不同核酸提取方法对HBV-DNA检测性能验证情况分析

目的评估2种乙型肝炎病毒(HBV)-DNA提取方法及2家检测试剂的性能,有助于选择优化提取试剂和检测试剂。方法2023年4月采用达安全自动核酸提取仪提取法(磁珠法)和手工提取法(一步法),并用达安和圣湘2种HBV-DNA试剂检测,对其进行精密度、正确度、线性范围、检出限及抗干扰能力等性能进行验证和评价。结果达安全自动核酸提取仪提取达安试剂检测、手工提取达安试剂检测和手工提取圣湘试剂检测在精密度、正确度、线性范围、检出限方面验证结果均达标;达安全自动核酸提取仪提取圣湘试剂检测在低值检测中变异系数大于5%,最低检测限验证不合格;抗干扰能力方面,全自动核酸提取仪提取的2.0 g/dL血红蛋白浓度的样本用达安和圣湘试剂检测结果均不受影响。手工提取甘油三酯浓度达3000 mg/dL的样本用达安和圣湘试剂检测的结果均不受影响。结论不同厂家的提取和检测试剂避免混用,达安和圣湘试剂对HBV-DNA定量检测的结果均符合要求。

精神分裂症患者血清反式激活反应-DNA结合蛋白表达水平与临床症状的相关性研究

目的:探讨精神分裂症患者血清反式激活反应-DNA结合蛋白(trans activated response DNA binding protein,TDP43)表达水平与临床症状的相关性研究。方法:选取2020年10月至2021年10月于本院确诊收治的54例精神分裂症患者为研究对象,记为研究组,同时以80名健康体检者作为对照组。收集研究组、对照组的一般临床资料和阳性与阴性症状量表(positive and negative syndrome scale,PANSS)评分进行比较,采集两组静脉血,分析血清TDP43水平和生化指标;Pearson法和Logistic回归分析一般病理症状评分、阴性症状量表评分、阳性症状量表评分及PANSS总分与血清TDP43水平的相关性及精神分裂症患者发生的危险及保护因素。结果:研究组、对照组在高密度脂蛋白、性别、受教育时间、年龄、总胆固醇、体质量指数、吸烟、三酰甘油及血糖方面比较,差异均无统计学意义(P均>0.05);与对照组相比,研究组人员低密度脂蛋白显著降低,患者血清TDP43水平以及一般病理症状评分、阴性症状量表、阳性症状量表评分及PANSS总分、同型半胱氨酸均显著增加(P均<0.05)。相关性分析显示,血清TDP43水平与一般病理症状评分、阴性症状量表评分、阳性症状量表评分及PANSS评分均呈正相关性(P均<0.05)。多因素Logistic分析显示,血清TDP43水平、PANSS评分、低密度脂蛋白、同型半胱氨酸为精神分裂症患者发生的影响因素(P均<0.05)。结论:精神分裂症患者血清TDP43水平显著升高,与临床症状有关。

非小细胞肺癌患者组织MutS同种组织蛋白2、O6-甲基鸟嘌呤-DNA甲基转移酶表达分析

目的探讨非小细胞肺癌(NSCLC)患者癌组织MutS同种组织蛋白2(MSH2)、O6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)表达情况及与临床病理参数、预后的关系。方法2021年7月至2022年7月我院收治的96例NSCLC患者,取其手术切除的NSCLC组织标本(NSCLC组)及距癌边缘3 cm处的癌旁正常组织(对照组)。检测两组MSH2和MGMT的表达水平,分析MSH2和MGMT表达水平与患者临床病理参数及预后的关系。结果与对照组比较,NSCLC组MSH2和MGMT阳性率更低(P<0.05);MSH2阳性与患者分化程度有关(P<0.05);MGMT阳性与患者吸烟史和分化程度有关(P<0.05);与MSH2和MGMT阴性患者比较,阳性患者1年生存率均更高(P<0.05)。结论MSH2和MGMT均在NSCLC组织中存在较低表达,其表达水平与临床病理参数、预后密切相关。

