脑卒中患者高敏C反应蛋白检测的意义

目的了解脑卒中患者高敏C反应蛋白(hs-CRP)的浓度变化.方法收集81例住院的脑卒中患者,其中脑出血30例,脑梗死51例,同时选择年龄、性别比较相似的42名正常健康体检者,空腹抽血测定hs-CRP.结果脑卒中患者血清hs-CRP的水平为(5.10±3.90) mg/L,与正常对照组[(1.08±0.56) mg/L]比较差异有显著性(P<0.01),脑梗死组和脑出血组hs-CRP分别为(3.64±2.80) mg/L、(6.12±3.20) mg/L,脑出血组显著高于脑梗死组,大梗死患者的hs-CRP比小梗死升高明显(P<0.05),分别为(5.61±2.40) mg/L、(3.48±2.70) mg/L.结论脑卒中患者测定血清hs-CRP浓度可以为临床评价脑血管病病情的变化提供有意义的参考指标,临床在治疗时应充分考虑炎症反应这一危险因素.应该注意的是,hs-CRP浓度的变化是组织受损时的一项非特异性反应,必需在排除了引起CRP变化的其他原因后才能作出正确的判断.     

急性脑梗死、脑出血患者血清E-选择素、超敏C-反应蛋白水平的对比研究

目的观察血清E-选择素、血清超敏C-反应蛋白(hs-CRP)水平在急性脑梗死、脑出血患者中的变化,并探讨其与疾病的关系。方法收集135例住院的脑血管病患者,急性脑卒中患者120例,其中脑出血43例,脑梗死77例,脑短暂性供血不足患者15例,同时选择年龄、性别比较相似的42例正常健康体检者。空腹抽血均以酶联免疫吸附法(ELISA)检测其E-选择素,免疫速率散射比浊法测定其Hs-CRP的水平。结果脑血管病患者两项阳性率为82.70%、77.78%,脑梗死阳性率分别83.56%、61.01%,脑出血阳性率78.90%、79.06%。脑卒中患者血清E-选择素(71.78±6.8)μg/L、超敏C-反应蛋白的水平为(9.10±7.60)mg/L,与正常对照组(33.78±7.75)μg/L、(1.08±0.56)mg/L比较差异有统计学意义(P<0.01)。脑梗死组和脑出血组血清E-选择素分别为(66.15±7.66)μg/L、(77.36±6.27)μg/L;hs-CRP分别为(8.48±7.34)mg/L、(10.0±7.89)mg/L,脑出血组显著高于脑梗死组。大梗死患者的E-选择素、hs-CRP比小梗死升高明显(P<0.01),分别为(72.23±6.76)μg/L、(58.13±6.36)μg/L;(10.61±2.40)mg/L、(5.48±2.70)mg/L。结论E-选择素、hs-CRP可能与脑卒中发病有关,脑卒中患者测定E-选择素、hs-CRP浓度可以为临床评价脑血管病病情的变化提供有意义的参考指标,临床在治疗时应充分考虑炎症反应这一危险因素。应该注意的是hs-CRP浓度的变化是组织受损时的一项非特异性反应,必须在排除了引起CRP变化的其他原因后才能做出正确的判断。     

颈动脉粥样硬化斑块内新生血管密度与血清超敏C反应蛋白浓度的相关性研究

目的应用超声造影研究颈动脉粥样硬化斑块内新生血管密度与血清超敏C反应蛋白(hs-CRP)浓度的关系。方法颈动脉硬化伴斑块形成患者96例,按脑梗死及斑块超声造影增强情况将其分为梗死组68例和非梗死组28例,采用免疫散射比浊法测定血清hs-CRP浓度,比较两组hs-CRP水平。结果梗死组血清hs-CRP浓度(7.51±2.13)mg/L高于非梗死组(3.15±1.08)mg/L,差异有统计学意义(P﹤0.01),斑块增强0~Ⅱ级的血清hs-CRP浓度分别为(0.89±0.23)mg/L、(6.52±1.83)mg/L及(8.51±2.25)mg/L,各组间两两比较差异均有统计学意义(P﹤0.01)。结论血清hs-CRP浓度可间接反映斑块内新生血管密度,临床上可通过检测血清hs-CRP水平,间接了解斑块内新生血管情况,评估斑块易损性。     

