Antinuclear autoantibodies in chronic schizophrenia

We determined the presence of antinuclear autoantibodies (ANA), antinative DNA and histone-reactive ANA in 3 groups of chronic schizophrenic patients (n= 85): haloperidol-treated patients (for at least 3 months) (n= 35), drug-free for at least 3 months (n= 35) and neuroleptic-naive patients (n= 15). The autoantibody titers were compared with those of healthy controls (n= 37). A significantly higher frequency of positive ANA was found among chronic schizophrenic patients (～20%) as compared with the controls (～5 %), irrespective of drug treatment, sex and age. No antinative ANA autoantibodies or histone reactive ANA were detected in either schizophrenic patients or controls. Further studies are needed to isolate and characterize in ANA-positive schizophrenic patients 1 a putative specific ANA profile.     

Protective immunity to malaria: studies with cloned lines of rodent malaria in CBA/Ca mice. IV. The specificity of mechanisms resulting in crisis and resolution of the primary acute phase parasitaemia of. Plasmodium chabaudi chabaudi and P. yoelii yoelii

Low numbers of parasites from cloned lines of the rodent malaria parasites, Plasmodium chabaudi chabaudi AS and P. yoelii yoelii A, injected into CBA/Ca mice produce acute but usually self-limiting infections. During crisis, i.e. 1-2 days after peak parasitaemia, 'pre-immune' mice experiencing such 'background' infections were reinfected intravenously with homologous parasites or parasites of heterologous strains or species. P. c. chabaudi AS pre-immune mice controlled an AS challenge with essentially the same kinetics as the background infection. Reinfection of AS pre-immune mice with the heterologous (CB and IP-PCI) P. c. chabaudi strains or P. chabaudi adami DS had little effect on the initial growth of these parasites, although eventually the parasitaemia was controlled. In contrast, a partial inhibitory effect on the growth of P. vinckei lentum DS was evident. Challenge with the non-lethal (A) or lethal (YM) variants of P. y. yoelii resulted in an increase in both the growth and virulence of these parasites. P. y. yoelii A pre-immune mice controlled a homologous challenge, but were less effective at controlling the YM variant. In addition, they were unable to clear rapidly a P. c. chabaudi AS or P. v. lentum DS challenge. Both the multiplication and virulence of P. berghei ANKA were enhanced. These findings demonstrate that resolution of the primary acute parasitaemia in P. c. chabaudi AS- and P. y. yoelii A-infected mice is predominantly mediated by species- and strain-specific mechanisms.     

Anti-mitochondrial antibodies in patients with dilated cardiomyopathy (anti-M7) are directed against flavoenzymes with covalently bound FAD

Anti-mitochondrial antibodies (anti-M7) in sera from patients with dilated cardiomyopathy and myocarditis recognize, besides mitochondrial antigens, bacterial sarcosine dehydrogenase. The common target antigen was identified as the covalently bound FAD of mitochondrial and bacterial flavoenzymes. Thus, anti-M7-positive serum reacted on Western blots exclusively with covalently flavinylated enzymes. The antigenic specificity of anti-M7 sera was reproduced by an antiserum raised in rabbits with 6-hydroxy- D -nicotine oxidase. The heart mitochondrial membrane antigen recognized by anti-M7 serum was identified as the flavoprotein subunit of succinate dehydrogenase, the antigens in rat liver mitochondrial matrix as the flavoenzymes dimethylglycine dehydrogenase and sarcosine dehydrogenase. Anti-M7 serum contained a specific anti-flavoenzyme antibody fraction. Nanomolar concentrations of FAD and riboflavin inhibited the immune reaction on Western blots and in ELISA, and incubation with FAD-agarose depleted the anti-M7 activity of the serum. N-terminally deleted dimethylglycine dehydrogenase proteins were only immunoprecipitated by anti-M7 sera when the FAD was covalently incorporated. An affinity constant (K_D) of 10^?8 M was established for the anti-flavoenzyme antibodies by competitive ELISA. Of patients with cardiomyopathy and myocarditis, 36% and 25%, respectively, were anti-flavoenzyme-positive by Western blot and ELISA, but only two of 15 patients with other heart diseases and none of 50 healthy controls.     

