42例失代偿期肝硬化的骨髓细胞学特征分析

目的:探讨42例失代偿期肝硬化患者的骨髓细胞学特征。方法:选取2014年9月至2016年9月于我院失代偿期肝硬化行骨髓细胞学检查的患者42例为观察组,另选取42例我院的健康体检者为对照组。对两组受检者检查结果进行线性回归分析,比较骨髓细胞增生程度、血液细胞计数、骨髓细胞学构成。结果:观察组与对照组相比,骨髓细胞增生程度明显降低;与对照组相比,观察组粒细胞系、巨核细胞数、红细胞数明显增高,粒红比明显降低(P0.05);与对照组相比,观察组骨髓细胞学诊断异常率明显增加(P0.05)。结论:失代偿期肝硬化的骨髓细胞学特征的有效分析可为帮助医生辨别患者发病所处阶段,易于临床对症治疗,对临床诊断、预测具有重要意义。     

阴道镜检查在妇科的应用价值

目的：探讨阴道镜检查在妇科疾病诊断中的应用价值。方法：随机抽取268例患者的阴道镜检查资料并结合细胞学检查进行回顾性分析。结果：268例阴道镜检查结合病理学检查中，阳性结果240例(占89．56％)，其中慢性宫颈炎191例(79．58％)，宫颈尖锐湿疣32例(13．33％)，宫颈不典型增生6例(2．50％)，宫颈原位癌6例(2．50％)，宫颈浸润癌4例(1．67％)，宫颈结核1例(0．42％)。结论：阴道镜检查结合细胞学检查为早期宫颈癌和宫颈尖锐湿疣早期阶段的诊断提供了可靠依据，对慢性宫颈炎的鉴别诊断有一定临床价值，可作为妇科疾病常规检查和宫颈癌普查项目之一。     

液基细胞学与人乳头瘤病毒检查用于宫颈癌筛查的意义研究

目的：探讨液基细胞学与人乳头瘤病毒检查用于宫颈癌筛查的临床意义。方法选取来我院进行宫颈癌癌前病变和宫颈癌筛查的女性1820例,将进行筛查的女性进行随机分组,分为观察组和对照组两组,每组各910例。两组筛查者首先都进行液基超薄细胞学检查进行阳性筛查,观察组在此基础上再进行高危型人乳头瘤病毒检查,结合两种检查方式的结果,进行阳性筛查。结果观察组患者经筛查检出高危型人乳头瘤病毒与液基超薄细胞学检查同时阳性共61例,经病理检查为阳性者共51例,临床诊断符合率为83.61%,对照组患者经筛查检出阳性者共116例,经病理检查为阳性者共68例,临床诊断符合率为58.62%,两组患者的阳性符合率比较差异具有统计学意义(2=11.923,<0.01)。结论液基超薄细胞学检查与高危型人乳头瘤病毒检查,在宫颈癌筛查中,两种方式互为补充,能够显著提高临床诊断符合率,降低漏诊率。     

促肝细胞生长素治疗重症肝炎疗效观察

中对所收治的78例重症病毒性肝炎进行了分组治疗，A组(观察组)36例．B组(对照组)42例，两组均采用积极的综合治疗，A组在原基础上加用促肝细胞生长素(PHCF)80mg加入10％葡萄糖溶液中每日静滴1～2次，疗程9～35天，进行观察后发现A组病死率为38.9％，B组为54.8％，两组比较有显性差异(P<0.05)，说明PHGF治疗重症肝炎确有一定疗效。中对PHGF作用机理、临床使用注意事项等进行了分析说明，并经初步观察发现使用促肝细胞生长素短期无诱发癌变现象。     

骨髓细胞学与WBC、SF联合诊断再生障碍性贫血的效果

目的:分析骨髓细胞学与白细胞计数(WBC)、铁蛋白(SF)联合诊断再生障碍性贫血(AA)的效果.方法:选取自 2017 年 5 月-2022 年 5 月本院收治的 202 例AA患者,将其纳入观察组.另选取同期体检的198 例健康志愿者纳入对照组.所有患者均进行骨髓细胞学检查,对比两组WBC、SF及骨髓细胞内外铁测定结果,并分析三者联合使用的诊断价值.结果:观察组患者WBC、SF水平及细胞内铁含量明显低于对照组,而细胞外铁明显高于对照组(P＜0.05).202 例AA患者均进行WBC、SF、细胞内铁联合检查后,结果显示有 193 例阳性患者、9 例阴性患者,198 例健康志愿者进行WBC、SF、细胞内铁联合检查后,结果显示有 11 例阳性患者、187 例阴性患者.三者联合检测后诊断准确率为 95.00％,特异度为 94.44％,灵敏度为95.54％.三者联合检测的诊断准确率、特异度、灵敏度均高于三者单独检测(P＜0.05).结论:骨髓细胞学、WBC、SF联合检测在AA的诊断中具有较高的应用价值,能显著提高诊断准确率,为临床诊疗提供可靠依据     

