慢性鼻窦炎指南的评价与内容分析

背景　慢性鼻窦炎是耳鼻喉科高发疾病，对患者造成严重的影响和经济负担，但目前国内外慢性鼻窦炎诊疗指南推荐意见存在差异。目的　对慢性鼻窦炎诊疗指南进行质量评价并分析其治疗意见，为指南制定和推荐意见的采纳提供建议。方法　于2019年2月检索中英文数据库和各专业指南网站获取相关文献，同时追踪参考文献，筛选适用于青少年及成年人的推荐意见中包含对慢性鼻窦炎的治疗意见的指南。检索时间为建库至检索日期。使用临床指南研究与评估系统Ⅱ（AGREE Ⅱ）和卫生保健实践指南报告清单（RIGHT）对纳入指南的方法学质量和报告质量进行评价，并绘制气泡图和思维导图，对比分析关于慢性鼻窦炎治疗的推荐意见。结果　最终纳入8部指南，AGREE Ⅱ评价总分平均为48.76%（30.90%~73.09%），仅2部指南强烈推荐使用（得分>60%），其余6部需修订后推荐。RIGHT条目总体报告率为34.29%~65.71%，其中评审和质量控制方面报告率均为0。指南推荐一致的治疗方法包括皮质类固醇、鼻腔盐水冲洗和手术治疗，以及过敏者口服抗组胺药，可选用的措施包括细菌溶解物、黏痰溶解药、质子泵抑制剂、植物疗法、辣椒素、亮氨酸拮抗剂、鼻用呋塞米、木糖醇盐水冲洗液、次氯酸钠盐水冲洗液、含婴儿香波的盐水冲洗液，尚无统一观点的治疗措施包括抗生素、减充血剂、白三烯受体拮抗剂、IgE拮抗剂及阿司匹林加重呼吸系统疾病患者阿司匹林脱敏治疗。结论　现有慢性鼻窦炎诊疗指南制定方法及其报告质量需提高，建议纳入患者的偏好、使用统一的评价工具和考虑运用性。推荐意见有冲突时，建议参考制定方法更为严谨的指南。     

基于Oncomine数据库分析PD-L1基因在头颈部癌中的表达及预后

目的:研究程序性死亡因子配体1(programmed death factor 1,PD-L1/CD274)在头颈部癌中的表达情况,并分析其与临床病理特征及预后的相关性。方法:挖掘Oncomine数据库中关于PD-L1基因在头颈部癌中的相关数据,进行PD-L1表达量与头颈部癌临床生物学特性的相关分析,并利用数据库中生存数据进行生存分析。结果:Oncom-ine数据库中有关PD-L1基因癌组织/正常组织表达量的分析共176项,其中高表达的癌种共4项,低表达2项;在头颈部癌组织中,显著高表达1项。Meta分析显示,PD-L1在头颈部癌中呈现高表达,显著高于正常组织。在人乳头瘤病毒(human papillomavirus,HPV)阳性的HNC患者中PD-L1的表达显著高于HPV阴性HNC患者(0.38 vs 0.16,P=0.018),有远处转移的患者显著高于无转移者(1.36 vs 0.55,P=0.004)。生存分析显示PD-L1表达量与生存期无显著相关。结论:PD-L1在头颈部癌中表达水平高,与人乳头瘤病毒状态及肿瘤转移相关,与生存期不相关。     

丝棉木种子化学成分及其抗肿瘤活性

目的 研究丝棉木Euonymus maackii Rupr.种子的化学成分及其抗肿瘤活性.方法 丝棉木种子95%乙醇提取物乙酸乙酯部位采用硅胶、D101、反相HPLC进行分离纯化,根据理化性质及波谱数据鉴定所得化合物的结构.MTT法测定其抗肿瘤活性.结果 从中分离得到10个化合物,分别鉴定为1β-甲基正丁酰氧基-2β-苯甲酰氧基-4α-羟基-6α-呋喃酰氧基-9β,12-二乙酰氧基-β-二氢沉香呋喃(1)、6α,9β,12-三乙酰氧基-1β,2β,8β-三苯甲酰氧基-β-二氢沉香呋喃(2)、6α,9β,12-三乙酰氧基-1β,8β-二苯甲酰氧基-2β-正己酰氧基-β-二氢沉香呋喃(3)、6α,9β,12-三乙酰氧基-1β,8β-二苯甲酰氧基-2β-正辛酰氧基-β-二氢沉香呋喃(4)、6α,9β,12-三乙酰氧基-1β,8β-二苯甲酰氧基-2β-正癸酰氧基-β-二氢沉香呋喃(5)、卫矛羰碱(6)、6α,12-二乙酸基-1β,9α-二乙酸(β-呋喃羧氧基)-4α-羟基-2β-2-甲基丁酯-β-二氢沉香呋喃(7)、6α,9β,12-三乙酰氧基-1β,8β-二苯甲酰氧基-2β-羟基-β-二氢沉香呋喃(8)、6α,12-二乙酸基-1β,9 α-二乙酸(β-呋喃羧氧基)-4α-羟基-1β-2-甲基丁酯-β-二氢沉香呋喃(9)、6α,9β,12-四乙酰氧基-1β,8β-二苯甲酰氧基-β-二氢沉香呋喃(10).化合物6对Hela细胞有明显的抑制作用,IC50为9.76 μg/mL.结论 化合物1为新化合物.化合物6有一定的抗肿瘤活性.     

