脑干听觉诱发电位、CT在新生儿缺氧缺血性脑病中的诊断价值

目的:应用脑干听觉诱发电位(BAEP)结合CT为诊断新生儿缺氧缺血性脑病(HIE)及分度提供科学诊断依据。方法:采用ZABR—200型脑干反应测听仪及西德SomatomDR型高分辨全身扫描机对30例HIE患儿进行检测和扫描。结果:BAEP:正常4例(13.3％),异常26例(86.7％),CT:轻度异常8例,中度异常14例,重度异常8例。结论:本研究CT所示脑损伤程度与临床表现程度有密切关系,BAEP检查敏感性高,影响因素小,结果准确可靠,对诊断HIE,预测和评价预后,指导治疗均有一定的价值。     

电极间距与电极直径对恒功率下双极射频熔脂效果影响的研究

在双极射频应用于局部脂肪堆积的无创治疗的过程中,关于双极射频设备的部分设计参数目前还没有形成统一的规范。采用有限元方法和离体实验,分析双极射频熔脂时不同参数对组织熔脂效果的影响,寻求在双极射频尽量不会对皮肤层造成热损伤的同时,实现较大范围熔脂效果的熔脂参数配置。采用COMSOLMultiphysics进行生物组织热电耦合的有限元分析;为验证模型有效性,采用一种自研的单路双极射频输出设备,对离体猪腹部组织进行实验。有限元分析结果显示:经双极射频加热30min后,在功率为10W,电极球直径分别为3、5、8mm,电极间距分别为2和3cm的熔脂参数配置下,皮肤层的最终温度低于热损伤阈值温度,且部分脂肪层在热损伤区域内;域点探针所显示的脂肪层热损伤区域内的温度变化曲线满足熔脂温度要求。不同熔脂参数配置,对双极射频加热下组织内的温度分布具有显著影响。在10W功率下,采用直径为8mm的球型电极,电极按压皮肤的深度为1mm,在电极间距分别为2和3cm的条件下,脂肪层内产生最大面积的连续热损伤区域和点状热损伤区域,热损伤区域的面积分别为2.84和2.55cm²。相同熔脂参数配置的离体实验表明,与组织模型相同位置处的热电偶探针的最终温度和对应的域点探针相差0.92℃±0.43℃。有限元分析结果和实验结果基本一致。由仿真结果和实验结果可知,上述熔脂参数配置可使双极射频不会对皮肤层造成热损伤,同时在脂肪层内产生有效的热损伤区域,并且热损伤区域内的温度达到了熔脂要求。合理的熔脂参数配置是决定双极射频熔脂是否成功的一项关键因素。     

三七皂苷R1保护四氯化碳诱导肝纤维化模型大鼠的作用

背景：前期研究发现,三七总皂苷对小鼠免疫性肝损伤具有一定的保护作用。 目的：探究三七皂苷R1对四氯化碳诱导的肝纤维化模型大鼠的治疗作用。 方法：用四氯化碳诱导SD雄性大鼠制备肝纤维化模型,给药组按照60 mg/kg的剂量给予30 g/L三七皂苷R1溶液, 1次/d,连续4周和6周。对照组及模型组给予同体积的生理盐水,采用苏木精-伊红染色及Masson染色观察肝脏组织结构和纤维化程度分期;反转录-定量聚合酶链反应(qRT-PCR)检测法检测Ⅰ型胶原、α-平滑肌激动蛋白和转化生长因子β1表达水平。实验方案经昆明医科大学动物实验伦理委员会批准(批准号为approval No. KMMU2018018)。 结果与结论：①肝组织病理学显示,与模型组相比,三七皂苷R1能显著减轻纤维增生程度;②与模型组相比,三七皂苷R1组Ⅰ型胶原、α-平滑肌激动蛋白和转化生长因子β1表达水平显著降低(P < 0.05),三七皂苷R1给药4周与6周组比较差异无显著性意义;③结果提示,三七皂苷R1对四氯化碳诱导的肝纤维化模型大鼠具有一定的治疗作用。 ORCID: 0000-0002-0755-1476(吴朕) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

脑电图在小儿抽搐诊断中的鉴别作用

本文分析384例小儿抽搐待查者的脑电图,阳性率62.8％。抽搐是一种临床常见的征候群,病因多、发作类型复杂,脑电图可定侧、定位,定性的动态观察脑生物电活动,对于鉴别有无脑机能障碍及抽搐病因探讨有很大的临床意义。     

脂多糖诱导的小鼠腹腔巨噬细胞基因表达谱分析

目的　利用基因芯片技术分析脂多糖 (LPS)活化的小鼠腹腔巨噬细胞基因表达谱 ,以更全面地了解LPS诱导的巨噬细胞反应。方法　以未刺激的和用 1mg/LLPS刺激的小鼠腹腔巨噬细胞制备3 3 P标记的cDNA探针 ,分别与含有 1176个已知基因的小鼠cDNA芯片杂交。结果　活化组和未刺激组间的 2倍差异表达基因为 118个 ,3倍差异表达基因为 6 9个 ,其中 4 4个上调 ,2 5个下调。转录因子、细胞内信号调节蛋白、炎症细胞因子和细胞凋亡相关基因的转录发生明显的调节变化。结论提供了LPS活化的巨噬细胞综合基因表达信息 ,并筛选出一些新的可能与LPS活化相关的基因。     

A rapid lung de-cellularization protocol supports embryonic stem cell differentiation in vitro and following implantation

