医务人员与SARS患者免疫指标的对比研究

目的 :研究严重急性呼吸道综合征 (SARS)病毒对医务人员免疫功能可能产生的影响 ,为传染病的防治提供理论依据。方法 :采用胶体金法和ELISA法检测SARS患者 (SARS患者组 )及与患者密切接触的医务人员 (小汤山医院组与非SARS定点医院组 )血清中SARSIgG抗体含量 ,并用特种蛋白分析仪测定CRP、补体C3、C4及CIC含量 ,同时选取 13例正常人作为对照组。结果 :对照组血清SARSIgG抗体均阴性 ;非SARS定点医院组医务人员血清中 ,胶体金法 1例阳性 ,ELISA法 1例阳性 ,阳性率为 1 14 % ;SARS患者组IgG抗体均阳性 ,阳性率 10 0 %。SARS患者组CRP分别是对照组、非SARS定点医院组、小汤山医院组的 3 1倍、3 5倍和 2 8倍(P <0 0 1)。与对照组比较 ,非SARS定点医院组补体C3、C4下降了 2 5 2 0 %和 2 7 5 9% ,小汤山医院组补体C3下降了 13 3 9% (P <0 0 5 )。非SARS定点医院组补体C3、C4与小汤山医院组比较 ,分别下降了 13 64 %和 2 2 2 2 % (P <0 0 5 ) ,CIC含量增高了 2 0 0 2 % (P<0 0 5 )。结论 :SARS可能存在隐性感染 ,CRP与患者的临床症状相关 ,可作为SARS病情监测的指标 ;而病毒对医务人员免疫功能的影响显示 ,小汤山医院组小于非SARS定点医院组 ,表明小汤山医院的隔离防护体系较为完善     

系统性红斑狼疮患者免疫功能与自身抗体的关系研究

目的:探讨系统性红斑狼疮(SLE)患者血清免疫功能相关指标(免疫球蛋白IgG、补体C3、补体C4)与自身抗体之间的关系。方法:选取94例SLE患者,81例其他自身免疫系统疾病患者及66例健康对照者分别作为SLE组、非SLE疾病组、健康对照组三组,检测各组血清自身抗体的表达。将SLE组按SLE疾病活动指数(SLEDAI)评分标准分成活动期组和稳定期组,按抗SmD1抗体、抗双链DNA(dsDNA)抗体阴阳性分别分成抗SmD1(+)组、抗SmD1(-)组、抗dsDNA(+)组、抗dsDNA(-)组,与健康对照组一起检测各组血清免疫球蛋白IgG、补体C3、补体C4水平。将以上各组指标进行比较分析。结果:与健康对照组相比,SLE组和非SLE疾病组自身抗体谱中各指标(除Jo-1外)阳性率差异具有统计学意义(P<0.05)。SLE组中抗SmD1抗体、抗dsDNA抗体、抗核小体抗体(AuNA)、抗组蛋白抗体(AHA)、抗核糖体P蛋白(Rib-P)抗体阳性率均比非SLE疾病组高(P<0.05)。SLE活动期组血清免疫球蛋白IgG水平高于SLE稳定期组和健康对照组,而血清补体C3,C4水平低于SLE稳定期组和健康对照组(均P<0.05),SLE稳定期组血清IgG,C3,C4水平和健康对照组相比,血清补体C3,C4水平更低,IgG水平则要高,差异有统计学意义(P<0.05)。SLE组中抗SmD1抗体、抗dsDNA抗体阳性组血清补体C3,C4水平分别低于抗SmD1抗体、抗dsDNA抗体阴性组(均P<0.05)。结论:联合检测免疫球蛋白IgG、补体C3,C4及自身抗体谱可有助于SLE的早期诊断、治疗监测及预后评估。     

类风湿性关节炎患者血清免疫球蛋白和补体水平变化及其临床意义

目的 探讨类风湿性关节炎(RA)患者血清免疫球蛋白(IgG、IgA、IgM)和补体(C3、C4)水平变化及其临床意义.方法 选择初诊RA患者41例,其中活动期27例,非活动期14例,并选择同期体检健康者20例作为对照组,采用免疫比浊法检测3组血清免疫球蛋白(IgG、IgA、IgM)和补体(C3、C4)水平.结果 RA活动组、RA非活动组血清IgG水平均高于对照组,差异均有统计学意义(P＜0.01,0.05),RA活动组与RA非活动组血清IgG水平差异无统计学意义(P＞0.05);RA活动组血清C3水平均高于RA非活动组和对照组,差异均有统计学意义(P ＜0.05,0.01),RA非活动组与对照组血清C3水平差异无统计学意义(P＞0.05);3组间血清IgA、IgM、C4水平差异均无统计学意义(P＞0.05).结论 血清IgG可作为RA的辅助诊断指标,血清C3可作为观察RA活动状态的指标.     