Cisplatin-induced activation of TGF-βsignaling contributes to drug resistance

Growing evidence suggests an association between epithelial-mesenchymal transition(EMT),a hallmark of tumor malignancy,and chemoresistance to a number of anti-cancer drugs.However,the mechanism of EMT induction in the process of acquiring anti-cancer drug resistance remains unclear.To address this issue,we obtained a number of cisplatin-resistant clones from LoVo cells and found that almost all of them lost cell-cell contacts.In these clones,the epithelial marker E-cadherin was downregulated,whereas the mesenchymal marker N-cadherin was upregulated.Moreover,the expression of EMT-related transcription factors,including Slug,was elevated.On the other hand,the upregulation of other mesenchymal marker Vimentin was weak,suggesting that the mesenchymal-like phenotypic changes occurred in these cisplatin-resistant clones.These mesenchymal-like features of cisplatin-resistant clones were partially reversed to parental epithelial-like features by treatment with transforming growth factor-β(TGF-β)receptor kinase inhibitors,indicating that TGF-βsignaling is involved in cisplatin-induced the mesenchymallike phenotypic changes.Moreover,cisplatin was observed to enhance the secretion of TGF-βinto the culture media without influencing TGF-βgene transcription.These results suggest that cisplatin may induce the mesenchymal-like phenotypic changes by enhancing TGF-βsecretion,ultimately resulting in drug resistance.

miR-125b reverses cisplatin resistance by regulating autophagy via targeting RORA/BNIP3L axis in lung adenocarcinoma

The platinum-based chemotherapy is one of the most frequently used treatment protocols for lung adenocarcinoma(LUAD),and chemoresistance,however,usually results in treatment failure and limits its application in the clinic.It has been shown that microRNAs(miRNAs)play a significant role in tumor chemoresistance.In this study,miR-125b was identified as a specific cisplatin(DDP)-resistant gene in LUAD,as indicated by the bioinformatics analysis and the real-time quantitative PCR assay.The decreased serum level of miR-125b in LUAD patients was correlated with the poor treatment response rate and short survival time.MiR-125b decreased the A549/DDP proliferation,and the multiple drug resistance-and autophagy-related protein expression levels,which were all reversed by the inhibition of miR-125b.In addition,xenografts of human tumors in nude mice were suppressed by miR-125b,demonstrating that through autophagy regulation,miR-125b could reverse the DDP resistance in LUAD cells,both in vitro and in vivo.Further mechanistic studies indicated that miR-125b directly repressed the expression levels of RORA and its downstream BNIP3L,which in turn inhibited autophagy and reversed chemoresistance.Based on these findings,miR-125b in combination with DDP might be an effective treatment option to overcome DDP resistance in LUAD.

Loss of Fascin2 increases susceptibility to cisplatin-induced hearing impairment and cochlear cell apoptosis in mice

Objectives:Deletion of Fscn2 gene in mice has been linked to progressive hearing loss and degeneration of cochlear cells.Cisplatin,an antitumor drug,can cause various side effects,including ototoxicity.The aim of this study was to investigate the effects of Fscn2 on cisplatin-induced hearing impairment in mice and to explore the possible mechanism.Methods:Two-week-old Fscn2^(+/+)mice and Fscn2^(−/−)mice were treated with two doses of cisplatin,with a 3-day recovery period in between.ABR(auditory evoked brain stem response)thresholds were measured and cochlear pathology was observed at 3 weeks of age.Results:Both Fscn2^(+/+)and Fscn2^(−/−)mice showed hearing loss under the effect of cisplatin,but the impairment was more severe in Fscn2^(−/−)mice.Further experiments showed that the percentages of outer hair cell(OHC)and spiral ganglion neuron(SGN)loss were significantly higher in cisplatin-treated Fscn2^(−/−)mice compared to Fscn2^(+/+)mice.Additionally,knockdown of Fscn2 in HEI-OC1 cells worsened cisplatin-induced cell apoptosis.Conclusion:FSCN2 mediates reduction of CDDP induced ototoxicity by inhibiting cell apoptosis.

TGF-β-regulated different iron metabolism processes in the development and cisplatin resistance of ovarian cancer