Inhibition of Complement Regulation Is Key to the Pathogenesis of Active Heymann Nephritis

Crry (complement receptor 1–related protein/gene y) is a key cellular complement regulator in rodents. It is also present in Fx1A, the renal tubular preparation used to immunize rats to induce active Heymann nephritis (HN), a model of membranous nephropathy. We hypothesized that rats immunized with anti-Fx1A develop autoantibodies (auto-Abs) to Crry as well as to the megalin-containing HN antigenic complex, and that anti-Crry Abs promote the development of injury in HN by neutralizing the complement regulatory activity of Crry. Rats immunized with Fx1A lacking Crry remained free of proteinuria and glomerular deposits of C3 during a 10-wk follow-up despite typical granular immunoglobulin (Ig)G deposits in glomeruli. Anti-Fx1A auto-Abs were present in their sera at levels that were not different from sera pooled from proteinuric rats with HN induced with nephritogenic Fx1A. Passive administration of sheep anti-Crry Abs to rats immunized with Crry-deficient Fx1A led to proteinuria and glomerular C3 deposition, which were not seen in such rats injected with preimmune IgG, nor in rats with collagen-induced arthritis injected with anti-Crry IgG. To directly examine the role of Crry in HN, rats were immunized with Crry-deficient Fx1A reconstituted with rCrry. This led to typical HN, with 8 out of 15 rats developing proteinuria within 14 wk. Moreover, the extent of glomerular C3 deposition correlated with proteinuria, and anti-Crry Abs were present in glomerular eluates. Thus, Crry is a key nephritogenic immunogen in Fx1A. Formation of neutralizing auto-Abs to Crry impairs its function, leading to unrestricted complement activation by Abs reactive with the HN antigenic complex on the epithelial cell surface.     

肾综合征出血热特异性抗体的检测与中西医结合治疗的研究

目的探索一种更为简便、快速、特异、灵敏的肾综合征出血热(hemorrhagic fever with renal syndrome, HFRS)抗体的检测方法及更为有效的中西医结合治疗手段.方法559例HFRS患者血清同时采用免疫滴金法(colloidal gold immuno-dot assay,CGIDA)与酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)对比检测特异性免疫球蛋白M抗体(抗HFRS-IgM),间接免疫荧光法(indirect fluorescent antibody test,IFAT)对比检测特异性免疫球蛋白G抗体(抗HFRS-IgG).101例HFRS患者分组进行中西医结合治疗,治疗组50例用苦黄注射液、参麦注射液联合黄芪口服液,对照组51例用利巴韦林注射液联合甘利欣注射液,针对老年患者的临床特点,及早采用综合性防治措施.结果559例HFRS患者血清,以CGIDA法检测抗HFRS-IgM,阳性396例(70.8%);以CGIDA法检测抗HFRS-IgG,阳性489例(87.5%).治疗组与对照组用药后退热天数、主要症状和体征缓解天数相似(P＞0.05);肾功能恢复天数,对照组优于治疗组(P<0.01);在越期方面,治疗组越休克期数明显高于对照组(P<0.01). 结论CGIDA法检测HFRS特异性抗体分别与ELISA法及IFAT法对照,均有简便、快速、特异、灵敏之优点,检测抗HFRS-IgM,CGIDA法敏感性差于ELISA法,但是无假阳性;检测抗HFRS-IgG,CGIDA法的灵敏度高于IFAT法.苦黄注射液、参麦注射液联合黄芪口服液与利巴韦林注射液联合甘利欣注射液相比较,疗效无明显差别,但前者优于改善休克情况,后者强于改善肾功能.     