输注辐照血小板后患者体液免疫参数的变化及与血小板输注无效的相关性

目的 研究输注辐照血小板后患者体液中各项免疫参数的变化及其变化情况与血小板输注无效(PTR)的相关性.方法 选取两次以上输血的患有恶性血液疾病的患者126例,采用随机单盲的分配方式将其随机分为观察组和对照组,各63例.观察组患者采用输注γ辐照机采血小板,对照组患者采用输注普通机采血小板.分别检测患者输血前后机体内补体(C3、C4)、免疫球蛋白(IsG、IgM、IgA)、C反应蛋白(CRP)和循环免疫复合体(CIC)的变化情况,比较两组患者血小板输注的有效率并分析免疫参数变化情况与发生无效输注之间的相关性.结果对照组患者C3、C4、IgG、IgM以及CIC均较观察组明显升高(均P＜0.05)；两组患者在输血后IsA无明显变化,但CRP有明显升高趋势；观察组的输注有效率为87.3％,明显高于对照组的61.9％(χ2=8.92,P＜0.05)；输血后PTR患者免疫参数C3、C4、IgG、lgM、CRP以及CIC较输血前均明显升高(均P＜0.05).结论患者机体中相关免疫参数与PTR密切相关,输注γ辐照血小板后可在一定程度上减轻患者体液免疫相关参数的反应情况,进一步提高临床输注有效率.     

SLE患者血清免疫球蛋白及补体水平与自身抗体相关性研究

目的探讨SLE患者血清免疫球蛋白及补体与自身抗体的相关性。方法采用速率散射免疫比浊法检测109例SLE患者和30例体检健康对照者的血清Ig及C3、C4水平并与自身抗体结果进行比较。结果SLE患者血清IgG、IgA水平高于对照纽（P〈0．05）;血清IgM水平与对照组比较差异无统计学意义（P〉0．05）;补体C3、C4水平低于对照组（P〈0．05）。ANA高滴度组与低滴度组相比较,IgG明显升高,补体C3明显降低（P〈0．01）;而IgA、IgM及c4差异无统计学意义（P〉0．05）。抗Sm及抗ds-DNA抗体阳性组分别与其对应的阴性组血清Ig及c3、C4水平相比较,Ig水平差异无统计学意义（P〉0．05）,而C3水平明显降低（P〈0．叭）。结论SLE患者存在血清IgG水平升高,血清补体C3、C4降低的现象;随自身抗体滴度升高差异更为显著,且IgG与疾病活动呈正相关,C3、C4与疾病活动呈负相关;C3可作为反映SLE疾病活动的参考指标。     

重症流感患儿血清免疫球蛋白及补体检测的临床意义

目的:探讨重症流感患儿血清免疫球蛋白(IgA、IgM、IgG)及补体(C3、C4,CH50)的临床意义.方法:80例流感患儿(观察组)和80例健康儿童(正常对照组)为研究对象,采用速率散射比浊法测定血清免疫球蛋白(Ig)和补体(C).结果:观察组IgA、lgM、IgG水平、补体C水平与正常对照组比较上升(P＜0.05).结论:IgA、IgM、IgG,补体C3、4,CH50在流感中起着重要作用,检测这些指标可以较准确地判定重症流感患儿病情和预后.     

