肿瘤细胞中的表观遗传编码紊乱

不改变基因的DNA编码,通过改变DNA双链与组蛋白间紧密度来决定基因是否转录表达,这称为表观遗传编码机制。表观遗传编码的生理作用是通过组蛋白修饰和DNA甲基化,调控细胞在适当的时间、空间位置表达适当的基因,从而控制细胞的增殖状况和分化方向。在细胞发育过程中,细胞内DNA甲基化水平增龄性增高,基因转录活性逐渐降低,使细胞从幼稚增殖进入成熟分化。肿瘤细胞中出现表观遗传编码紊乱,致细胞增殖失控,不能进入分化成熟阶段。基因启动子出现甲基化重排,阻碍转录因子与启动子结合,导致基因转录丧失正常调控,合成成熟功能蛋白受阻。利用表观遗传机制(如,RNA干涉)可成为肿瘤治疗的新方法。     

Mutations in VMK1, a mitogen-activated protein kinase gene, affect microsclerotia formation and pathogenicity in Verticillium dahliae

Verticillium dahliae is an important soil-borne fungal pathogen that causes vascular wilt diseases in a large variety of important crop plants. Due to its persistence in the soil, control of Verticillium wilt relies heavily on soil fumigation. The global ban on methyl bromide, a highly effective soil fumigant, poses an urgent need to develop alternative control measures against Verticillium wilt; and these might be more forthcoming with a better understanding of the molecular and cellular mechanisms that underpin the pathogenicity of V. dahliae. In this study, we assessed the role in growth, development, and pathogenicity of VMK1, a gene encoding a mitogen-activated protein (MAP) kinase (hence, Verticillium MAP Kinase 1). Disruption of VMK1 via Agrobacterium tumefaciens-mediated transformation, in two V. dahliae isolates, one from lettuce and the other from tomato, resulted in severely reduced virulence in diverse host plants, suggesting that VMK1 is essential for pathogenicity and that the MAP kinase-mediated signaling pathway has a conserved role in fungal pathogenicity. The vmk1 mutants also exhibited reduced conidiation and microsclerotia formation, suggesting that the gene is important for multiple cellular processes. P.R. and R.G.B. equally contributed to the work     

带蒂股后皮神经营养血管皮瓣的解剖与临床应用

目的：报道股后皮神经营养血管带蒂皮瓣的解剖特点与临床应用疗效。方法：在10侧经动脉灌注红色乳胶成人新鲜下肢标本上，解剖观测股后皮神经血供及其筋膜皮支的分布范围，设计股后皮神经营养血管岛状皮瓣转移修复腘窝、髋关节周围软组织缺损6例。结果：股后皮神经营养血管主要来源臀下动脉、穿动脉和腘动脉后侧穿支的升皮支，并在股后区形成网状吻合营养股后侧皮肤。皮瓣5例全部成活，1例皮瓣远端少量坏死，换药后愈合。经12～44个月随访，皮瓣无破溃，膝、髋关节功能活动良好。结论：股后皮神经营养血管岛状皮瓣转位是一种修复腘窝、髋关节周围软组织缺损良好的方法。     

HPI毒力岛缺失的EAggEC17-2突变菌株的构建及其功能研究

目的 构建HPI毒力岛缺失的EAggEC17-2突变株，初步研究EAggEC菌株携带的耶尔森菌HPI毒力岛合成铁载体Ybt的功能。方法以EAggEC17-2为出发菌株，irp8基因部分序列作为同源重组的一侧序列，irp5基因序列作为同源重组的另一侧序列，中间插入有氯霉素（Can）抗性基因（cat基因）标记。通过接合转移和同源重组，构建了缺失约24kb的HPI毒力岛功能核心区区域EAggEC17-2的仝岛缺失株EA85。应用流式细胞技术（FACS）检测指示菌株WA-CS irp1：：KN（pC3G3．3N）荧光强度的变化情况，对EA85缺失株和出发菌株进行了合成Ybt的功能比较研究。结果成功构建了EAggEC17-2HPI全岛缺失株EA85。EAggEC17-2菌株具有表达Ybt的功能，而缺失株EA85丧失了合成Ybt的能力。结论EAggEC17-2HPI毒力岛的缺失，使Ybt的合成彻底阻断。EAggEC17-2具有的合成Ybt的功能是由其染色体携带的HPI毒力岛所决定的。     

拇指背动脉岛状皮瓣再造拇指的解剖学研究

作者在18只尸体手标本上,对拇指背动脉进行了显微解剖研究,发现该动脉出现率较恒定,起始部血管外径平均为0.63mm,动脉可解剖长度为7.2cm,血管分布范围包括第一掌骨背侧、部份鱼际区及拇指近节背桡侧5×10cm 的皮肤。以拇指背动脉及与其相连的桡动脉远段为蒂,可以游离成一个理想的岛状皮瓣,适用于拇指再造及邻近的组织缺损修复。     