柴胡加龙骨牡蛎汤联合腹针治疗脑卒中后抑郁疗效观察

目的:观察柴胡加龙骨牡蛎汤联合腹针治疗脑卒中后抑郁的临床疗效。方法:将94例失眠患者随机分为对照组和治疗组各47例,对照组采用氟哌噻吨美利曲辛片治疗,治疗组采用柴胡加龙骨牡蛎汤联合腹针治疗,两组均连续治疗6周后判定临床疗效,比较两组患者治疗前后汉密尔顿抑郁量表(HAMD)评分及Barthel指数(BI)变化。结果:两组患者治疗后HAMD评分较本组治疗前明显降低(P<0.05),BI评分较治疗前明显升高(P<0.05),且治疗组治疗后HAMD评分低于对照组(P<0.05),BI评分高于对照组(P<0.05)。两组患者治疗后中医证候积分与治疗前比较,差异有统计学意义(P<0.05);两组患者中医证候积分差值比较,差异有统计学意义(P<0.05)。结论:柴胡加龙骨牡蛎汤联合腹针治疗脑卒中后抑郁可改善患者抑郁症状。     

Novel intronic variant in PALB2 gene and effective prevention of Fanconi anemia in family

Familial Cancer - Despite the acceptance of NextGen sequencing as a diagnostic modality suitable for probands and carriers of Mendelian diseases, its efficiency in identifying causal mutations is...     

Effect of rifampin and itraconazole on the pharmacokinetics of zanubrutinib (a Bruton's tyrosine kinase inhibitor) in Asian and non-Asian healthy subjects

Cancer Chemotherapy and Pharmacology - Zanubrutinib (BGB-3111) is a potent Bruton’s tyrosine kinase inhibitor with promising clinical activity in B-cell malignancies. Zanubrutinib was shown...     

CDC42 promotes vascular calcification in chronic kidney disease

Vascular calcification is prevalent in patients with chronic kidney disease (CKD) and a major risk factor of cardiovascular disease. Vascular calcification is now recognised as a biological process similar to bone formation involving osteogenic differentiation of vascular smooth muscle cells (VSMCs). Cell division cycle 42 (CDC42), a Rac1 family member GTPase, is essential for cartilage development during endochondral bone formation. However, whether CDC42 affects osteogenic differentiation of VSMCs and vascular calcification remains unknown. In the present study, we observed a significant increase in the expression of CDC42 both in rat VSMCs and in calcified arteries during vascular calcification. Alizarin red staining and calcium content assay revealed that adenovirus-mediated CDC42 overexpression led to an apparent VSMC calcification in the presence of calcifying medium, accompanied with up-regulation of bone-related molecules including RUNX2 and BMP2. By contrast, inhibition of CDC42 by ML141 significantly blocked calcification of VSMCs in vitro and aortic rings ex vivo. Moreover, ML141 markedly attenuated vascular calcification in rats with CKD. Furthermore, pharmacological inhibition of AKT signal was shown to block CDC42-induced VSMC calcification. These findings demonstrate for the first time that CDC42 contributes to vascular calcification through a mechanism involving AKT signalling; this uncovered a new function of CDC42 in regulating vascular calcification. This may provide a potential therapeutic target for the treatment of vascular calcification in the context of CKD. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Effect of Electroconvulsive Therapy on Anxiety in Linear and Non-Linear Rats with Depressive-Like Disorders Induced by Ultrasound Stimulation

Bulletin of Experimental Biology and Medicine - We performed a comparative study of the effect of electroconvulsive therapy on anxiety in outbred rats and Sprague-Dawley rats with depressive-like...