血清超敏C反应蛋白和低密度脂蛋白测定对糖尿病并发动脉粥样硬化的价值

目的研究血清超敏C反应蛋白(hs-CRP)和血清低密度脂蛋白胆固醇(LDL-C)对糖尿病并发动脉粥样硬化的预示作用。方法用胶乳增强免疫比浊法检测血清hs-CRP,一步法检测LDL-C。结果糖尿病患者LDL-C正常组,血清hs-CRP浓度为(10.63±6.21)mg/L,LDL-C为(2.74±0.31)mmol/L;LDL-C升高组hs-CRP为(17.39±2.31)mg/L,LDL-C为(3.91±0.58)mmol/L。正常对照组血清hs-CRP为(2.83±1.35)mg/L,LDL-C为(2.57±0.30)mmol/L。LDL-C正常组和LDL-C升高组hs-CRP明显高于正常对照组(P<0.01)。hs-CRP在LDL-C正常组和LDL-C升高组之间也存在明显差异(P<0.01)。糖尿病组hs-CRP浓度与LDL-C浓度呈正相关(r=0.46,P<0.01)。结论hs-CRP参与糖尿病并发动脉粥样硬化过程,对其发病机制有一定的预示作用。     

复发性脑梗死与超敏C反应蛋白关系的探讨

目的 观察脑梗死初发、复发患者血清超敏C反应蛋白(hs-CRP)浓度,探讨脑梗死复发与血清hs-CRP的关系.方法 用免疫放射比浊法测定200例急性脑梗死患者及100例非急性脑卒中患者的血清hs-CRP浓度,并进行分析.结果 急性脑梗死患者血清hs-CRP浓度高于非急性脑卒中患者(P＜0.01);各类型脑梗死患者之间血清hs-CRP浓度差异无统计学意义(P＞0.05),脑梗死复发患者血清hs-CRP[(18.035±10.684) mg/L]高于初发患者[(14.567±8.510)mg/L] (P ＜0.01),且高血清hs-CRP比率(54％)亦高于初发患者(37％)(P＜0.05).各类型脑梗死复发患者之间血清hs-CRP浓度差异无统计学意义(P＞0.05).结论 脑梗死复发患者血清hs-CRP浓度高于初发患者,提示脑梗死复发与血清hs-CRP升高有一定关系.     

缺血性脑卒中患者血清LP(a)和CRP水平与预后的相关性

目的:探讨缺血性脑卒中患者血清脂蛋白a[liporotein-a,LP(a)]和C-反应蛋白(C-reactiveprotein,CRP)水平与疾病预后的相关性。方法:采用透射比浊法分别在急性期和恢复期检测46例脑梗死患者的血清LP(a)和超敏CRP的浓度,并与30例正常人进行对照。结果:(1)缺血性脑卒中组急性期和恢复期LP(a)分别为(315.05±142.16)mg/L和(311.68±169.20)mg/L,与正常对照组(189.57±152.49)mg/L比较,两次结果差异均有显著性(P<0.05),但是急性期与恢复期LP(a)差异无显著性(P>0.05)。(2)与正常对照组(4.93±1.39)mg/L比较,缺血性脑卒中组急性期CRP(15.32±1.73)mg/L和恢复期CRP(6.17±1.45)mg/L差异有显著性(P<0.05),而其恢复期CRP与急性期比较差异有显著性(P<0.05)。结论:LP(a)与CRP可作为缺血性脑卒中的观察指标。     

血清S100β蛋白及超敏C-反应蛋白含量与急性脑梗死患者病情及预后关系的研究

目的 探讨急性脑梗死(ACI)患者血清S100β蛋白及超敏C-反应蛋白(hs-CRP)水平变化与预后的关系.方法 采用双抗体夹心ELISA法测定33例脑梗死患者及25例健康对照组的血清S100β蛋白水平;用散射比浊法测定血清超敏C-反应蛋白含量.现察并比较ACI患者在不同程度病情、不同梗死面积时,血清S100β蛋白和hs-CRP含量变化,采用Pearson法进行相关性分析.结果 脑梗死组患者血清S1006蛋白(0.025±0.017μg/L)和hs-CRP(7.147±10.503 mg/L)水平均显著高于正常对照组(0.017±0.009 μg/L,2.679±1.678 mg/L),均P<0.05,并且随着神经功能损伤程度的增高和梗死面积的增加,血清S100β蛋白和hs-CRP含量亦明显升高;S100蛋白水平和hs-CRP水平呈正相关(P<0.05).结论 急性脑梗死患者血清s100β和hs-CRP浓度均明显增高.S100β蛋白和hs-CRP蛋白浓度高低不仅可以给神经元和神经胶质细胞的损伤程度提供定量信息,而且也是判断病情,评估预后的重要指标.     

