a-1, 2岩藻糖基转移酶II在肺鳞癌组织中的表达及对肺鳞癌细胞增殖的影响

目的：探讨a-1，2岩藻糖基转移酶II（FUT2）在肺鳞癌中的表达情况及其对肺鳞癌细胞增殖的影响。方法：应用UALCAN数据库分析FUT2在临床肺鳞癌患者组织中的差异表达及其与肺鳞癌患者临床TNM分期、年龄及性别因素的相关性；采用瞬时转染技术，将FUT2的shRNA质粒转染进H226细胞株中构建FUT2低表达的肺鳞癌细胞模型；利用CCK-8、平板克隆及Western blot实验检测FUT2对肺鳞癌细胞的生长、单克隆细胞团形成及PCNA蛋白表达的影响。结果：FUT2在肺鳞癌尤其是肺鳞癌TNM早中期呈现高表达趋势（P＜0.05），而与年龄和性别无关。低表达FUT2可以抑制肺鳞癌细胞的生长速率和单克隆细胞团的形成数，同时，可以抑制肺鳞癌细胞PCNA蛋白的表达水平，差异均有统计学意义（P＜0.05）。结论：FUT2在肺鳞癌中高表达且促进肺鳞癌细胞的增殖能力，有望成为肺鳞癌的早期诊断指标。     

经前侧入路达芬奇机器人辅助肺段切除术的临床分析

目的总结经前侧入路达芬奇机器人辅助肺段切除术治疗肺部结节的临床价值。方法回顾性分析2018年6月至2019年10月于我科行前侧入路达芬奇机器人辅助肺段切除术77例患者的临床资料,其中男22例、女55例,年龄53(30~71)岁。对患者症状、一般情况、术前影像学资料、切除肺段分布、手术时间、出血量、淋巴结清扫数、术后带管时间、引流量、术后住院时间、术后并发症以及围术期死亡等指标进行分析。结果所有患者均顺利完成手术,无中转开胸,无严重并发症,无围术期死亡。术后病理48例为早期肺癌,29例为良性肿瘤。机器人Docking时间4(1~30)min,机器人腔内操作时间76(30~170)min,出血量30(20~400)mL,术后胸腔闭式引流管引流时间4(2~15)d,术后总引流量780(200~3980)mL;术后住院时间7(3~19)d。结论经前侧入路机器人辅助肺段切除治疗肺部结节安全、便捷和有效,值得临床推广应用。     

Crystalloids,colloids, blood products and blood substitutes

Understanding the physiology of fluid distribution in the human body is fundamental to good clinical practice in anaesthesia and intensive care. Intravenous fluid therapies have a range of clinical and metabolic consequences, and they should be context and patient specific. Inadequate or excessive fluid treatment is harmful to patients. There are numerous trials, both historical and current, investigating best practice in fluid therapy. New paradigms and guidelines are being published, and it is important for clinicians to keep up to date with current practice. There is also a continued drive to improve the safety of donor blood products and prevent transfusion errors. Knowledge of how blood products are collected, separated, stored and administered is essential to prevent harm to patients through transfusions. The development of blood substitutes is progressing, and multinational trials are ongoing.     

Optimisation of the organ donor and effects on transplanted organs: a narrative review on current practice and future directions

Mortality remains high for patients on the waiting list for organ transplantation. A marked imbalance between the number of available organs and recipients that need to be transplanted persists. Organs from deceased donors are often declined due to perceived and actual suboptimal quality. Adequate donor management offers an opportunity to reduce organ injury and maximise the number of organs than can be offered in order to respect the donor's altruistic gift. The cornerstones of management include: correction of hypovolaemia; maintenance of organ perfusion; prompt treatment of diabetes insipidus; corticosteroid therapy; and lung protective ventilation. The interventions used to deliver these goals are largely based on pathophysiological rationale or extrapolations from general critical care patients. There is currently insufficient high-quality evidence that has assessed whether any interventions in the donor after brain death may actually improve immediate post-transplant function and long-term graft survival or recipient survival after transplantation. Improvements in our understanding of the underlying mechanisms following brain death, in particular the role of immunological and metabolic changes in donors, offer promising future therapeutic opportunities to increase organ utilisation. Establishing a UK donor management research programme involves consideration of ethical, logistical and legal issues that will benefit transplanted patients while respecting the wishes of donors and their families.     