The impact of different iron metabolism processes(DIMP)on ovarian cancer remains unclear.In this study,we employed various gene chips and databases to investigate the role of DIMP in the initiation and development of ovarian cancer.cBioPortal was used to determine mutations in DIMP-associated genes in ovarian cancer.Kaplan-Meier plotter was used to examine the influence of DIMP on the prognosis of ovarian cancer.By analyzing 1669 serous ovarian cancer cases,we identified a range of mutations in iron metabolism genes,notably in those coding for the transferrin receptor(19%),melanotransferrin(19%),and ceruloplasmin(10%)in the iron import process,and glucose-6-phosphate isomerase(9%),hepcidin antimicrobial peptide(9%),metal regulatory transcription factor 1(8%),and bone morphogenetic protein 6(8%)in the iron regulation process.Compared to the unaltered group,the group with gene alterations exhibited a higher tumor mutation burden count(43 vs.54)and more advanced histologic grade(78.19%vs.87.90%).Compared to the normal ovarian counterparts,a reduction in expression was observed in 9 out of the 14 genes involved in iron utilization and 4 out of the 5 genes involved in iron export in ovarian cancer;in contrast,an increase in expression was observed in 2 out of the 3 genes involved in iron storage in ovarian cancer.Furthermore,in cisplatin-resistant cells compared to cisplatin-sensitive ones,the expression of all genes in iron storage and 13 out of 14 genes in iron import was decreased,while that of 8 out of the 10 genes in iron utilization was increased.In addition,survival curve analysis indicated that a higher expression in the majority of genes in the iron import process(12/21),or a reduced expression in most genes in the iron export process(4/5)correlated with poor progression-free survival.Additionally,TGF-βcould regulate the expression of most iron metabolism-associated genes;particularly,expression of genes involved in the iron storage process(2/2)was inhibited after TGF-β1 or TGF-β2 treatment.In conclusion,DIMP plays multifaceted roles in the initiation,chemo-resistance,and prognosis of ovarian cancer.Therapeutically targeting DIMP may pave the way for more tailored treatment approaches for ovarian cancer.

Celecoxib enhances the response of tumor cells to cisplatin through upregulating PUMA in non–small cell lung cancer carrying wild-type p53

Celecoxib,a cyclooxygenase-2 inhibitor,can enhance the efficacy of chemotherapy;however,its effect seems inconsistent.In this study,we investigated whether celecoxib would increase the antiproliferative effects of cisplatin in human lung cancer cells.Our data demonstrated the synergistic effects of celecoxib with cisplatin in wild-type p53 cells and their antagonistic effects inmutated or deleted p53 cells.Combination indices of 0.82 to 0.93 reflected a synergistic effect between celecoxib and cisplatin in lung cancer cells with wild-type p53.Combination indices of 1.63 to 3.00 reflected antagonism between celecoxib and cisplatin in lung cancer cells with mutated or deleted p53.Compared with that in cells with mutated or deleted p53,apoptosis significantly increased with the addition of celecoxib and cisplatin in wild-type p53 cells(P<0.05).Moreover,the results in vivo were similar to those in vitro:celecoxib combinedwith cisplatin slowed tumor growth in wild-type p53 groups and not in mutated or deleted p53 groups.In addition,celecoxib promoted p53 translocation into the nucleus and upregulated active p53 expression in wild-type p53 cells.Celecoxib combined with cisplatin upregulated PUMA(PUMA is a downstream gene of p53)after active p53 increased in wild-type p53 cells.In summary,the combination of celecoxib and cisplatin demonstrates clear synergistic effects in wild-type p53 cells and antagonistic effects inmutated or deleted p53 cells.The synergistic effect was achieved by apoptosis,induced by upregulating PUMA.Our results will provide a new treatment strategy for patients carrying wild-type p53,insensitive to cisplatin.

CES1 is associated with cisplatin resistance and poor prognosis of head and neck squamous cell carcinoma

Background:Head and neck squamous cell carcinoma(HNSCC)is a prevalent form of cancer globally,with chemoresistance posing a major challenge in treatment outcomes.The efficacy of the commonly used chemotherapeutic agent,cisplatin,is diminished in patients with poor prognoses.Methods:Various bioinformatics databases were utilized to examine Carboxylesterase 1(CES1)gene expression,clinicopathologic features,patient survival analysis,and gene function.An organoid model of HNSCC was established,along with the induction of drug-resistant HNSCC in the organoid model.CES1 expression was assessed using qRT-PCR and Western Blot,and differential markers were identified through transcriptome sequencing.Knockdown and overexpression models of CES1 were created in SCC-9 and patient-derived organoid(PDO)cells using shRNA and lentivirus to investigate the tumor biology and cisplatin resistance associated with CES1.Results:Research in bioinformatics has uncovered a strong correlation between the expression level of CES1 and the prognosis of HNSCC.The data suggests a significant link between CES1 expression and tobacco smoking.RNA-sequencing revealed a notable increase in CES1 expression in HNSCC-PDOcis-R cells compared to the parental PDO cells.Subsequently,we performed in vitro studies by HNSCC-PDO and SCC-9 and found that CES1-overexpressing cells exhibited reduced sensitivity to cisplatin and stronger tumor malignant biological behavior compared with CES1-knockdown cells.Conclusion:The observed association between CES1 expression and tobacco smoking implies a potential influence of smoking on the efficacy of cisplatin-based chemotherapy in HNSCC through the regulation of CES1 expression.