急性脑卒中患者血清及脑脊液中神经元特异性烯醇化酶水平与神经功能缺失的关系

目的:观察急性期和恢复期脑出血和脑梗死患者血清和脑脊液的神经元特异性烯醇化酶(neuronspecificenolase,NSE)的变化,探讨其与神经功能缺损程度的相关性。方法:分别收集2002-06/2004-06甘肃省人民医院脑系科收治的50例急性期和恢复期脑出血患者、50例急性期和恢复期脑梗死患者及20例正常人的血清、脑脊液标本,采用酶联免疫分析方法测定NSE,并进行统计学分析。结果:脑梗死组急性期血清NSE质量浓度是(26.82±7.03)μg/L,脑脊液NSE质量浓度是(33.28±11.34)μg/L;脑出血组急性期血清NSE质量浓度是(22.44±6.06)μg/L,脑脊液NSE质量浓度是(28.48±8.97)μg/L;并且病情越重、血清和脑脊液中NSE的质量浓度越高。急性期脑出血和脑梗死患者血清和脑脊液中NSE质量浓度呈显著正相关(脑出血组r=0.920,P<0.01;脑梗死组r=0.865,P<0.01);脑出血和脑梗死患者血清和脑脊液中NSE质量浓度与出院时神经功能缺损程度呈显著正相关(脑出血组r=0.893,P<0.01;脑梗死组r=0.736,P<0.01)。结论:血清和脑脊液中NSE的质量浓度能反映脑损害的程度,是判断脑损害程度的定量信息,对预测患者出院后神经症状和体征的恢复程度也具有较大的价值。     

糖尿病患者血清超敏C反应蛋白、白细胞介素-6及白细胞介素-10的变化

目的:研究血清超敏C反应蛋白(hs-CRP)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)在糖尿病患者中的变化,及其对心血管并发症的预示作用.方法:收集99例糖尿病患者血清,其中胆固醇正常者68例,胆固醇升高者31例,及50例正常体检人员的血清.使用乳胶增强免疫透射比浊法检测hs-CRP,一步酶法检测胆固醇,同时采用ELISA双抗体夹心法测定血清IL-6、IL-10.结果:正常对照组血清hs-CRP、IL-6和IL-10浓度分别为(1.66±0.95)mg/L、(24±8)ng/L和(27±7)ng/L,胆固醇正常糖尿病组血清hs-CRP、IL-6和IL-10浓度分别为(2.77±1.19)mg/L、(25±10)ng/L和(28±8)ng/L,胆固醇升高糖尿病组血清hs-CRP、IL-6和IL-10浓度分别为(5.70±1.81)mg/L、(34±10)ng/L和(21±5)ng/L.与正常对照组、胆固醇正常糖尿病组相比,胆固醇升高糖尿病组hs-CRP、IL-6和IL-10表达水平差异均有统计学意义(分别为P＜0.01、P＜0.05、P＜0.05).与正常对照组比较,胆固醇正常糖尿病组hs-CRP高表达(P＜0.05),而这两组间IL-6和IL-10表达水平差异无统计学意义(P＞0.05).结论:炎症因子hs-CRP在预测糖尿病患者并发冠心病中具有重要的临床意义.     

血清hs-CRP与脑小血管病的相关性分析

将我院收治的腔隙性脑梗死患者53例作为观察组,选择同期在我院进行健康体检者53例作为对照组。对两组患者均进行血清hs-CRP的检测。结果观察组的血清hs-CRP含量为7.91±1.75mg/L,明显高于对照组的血清hs-CRP含量1.86±0.67mg/L,P<0.05。观察组,20例轻度神经缺损患者的血清hs-CRP含量为3.42±0.82mg/L,20例中度神经缺损患者的血清hs-CRP含量为6.95±1.24mg/L,13例重度神经缺损患者的血清hs-CRP含量为12.89±2.35mg/L。神经缺损严重的患者的血清hs-CRP含量明显高于神经缺损较轻的患者(P<0.05)。血清hs-CRP与脑小血管病的病情严重程度具有密切的关系,可以用来评估患者病情的严重程度,值得临床推广。     

