非那雄胺在慢性中心性浆液性脉络膜视网膜病变患者中的应用

目的评估非那雄胺治疗慢性中心性浆液性脉络膜视网膜病变(central serous chorioretinopathy,CSC)的有效性及安全性。方法选取2017年3月至2019年6月在本院确诊的慢性CSC患者31例40眼,采用单臂试验对患者进行非那雄胺治疗。使用非那雄胺治疗后6个月,对患者的视网膜神经上皮层(retinal neuroepithelial layer,RNL)下积液状况,ETDRS视力以及黄斑中心凹视网膜厚度(central foveal thickness,CFT)进行检查。结果非那雄胺治疗后1个月,有10眼(25.0%)RNL下积液完全消退。持续治疗2个月、3个月、4个月、5个月、6个月,分别有7眼(17.5%)、6眼(15.0%)、7眼(17.5%)、3眼(7.5%)及3眼(7.5%)RNL下积液消退,仅有4眼(10.0%)在治疗后6个月RNL下积液仍存在。患眼EDTRS视力非那雄胺治疗后1个月为(50.00±16.11)个字母,与治疗前(46.16±16.67)个字母差异无统计学意义(P=0.2213);治疗后2个月(53.39±14.67)个字母,较治疗前显著升高(P=0.0003);治疗后3个月、4个月、5个月、6个月,分别为(57.39±12.76)个字母、(58.52±12.39)个字母、(59.13±10.76)个字母及(60.42±10.96)个字母,与治疗前相比差异均有统计学意义(均为P<0.0001)。而患眼CFT自治疗后1个月、2个月、3个月、4个月、5个月、6个月分别为(274.10±22.74)μm、(273.00±17.22)μm、(263.50±12.81)μm、(263.90±10.62)μm、(259.70±12.48)μm及(252.60±11.00)μm,与治疗前(296.60±35.41)μm相比,差异均有统计学意义(均为P<0.05)。所有患者均无服药后身体不适或并发症发生。结论非那雄胺对于慢性CSC的治疗安全且有效,有望成为慢性CSC的治疗选择。     

鼠巨细胞病毒感染C57BL/6小鼠急性肝炎动物模型的建立与鉴定

目的：建立鼠巨细胞病毒（MCMV）感染C57BL/6小鼠急性肝炎模型并对其感染特点进行分析及鉴定。方法：将24 只C57BL/6小鼠随机分为阴性对照组（n =12）及病毒感染组（n =12），病毒感染组腹腔注射1.0×106 PFU（200 μL）MCMV悬液，阴性对照组注射等体积小鼠胚胎成纤维细胞（MEF）悬液。于感染后第3天和第7天取外周血分离血清检测谷丙转氨酶（ALT）及谷草转氨酶（AST）。同时进行肝组织病毒分离、组织病理学及MCMV IE和M55基因、细胞因子白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、肿瘤坏死因子α（TNF-α）的检测。结果：病毒感染组肝组织匀浆病毒分离均为阳性，肝炎发生率为100%。在感染后第3天即发生肝炎病理改变，病毒感染组血清ALT及AST较阴性对照组明显升高（P ＜0.01）；病毒感染组肝脏HE染色第3天可见局灶性炎性细胞浸润及肝脏点灶状坏死，持续至第7天，Ishak评分较阴性对照组明显升高（P ＜0.01）；在感染后第3天病毒感染组肝组织内可检测到MCMV IE及M55基因，且在感染后第7天仍可测得IE基因；感染后第3天及第7天病毒感染组炎性细胞因子IL-6、TNF-α及IL-1β mRNA表达水平明显升高（P ＜0.05）。 结论：成功建立MCMV感染C57BL/6小鼠急性动物肝炎模型，其感染表现主要集中在急性感染前期。     