间接荧光抗体试验检测日本血吸虫感染家兔血清中特异性抗体水平的动态变化

用尾蚴、雌虫、雄虫和血吸虫感染兔肝组织内虫卵冰冻切片抗原进行间接荧光抗体试验（ＩＦＡＴ），观察日本血吸虫感染家兔血清中特异性抗体的动态变化。抗尾蚴、成虫（雌、雄虫）、虫卵抗体检出的最早时间分别为３ｗｋ、３ｗｋ、４ｗｋ，其抗体滴度高峰分别在感染后７ｗｋ、１０～１２ｗｋ和１０ｗｋ。以抗尾蚴抗体水平最高，抗虫卵抗体次之，抗雌、雄虫抗体较低。这为全面了解感染宿主对血吸虫各期抗原（尾蚴、雌、雄虫、虫卵）的免疫反应及免疫学诊断提供了新的资料     

Use of a synthetic peptide-based elisa for the diagnosis of infectious mononucleosis and other diseases

A simple enzyme immunoassay has been developed based on measuring antibodies to synthetic peptides corresponding to sequences in the Epstein-Barr nuclear antigen (EBNA). This assay, which is reproducible, quantitative, and simple to perform and interpret, can be an effective tool to aid in the diagnosis of infectious mononucleosis and nasopharyngeal carcinoma.     

母婴ABO血型不合母体高效价IgG的低温分离与纯化

目的 分离和纯化母婴血型不合母体的特异性高效价的IgG抗体。方法 采用半饱和硫酸铵低温沉淀法分离IgG抗体，SephedexA50层析柱纯化，然后用B型红细胞(RBC)吸收放散IgG，用聚乙二醇(PEG)沉淀，真空泵脱水回收IgO。结果 200ml血浆经半饱和硫酸铵低温沉淀后得IgG粗制品2．26g，Sephedex A50层析柱纯化后得纯制品1．84g，经B型RBC吸收放散后得特异性IgG 0．55g，回收率达29．89％(0．55／1．84)。结论 采用半饱和硫酸铵低温沉淀法分离高效价IgG抗体，可以获得高纯度的IgG。     

个性化护理干预对妇科恶性肿瘤手术后生活质量的影响

[目的]探讨个性化护理干预对妇科恶性肿瘤手术后生活质量的影响。[方法]将46例在我科因妇科恶性肿瘤手术的患者随机分为实验组和对照组，通过实施个性化护理干预，对两组患者进行SF-36量表和Olson婚姻质量问卷进行测评。[结果]对妇科恶性肿瘤手术后患者进行个性化护理干预后其生活质量明显提高，差异有显著性意义（P〈0．01）。[结论]个性化护理干预能提高妇科恶性肿瘤手术后生活质量。     

流行性出血热病毒特异性转移因子的研究

对流行性出血热病毒(EHFV)特异性转移因子(EHFV-TF)的制备、特性及在小鼠体内的活性作用进行了研究。其理化性状与普通 TF 非常相似,能激活淋巴细胞的 E 受体(激活率为65.54%),明显提高 Et-RFC 的形成率。E-HFV-TF 还具有特异性抗原依赖活性:①促进 BALB/C 小鼠和 NIH 裸鼠特异性抗体的产生;②促进 LACA 小鼠脾细胞对 EHFV 反应的特异性应答;③促进脾细胞在 EHVF 存在时对 PHA 诱导下的增殖反应(促时率为151.3%)。EHFV—TF可推迟动物感染 HEFV 后的发病期,延长病程和推迟死亡时间;减轻发病动物脑肺充血、出血、水肿现象和肝肾病理损害程度。结果表明 EHFV-TF 不仅具有提高细胞免疫的非特异活性,而且具有对 EHFV 抗原的依赖活性。本研究提示,E-HFV-TF 可用于 EHFV 感染病人的治疗。