Pulmonary diseases represent a large portion of neonatal and adult morbidity and mortality. Many of these have no cure, and new therapeutic approaches are desperately needed. De-cellularization of whole organs, which removes cellular elements but leaves intact important extracellular matrix (ECM) proteins and three-dimensional architecture, has recently been investigated for ex vivo generation of lung tissues. As specific cell culture surfaces, including ECM composition, profoundly affect cell differentiation, this approach offers a potential means of using de-cellularized lungs to direct differentiation of embryonic and other types of stem/progenitor cells into lung phenotypes. Several different methods of whole-lung de-cellularization have been reported, but the optimal method that will best support re-cellularization and generation of lung tissues from embryonic stem cells (ESCs) has not been determined. We present a 24-h approach for de-cellularizing mouse lungs utilizing a detergent-based (Triton-X100 and sodium deoxycholate) approach with maintenance of three-dimensional lung architecture and ECM protein composition. Predifferentiated murine ESCs (mESCs), with phenotypic characteristics of type II alveolar epithelial cells, were seeded into the de-cellularized lung scaffolds. Additionally, we evaluated the effect of coating the de-cellularized scaffold with either collagen or Matrigel to determine if this would enhance cell adhesion and affect mechanics of the scaffold. Finally, we subcutaneously implanted scaffolds in vivo after seeding them with mESCs that are predifferentiated to express pro-surfactant protein C (pro-SPC). The in vivo environment supported maintenance of the pro-SPC-expressing phenotype and further resulted in vascularization of the implant. We conclude that a rapid detergent-based de-cellularization approach results in a scaffold that can maintain phenotypic evidence of alveolar epithelial differentiation of ESCs and support neovascularization after in vivo implantation.     

黏液瘤病毒体外对胶质瘤细胞杀灭作用的研究

目的了解C6细胞在体外对黏液瘤病毒的易感性,并测定黏液瘤病毒对体外C6胶质瘤细胞的杀灭作用。方法以黏液瘤病毒感染体外培养的C6胶质瘤细胞,以灭活病毒作为阴性对照,5-Fu作为阳性对照,DEMD液做空白对照,应用Western—Blot法、倒置显微镜及MTT法观察各组细胞的形态、成活率。结果病毒感染组及5-Fu组24h后细胞成活率明显低于空白对照组及阴性对照组,同时病毒感染组细胞出现明显细胞病变。结论C6胶质瘤细胞在体外对黏液瘤病毒易感,黏液瘤病毒在体外对C6胶质瘤细胞有杀灭作用。     

DNA methylation studies on imprinted loci in a male monozygotic twin pair discordant for Beckwith–Wiedemann syndrome

Tierling S, Souren NY, Reither S, Zang KD, Meng‐Hentschel J, Leitner D, Oehl‐Jaschkowitz B, Walter J. DNA methylation studies on imprinted loci in a male monozygotic twin pair discordant for Beckwith–Wiedemann syndrome. Beckwith–Wiedemann syndrome (BWS) is one of the most prevalent congenital disorders predominantly caused by epigenetic alterations. Here we present an extensive case study of a monozygotic monochorionic male twin pair discordant for BWS. Our analysis allows to correlate BWS symptoms, like a protruding tongue, indented ears and transient neonatal hypoglycaemia, to an abnormal methylation at the KvDMR1. DNAs extracted from peripheral blood, skin fibroblasts, saliva and buccal swab of both twins, their sister and parents were analysed at 11 differentially methylated regions (DMRs) including all four relevant DMRs of the BWS region. The KvDMR1 was exclusively found to be hypomethylated in all cell types of the affected BWS twin, while the unaffected twin and the relatives showed normal methylation in fibroblasts, buccal swab and saliva DNA. Interestingly, the twins share a common blood‐specific hypomethylation phenotype most probably caused by a feto‐fetal transfusion between both twins. Because microsatellite analysis furthermore revealed a normal biparental karyotype for chromosome 11, our results point to an exclusive correlation of the observed BWS symptoms to locally restricted epimutations at the KvDMR1 of the maternal chromosome.     

脂多糖对核转录因子-κB的激活在人肺非小细胞肺癌获得性耐药细胞中的作用

目的 本研究旨在通过检测脂多糖(lipopolysaccharide ,LPS)作用后人非小细胞肺癌耐药株细胞内核转录因子(nuclear factor-κB,NF)-κB p65表达量的变化,探讨LPS作用下NF-κB表达量的增高与吉非替尼获得性耐药产生的相关性.方法 成功诱导非小细胞肺癌细胞株HCC827对吉非替尼产生稳定的获得性耐药后,按设置的分组用LPS及吉非替尼处理细胞,采用CCK-8法检测处理后吉非替尼对细胞的半数抑制浓度(IC50值),并与各自对照组相比较.细胞增殖曲线显示LPS作用对细胞增殖的影响.采用克隆形成实验显示LPS作用后对细胞增殖的影响.采用蛋白质印迹法检测LPS及吉非替尼处理后耐药株HCC827/GR-8-1细胞中凋亡相关蛋白caspase-3、Bcl-2等蛋白的表达量,并检测NF-κB蛋白的表达量,探讨LPS作用后激活的NF-κB对细胞吉非替尼敏感性的调节.结果 LPS处理后,可以显著降低耐药细胞对吉非替尼的敏感性,细胞克隆形成实验及增殖曲线显示LPS并无明显促进细胞的增殖作用,但可以降低细胞对吉非替尼的敏感性.蛋白质免疫印迹结果显示,与对照组相比较,LPS可抑制Caspase-3等相关促凋亡蛋白的表达,而相应凋亡抑制蛋白Bcl-2的表达上升.LPS处理48 h后NF-κB的表达量显著上调.LPS通过调节NF-κB表达量上升而参与细胞耐药机制的产生.结论 经LPS作用后的非小细胞肺癌细胞对吉非替尼敏感性降低,LPS处理后细胞的NF-κB表达量显著增高,增高的NF-κB表达量与细胞对吉非替尼的药物敏感性下降相关.