改善微循环障碍对肺心病急性加重期的影响

肺心病急性加重期病人58例,随机分为治疗组30例,男18例,女12例.年龄54～81岁,平均65.6岁.肺心病病史6～16年,平均10.2年.     

肺心病患者急性加重期救治与护理体会

目的：研究肺心病患者急性加重期救治与护理体会。方法从2013年3月~2014年4月,于我院共有112例肺心病急性期患者。以数字法随机分成观察组(56例)和对照组(56例)。其中观察组在治疗的同时采用护理干预,而对照组则仅采用药物治疗。结果观察组为"满意"者占比,显著高于对照组,电解质紊乱发生率,心律失常发生率,弥散性血管内凝血发生率。均显著低于对照组,差异均有统计学意义(均<0.05)。结论药物治疗配合有效的护理,可明显提高治疗效果,安全性较好,值得临床推荐。     

肺心病急性加重期HPAA与细胞免疫变化的关系

为了探讨肺心病急性加重期患者下丘脑－垂体－肾上腺皮质轴（HPAA）激素水平与细胞免疫变化的关系。本研究同步检测了36例肺心病患者急性加重及解缓解期血浆促肾上腺激素（ACTH）、β－内啡肽（β－EP）、糖皮质激素（GC）及外周血T淋巴细胞亚群的变化,并分析它们之间的相互关系。结果显示肺心病急性加重期ACTH、β－EP、GC均显著升高,CD2、CD4、CD8及CD4／CD8比值显著下降（P＜0．01）,相关分析显示ACTH、β－EP、GC分别与CD3、CD4、CD4／CD8呈显著负相关。本研究提示肺心病急性加重期机体内发生了神经内分泌免疫调节紊乱。显著升高的ACTH、β－EP、GC对细胞免疫产生抑制作用。     

大肠癌患者围手术期免疫状态变化的临床意义

目的 研究大肠癌患者围手术期的免疫状态。方法 应用ＡＰＡＡＰ夹心法ＥＬＩＳＡ和比色法分别测定大肠癌患者手术前后Ｔ细胞亚群变化,血浆可溶性白介２受体（ｓＩＬ－２Ｒ）及一氧化氮（ＮＯ）和癌组织的ＳＩＬ－２Ｒ,ＮＯ含量。结果 大谫ＣＤ３,ＣＤ４细胞、ＣＤ４／ＣＤ８比值和血浆ＮＯ水平明显低于正常,血浆ＳＩＬ－２Ｒ、ＣＤ８细胞较正常显著增高,肿瘤切除后３周左右ＣＤ３、ＣＤ４细胞、ＣＤ４／ＣＤ８和血浆术前有明     

疏血通注射液治疗慢性肺心病急性加重期血液流变学的影响

目的观察疏血通注射液治疗慢性肺心病急性加重期对血液流变学的影响。方法将60例慢性肺心病急性加重期患者随机分为对照组和疏血通组 ,每组30例。对照组采用常规治疗。疏血通组在常规治疗基础上给予疏血通注射液6ml加入5%葡萄糖200ml中静滴 ,每日1次 ,10d一疗程 ,共两疗程。结果疏血通组治疗后全血高切粘度、低切粘度、血浆粘度、细胞压积、红细胞聚集指数及纤维蛋白原等指标较治疗前明显下降 ,与常规治疗组比较有显著差异 ,临床症状的改善也与血液流变性的改善一致。结论疏血通注射液具有良好的降粘、解聚、溶纤的功能 ,并能显著提高肺心病的临床疗效     

传染性单核细胞增多症患儿免疫功能变化及其临床意义

目的研究传染性单核细胞增多症（IM）患儿血清中的免疫球蛋白和外周血T淋巴细胞亚群变化及其临床意义。方法采用透射比浊法和APAAP法检测了36例生长发育正常的IM患儿血清Ig和T淋巴细胞亚群。结果IgG、IgA、CD4、CD4/CD8比值明显低于对照组（P〈0.01）,CD3、CD8明显高于对照组（P〈0.01）,IgM与对照组比较无显著性差异（P〉0.05）。结论EB病毒感染后引起机体体液和细胞免疫功能异常是IM发病的关键,为临床IM患儿的免疫治疗提供了理论依据。     

慢性肺心病急性加重期患者CD41、CD62p和血小板数的变化

以往研究显示血小板激活在肺心病急性加重期的血栓形成中起着重要作用[1,2],我们采用流式细胞仪和特异性抗体对肺心病患者急性加重期血小板表面CD41、CD62p的表达和血小板数的变化进行了研究,以探讨肺心病急性加重期血小板功能的变化及其临床意义.     