红参发酵产物联合长春瑞滨及顺铂化疗方案治疗晚期非小细胞肺癌患者的疗效

目的探讨红参发酵产物联合长春瑞滨及顺铂化疗方案治疗晚期非小细胞肺癌患者的疗效。方法将104例晚期非小细胞肺癌患者随机分为治疗组及对照组,每组52例。对照组患者给予单纯长春瑞滨^+顺铂化疗方案,治疗组患者在对照组基础上联合应用红参发酵产物。分别在治疗前后采用疲劳症状量表(FSI)、肺癌治疗功能评价量表(FACT-L)评价两组患者疲劳症状及生活质量,并比较治疗前后两组患者血清肿瘤标志物水平、免疫功能指标水平、药物不良反应及生存情况。结果治疗前,两组患者FSI各维度评分及总分,FACT-L各维度评分及总分,细胞角质蛋白19片段抗原21-1(CYFRA21-1)、神经元特异性烯醇化酶(NSE)、癌胚抗原(CEA)、自然杀伤(NK)细胞、CD3^+、CD4^+、CD8^+、CD4^+/CD8^+水平比较,差异均无统计学意义(P﹥0.05)。治疗后,对照组患者FSI各维度评分及总分均高于治疗前及治疗组;治疗组患者生理状态、情绪状态、对疾病关注度评分及总分均高于治疗前,且生理状态、社会家庭状态、情绪状态、功能状态、对疾病关注度评分及总分均高于对照组;两组患者CEA、CYFRA21-1及NSE水平均较治疗前下降,且治疗组患者均低于对照组患者;治疗组患者NK细胞、CD3^+、CD4^+及CD4^+/CD8^+水平均较治疗前上升,且均高于对照组患者,差异均有统计学意义(P﹤0.05)。治疗组患者血液学不良反应发生例数少于对照组,差异有统计学意义(P﹤0.05)。结论红参发酵产物联合长春瑞滨及顺铂化疗方案能够有效提高晚期非小细胞肺癌患者的免疫功能及生活质量,降低血清肿瘤标志物水平,并减轻血液学不良反应。     

福建省新型冠状病毒肺炎中医证型探讨

按中医因地制宜的理论,根据武汉市与福建省不同的地理气候,福建省与武汉市新型冠状病毒肺炎中医证候差异,提出国家新型冠状病毒肺炎指南的证型不能完全覆盖福建省的全部病例,福建省应增加"湿热郁肺证",并提出"湿热郁肺证"的临床表现、治则治法与方药。     

Efficacy of immunotherapy targeting the neoantigen derived from epidermal growth factor receptor T790M/C797S mutation in non–small cell lung cancer

Lung cancer is the leading cause of cancer‐related deaths worldwide. Epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI) often have good clinical activity against non–small cell lung cancer (NSCLC) with activating EGFR mutations. Osimertinib, which is a third‐generation EGFR‐TKI, has a clinical effect even on NSCLC harboring the threonine to methionine change at codon 790 of EGFR (EGFR T790M) mutation that causes TKI resistance. However, most NSCLC patients develop acquired resistance to osimertinib within approximately 1 year, and 40% of these patients have the EGFR T790M and cysteine to serine change at codon 797 (C797S) mutations. Therefore, there is an urgent need for the development of novel treatment strategies for NSCLC patients with the EGFR T790M/C797S mutation. In this study, we identified the EGFR T790M/C797S mutation‐derived peptide (790‐799) (MQLMPFGSLL) that binds the human leukocyte antigen (HLA)‐A*02:01, and successfully established EGFR T790M/C797S‐peptide‐specific CTL clones from human PBMC of HLA‐A2 healthy donors. One established CTL clone demonstrated adequate cytotoxicity against T2 cells pulsed with the EGFR T790M/C797S peptide. This CTL clone also had high reactivity against cancer cells that expressed an endogenous EGFR T790M/C797S peptide using an interferon‐γ (IFN‐γ) enzyme‐linked immunospot (ELISPOT) assay. In addition, we demonstrated using a mouse model that EGFR T790M/C797S peptide‐specific CTL were induced by EGFR T790M/C797S peptide vaccine in vivo. These findings suggest that an immunotherapy targeting a neoantigen derived from EGFR T790M/C797S mutation could be a useful novel therapeutic strategy for NSCLC patients with EGFR‐TKI resistance, especially those resistant to osimertinib.