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目的研究同型半胱氨酸(Hcy)、高敏C反应蛋白(hs-CRP)及低密度脂蛋白胆固醇(LDLC)联合检测对冠心病(CHD)的诊断价值。方法回顾性分析90例CHD患者临床资料,根据病情将其分为稳定型心绞痛(SAP)组42例、不稳定型心绞痛(UAP)组29例及急性心肌梗死(AMI)组19例;将同期30例行冠状动脉造影检查排除CHD的非心脑血管疾病患者纳入对照组。应用受试者工作曲线(ROC曲线)评价Hcy、hs-CRP、LDLC及三者联合对CHD的诊断价值。结果Hcy、hs-CRP、LDLC ROC曲线显示AUC分别为0.832、0.895、0.747(P均<0.05),灵敏度分别为0.667、0.867、0.767,特异度分别为0.900、0.800、0.667。3者联合预测AUC为0.971,灵敏度、特异度分别为0.878、1.000,优于各自单独预测(P<0.05)。肌酸激酶同工酶(CKMB)、肌钙蛋白T(cTnT)、肌钙蛋白Ⅰ(cTnⅠ)诊断CHD的灵敏度分别为0.889、0.867、0.878,特异度分别为0.667、0.633、0.600,与上述Hcy、hs-CRP、LDLC诊断价值相近;3种心肌酶谱联合诊断CHD的灵敏度、特异度分别为0.889、0.833略低于Hcy、hs-CRP、LDLC联合诊断价值。结论血清Hcy、hs-CRP、LDLC水平与CHD发生、发展密切相关,联合检测对CHD诊断有一定价值。 相似文献
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《Journal of thoracic oncology》2021,16(5):827-839
IntroductionBy implementing dynamic circulating tumor DNA (ctDNA) analysis, we explored the impact of TP53 mutations on tumor evolution and resistance mechanisms to ensartinib in patients with ALK-positive NSCLC.MethodsIn a multicenter phase 2 trial, patients with ALK-positive NSCLC who progressed on crizotinib were treated with ensartinib. Blood samples for ctDNA analysis were collected at baseline, cycle 3 day 1, and progression disease (PD) and analyzed with a 212-gene panel.ResultsA total of 440 samples were collected from 168 patients. Baseline TP53 mutations (20.2%) significantly correlated with inferior progression-free survival (4.2 mo versus 11.7 mo, p < 0.0001). Patients with TP53 mutations had higher mutation load than those without TP53 mutations at baseline (13.79 ± 3.72 versus 4.67 ± 0.39, p < 0.001). Although there was no significant difference in mutation load between these groups at cycle 3 day 1 (5.89 ± 2.25 versus 3.72 ± 0.62, p = 0.425), patients with mutated TP53 developed more mutations at PD (7.07 ± 1.25 versus 3.20 ± 0.33, p = 0.003). Frequency and abundance of secondary ALK mutations G1269A, G1202R, and E1210K increased markedly at PD than baseline. In patients without secondary ALK mutations, we identified ALK-independent resistance mechanisms including bypass signaling activation, downstream effector protein reactivation, epithelial-mesenchymal transformation, and epigenetic dysregulation.ConclusionsOur study highlighted the advantage of ctDNA analysis for monitoring tumor evolution. TP53 mutations promoted genetic evolution and accelerated occurrence of resistance. We also unveiled ALK-dependent resistance mechanisms, mainly by G1269A, G1202R, and E1210K mutations, and ALK-independent resistance mechanisms to ensartinib. 相似文献
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目的 研究改良式体位结合0.02%氯己定口腔护理对重症呼吸机相关性肺炎(ventilator associated pneumonia,VAP)的防治效果。 方法 选取2016年2月-2018年2月在成都医学院附属第二医院进行治疗的经口气管插管行机械通气时间>48 h的VAP患者170例,采用随机数字法分为2组。给予常规护理组患者常规口腔护理,给予结合护理组患者改良体位联合浓度为0.02%氯己定溶液进行口腔护理,比较患者护理后的肺部感染情况、ICU住院时间、口腔炎症情况、机械通气时间及GCS评分,对患者病菌发生率、痰痂形成率、VAP发生率进行统计。 结果 结合护理组患者在护理后的肺部感染评分和ICU住院时间显著低于常规护理组患者(P<0.05);结合护理组的口腔炎症发生率显著低于常规护理组(P<0.05);结合护理组的口咽定植菌和气管内定植菌发生率均显著低于常规护理组(P<0.05);结合护理组患者在护理后的痰痂形成率和VAP发生率显著低于常规护理组患者(P<0.05)。 结论 使用改良式体位和浓度为0.02%氯己定溶液能更好地降低重症患者在机械通气的情况下发生呼吸机相关性肺炎的几率,对患者的康复及疾病治疗提供很大的帮助。 相似文献
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《Forensic science international. Genetics》2013,7(2):e23-e26