从武汉抗疫看中医药文化认同与新的医学模式

从武汉抗疫中医药的投入使用情况,反思现代临床和国人所呈现出的中医药文化认同和就医习惯,探索其历史文化根源及社会因素与医学发展的内在关联。回顾历史,中医屡次临危受命,不负重托,如今大疫当前,中医药再次发挥了重要作用。故新时代探讨如何遵循中医药发展规律,传承精华、守正创新,坚持中医药原创优势,形成中医药学科优势整体化呈现的新模式医学,对提升全社会的中医药认知度具有重要意义。     

改进软腭牵拉暴露鼻咽手术治疗腺样体肥大

2013年5月至2014年2月对解放军107医院收治的80例腺样体肥大患者采用吸痰管牵拉软腭暴露鼻咽部,并在70°鼻内镜辅助下行肥大腺样体切除术,效果良好,现报告如下。1资料与方法1.1临床资料本组80例中,男43例,女37例,5~13岁,平均7岁,病程9个月~4年。临床症状均有不同程度夜寐打鼾、张口呼吸,伴有鼻塞。其中     

Helicobacter pylori induces epithelial-mesenchymal transition in gastric carcinogenesis via the AKT/GSK3β signaling pathway

Helicobacter pylori (H. pylori) is a main risk factor for gastric cancer (GC). Epithelial-mesenchymal transition (EMT) is involved in the development and progression of H. pylori-associated GC. However, the exact molecular mechanism of this process remains unclear. The AKT/GSK3β signaling pathway has been demonstrated to promote EMT in several types of cancer. The present study investigated whether H. pylori infection induced EMT, and promoted the development and metastasis of cancer in the normal gastric mucosa, and whether this process was dependent on AKT activation. The expression levels of the EMT-associated proteins, including E-cadherin and N-cadherin, were determined in 165 gastric mucosal samples of different disease stages by immunohistochemical analysis. The expression levels of E-cadherin, N-cadherin, AKT, phosphorylated (p-)AKT (Ser473), GSK3β and p-GSK3β (Ser9) were further determined in H. pylori-infected Mongolian gerbil gastric tissues and cells co-cultured with H. pylori by immunohistochemical analysis and western blotting. The results indicated that the expression levels of the epithelial marker E-cadherin were decreased, whereas the expression levels of the mesenchymal marker N-cadherin were increased during gastric carcinogenesis. Their expression levels were associated with H. pylori infection. Furthermore, H. pylori infection resulted in downregulation of E-cadherin expression and upregulation of N-cadherin expression in Mongolian gerbils and GES-1 cells. In addition, an investigation of the associated mechanism of action revealed that p-AKT (Ser473) and p-GSK3β (Ser9) were activated in GES-1 cells following co-culture with H. pylori. Furthermore, following pretreatment of the cells with the AKT inhibitor VIII, the expression levels of E-cadherin, N-cadherin, p-AKT and p-GSK3β did not show significant differences between GES-1 cells that were co-cultured with or without H. pylori. The levels of p-AKT and p-GSK3β were increased in H. pylori-infected Mongolian gerbils. In conclusion, the present study demonstrated that H. pylori infection activated AKT and resulted in the phosphorylation and inactivation of GSK3β, which in turn promoted early stage EMT. These effects were AKT-dependent. This mechanism may serve as a prerequisite for GC development.     

PS联合CPAP治疗新生儿呼吸窘迫综合征临床研究

目的通过研究肺表面活性物质(PS)结合持续气道正压通气(CPAP)治疗新生儿呼吸窘迫综合征(NRDS)的治疗效果,进一步指导NRDS的临床治疗。方法选取于2017年4月-2018年10月间在本院收治的80例确诊为新生儿呼吸窘迫综合征的患儿作为研究对象,随机将患儿分为试验组和对照组,对照组给予持续气道正压通气治疗,试验组在对照组的基础上联合使用PS治疗。结果试验组对于呼吸窘迫缓解的有效率明显高于对照组,在气管插管内滴入PS治疗后试验组的血气情况明显优于对照组,且试验组患儿副作用发生率明显低于对照组,以上指标差异具有统计学意义,P <0.05。结论 PS结合CPAP在新生儿呼吸窘迫综合征的治疗中疗效很好。