肺心病急性加重期患者血清T3、T4和胃泌素RIA的变化

本文采用放射免疫分析测定法对39例慢性肺心病急性加重期患者及73例健康人进行血清T3、T4及胃泌素测定，同时作血气分析以探讨其临床意义。     

孕妇免疫功能检测及临床意义

目的：探讨孕妇免疫功能与妊娠的关系。方法：采用免疫荧光法和透射比浊法分别测定60例孕妇和20例正常人的细胞免疫及体液免疫功能。结果：T淋巴细胞与B淋巴细胞的比例虽无明显变化，但T淋巴细胞亚群的比率有明显改变。结论：孕妇存在免疫功能抑制。测定孕妇的免疫功能可以判断妊娠发展情况与预后。     

乙型肝炎患者免疫功能的检测及其临床意义

研究乙型肝炎患者外周血T淋巴细胞亚群、NK细胞和血清免疫球蛋白的变化及临床意义.采用流式细胞仪检测150例乙肝患者和30名健康者(对照组)外周血T淋巴细胞亚群(CD3 CD4 、CD3 CD8 )、NK细胞,免疫散射法检测血清免疫球蛋白(IgG、IgM、IgA)变化.结果表明各临床类型乙肝患者NK细胞降低,与对照组比较有显著性差异(P<0.01);慢性乙型肝炎组、慢性重型乙型肝炎组、肝硬化组外周血CD3 CD4 、CD3 CD8 T细胞均下降,其中慢性重型乙型肝炎组外周血CD3 CD8 与对照组比较有显著性差异(P<0.01),急性乙型肝炎组外周血T细胞亚群变化不明显(P>0.05);各临床类型乙型肝炎患者血清免疫球蛋白IgG、IgA随着病情的进展逐渐升高,与对照组比较有显著性差异(P<0.01).因此认为慢性乙肝患者存在细胞免疫和体液免疫功能紊乱,免疫功能的检测对乙肝的诊断、治疗及预后的判断有着一定临床意义.     

Acid-base changes in acute exacerbation of chronic hypercapnia in man.

Acid-base parameters were studied in 10 adult patients with chronic respiratory failure during spontaneous acute exacerbations of chronic hypercapnia and after return and stabilization of PaCO2 values at previous levels with improvement of clinical conditions. All factors interfering with acid-base equilibrium were carefully avoided. The results of this investigation confirm qualitatively those obtained by GOLDSTEIN et al. [7] in dog studies and those of INGRAM et al. [9]in human studies: increasing degrees of chronic hypercapnia tend to minimize the pH reduction induced by acute PACO2 changes. From a quantitative standpoint INGRAM's data in humans are considerably different from GOLDSTEIN's data obtained in dogs. Our data, although numerically limited, confirm the acute deltaH+/deltaPaCO2 slope obtained from dogs by GOLDSTEIN et al. As data are not yet sufficient, definitive conclusions cannot be drawn. However the pattern of acid-base equilibrium changes in man in this situation seems to be similar to that observed by GOLDSTEIN et al. in the dog and could be described with reasonable accuracy by the theoretical model of LEUENBERGER et al.[13].     

慢性阻塞性肺疾病急性加重患者呼吸道病毒的检测分析

目的 探讨呼吸道病毒感染与慢性阻塞性肺疾病急性加重(AECOPD)的相关性.方法 随机选择140例慢性阻塞性肺疾病急性加重(AECOPD)患者,60例健康老年志愿者为对照组,分别检测呼吸道合胞病毒(RSV)、单纯疱疹病毒(HSV)、腺病毒(ADV)、巨细胞病毒(CMV)、副流感病毒(PIV)、流感病毒A/B(FluA/B)特异性抗体IgM水平,对组间阳性率进行比较.结果 AECOPD组患者中IgM阳性率依次为RSV＞PIV＞ FluA/B＞CMV＞ADV＞ HSV.AECOPD组与对照组各病毒抗体阳性率比较差异有统计学意义(P＜0.05).结论 病毒感染是AECOPD重要因素,病毒感染参与了AECOPD病情的进展过程,在呼吸道病毒流行的季节应做好预防工作.     

