肿瘤性复杂性胸壁缺损的修复策略及对肿瘤治疗的积极影响

复杂性胸壁缺损的修复一直是一项极具挑战性的工作。肿瘤性复杂性胸壁缺损的修复决策及其执行困难是限制胸壁肿瘤治疗方法选择及影响预后的重要因素之一。皮瓣解剖学研究的深入、胸壁支持结构重建技术的进步、显微外科技术的发展、麻醉护理的发展、对综合治疗的重视和治疗手段的进步等,使传统认为不可切除的胸壁肿瘤得以彻底地切除和安全有效地修复,从而使与缺损修复相关的肿瘤切除及辅助治疗的禁忌证缩减到最小程度,有效地提高了胸壁肿瘤患者的生存质量,并很大程度上延长了生存率。作者以湖南省肿瘤医院整形外科15年565例胸壁肿瘤切除后修复重建的临床资料为依据,充实了胸壁肿瘤切除及修复的策略:(1)可靠的胸壁骨性支架重建;(2)有效的软组织修复;(3)麻醉及护理与手术团队的合作;(4)系统有序的综合治疗。并进一步明确了复杂胸壁肿瘤切除及重建的细节理念,包括胸部肿瘤治疗中加强多学科合作的密切性和科学性,整形外科医生参与肿瘤治疗整体规划的主动性和时机前移等。     

乳腺密度对浸润性小叶癌术前MRI评估的影响

目的:探讨MRI在浸润性小叶癌(ILC)术前诊断中的应用价值，并评估乳腺密度对其影响。方法:选取75例术前30天内行MRI检查的I-Ⅲ期ILC患者列入本项研究，根据腺体含量评估乳腺密度，在MRI下测量肿瘤大小，并对比其与病理大小的一致性。结果:75例入组患者中26例（34.7%）患者经MRI评估发现新的可疑病灶，20例（26.7%）患者改变了手术方式。高密度乳腺型患者额外病灶检出率明显高于低密度乳腺型患者（51.6% vs 22.7%，P=0.010）。MRI评估肿瘤大小在低密度乳腺型患者中容易被低估（36.4% vs 12.9%，P=0.024），在高密度乳腺型患者中容易被高估（6.8% vs 29.0%，P=0.010），但两组患者与病理大小一致性的比例无明显差异。结论:ILC患者术前乳腺MRI检查能够提高额外恶性肿瘤的检出率，而乳腺密度是影响MRI评估的重要因素。     

POLG 基因变异致线粒体病一家系分析

目的分析POLG基因变异致线粒体病的临床表型及基因变异。方法回顾分析于2019年5月就诊,并经采集外周血DNA进行医学外显子、外显子-内含子交界区靶向二代测序和一代验证,1个确诊为POLG基因变异致线粒体病家系的临床资料。结果先证者,男,10岁,与其同卵双胎哥哥均有相同的体征,深感觉受损、腱反射消失、肌肉可疑萎缩。先证者3个兄姐先后于1岁多夭折。提取患儿及其父母的外周血,先证者及同卵双胎哥哥POLG基因均存在G.2558A(p.R853Q)、c.2890T(p.R964C)复合杂合变异,分别来源于患儿父母亲。结论 POLG基因复合杂合变异线粒体病家系成员有不同的表型;POLG相关疾病,即使同种基因变异,其临床异质性也较大。     

甘肃省和政县农村老年性白内障防盲项目的卫生经济学评价研究

目的 对2014-2016年在甘肃省和政县开展的白内障综合防盲干预项目进行卫生经济学评价。设计 横断面调查。 研究对象 甘肃省和政县2014-2016年老年性白内障手术前407例患者及术后半年109例患者。方法 对所有调查对象进行卫生经济学问卷调查。通过净效益法、成本效益分析法和成本效果分析法评价项目产生的经济效益和总成本。主要指标 直接成本、间接成本、直接经济效益、间接经济效益、总成本、总效益、净效益、成本效益比、成本效果比。结果 2014-2016年项目期间甘肃省和政县白内障所致总体疾病经济负担为2142.28万元。白内障手术产生的总效益为3398424.98元，总成本为2939125.20元，净效益为459299.78元，效益成本比为1.16:1。项目每投入1万元可降低50岁以上白内障患者导致的0.027%的致盲率和0.164%致残率；项目每降低1%的50岁以上白内障患者的盲率，需投入36.47万元；每降低1%50岁以上白内障患者的残率，需投入6.11万元。结论 在甘肃省和政县开展的老年性白内障防盲综合干预项目具有较好的产出回报比和较高的防盲技术效率。（眼科，2020，29： 298-303）     

Five-year clinical outcomes using the bioresorbable vascular scaffold: Insights from the FRANCE ABSORB registry

Central illustration: cumulative major adverse cardiac events (MACE) and bioresorbable vascular scaffold (BVS) thrombosis rates after 1, 2, 3, 4 and 5 years.

     

Immunisation with the BCG and DTPw vaccines induces different programs of trained immunity in mice

In addition to providing pathogen-specific immunity, vaccines can also confer nonspecific effects (NSEs) on mortality and morbidity unrelated to the targeted disease. Immunisation with live vaccines, such as the BCG vaccine, has generally been associated with significantly reduced all-cause infant mortality. In contrast, some inactivated vaccines, such as the diphtheria, tetanus, whole-cell pertussis (DTPw) vaccine, have been controversially associated with increased all-cause mortality especially in female infants in high-mortality settings. The NSEs associated with BCG have been attributed, in part, to the induction of trained immunity, an epigenetic and metabolic reprograming of innate immune cells, increasing their responsiveness to subsequent microbial encounters. Whether non-live vaccines such as DTPw induce trained immunity is currently poorly understood. Here, we report that immunisation of mice with DTPw induced a unique program of trained immunity in comparison to BCG immunised mice. Altered monocyte and DC cytokine responses were evident in DTPw immunised mice even months after vaccination. Furthermore, splenic cDCs from DTPw immunised mice had altered chromatin accessibility at loci involved in immunity and metabolism, suggesting that these changes were epigenetically mediated. Interestingly, changing the order in which the BCG and DTPw vaccines were co-administered to mice altered subsequent trained immune responses. Given these differences in trained immunity, we also assessed whether administration of these vaccines altered susceptibility to sepsis in two different mouse models. Immunisation with either BCG or a DTPw-containing vaccine prior to the induction of sepsis did not significantly alter survival. Further studies are now needed to more fully investigate the potential consequences of DTPw induced trained immunity in different contexts and to assess whether other non-live vaccines also induce similar changes.