腓肠外侧皮神经营养血管岛状筋膜皮瓣的解剖学基础

目的 :为腓肠外侧皮神经营养血管岛状筋膜皮瓣提供解剖学依据。方法 :采用巨微解剖、全身动脉放射显影及电脑图像分析技术 ,解剖观察了腓肠外侧皮神经及其营养血管的起始、走行、分支与分布情况。结果 :腓肠外侧皮神经于腓骨头上方 ( 7.1± 1.3 )cm ,中线外侧 ( 1.8± 0 .6)cm起自腓总神经 ,分支分布于小腿后外侧上 2 /3部 ,末端与腓肠内侧皮神经相吻合。其营养动脉主要为窝外侧皮动脉 ,于腓骨头水平面上方 ( 4 .6± 2 .3 )cm处发自动脉 ,并于腓骨头上 ( 4 .6± 1.2 )cm ,中线外侧 ( 2 .1± 0 .5 )cm处开始伴行腓肠外侧皮神经下降 ,下端主要与腓动脉穿支吻合 ,形成一营养血管链。结论 :以腓肠外侧皮神经及其营养血管链为蒂可以设计近端或远端蒂岛状筋膜皮瓣。     

血清叶酸与RAR - β、MGMT甲基化在宫颈上皮内瘤变中的交互效应

目的 探讨血清叶酸与RAR - β、MGMT 启动子区CpG岛甲基化在宫颈上皮内瘤变（CIN）中的交互效应。方法 基于课题组建立于山西省（介休市和阳曲县）的已婚妇女人群队列,选取2014年6月 - 9月病理学确诊的CIN患者（CINⅠ147例、CINⅡ/Ⅲ 134例）及正常宫颈妇女（156例）为研究对象。收集全部对象人口学特征及相关因素,采集空腹静脉非抗凝血与宫颈脱落细胞。采用化学发光免疫法检测血清叶酸浓度,甲基化特异性PCR法检测基因CpG岛甲基化状态,导流杂交法判定HPV感染状况。采用Kruskal - Wallis H检验、χ2检验、趋势χ2检验进行资料分析,非条件logistic回归模型和交互作用指标评价交互效应。结果 血清叶酸在NC、CINⅠ和CINⅡ/Ⅲ组总体分布差异有统计学意义（P＜0.001）。低血清叶酸（≤23.13 nmol/L）可增加CINⅠ和CINⅡ/Ⅲ的发生风险（OR = 6.78,95%CI:3.75～12.26;OR = 64.13,95%CI:18.34～224.20）,且随病变进展,血清叶酸逐渐降低（χ2趋势 = 92.69,P＜0.001）。CIN组RAR - β、MGMT CpG岛甲基化率均高于NC组,且甲基化率随病变进展逐渐上升（χ2趋势 = 20.19,P＜0.001;χ2趋势 = 15.35,P＜0.001）。在各组中低血清叶酸与RAR - β、 MGMT CpG岛高甲基化均呈正相加交互作用（CINⅠ:S = 2.23,95%CI:1.63～8.08,S = 1.21,95%CI:1.01～10.01;CINⅡ/Ⅲ:S = 2.43,95%CI:1.72～6.80,S = 2.83,95%CI:1.55～8.10）,但未显示相乘交互作用（P＞0.05）。结论 低血清叶酸和RAR - β、 MGMT CpG岛高甲基化均可增加CIN的风险,且可能存在相加交互作用。     

Bone island (enostosis): current concept — a review

An enostosis or bone island represents a focus of mature compact (cortical) bone within the cancellous bone (spongiosa). Thought by some to be a tumor-like condition and by others a hamartoma, this benign lesion is probably congenital or developmental in origin and reflects failure of resorption during endochondral ossification. A bone island can be virtually diagnosed based on its characteristic clinical and radiologic features. Typically asymptomatic, the lesion is usually an incidental finding, with a preference for the pelvis, femur, and other long bones, although it may be found anywhere in the skeleton, including the spine. Plain radiography reveals a homogeneously dense, sclerotic focus in the cancellous bone with distinctive radiating bony streaks (thorny radiation) that blend with the trabeculae of the host bone, creating a feathered or brush-like border. On CT scan, a bone island appears as a low-attenuation focus, and on MRI sequences it shows low signal intensity like cortical bone. A distinguishing feature of bone islands is that they are usually cold on skeletal scintigraphy. Thus, bone scan has been and continues to be the means of differentiating bone islands from the more aggressive entities. However, reports of histologically confirmed bone islands that were scintigraphically active have raised a note of caution about relying on this modality in the differential consideration of lesions otherwise characteristic of bone islands. Guides to the correct diagnosis should be looked for in the individual clinical situation and in the morphologic features of the lesion on plain radiography, CT, and MRI, without regard to the lesion's activity on bone scan. If such a lesion, however, is symptomatic and hot on scintigraphy, it demands close observation with follow-up imaging studies.