Colti病毒抗原制备、保存及其在检测患者血清Colti病毒抗体中的应用

目的 获得较高滴度和稳定的Colti病毒抗原，进一步开展Colti病毒感染的血清学诊断。方法 用C6／36细胞培养Colti病毒，于不同时间收获后进行病毒滴度测定。病毒经聚乙二醇(PEG)纯化浓缩后抗原分别保存于-20℃和4℃备用。利用该抗原采用ELISA法检测患者血清标本的Colti病毒抗体。结果 在制备Colti病毒抗原时，以细胞培养3—4周的病毒滴度最高，经PEG纯化浓缩的抗原于-20℃和4℃条件下，保存6个月，其抗原滴度仍保持在较高水平。特别是加入甘油的抗原无论在-30℃，还是在4℃下，甚至可保存2年。用这些抗原，检测疑似乙型脑炎或病毒性脑炎患者标本1141份，Colti病毒IgM抗体阳性130例，阳性率为11．4％(130／1141)，特别是检测广州市儿童医院患者标本41份，9份Colti病毒抗体阳性，阳性率为22．0％，其中5例临床诊断为病毒性脑炎。结论 为建立检测Colti病毒抗体及诊断试剂盒提供了较稳定的抗原，Colti病毒可能是引起我国夏、秋季脑炎的又一重要病原。     

RT-PCR扩增汉滩病毒及其核苷酸序列的发生树分析

目的：用RT－PCR方法扩增肾综合征出血热病人血样品的汉滩病毒RNA，对扩增产物进行测序并分析汉滩病毒基因组的变异，方法：用引物PⅠ/PⅡ对22例血样品中的汉滩病毒RNA进行第一次PCR扩增，PⅠ/PⅡ扩增样品有再PⅠ1/PⅡ2引物进行槽式RT－PCR扩增，将扩增效果良好的PCR产物进行测序，对测序结果用生物化学软件进行同源性比较和进化树分析，其中HV226样品用引物P1／P2进行RT－PCR扩增。结果：22例肾综合征病人血样品用PⅠ/PⅡ和P1／P2引物扩增有19例阳性，其中编号W613、W1141样品用PⅠ1／PⅡ2进行槽式增后对其扩增产物直接进行测序。HV226号样品用引物P1／P2进行扩增后，其扩增物也直接进行测序，对该3株序列测定结果进行比较分析发现，编号W613、W1141样品核苷酸序列与HV114株的同源性为84％，而与HTN76－118株的同源性为99％，HV226号样品与HV114有95％的同源性，而与HTN76－118有82％的同源性。进化树分析表明，W613，W1141与HTN76－118株立同一分枝，而HV226与HV114、A9株处于同一分枝。结论：湖北地区汉滩病毒至少存在2个亚型，其中W613、W1141与HTN76－118的核苷酸序列高度同源，属于同一亚型，而HV226与HV114属于另一亚型。     

巨细胞病毒在冠心病发病及发展中的作用及相关性研究

目的 分析讨论巨细胞病毒(HCMV)在冠心病发病及发展中的作用与相关性.方法 选取本院收治的40例冠心病患者作为研究对象,将其按照疾病类型分为2组,观察组A有22例急性冠脉综合征患者,观察组B有18例稳定心绞痛患者,并选取同期于本院进行健康体检者20名为对照组,对各组HCMV-IgG、HCMV-IgM与白细胞计数等检测结果进行观察比较分析.结果 观察组A的HCMV-IgG阳性率为90.9％、HCMV-IgM阳性率为40.9％,明显高于对照组(P＜0.05),且观察组A的hs-CRP、LPA和白细胞计数等检测值均与观察组B和对照组具有显著性差异(P＜0.05),观察组A患者的hs-CRP、LPA和HCMV-IgM具有正相关性(P＜0.05).结论 巨细胞病毒(HCMV)可导致冠心病炎症加重,其感染程度与冠心病发展具有密切相关性,且为激发其发病的独立危险因素.     

