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1.
A review of negative split-sample cervical cytology cases revealed five cases reported as chronic follicular cervicitis. These cases showed characteristic morphological features in conventional smears with lymphoid cells, plasma cells and tingible body macrophages smeared across the slides. This contrasts with the presentation of ThinPrep samples (Cytic Corporation, Boxburgh, MA, USA), where cells were observed aggregated in clumps. The different presentation noted in liquid-based samples may require careful microscopic evaluation at high-power magnification.  相似文献   
2.
Summary Although serological reactivity to human papillomavirus type 16 (HPV-16) proteins has been demonstrated in patients with invasive cervical carcinoma, the degree of seroreactivity to these proteins in women with preinvasive disease and its relationship to the HPV type associated with the disease are unclear. We obtained sera from 27 women undergoing cone biopsy for cervical precursor lesions and 22 controls and analyzed seroreactivity by Western blot to fusion proteins containing portions of the HPV-16 E4, L1 and L2 open-reading frames (ORFs). Positives were analyzed by scanning densitometry and intensity values for each case plotted relative to controls. Cervical biopsy specimens from patients were analyzed for HPV-16 nucleic acids by DNA · DNA in situ hybridization. Mean intensity values for seroreactivity to the pATH-E4 protein approached significance (P = 0.058) and a significantly higher proportion of cases vs controls registered values over 4.0 for pATH-E4 (26% vs 4.5%;P = 0.04) and pATH-L2 (48% vs 18%;P = 0.03) proteins. A significantly higher mean intensity value for E4 was observed for cases containing HPV-16 DNA vs HPV-16 negative cases or controls. Thus, seroreactivity to HPV-16-derived proteins may be more common in women with preinvasive cervical disease, and for some protein targets (E4) may indicate a relatively type-specific response.Supported in part by grants from the National Cancer Institute [CA 47676 (C.P.C.)], American Cancer Society [MV-395 (C.P.C.)] and an institutional support grant (J.K.R.). Dr. Crum is a recipient of a Physician Scientist Award from the National Institute of Allergy and Infectious Disease (AI00628)  相似文献   
3.
采用聚合酶链式反应(PCR)技术,对HPV-18序列中引物HP_1、HP_2之间的片段(F)进行扩增,通过两组阴、阳性对照实验证明扩增片段的特异性。用不同Mg浓度的缓冲系统进行PCR反应发现,缓冲系统中Mg浓度高低是影响HPV-18/HP_1、HP_2特异扩增的重要因素,高浓度Mg导致扩增特异性降低。对17例宫颈癌组织DNA进行PCR检测,有9例检出F片段,其检出率是53%,为HPV-18与宫颈癌的相关性提供证据。  相似文献   
4.
Cervical cancer is still an important cause of death in countries like Colombia. We aimed to determine whether socioeconomic status of residential address (SES) and type of health insurance affiliation (HIA) might be associated with cervical cancer survival among women in Bucaramanga, Colombia. All patients residing in the Bucaramanga Metropolitan Area diagnosed with invasive cervical cancer (ICD-0–3 codes C53.X) between 2008 and 2016 (n = 725) were identified through the population-based cancer registry, with 700 women having follow-up data for >5 years (date of study closure: Dec 31, 2021), yielding an overall 5-year survival estimate (95 % CI) of 56.4 % (52.7 – 60.0 %). KM estimates of 5-year overall survival were obtained to assess differences in cervical cancer survival by SES and HIA. Multivariable Cox-proportional hazards modeling was also conducted, including interaction effects between SES and HIA. Five-year overall survival was lower when comparing low vs. high SES (41.9 % vs 57.9 %, p < 0.0001) and subsidized vs. contributive HIA (45.1 % vs 63.0 %, p < 0.0001). Multivariable Cox modeling showed increased hazard ratios (HR) of death for low vs. high SES (HR = 1.78; 95 % CI = 1.18–2.70) and subsidized vs. contributive HIA (HR = 1.44; 95 % CI = 1.13–1.83). The greatest disparity in HR was among women of low SES affiliated to subsidized HIA (vs. contributive HIA and high SES) (HR=2.53; 95 % CI = 1.62–3.97). Despite Colombia’s universal healthcare system, important disparities in cervical cancer survival by health insurance affiliation and socioeconomic status remain.  相似文献   
5.
摘要 目的:探讨宫颈癌组织微小核糖核酸(miRNA)-200b-5p、miR-424-5p表达与临床病理特征、磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白(PI3K/AKT/mTOR)信号通路和预后的关系。方法:选取2016年7月~2019年6月西安市中心医院收治的123例宫颈癌患者,采用定量聚合酶链式反应(qPCR)检测癌组织与癌旁组织中miR-200b-5p、miR-424-5p、PI3K信使RNA(mRNA)、AKT mRNA、mTOR mRNA表达。分析miR-200b-5p、miR-424-5p表达与PI3K mRNA、AKT mRNA、mTOR mRNA表达的相关性及与临床病理特征的关系。采用K-M法绘制不同miR-200b-5p、miR-424-5p表达宫颈癌患者生存曲线。结果:与癌旁组织比较,宫颈癌组织中miR-200b-5p、miR-424-5p表达降低,PI3K mRNA、AKT mRNA、mTOR mRNA表达升高(P<0.05)。Pearson相关性分析显示,宫颈癌组织中miR-200b-5p、miR-424-5p表达与PI3K mRNA、AKT mRNA、mTOR mRNA表达均呈负相关,PI3K mRNA、AKT mRNA、mTOR mRNA表达呈两两相关(P<0.05)。miR-200b-5p、miR-424-5p表达与宫颈癌分化程度、国际妇产科联盟(FIGO)分期和淋巴结转移有关(P<0.05)。随访3年,123例宫颈癌患者累积生存率为62.60%(77/123)。K-M生存曲线分析显示,miR-200b-5p、miR-424-5p高表达组累积生存率分别高于miR-200b-5p、miR-424-5p低表达组(P<0.05)。结论:宫颈癌组织中miR-200b-5p、miR-424-5p低表达,与分化程度、FIGO分期、淋巴结转移、PI3K/AKT/mTOR信号通路和预后有关。  相似文献   
6.
