基于网络药理学和实验验证研究柴胡疏肝散治疗慢性萎缩性胃炎的作用机制＊

目的 通过网络药理学的方法进行预测，再深一步进行动物实验验证来研究柴胡疏肝散治疗CAG的作用机制。方法 首先在TCMSP数据库中检索柴胡疏肝散的所有活性成分与药物靶点；通过收集PharmGkb、OMIM、GeneCards和DrugBank数据库中收录的慢性萎缩性胃炎的相关靶点。将药物靶点与疾病靶点进行映射筛选出交集靶点，将得到的交集靶点构建PPI网络与活性成分-共同靶点网络，并对其进行GO和KEGG富集分析。最后利用Vina软件进行分子对接实验验证，并通过免疫印迹法验证柴胡疏肝散对两种受体蛋白EGFR和STAT1的影响。结果 最终筛选得到柴胡疏肝散活性成分104个，潜在靶点238个，与慢性萎缩性胃炎的交集靶点52个；GO与KEGG富集分析分别得到2166条目和148条目，主要涉及到JAK-STAT信号通路、TNF信号通路、HIF-1信号通路等；分子对接结果显示EGFR、STAT1两个靶点能够与核心活性成分能够自发结合成较为稳定的构像；免疫印迹法实验证明柴胡疏肝散能够降低大鼠胃黏膜组织EGFR和STAT1蛋白表达。结论 通过网络药理学和实验验证，发现柴胡疏肝散可能通过调节EGFR和STAT1蛋白表达来共同调控胃黏膜细胞增殖与凋亡，进而发挥着治疗慢性萎缩性胃炎的效果，为深入进行柴胡疏肝散治疗慢性萎缩性胃炎的作用机制研究提供新思路和新方法。     

Dexamethasone potentiates in vitro blood-brain barrier recovery after primary blast injury by glucocorticoid receptor-mediated upregulation of ZO-1 tight junction protein

Owing to the frequent incidence of blast-induced traumatic brain injury (bTBI) in recent military conflicts, there is an urgent need to develop effective therapies for bTBI-related pathologies. Blood-brain barrier (BBB) breakdown has been reported to occur after primary blast exposure, making restoration of BBB function and integrity a promising therapeutic target. We tested the hypothesis that treatment with dexamethasone (DEX) after primary blast injury potentiates recovery of an in vitro BBB model consisting of mouse brain endothelial cells (bEnd.3). DEX treatment resulted in complete recovery of transendothelial electrical resistance and hydraulic conductivity 1 day after injury, compared with 3 days for vehicle-treated injured cultures. Administration of RU486 (mifepristone) inhibited effects of DEX, confirming that barrier restoration was mediated by glucocorticoid receptor signaling. Potentiated recovery with DEX treatment was accompanied by stronger zonula occludens (ZO)-1 tight junction immunostaining and expression, suggesting that increased ZO-1 expression was a structural correlate to BBB recovery after blast. Interestingly, augmented ZO-1 protein expression was associated with specific upregulation of the α⁺ isoform but not the α⁻ isoform. This is the first study to provide a mechanistic basis for potentiated functional recovery of an in vitro BBB model because of glucocorticoid treatment after primary blast injury.     

Iliopsoas Abscess Due to Brenner Tumor Malignancy: A Case Report

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SMYD3 promotes implant metastasis of ovarian cancer via H3K4 trimethylation of integrin promoters

Detachment of cancer cells from the primary tumor and formation of spheroids in ascites is required for implantation metastasis in epithelial ovarian cancer (EOC), but the underlying mechanism of this process has not been thoroughly elucidated. To mimic this process, ovarian cancer cells were grown in 3D and 2D culture. Hey and OVCA433 spheroids exhibited decreased cell proliferation and enhanced adhesion and invasion. SMYD3 expression was elevated in ovarian carcinoma spheroids in association with increased H3K4 methylation. Depletion of SMYD3 by transient siRNA, stable shRNA knockdown and the SMYD3 inhibitor BCI-121 all decreased spheroid invasion and adhesion. Gene expression arrays revealed downregulation of integrin family members. Inhibition assays confirmed that invasion and adhesion of spheroids are mediated by ITGB6 and ITGAM. SMYD3-deficient cells regained the ability to invade and adhere after forced overexpression of SMYD3, ITGB6 and ITGAM. However, this biological ability was not restored by forced overexpression of SMYD3 in ITGB6- and/or ITGAM-deficient cancer cells. SMYD3 and H3K4me3 binding at the ITGB6 and ITGAM promoters was increased in spheroids compared to that in monolayer cells, and the binding was decreased when SMYD3 expression was inhibited, consistent with the expression changes in integrins. SMYD3 expression and integrin-mediated adhesion were also activated in an intraperitoneal xenograft model and in EOC patient spheroids. In vivo, SMYD3 knockdown inhibited tumor metastasis and reduced ascites volume in both the intraperitoneal xenograft model and a PDX model. Overall, our results suggest that the SMYD3-H3K4me3-integrin pathway plays a crucial role in ovarian cancer metastasis to the peritoneal surface.     