不明原因习惯性流产与HLA相关研究

目的 探讨不明原因习惯性流产(RSA)与HLA的关系。方法 用血清学方法对20例不明原因习惯性流产的夫妇和20例正常妊娠夫妇进行HLA-A.B.C抗原位点检测。结果 RSA夫妇无抗原共享率10％,对照组40％。有显著差异;一个抗原共事率RSA组15％,对照组35％,无显著差异;两个抗原共事率RSA组50％,对照组20%,有显著差异;三个位点以上抗原共事率25％,对照组0％,差异更正著。结论 HLA相容性可能是导致RSA的免疫因素。     

抗家鼠型肾综合征出血热病毒单克隆抗体对感染乳鼠保护作用的初步研究

以家鼠型HFRS病毒R22株100LD_(50)感染2～4日龄乳鼠。于感染后0、48、96及120h分别经腹腔注射对该株病毒具有中和活性的单一McAb或混合McAb,同时设该病毒免疫血清、单注射该病毒和Sp2/0腹水3种对照,观察McAb对感染乳鼠的保护作用,观察时间为35d。结果在感染后96h内注射单一McAb、混合McAb及免疫鼠血清的保护率均可达100％,而Sp2/0腹水对照组与病毒对照组的乳鼠均在感染后第13～16d发病死亡。在死亡乳鼠的脑,肺组织中检出了HFRS病毒抗原,而在保护存活乳鼠的脑、肺组织中均未检出病毒抗原。McAb对感染乳鼠的保护率与其浓度相关。在感染后24h分别注射不稀释、10~(-1)、10~(-2)和10~(-3)稀释的混合McAb,其保护率依次为100％、88.7％、55.6％和16.7％。     

Study of the cultured human endothelial cells infected by epidemic hemorrhagic fever virus]

Virus antigen could be detected in the cytoplasm of infected human endothelial cells (HEC) by immunofluorescent assay (IFA) 2 to 10 days after the inoculation of epidemic hemorrhagic fever virus (EHFV), but no apparent histologic changes could be found by phase contrast light microscopy, as well as no mature virus particles could be detected under the transmission electron microscope. Reinoculation of the freeze-melt supernatant of HEC 8 days after the inoculation of EHFV to EHFV susceptible Vero E-6 cells, viral antigen could be detected in most of these cells and mature EHFV particles or viral inclusion bodies could also be obtained in the cytoplasm under transmission electron microscope. The results show that HEC is a susceptible target cell to EHFV and infection by this virus may not give apparent cytopathogenic effect in HEC.     

Occurrence and distribution of Hantavirus in wild living mammals in Belgium

Small mammals were screened for the presence of antibodies to Hantaan virus (HTN) and Hantavirus (HV) antigen in Belgium. Antibody and antigen-positive animals were found in different parts of the country. One insectivore and five rodent species were found positive. The highest prevalence of infection was found in the bank vole (Clethrionomys glareolus). A relation between infected animals and wet habitats was observed. It was obvious that in bank vole the likelihood of infection increased with age.     

Sensitive solid-phase immune electron microscopy double-antibody technique with gold-immunoglobulin G complexes for detecting rotavirus in cell culture and feces.

A new solid-phase immune electron microscopy double-antibody colloidal-gold technique (SPIEMDAGT) was developed and compared with direct electron microscopy, direct immune electron microscopy, and enzyme immunoassay for detecting rotavirus. Guinea pig and rabbit antirotavirus antisera were used as capture and detector antibodies, respectively, and goat anti-rabbit immunoglobulin G-gold complexes were employed as a label. Animal rotavirus in cell culture media and human virus in stool specimens were detected by this method. On average, SPIEMDAGT detected 800 times more virus particles than direct electron microscopy and 45 times more particles than direct immune electron microscopy and yielded 20% more positives than enzyme immunoassay. SPIEMDAGT could detect not only viral antigen associated with morphologically recognizable particles but also antigen present when whole virus particles were not visible.     