系统性红斑狼疮患者血循环免疫复合物和补体水平变化及其临床意义

目的探讨定量检测血循环免疫复合物（circulating immune complexes,CIC）以及补体C3、C4在系统性红斑狼疮（systemic lupus erythematosus,SLE）诊断及评价活动性中的意义。方法用ELISA法定量检测SLE患者和其他风湿病患者血清中的CIC,散射比浊法检测补体C3、C4。据SLEDAI积分表,将SLE患者分为Ⅰ组（SLEDAI评分0．4分）、Ⅱ组（SLEDAI评分5—9分）和Ⅲ组（SLEDAI评分≥10分）。结果SLE患者CIC明显高于疾病对照组（P值〈0．05）,补体C3、C4明显低于疾病对照组（P值〈0．05）;CIC和补体C3：Ⅱ组、Ⅲ组与Ⅰ组比较差异有显著性（P值〈0．05）,而补体C4仅Ⅲ组与Ⅰ组比较差异有显著性（P值〈0．05）。相关分析显示CIC与SLEDAI积分呈正相关,补体C3、C4与SLEDAI积分呈负相关。结论血清CIC和补体C3、C4可作为SLE诊断及评价活动性的有用指标,动态观测CIC和补体C3来评价SLE活动性优于补体C4。     

肺炎支原体感染与急性心肌梗死的临床关系分析

目的:探讨肺炎支原体(MP)感染与急性心肌梗死(AMI))的关系及外周血清MP抗体Igc检测的临床意义.方法:采用固相酶联免疫吸附(ELISA)方法,对30例冠心病病人和对照组30例健康人进行外周血MP抗体检测.结果:冠心病组30例,外周血清MP抗体IgG阳性6例(20.0%),对照组30例中MP抗体IgG阳性1例(3.3%),两组比较差异有显著意义(P＜0.05).结论:肺炎支原体感染与冠心病急性心肌梗死发生发展明显相关.     

原发性干燥综合征患者B细胞活化因子受体的表达

目的 检测原发性干燥综合征(pSS)患者血清中B细胞活化因子受体(BAFF-R)的表达,探讨其在pSS发病中的作用.方法 pSS患者120例,采用酶联免疫吸附法(ELISA)检测血清BAFF-R水平,对照组62例为健康体检者,性别、年龄构成与患者组匹配.分析血清BAFF-R表达与免疫指标、炎性指标及自身抗体的相关性.结果 血清BAFF-R平均水平pSS组为(692.7±536.9)ng/L,对照组为(279.7±186.9)ng/L,pSS组明显高于对照组(P＜0.01).血清BAFF-R水平与免疫球蛋白IgG呈正相关(r=0.429,P＜0.01),与免疫球蛋白IgA、IgM、补体C3、C4、类风湿因子、红细胞沉降率、C反应蛋白无明显相关性.抗核抗体、抗SSA抗体、抗SSB抗体阳性者血清BAFF-R水平高于阴性者.随着抗核抗体滴度的增加,血清BAFF-R水平呈平行增高趋势.结论 pSS患者中BAFF-R表达增高,并与免疫球蛋白定量、自身抗体表达呈相关性.BAFF-R的异常表达参与了pSS的发病.     

免疫功能在百草枯导致的ARDS中的作用研究

目的 研究免疫功能在百草枯(PQ)导致的急性呼吸窘迫综合征(ARDS)中的作用.方法 将医院从2018年1月2月-2020年1月30日收治的PQ所致ARDS患者30例纳入研究.将其按照ARSD分级的差异分作轻度组8例,中度组12例,重度组10例.另取同期于医院接受体检的健康志愿者30例作为对照组.分析各组人员血清补体C3、C5以及IgG、IgM、IgA水平等方面的差异.此外,将PQ所致ARDS患者按照发病后30d内结局的差异分作死亡组21例和存活组9例.比较两组血清补体C3、C5以及IgG、IgM、IgA水平.结果 轻度组、中度组以及重度组血清补体C3、C5水平均高于对照组,且轻度组、中度组以及重度组治疗前、治疗后第1d以及治疗后第8d时的血清补体C3、C5水平均呈逐渐升高趋势,各组间对比差异有统计学意义(均P<0.05).轻度组、中度组以及重度组血清IgG、IgM及IgA水平均高于对照组,且轻度组、中度组以及重度组治疗前、治疗后第1d以及治疗后第8d时的血清IgG、IgM及IgA水平均呈逐渐升高趋势,各组间对比差异有统计学意义(均P<0.05).死亡组血清补体C3、C5以及IgG、IgM、IgA水平均高于存活组(均P<0.05).结论 免疫功能在PQ导致的ARDS过程中起着至关重要的作用.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.