Cisplatin-coordinated copolythiophene for synergistic chemotherapy and sonodynamic therapy of tumor

Sonodynamic therapy(SDT)is a novel cancer treatment type showing the advantages of high tissue penetration ability,non-invasion,low systemic toxicity,and high selectivity.However,SDT depends on ultrasound(US)irradiation;once US is turned off,the sonosensitizer will stop producing reactive oxygen species(ROS).Moreover,most sonosensitizers generate oxygen-dependent ROS,that is,singlet oxygen(^(1)O_(2)),significantly limiting the therapeutic effect of SDT in treating deep and hypoxic tumor.Therefore,combining SDT with other treatment modalities is essential.Here,we designed and synthesized a series of cisplatin-coordinated copolythiophenes(CPT-Pts),simultaneously generating^(1)O_(2),superoxide anion,and hydroxyl radicals for synergistic chemotherapy and SDT of tumor.The sonodynamic toxicity and cytotoxicity of CPT-Pts were accurately regulated by tuning the monomer ratio of the polythiophene.This copolymerization strategy avoids the side effects originating from the high-dose chemotherapy drug while making up for limiting SDT relying on ultrasonic activation,effectively inhibiting cancer cells and tumors.

结核菌培养联合结核分枝杆菌-DNA检测对菌阴肺结核诊断效能的研究

目的探究结核菌培养联合结核分枝杆菌-DNA检测对菌阴肺结核的诊断效能。方法选取2021年9月至2022年9月阳江市公共卫生医院收治的188例疑似菌阴肺结核患者,均进行结核菌培养、结核分枝杆菌-DNA检测。以组织培养及病理检查为“金标准”。比较结核菌培养、结核分枝杆菌-DNA检测单独检测、联合检测菌阴肺结核的诊断结果以及诊断效能。结果188例疑似菌阴肺结核患者中132例确诊为阳性,结核菌培养检测检出阳性115例,阴性73例;结核分枝杆菌-DNA检测检出阳性107例,阴性81例;联合检测检出阳性134例,阴性54例。结核菌培养联合结核分枝杆菌-DNA检测对菌阴肺结核的灵敏度、阴性预测值、准确率(91.67%、79.63%、87.23%)高于结核菌培养检测(78.79%、61.64%、79.26%)、结核分枝杆菌-DNA检测(75.00%、59.26%、78.19%),差异有统计学意义(P<0.05)。结核菌培养联合结核分枝杆菌-DNA检测对菌阴肺结核的特异度、阳性预测值(76.79%、90.30%)与结核菌培养检测(80.36%、90.43%)、结核分枝杆菌-DNA检测(85.71%、92.52%)比较,差异无统计学意义(P>0.05)。结论结核菌培养联合结核分枝杆菌-DNA检测对菌阴肺结核进行诊断,有利于提升诊断灵敏度、阴性预测值、准确率,诊断效能较高。

HPV-DNA联合肿瘤标志物检测在宫颈癌诊断中价值分析

分析人乳头瘤病毒(HPV)-DNA联合肿瘤标志物检测在宫颈癌诊断中价值。方法 选取2021年3月至2023年3月间在本院就诊的宫颈癌患者作为研究对象(n=60),均进行宫颈癌活检后确诊,同时选取同期健康体检者为健康组(n=61)。对两组患者分别采取HPV-DNA单一检测,及联合肿瘤标志物检测,对比两组检测结果、检出率以及宫颈癌诊断效能。结果 联合检测宫颈癌检出率高于单一检测(P<0.05)。癌变组肿瘤标志物水平较健康组显著上升(P<0.05)。联合检测较单一检测临床诊断效能更高(P<0.05)。结论 相较于单一HPV-DNA检测,联合肿瘤标志物检测宫颈癌β2-可提高宫颈癌患者临床诊断准确性。