Seroepidemiology of Hantaan virus infection in Taiwan

In order to investigate the infection rate of Hantaan virus in Taiwan, a total of 6,536 human serum samples were collected from residents, selected by stratified random sampling, from 19 townships covering four different ethnic groups: Aborigines, Fukien Taiwanese, Hakka Taiwanese, and Mainland Chinese. Serum samples were screened for Hantaan virus antibodies by indirect immunofluorescence. The prototype Hantaan virus (76/118)-infected Vero E6 cells were used as the viral antigen for the antibody detection. Among 6,536 human serum samples, 403 (6.2%) samples had Hantaan virus antibodies. The seropositive rates for males and females were 6.1% and 6.2%, respectively. A higher seropositive rate was found among Aborigines on the Orchid Islets (11.5%) and Fukien Taiwanese on the Penghu Islets (11.6%), while the lowest rate was observed among Hakka Taiwanese in the south of Taiwan (2.5%). In comparing with different ethnic groups, the highest prevalence was found among Fukien Taiwanese (8.1%) and the lowest among Mainland Chinese (4.9%). Among the different geographical areas, the highest positive rate was found in western Taiwan (7.1%) and the lowest in southern Taiwan (5.4%). Hantaan virus antibodies were also detected in 22 of 548 (4.0%) rat serum samples. The highest seropositive rate was found in rat sera collected from the Orchid Islets (21.4%). None of the rat sera collected from Hsinchu, Miaoli, Changhua, Nantu, Yunlin, Chi-ayi, Tainan, and Penghu Counties were positive. Hantaan virus antibodies were found in rats: Rattus rattus (20%), Bandicota indica (9.0%), Rattus norvegicus (8.3%), Bandicota nemorivaga (6.3%), Rattus losea (4.2%), and Apodemus agrarius (1.6%). Hantaan virus antibodies were not detected in rat sera collected from species of Rattus coxinga, Rattus culturatus, Mus musculus, Mus caroli, Suncus murinus, and Apodemus semotus. The results show that the Hantaan or Hantaan-related virus exists and is distributed widely in both human and rats in Taiwan. © 1996 Wiley-Liss, Inc.     

Identification of Hantaan virus-related structures in kidneys of cadavers with haemorrhagic fever with renal syndrome

Summary The etiologic agent of haemorrhagic fever with renal syndrome (HFRS), Hantaan virus, was first isolated in 1976. Since then numerous Hantaan-like viruses have been isolated and five serotypes of Hantavirus have been recognized. Serological studies indicate that these viruses are globally distributed, with each serotype occurring in specific areas. Hantaan virus has been intensively studied antigenically, biochemically, and genetically. However there is still a paucity of information on the pathogenesis of Hantaan virus in the human host.In this paper, we report the detection by thin section immune electron microscopy of the occurrence of numerous dense precipitates, typical inclusion bodies, a surface antigen layer, as well as Hantaan virion-like structures in the kidneys of patients that died during the acute phase of HFRS. These findings may shed some light on understanding the pathogenesis of HFRS in target organs most affected by the disease, such as the kidneys.     

Protective immunity of Hantaan virus nucleocapsid and envelope protein studied using baculovirus-expressed proteins

Summary Recombinant Hantaan virus nucleocapsid protein (rNP) and recombinant envelope (rEnv) proteins were prepared using a baculovirus expression system to examine the role of Hantaan virus structural proteins in protective immunity. Passive transfer of spleen cells from mice immunized with rNP conferred partial protection or prolongation of time to death from fatal Hantaan virus infection in suckling mice which were challenged with Hantaan virus at 40 LD₅₀ (survival rate: 43%) or 4 LD₅₀ (survival rate: 43%). The T cell-enriched fraction protected one mouse from lethal infection but the B cell-enriched fraction had no such effect on fatal HTN infection. The protective effects of the antibody against HTN challenge were examined by passive immunization. The monoclonal antibody ECO 2 directed to NP also conferred partial survival and significant difference in time to death. Although rEnv antigen failed to induce neutralizing antibody, both immune spleen cells and immune serum to rEnv conferred partial protection upon suckling mice. These results indicate that both nucleocapsid and envelope proteins of Hantaan virus were responsible for induction of cell mediated protective immunity. Vero E 6 cells infected with Hantaan virus expressed envelope protein on the surface, as determined by flow cytometry. However, there was only negligible expression of nucleocapsid protein.     

