要作用，是预测未来心血管危险最有力的炎症标记物。

C-反应蛋白在临床上的应用价值

C-反应蛋白（C-reactlvc protein,CRP）是由细胞因子白细胞介素-6（IL-6）诱导肝脏合成的急性时相蛋白,近年来,随着分子生物学和免疫学的发展,新的检测方法和仪器得到广泛的应用,这对CRP的研究进展起到了推动作用。CRP的临床应用价值引起了人们的特别关注，CRP在临床上得到广泛的应用，特别是它在鉴别感染性疾病以及心血管疾病的诊断、鉴别、

脑梗死急性期与C-反应蛋白相关分析

血清C-反应蛋白fC—reactive Protein，CRP）是人体非特异炎症反应的敏感性标志物之一，在急性心脑血管事件中所起的作用已日益得到重视。CRP在动脉粥样硬化的形成和发展过程中起着关键作用，在多种疾病时各有其变化。CRP是造成和加速动脉粥样硬化的一个重要的独立危险因素，国内外多项研究表明炎症可以通过多途径和一系列病理、

两种C-反应蛋白分析方法的验证比对

目的：实验室对同一个测定项目CRP存在不同检测系统时,应对于不同检测系统进行数据比对和偏差评估,以确保检测结果的可比性,也便于临床医生的决策.方法：采用两种不同水平（高、 中、 低值）质控品和各个不同浓度的患者的抗凝全血和分离血清用于我室QuikRead CRP分析仪以及BNP全自动特定蛋白仪检测CRP进行方法对比和偏差的评估,为本实验室内不同检测系统测定结果可比性提供数据.结果：两种检测系统的的r=0.991,r2=0.981.在3个医学决定水平上的系统误差都在10％以内,可以适应临床对于CRP测定的要求.结论：门诊使用的QuikRead CRP分析仪以及免疫室使用的BNP全自动特定蛋白仪检测同一标本时具有良好的相关性其预期偏差也是可以接受的.

血清C-反应蛋白在尿路感染中的临床价值

血清C-反应蛋白（c-reactive protein,CRP）是机体有核细胞合成的一种低分子量蛋白,能与广谱细菌和组织结合,提高吞噬和运动能力,促进各种细菌和异物的吞噬,自由透过肾小球基底膜,且被近曲小管吸收,是炎症反应过程中较早出现的敏感指标之一,是反映肾小球滤过率（GFR）理想的内源性标志物[1],对尿路感染的定位诊断、肾功能损害程度判断有一定的临床价值。

C-反应蛋白水平与老年急性冠状动脉综合征预后的关系

急性冠状动脉综合征（acute coronary syndrome,ACS）是冠心病病情较重的一种类型，虽目前治疗上有很大进展，但仍是威胁人类健康尤其是老年人的主要疾病。因此，寻找对其预后有影响的因素及时发现并给予患者干预治疗有重要临床意义。近年来，大量的血清学、病理学以及动物模型等研究提示，感染与冠心病的发生、发展有关，感染可能是冠心病的病因或危险因素之一。我们检测50例老年ACS患者血清C-反应蛋白（C-reactive protein,CRP）水平，旨在探讨其对预后的影响。