跖跗关节骨折脱位手术治疗21例报告

我院自 1993年 5月 - 2 0 0 1年 5月采用闭合复位或切开复位克氏针内固定治疗跖跗关节骨折脱位2 1例 ,取得满意疗效 ,现报告如下。1　临床资料　　本组 2 1例 ;男 14例 ,女 7例 ;左侧 12例 ,右侧 8例 ,双侧 1例 ;年龄 2 1～ 6 8岁 ,平均 4 0 5岁 ;闭合性骨折脱位 16例 ,开放性骨折脱位 5例 ;按照Kuss分类法 :同向性脱位 15例 ,分离性脱位 6例 ;伤因 :车祸伤 12例 ,高处坠落伤 5例 ,重物压伤 3例 ,扭伤 1例。同时伴肢体骨折 6例 ,胸腹伤 3例。2　治疗方法本组 16例闭合性损伤均采用闭合复位克氏针内固定。一般在硬麻下进行 ,取平卧位 ,膝关…     

逼尿肌收缩强度与膀胱排空能力关系的研究

目的：研究逼尿机收缩强度[detrusor contraction strength，又称Watts factor（WF），瓦特因子]与膀胱排空能力的关系。方法：126例患埏，年龄13－78岁，平均56岁。包括良性前列腺增生61例，女性下尿路综合征39例，压力性尿失禁19例，尿道狭窄7例。常规方法行尿流率、压力－流率测定。采用WF等为研究参，将患者按照有无梗阻分组，比较最大尿流率（Qmax)、剩余尿（PVR）、最大尿流率时逼尿肌压（PQmax）、最大逼尿肌收缩强度（WFmax），将患者按照有无剩余尿分组，比较最大逼尿肌收缩强度。结果：有梗阻组最大尿流率低，剩余尿多，PQmax及WFmax明显增高；有剩余尿组WFmax值明显低于无剩余尿组。结论：膀胱出口梗阻时，WF增加但作用有限。剩余的产生与梗阻密切相关，也与逼尿肌活动低下密切相关。研究WF或收缩力时要考虑梗阻因素。     

双钢板内固定治疗浮肩损伤

目的总结浮肩损伤(FSI)的临床特征和治疗效果。方法1997年1月~2006年5月收治浮肩损伤患者17例,均行手术治疗,锁骨、肩胛骨一期行钢板内固定术,术后6个月对患肩功能进行Constant评分判定疗效。结果17例患者经过6个月~4年(平均17.6个月)的随访,锁骨和肩胛骨骨折均愈合,肩关节活动范围无明显受限13例,4例患者上举时有轻度的疼痛。结论浮肩损伤多为高能量暴力所致的不稳定性肩胛带损伤,行手术治疗是必要的。     

KMT2C通过c-Myc/CDK4信号通路调控胃癌细胞的生长与增殖

摘要:目的 探究赖氨酸特异性甲基转移酶2C(lysine specific methyltransferase 2C,KMT2C)在胃癌发生发展中的 作用及机制。方法 通过 TCGA 数据库分析 KMT2C在胃癌与癌旁的表达差异。采用 Western blot检测 KMT2C在胃 癌与癌旁临床样本中的表达差异。通过 Kaplan-Meier Plotter数据库分析 KMT2C 对胃癌患者预后的影响。采用细胞 实验(克隆形成、EdU 及 CCK-8检测)及皮下瘤负荷模型检测 KMT2C 在体内外对胃癌细胞增殖能力的影响。结果 KMT2C在胃癌中高表达。胃癌患者中 KMT2C高表达组相对于 KMT2C低表达组预后较差。敲减 KMT2C在体内外 均有抑制胃癌 细 胞 增 殖 的 作 用。基 因 集 富 集 分 析 (GSEA)发 现 KMT2C 影 响 c-Myc信 号 通 路。敲 减 KMT2C 后, H3K4me1蛋白表达水平降低,同时,CDK4的 mRNA 与蛋白表达水平降低。KMT2C与c-Myc核内结合促进了c-Myc 与 CDK4的启动子区域的结合。结论 KMT2C通过影响c-Myc/CDK4信号通路促进胃癌细胞增殖。     

用PCR扩增tim基因检测蓝氏贾第鞭毛虫

采用聚合酶链反应 (PCR)对蓝氏贾第鞭毛虫 (Giardialamblia)的磷酸丙糖异构酶 (triosephosphateisomerase ,缩写为tim)基因进行特异性扩增 ,结果扩增出 1条 6 83bp的DNA片段。此方法的特异性可高达10 0 % ,而其它DNA样本 ,如日本血吸虫 (Schistosomajaponicum)、刚地弓形虫 (Toxoplasmagondii)、微小隐孢子虫 (Cryptosporidiumparvum)、溶组织内阿米巴 (Entamoebahistolytica)、旋毛虫 (Trichinellaspiralis)和阴道毛滴虫 (Trichomonasvaginalis) ,以及人体血细胞等均未出现扩增反应。本法的敏感性也很高 ,可检测到0 4pg贾第虫包囊的DNA。 13株来自不同地理位置和 或宿主的贾第虫DNA样本在PCR中均各产生 1条长为 6 83bp的目的片段。上述结果表明本实验建立的检测贾第虫的PCR方法有效     

我国三级公立医院护士薪酬满意度调查

目的调查我国三级公立医院护士薪酬满意度,分析其影响因素,为稳定护士队伍提供参考。 方法依托第5次“全国改善医疗服务行动第三方评估”项目,选取全国31个省（自治区、直辖市）及新疆生产建设兵团共136家三级公立医院护士进行调查。应用SPSS 23.0软件对数据进行统计学分析。结果护士薪酬满意度为43.6%。医院所在地区、医院类型、护士工作年限、职称、所在科室、聘用形式、行政职务和教学任务担任情况、工作负荷、休息室提供是否充足以及对子女从医态度等,是护士薪酬满意度的影响因素。结论三级公立医院护士薪酬总满意度较低。应从国家层面和医院层面完善绩效分配制度,切实体现护士劳动价值,从而稳定护理队伍。