Significance of secondary cytogenetic changes in patients with Ph-positive chronic granulocytic leukemia in the acute phase

The karyotypic abnormalities in 29 patients in the acute phase of Ph-positive chronic granulocytic leukemia are described. Of 18 Giemsa banded samples, 11 showed one or more of the typical additional abnormalities found in the acute phase, namely +Ph, +8, or i(17q). Survival data from these patients was combined with three published series providing 135 patients and the effect of one, two, or three of these abnormalities tested. The prognosis was significantly worse in patients with two or more additional abnormalities, compared with those with one or none. Analysis of the subset of patients with only one additional abnormality [+Ph or +8 or i(17q)] suggested a worse prognosis in those with +8 than in those with +Ph or i(17q), although the differences were not significant. There also was a trend for patients in whom all metaphases showed abnormalities in addition to the Ph chromosome to have a worse prognosis than those in whom some or all metaphases contained the Ph only. However, this trend just failed to reach a 5% level of significance.     

Detection and characterization of circulating immune complexes during acute exacerbation of chronic viral hepatitis

For the detection and characterization of circulating immune complexes (CIC) in various liver diseases, a Clq binding test was used. Though the CIC level was almost normal in HB surface antigen (HBsAg) positive asymptomatic carriers, the level increased in patients with liver diseases. During acute exacerbation of chronic viral hepatitis, the CIC level reached peaks 1 to 3 weeks before and after the hepatic cell necrosis. Study of the sedimentation rates of CIC in various liver diseases showed CIC in the 19s-22s region and in the 7s-19s region. In acid buffer, CIC was dissociated into 5 to 6 components by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). In one case of HBsAg positive severe chronic aggressive hepatitis, CIC was composed of HBsAg, IgG and another three or four undetermined components. During acute exacerbation of chronic hepatitis, minor changes of these dissociation patterns of CIC were observed.     

Elevated serum levels of thioredoxin in patients with acute exacerbation of asthma

The pathogenesis of bronchial asthma is chronic airway inflammation caused by immune cells such as T lymphocytes and eosinophils. Eosinophils release cytotoxic products including reactive oxygen species at the site of inflammation, leading to epithelial damage. Human thioredoxin (TRX), a redox-regulating protein with antioxidant activity, is induced and secreted from cells by oxidative stress. This study was undertaken to investigate the clinical significance of TRX in the pathogenesis of asthma. We collected blood samples from 48 patients with bronchial asthma with or without attack, and measured serum ECP and pulmonary function as well as serum TRX. The serum TRX levels in patients with asthma were significantly increased in patients with mild (34.63 [28.40-42.73] ng/ml, medians with 25 and 75% interquartiles, P=0.0064) and moderate (38.83 [35.14-50.80] ng/ml, P=0.0017) asthma attacks compared with those during the asymptomatic period. The serum TRX levels were inversely correlated with FEV(1.0)% (r=-0.44, P=0.039) and %PEF (r=-0.49, P=0.020) during attack. There was a significant correlation between the serum TRX and the serum eosinophil cationic protein (rs=0.32, P=0.016). These findings suggest that serum TRX is related to the state of asthma exacerbation and allergic inflammation.     

Detection and characterization of circulating immune complexes during acute exacerbation of chronic viral hepatitis.

For detection and characterization of circulating immune complexes (CIC) in various liver diseases, a C1q binding test (C1q BT) was used. While the CIC level was almost normal in HB surface antigen (HBsAg) positive asymptomatic carriers, it was relatively high in patients with liver diseases. The study of the sedimentation rate of CIC in various liver diseases showed two kinds of CIC; one greater than the other. During acute exacerbation of chronic active liver diseases, the CIC level reached its peak 1-5 weeks before and after the peak of sGPT. In acid buffer, CIC in one patient with HBsAg positive severe chronic aggressive hepatitis was dissociated into 5-6 fractions by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The two of these fractions proved to be HBsAg and IgG and another three or four undetermined components. At the acute exacerbation period of this case, the fraction pattern of CIC by SDS-PAGE was similar to each other at any of the four stages and HBsAg always composed one of the antigens.