严重感染患者急性时相蛋白的临床研究

目的 为了探讨急性时相蛋白在严重感染患者发病过程中的变化及其诊断价值。方法 采用全自动散射比浊定量分析法测定30例严重感染患者CRP.α_1—AT、α_1—AG及HP的含量和动态变化,并与30例轻症医院感染患者及30例正常人对照分析,结果 严重感染患者首次测定CRP、α_1—AT,α_1—AG及HP含量均显著高于轻症感染组和正常组(P值分别<0.01)。动态观察发现急性时相蛋白随着病情好转逐渐降至正常范围,轻症感染患者仅α_1—AG差异显著(P<0.05)。结论 CRP、α_1—AT、α_1—AG及HP的定量分析能尽早发现医院感染,准确判断其严重程度及预后具有重要价值。CRP持续升高、α_1—AG和HP迅速下降则提示病情恶化。     

C-反应蛋白与急性冠脉综合征的关系

目的：探讨C-反应蛋白（CRP）与急性冠脉综合症（ACS）的关系。方法：采用免疫比浊法测定126例ACS患者和100例健康对照者的外向学清CRP水平。结果：ACS组的血清CRP水平明显高于对照组，而急性心机梗塞组血清CRP水平显著高于不稳定性心绞痛组。结论：CRP是ACS危险因素。     

特定蛋白的理化特性与临床意义

血液中含有多种蛋白质执行着多重功能。这些蛋白质，如载体蛋白、抗体、酶、凝血因子等，它们在血液中的改变与多种疾病有着密切的关系。但由于这些特定蛋白质在血液巾含量少，因此检测比较困难。随着检测方法的不断改进，血浆蛋白的检测范围逐步扩大，不仪可检测血液中的特定蛋白，还可检测尿液、脑脊液、胸腹水中的特定蛋白。目前特定蛋白的检测已成为临床不可缺少的检验项目。[第一段]     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

阿托伐他汀对急性冠状动脉综合征患者C-反应蛋白的影响

目的探讨阿托伐他汀对急性冠状动脉综合征（ACS）患者C-反应蛋白（CRP）等的影响及机制。方法测脂，CRP等参数浓度，并与常规治疗119例作为定119例ACS患者在常规治疗基础上加服阿托伐他汀20mg／d，治疗1个月后测定血对照组。结果119例ACS患者经阿托伐他汀治疗1个月后CRP等测定值分别显著低于治疗前水平（P〈0．05），1个月后上述各项参数改变更加明显，与常规治疗对照组及治疗前比较，差异有显著性（P〈0．05）。结论阿托伐他汀通过降脂、抗炎等机制对防治ACS早期动脉硬化及稳定斑块起着重要作用。     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.     

Change of alveolar epithelial type Ⅱ cells and pulmonary surfactant protein A in young rats with acute lung injury

Objective To study the temporal changes of alveolar epithelial type Ⅱ cells and surfactant pro-tein A in young rats with acute lung injury induced by lipopolysaecharide. Method Totally 110 SD young rats (male:53, female : 57) were randomly divided into ALI and normal control groups (six subgroups in each group).LPS(4 mg/kg) was given intraperitoneally in ALI group. The same amount of normal saline was given in the con-trol groups. Eight rats in each subgroup were sacrificed at 6, 12, 24, 36, 48 and 72 hours after the injection.Lung samples were taken for transmission electron microscope examination. RT-PCR was epmloyed for the mea-surement of SP-A mRNA. Western blot was used for the detection of SP-A in the lung tissue. ANOVA and homo-geneity of variance test were performed by SPSS 12.0. Results The microvilli disappeared at 24 hours after the injection of LPS. The number of lamellar body (LBs) was provisionality increased at 24 hours and 48 hours. The ring-like an'angement of LBs around nucleus and the giant LB with vacuole-like deformity were found as the main characteristics of AEC- Ⅱ in ALI at 48 hours. The number of LBs reduced and broken and residual LB remained at 72 hours. SP-A elevated greatly from 24 to 48 hours (P < 0.01), reached peak at 36 hours (6.94 ± 0.80, P <0.01),reached the lowest level(3.87 ±0.50, P <0.01)at 72 hours. Conclusions The pathological changes of AEC-Ⅱ and SP-A in lung tissue wiht ALI are time-dependent. The typical alterations of AEC- Ⅱ occurs at 48 hours accompanied by the compensatory increase of SP-A. AEC- Ⅱ is seriously injuried with the typical changes of LBs and the diminishing of SP-A in lung tissue.