采用加端聚合酶链反应技术,从湖北地区一宫颈癌患者癌组织DNA中分离出人乳头瘤病毒16型(HPV16)E7基因,并在pUC18载体中克隆。经限制性核酸内切酶分析和DNA序列分析,确认了含HPV16E7重组克隆质粒,命名pHPV16E7─HB。DNA序列分析表明,HPV16E7─HB基因全长294bp(与报道的标准株基因长度相同),但其核苷酸顺序中有两处发生了C→T突变,即第43位密码子CAA变为TAA,第76位CGT变为TGT;前者使谷氨酰胺密码子变为终止密码,即无义奕变(nonsensemutation)。这种突变发生在294个碱基的DNA扩增产物之中,不像是PCR本身的错配,而很可能是湖北株与标准株之间的结构差异。  相似文献   
7.
In previous ultrastructural studies we have shown that at the tip of intestinal villi in guinea pigs, effete enterocytes are separated into two portions: a thin apical cytoplasm to be exfoliated into the lumen and a major basal portion to be ingested by lamina propria macrophages. During this process, intraepithelially disposed, large granular lymphocytes interdigitate with enterocytes in a complex manner. In the present study, the relation between the enterocytes and the lymphocytes in the villous epithelium of the guinea pig small intestine is described by use of transmission and scanning electron microscopy in an attempt to visualize the roles and activities of the lymphocytes more clearly. The lymphocytes project numerous pointed processes into effete enterocytes, even piercing them. Enterocytes are deeply indented or perforated, probably as a result of the encroaching lymphocyte processes. Some enterocytes are separated into apical and basal portions by numerous large excavations in the cytoplasm. These findings indicate that repeated perforating penetration of the lymphocytes induces cell cleavage. Supporting this supposition, our microcinematographic observations demonstrate the alternate protrusion and withdrawal of processes of lymphocytes. The processes advance with a pointed end, and subsequently, retract with a rounded end in a cycle of 8–18 seconds.  相似文献   
8.
The addition of carbachol to superior cervical ganglia causes a rapid increase in tyrosine hydroxylation in situ. The increase occurs in ganglia from both newborn and adult animals, and in ganglia from animals pretreated with reserpine. The increase is not due to increased transport of the substrate. The increase is dependent upon the presence of calcium, and is additive to the stimulation produced by dibutyryl cyclic AMP. The stimulation seems specific for tyrosine hydroxylation; dopamine beta-hydroxylation is not increased. Preincubation experiments suggest that the carbachol-induced stimulation is due to a change in the availability of, or the affinity of the enzyme for, reduced pterin cofactor. The stimulation is inhibited by atropine and also by low concentrations of phenoxybenzamine or haloperidol, which suggests that it is caused by an action of carbachol on the interneurons in the ganglia.  相似文献   
9.
目的:探讨mi R-5195-3p对人宫颈癌细胞系Si Ha增殖、迁移与侵袭的影响。方法:采用qRT-PCR检测人宫颈癌细胞SiHa和正常上皮细胞HaCaT中mi R-5195-3p的表达水平。将mi R-5195-3p mimic转染至Si Ha细胞中构建外源性过表达细胞株,阴性对照组中则转染NC mimic,并用q RT-PCR验证转染效率;通过MTT和集落形成实验检测细胞增殖能力;划痕愈合实验检测细胞横向迁移能力; Transwell小室实验检测细胞纵向迁移能力和侵袭能力;采用qRT-PCR和Western blot检测E-cadherin、Vimentin与snail m RNA转录水平及蛋白表达水平。结果:宫颈癌细胞Si Ha中的mi R-5195-3p表达水平较HaCaT偏低(P 0. 05)。与阴性对照组相比,转染mi R-5195-3p mimic的SiHa细胞中mi R-5195-3p水平显著增高(P 0. 01);并且其体外增殖(P 0. 001),迁移(P 0. 001)与侵袭能力(P 0. 001)明显减弱;同时E-cadherin表达水平上调而Vimentin、snail表达水平下调。结论:过表达mi R-5195-3p可能通过阻碍EMT通路抑制宫颈癌细胞Si Ha的增殖,迁移与侵袭。  相似文献   
10.
目的:筛选参与宫颈癌发生、发展的关键基因,为临床诊疗提供新的靶点。方法:在NCBI-GEO数据库中筛选多组宫颈癌基因表达检测数据集,利用GEO2R分析工具筛选各组数据集的差异表达基因;应用R分析筛选不同数据集之间共有的差异表达基因;利用DAVID在线分析对差异表达基因进行功能聚类和通路分析;利用STRING分析差异表达基因编码蛋白之间的相互作用关系。结果:共选择6组表达数据集,筛选得到59个差异表达基因(宫颈癌组织vs正常组织),表达差异至少达2倍,其中包含50个表达上调基因及9个表达下调基因。这些差异表达基因参与细胞周期、DNA复制、细胞分裂等生物进程。蛋白互作分析表明,这些差异表达基因多数存在相互作用。结论:利用生物信息学方法对不同来源的基因检测数据进行整合分析,有助于更准确的筛选对宫颈癌发生、发展过程具有重要作用的关键基因,本文筛选的宫颈癌差异基因为进一步研究宫颈癌发生、发展的分子机制及临床诊疗提供思路。  相似文献   
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