Scanning electron microscopy of lymphoid cells from leukemia virus-infected mice

Spleen, lymph node, bone marrow, and thymus cells from Friend leukemia virus (FLV)-infected mice were examined by scanning electron microscopy. Whereas splenocytes from normal, noninfected animals showed the expected morphological classes of lymphocytes, including cells with numerous villous projections and smoother cell types, spleen cells from mice infected with FLV showed a rapid alteration of surface morphology. Shortly after infection, a decrease in the number and percentage of villous cells occurred, with a concomitant increase in the number of cells that were larger and smoother. Within 10 to 20 days after infection, the majority of splenocytes were smooth, large cells showing many distinct morphological charges, including surface "holes" and a "spongy" appearance. By days 25 to 35 after infection, most splenocytes were abnormal in appearance. Similar changes occurred in the lymph nodes after FLV infection, but the rate of change was much lower. Abnormal and larger smooth-surfaced cells did not become prominent until after week 2 or 3 infection. Thymus and bone marrow cells showed little if any change in surface morphology until late in the infectious process. However, even at that time only a few of the cells were abnormal in appearance. The changes in cell population in the spleen but not the lymph nodes paralleled the rapid decrease in the percentage of cells which stained positive for surface immunoglobulin and theta antigen. Futhermore, FLV antigen rapidly appeared on spleen cells after infection; fewer lymph node cells were positive, and only low numbers of marrow and thymus cells stained positive for FLV antigen. The marked immunosuppression induced by FLV infection paralleled and in some instances preceded the marked morphological changes.     

Induction of apoptosis in a carp leucocyte cell line infected with turbot (Scophthalmus maximus L.) rhabdovirus

A rhabdovirus was observed from the diseased turbot (Scophthalmus maximus L.) with lethal syndrome. In this study, a carp leucocyte (CLC) cell line was used to investigate the infection process and cell death mechanism occurring during the virus infection. Strong cytopathogenic effect (CPE) and the morphological changes, such as extreme chromatin condensation, nucleus fragmentation, and apoptotic body formation, were observed under fluorescence microscopy after DAPI staining in the infected CLC cells. Transmission electron microscopy analysis showed cell shrinkage, plasma membrane blebbing, cytoplasm vacuolization, chromatin condensation, nuclear breakdown and formation of discrete apoptotic bodies. The bullet-shaped nucleocapsids were measured and ranged in size from 110 to 150 nm in length and 40 to 60 nm in diameter. And therefore the virus is called Scophthalmus maximus rhabdovirus (SMRV). Agarose gel electrophoresis analysis of the DNA extracted from infected cells showed typical DNA ladder in the course of SMRV infection. Flow cytometry analysis of SMRV infected CLC cells detected apoptotic peak in the virus infected CLC cells. Virus titre analysis and electron microscopic observation revealed that the virus replication fastigium was earlier than that of the apoptosis occurrence. No apoptosis was observed in the CLC infected with UV-inactivated SMRV. All these supported that SMRV infected CLC cells undergo apoptosis and the virus replication is necessary for apoptosis induction of CLC cells.     

Replication of murine cytomegalovirus in mast cells

Summary Mast cells purified from the peritoneal cell population and mast cells derived in culture from bone marrow cells were examined for their sensitivity to murine cytomegalovirus (MCMV) infection in vitro. While up to 70% of mast cells expressed viral antigens, less than 12% of the cells produced infectious virus. Transmission electron microscopy demonstrated nucleocapsids in the nuclei and in association with the cisternal elements of the Golgi apparatus. Some complete virions were found within small cytoplasmic vacuoles. In contrast with previous studies of macrophages and fibroblasts, the susceptibility of mast cells to MCMV infection in vitro was not influenced by the H-2 or non-H-2 genotype of the donor.     

On the absence of a cytopathogenic effect of the three poliovirus types on plasmocytoma cells and macrophages in bone marrow cultures

Summary The effect of the three poliovirus types have been examined in bone marrow cultures of 6 myeloma patients.Virus doses up to 2 × 10⁶ ID 50, which completely destroyed control cultures of human fibroblasts and monkey kidney cells in less than 48 hours, were inoculated.Plasmocytoma cells from cases with diminished as well as increased gammaglobulin synthesis proved to be resistant to the cytopathogenic effect of poliovirus. Macrophage cells proved equally resistant to the cytopathogenic effect. After titration experiments performed in one case plasmocytoma cells seem not to support propagation of infective virus to any significant extent.No definite conclusions regarding virus growth in macrophages could be drawn.Fibroblasts showed to be fully susceptible. No virus inhibiting factor neither of antibody nor of unspecific type could be found so far in culture fluid or plasmocytoma cell extracts.The authors express their gratitude to ProfessorS. Gard for his interest in this work and for helpful coitisisms.