注射用亚胺培南西司他丁钠用于儿童的分剂量及稳定性研究

目的考察注射用亚胺培南西司他丁钠(ICS)的分剂量对其主药亚胺培南(IPN)含量一致性的影响以及不同浓度药液的稳定性,为儿童安全、有效使用ICS提供参考。方法3名操作员按照临床儿童常用的2种分剂量方式(以10 mL或20 mL的0.9%氯化钠注射液制成ICS初溶药液,自初溶药液中吸取所需药量)制备ICS供试液,平行处理后通过超高效液相色谱-串联质谱联用法测定IPN的含量,根据IPN含量变异系数(CV)<15%判断每组供试液的含量一致性。按照说明书配制ICS供试液X1,再将X1以0.9%氯化钠注射液按1∶1和1∶2体积比稀释后制得供试液X2和X3,分别置于室温[(23.0±0.5)℃]、30℃恒温水浴锅以及2~8℃冰箱内保存,以规定放置温度和时间下测得的IPN质量浓度与初始(0 h)质量浓度之比判断药液稳定性(比值≥90%则认为药液稳定)。结果每位操作员以2种分剂量方式制得的每组药液中,IPN含量的CV均小于15%,表明IPN的含量偏差较小。3个质量浓度水平的药液在室温6 h或冷藏18 h条件下均较稳定;在30℃放置6 h时,供试液X1和X2也可保持稳定,但供试液X3中IPN的质量浓度较0 h时的质量浓度下降约20%。结论ICS在儿童常用的2种分剂量方式下,其主药IPN的含量一致性较好。ICS药液的稳定性受浓度、温度和时间的影响,更低的浓度在更高的温度下会导致IPN的稳定性降低。临床应注意控制医嘱溶媒量以及配制和使用过程中的环境温度与时间。

无机层状复合氢氧化物中顺铂-DNA模型分子的选择性插入(英文)

药物分子的选择性包裹和控制释放是药物研究领域中具有挑战性的研究方向。本文研究表明:顺铂-DNA模型分子cis-犤Pt(NH3)2(5'-GMP)2犦(5'-GMP5'-单磷酸鸟苷)可插入无机层状复合氢氧化物犤Zn0.68Al0.32(OH)2犦(NO3)0.32·mH2O。但另一种层状复合氢氧化物犤LiAl2(OH)6犦Cl·H2O由于其阳离子层中正电荷密度较高、阳离子层与层间阴离子之间静电作用较强,因而顺铂-DNA模型分子不能通过离子交换方式插入其层间。光谱数据证实插入层间的顺铂-DNA模型分子结构不变。这可能为铂-DNA分子的传递提供新的方法。

顺铂联合替莫唑胺治疗O^6-甲基鸟嘌呤-DNA甲基转移酶启动子甲基化胶质瘤的近期疗效观察

目的采用顺铂联合替莫唑胺方案与单用替莫唑胺方案对O^6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)启动子甲基化胶质瘤术后辅助化疗,比较两种化疗方案的近期疗效及不良反应的差异。方法选择2016年6月至2016年12月在安徽医科大学第一附属医院神经外科就诊,术后组织病理证实为胶质瘤(WHOⅡⅣ级)且分子病理示MGMT启动子甲基化阳性的患者18例为处理组;选择同期手术且符合纳入标准的患者16例为对照组,所有处理组和对照组患者都采取同步放化疗加6个周期序贯化疗。结果处理组与对照组患者的客观应答率分别为66.66%和31.25%,差异有统计学意义(P=0.042);癫痫发生率分别为22.22%和12.50%,差异无统计学意义(P=0.660);且未发生严重不良反应。结论 MGMT启动子甲基化胶质瘤术后采用同步放化疗+顺铂联合替莫唑胺化疗疗效优于同步放化疗+替莫唑胺单药化疗,两组患者癫痫发生率差异无统计学意义,且未发生严重不良反应。

阳离子脂质体-DNA复合物与脂质-鱼精蛋白-DNA复合物体外细胞转染率比较

采用薄膜-挤压法制备空白阳离子脂质体后,再分别制得阳离子脂质体-DNA复合物和脂质-聚阳离子-DNA复合物(Lipid-polycation-DNA lipopolyplexes,LPD);用凝胶阻滞实验,确定阳离子脂质体与质粒DNA的配比;用透射电镜观察阳离子脂质体-DNA复合物和LPD的形态,用激光粒度仪测定它们的粒径和zeta电位;用酶标仪测定它们对张氏(Chang)肝细胞、HepG2肝癌细胞的转染率。结果表明阳离子脂质体-DNA复合物和LPD的形态均近似于球体,但LPD的粒径明显较小;LPD对张氏(Chang)肝细胞和HepG2肝癌细胞的转染率均高于阳离子脂质体-DNA复合物。LPD是基因治疗的临床应用中一种更具前景的载体系统。