In this study, 17 Y-STR loci(AmpFISTR®Y-filerTM)—DYS456, DYS389I, DYS390, DYS389II, DYS458, DYS19, DYS385a/b, DYS393, DYS391, DYS439, DYS635, DYS392, Y-GATA H4, DYS437, DYS438, DYS448 were analyzed in 424 unrelated males from Luzhou Han ethnic group, Southwest China. 365 haplotypes were observed. The discrimination capacity was 0.8608 and the haplotype diversity was 0.9992. 相似文献
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目的从精浆中性α-1,4糖苷酶入手,探讨中药加电针改善弱精症患者精液质量的机制。方法将120例弱精症患者随机分为中药组、针药组各60例,疗程3个月,观察两组患者治疗前后精浆中性α-1,4糖苷酶和精子活力的变化。结果经统计学处理,两组患者治疗前后精浆中性α-1,4糖苷酶比较、精子活力比较,治疗后两组精浆中性α-1,4糖苷酶比较、两组精子活力比较差异均有统计学意义(P〈0.05)。结论中药加电针能明显提高弱精症患者精浆中性α-1,4糖苷酶水平并增强精子活力。 相似文献
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《Geriatric nursing (New York, N.Y.)》2021,42(5):1198-1203
This study explored if a self-management training program was feasible for a predominantly older rural Latino adults with chronic pain who had limited access to non-pharmacologically based pain treatment. Physical therapy doctoral students delivered the six-week low-literacy low-cost patient-centered program. The intervention was feasible to the participants (n=38) who showed improvement in a majority of the eight outcome measures at 6-week posttest and three measures at 18-week followup. The changes in pain severity, pain interference and pain-related physical functions reached minimally clinically important difference at follow-up. A randomized controlled trial with long-term follow-up is needed to test the program effectiveness in partnership with community health centers to increase access to pain management in rural communities. 相似文献
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Jing-Jing Guo Xue Ma Claire Q F Wang Yu-Fei Ge Qing-Quan Lian Dianne O Hard Yu-Fei Zhang Qiang Dong Yun-Fei Xu Ren-Shan Ge 《Asian journal of andrology》2013,15(5):685-691
Progenitor Leydig cells are derived from stem cells. The proliferation and differentiation of progenitor Leydig cells significantly contributes to Leydig cell number during puberty. However, the regulation of these processes remains unclear. The objective of the present study was to determine whether luteinizing hormone (LH) or androgen contributes to the proliferation and differentiation of progenitor Leydig cells. Fourteen-day-old male Sprague-Dawley rats were treated for 7 days with NalGlu, which is a gonadotropin- releasing hormone antagonist, to reduce the secretion of LH in the pituitary and thus, androgen in the testis. Rats were co-administered with LH or 7a-methyl-nortestosterone (MENT), which is an androgen resistant to metabolism by 5a-reductase 1 in progenitor Leydig cells, and the subsequent effects of LH or androgen were measured. 3H-Thymidine was also intravenously injected into rats to study thymidine incorporation in progenitor Leydig cells. Progenitor Leydig cells were examined. NalGlu administration reduced progenitor Leydig cell proliferation by 83%. In addition, LH or MENT treatment restored Leydig cell proliferative capacity to 73% or 50% of control, respectively. The messenger RNA levels of proliferation-related genes were measured using real-time PCR. The expression levels of Igfl, Lifr, Pdgfra, Bcl2, Ccnd3and Pcnawere upregulated by MENT, and those of Pdgfra, Ccnd3and Pcnawere upregulated by LH. Both LH and MENT stimulated the differentiation of progenitor Leydig cells in vitro. We concluded that both LH and MENT were involved in regulating the development of progenitor Leydig cells. 相似文献