血清中乙型肝炎5项标志表现模式与乙型肝炎病毒-DNA含量的关系

目的 探讨乙型肝炎血清学 5项指标与乙型肝炎病毒 - DNA(HBV- DNA)含量的关系 ,了解乙肝血清免疫学指标的各种组合模式的病毒含量情况 ,以此估计其传染性程度 ,为乙肝的预防、诊断和治疗提供实验室依据。方法 用美国 Abbott公司的 AXSYM全自动免疫分析系统和微粒子酶免疫检测试剂盒 ,检测血清乙型肝炎 5项指标 ;根据结果选出常见 6种组合模式 ,每种组合随机取样 5 0例 ,共 30 0例 ;并以聚合酶链反应 (PCR)定量检测血清 HBV- DNA含量。结果 在各种组合模式中 ,均能不同程度地检出 HBV- DNA,在乙肝表面抗原阳性标本其HBV- DNA含量明显高于乙肝表面抗原阴性的标本 ,其中以乙肝表面抗原 (HBs Ag) (+) /乙肝 e抗原 (HBe Ag)(+) /乙肝核心抗体 (HBc Ab) (+)形式病毒含量最高 (大于 10 6拷贝 / μl,占 84% ) ,阳性率为 10 0 % ;而乙肝表面抗体阳性的组合模式 ,HBV- DNA阳性率较低 ,且含量在 10 6拷贝 / μl以下。结论 血清乙肝 5项标志阳性者 。

产妇血清和乳汁HBV-DNA含量检测及意义

目的探讨 HBV 携带产妇血清、乳汁不同 HBV-DNA 含量母乳喂养的安全性,以指导母乳喂养。方法应用荧光定量 PCR(FQ-PCR)技术对93例 HBV 携带产妇血清、乳汁及婴儿血标本进行 HBV-DNA 定量检测。婴儿分别采用母乳和人工两种喂养方式。结果 68例血清 HBV-DNA 阳性产妇的乳汁中 HBV-DNA 阳性44例(64.71%),乳汁 HBV-DNA 阳性率随母血 HBV-DNA 载量的增加而增加,且2种标本 HBV-DNA 含量呈正相关(r=0.684,P<0.05);HBeAg 阳性和阴性产妇乳汁 HBV-DNA 阳性率差异有统计学意义(P<0.01);仅 HBsAg阳性产妇婴儿,母乳喂养组和人工喂养组均未发生 HBV 感染。结论血清 HBV-DNA 阳性产妇哺乳应结合乳汁HBV-DNA 检测;乳汁 HBV-DNA 检测对正确指导母乳喂养有一定的实用价值。[临床儿科杂志,2008,26(10):869-871]

探讨模式液基薄层细胞学检测(TCT)技术和高危型HPV-DNA检测与宫颈病变的相关性

目的:探讨模式液基薄层细胞检测(TCT)技术和高危型人乳头瘤病毒(HPV)-DNA检测与宫颈病变的相关性。方法:回顾性分析224例TCT异常患者资料,依据HPV-DNA检测结果将其分为A组(182例)与B组(42例)。A组患者HPV(HC2)检测阳性;B组患者HPV-DNA(HC2)检测阴性,两组以阴道镜下取活检病理结果为宫颈病变诊断的金标准进行比较。结果:A组患者筛查出宫颈上皮内瘤变(CIN)、鳞癌及腺癌121例(占66.48%);B组患者筛查出CIN、鳞癌及腺癌17例(占40.48%),两组比较差异有统计学意义(x^2=9.758,P<0.05)。结论:采用TCT技术联合HPVDNA(HC2)检测方法能够有效提高子宫颈病变的阳性检查率;随着宫颈病变级别的升高,HPVDNA的感染率也随之升高,两者联合对于宫颈病变的预防和早期诊治有重要的临床应用价值。

荧光定量PCR法检测HBV-DNA室内质控物的制备及质控图的应用

目的制备HBV-DNA荧光定量PCR检测室内质控物,建立室内质控管理体系,利用Excel表格进行质控图的绘制。方法取单一浓度HBV-DNA阳性血清,稀释至一定浓度后,分装数管,-70℃保存。连续检测20次,计算均值、标准差和变异系数,绘制质控图,进行室内质控动态监测。结果HBV-DNA室内质控均值的对数值为5.573,标准差为0.244,变异系数为4.4%,稳定性很好,有临床应用价值,质控图利用Excel表格标示出警告限和失控限,有利于动态监控。结论荧光定量PCR方法进行HBV-DNA检测的质控物制备简单,稳定性良好,质控图操作方便,一目了然,适合临床实验室应用和推广。