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目的探究脂代谢相关基因ABHD5在肿瘤中的表达水平及其与临床分期、预后、免疫浸润的关系。方法在本研究中，使用GTEx、TCGA、TIMER2.0、CPTAC数据库及免疫组织化学法、免疫印迹法探究ABHD5在泛癌中的表达模式及其与不同临床分期的相关性，使用Kaplan-Meier Plotter、Oncolnc、R2数据库探究ABHD5与预后的相关性，并使用TCGA、TIMER2.0数据库探究ABHD5与免疫细胞浸润之间的相关性，再用STRING、GEPIA数据库获取肿瘤中与ABHD5结合或共表达的基因，进行GO和KEGG富集分析。结果与正常组织相比，ABHD5在多种肿瘤中mRNA和蛋白表达水平下调，在少数肿瘤中升高。ABHD5高表达在8种肿瘤中与较好的预后相关，在2种肿瘤中与较差的预后相关，在9种肿瘤中与免疫细胞浸润水平呈正相关关系，并在泛癌中与中性粒细胞浸润及免疫检查点基因的表达具有显著正相关性。富集分析显示ABHD5与组蛋白去甲基化过程密切相关。结论ABHD5与中性粒细胞浸润、免疫检查点基因表达及组蛋白去甲基化过程相关，且与多种肿瘤的预后相关。

目的检测神经母细胞瘤（NB）患者组织中DNA去甲基化酶十一易位蛋白（TET） TET1、TET2、TET3的表达水平，探讨TET在神经母细胞瘤患者组织中的表达及临床意义。方法神经母细胞瘤患者组织标本46例，用免疫组织化学法（IHC）检测TET1、TET2、TET3在NB患者组织中的表达水平；使用Target数据库中的临床数据分析TET1、TET2、TET3的表达与NB患者预后的关系并进行批量相关性分析。用SPSS 25.0统计学软件进行分析，GraphPad Prism 8软件作图。结果①免疫组化结果显示，在不同级别有丝分裂-核碎裂指数（MKI）的NB患者组织中，TET3的表达存在差异且具有统计学意义（P=0.037）。TET3的表达水平在不同肿瘤细胞分化程度的各组间存在统计学差异（P=0.041），TET3高表达与NB患者预后良好呈正相关（P=0.020）。TET1表达与肾上腺素能受体2（β2-AR）表达呈正相关（r=0.347，P=0.023）。②生物信息学分析结果表明，TET3 mRNA表达水平与ADNP（神经保护蛋白）、ARID2（染色质重塑因子）等抑癌基因的mRNA表达水平呈正相关，与CD63（四次跨膜蛋白）、JOSD2（去泛素化酶）等癌基因的mRNA表达水平呈负相关；TARGET数据库中TET3 mRNA水平与神经母细胞瘤患者总生存期（OS）和无事件生存期（EFS）呈正相关（P=0.024， P=0.014）。结论TET3在NB患者组织中的表达与患者临床特征有一定的关系，且TET3高表达与NB患者预后良好呈正相关，提示TET3在神经母细胞瘤中可能作为肿瘤抑制因子发挥作用，TET3可以作为预测NB患者预后的一个潜在指标，对NB的临床评估有一定的价值。

目的探讨宫腔粘连（IUA）不同分类标准在预测其术后生殖结局方面的意义。方法搜集2017年1月至2018年2月在重庆市妇幼保健院诊断IUA并且进行宫腔镜手术的患者，最后纳入178名作为研究对象。所有入选患者均行宫腔粘连分离术，分别采用美国AFS评分、欧洲ESGE评级、Nasr评分以及国内评分系统进行完整评分，分析比较不同评分系统对IUA患者术后妊娠率和活产率的预测价值。结果① 术前不同月经类型、术后不同月经恢复情况及输卵管开口是否可见的妊娠率及活产率组间差异无统计学意义（P＞0.05）。不同粘连范围及粘连性质的妊娠率及活产率组间差异有统计学意义（P＜0.05）。② 在4种评分标准下，不同粘连程度间的妊娠率差异有统计学意义（P＜0.05）；AFS评分、ESEG评级、Nasr评分下不同粘连程度间的活产率差异有统计学意义（P＜0.05），而国内评分下不同粘连程度间的活产率异无统计学意义（P＞0.05）。③ 各评分系统对妊娠结局的预测效能：AFS评分、ESEG评级、Nasr评分内国内评分妊娠率曲线下面积（AUC）依次为0.609、0.602、0.645和0.588；活产率AUC依次为0.596、0.617、0.638和0.575。国内评分下妊娠率、活产率的AUC最小，Nasr评分下妊娠率、活产率的AUC最大，但均＜0.7。结论粘连范围越大、性质越偏肌性、程度越重，其生殖结局越差；AFS评分、ESGE评级、Nasr评分以及国内评分系统在预测生殖结局方面均存在一定缺陷。临床上需进一步探讨及制定更合理的评分标准来预测生殖结局。

血管新生是肿瘤发生发展中一个重要的病理特征，抗血管新生已经成为肿瘤治疗研究的一大热点。目前抗 血管新生的策略主要是应用血管新生刺激因子拮抗剂或血管新生抑制因子，以恢复肿瘤中被打破的血管新生平衡。相比 于血管新生刺激因子拮抗剂，内源性血管新生抑制因子展现了更好的治疗前景，但是其分子机制还有待进一步阐明。内 源性血管新生抑制因子包括两类，一类是前体蛋白的水解片段，如人纤溶酶原K5（plasminogen kringle 5，K5）、血管抑素 （angiostatin/ kringle 1-4）、内皮抑素（endostatin）等；另一类是细胞分泌性的蛋白质，如色素上皮衍生因子（pigment epitheliumderived factor，PEDF）、激肽释放酶结合蛋白（kallikrein-binding protein，KBP/kallistatin）、抗凝血酶（antithrombin）等。本文以 K5、PEDF、KBP为例，分别介绍其生物学功能、抗肿瘤血管新生机制及应用前景等方面的研究进展，希望这些研究能够为 未来抗肿瘤血管新生治疗提供借鉴。

摘要：【目的】探讨血小板O2·- 和H2O2水平变化导致2型糖尿病患者血小板异常活化的分子机制。【方法】检测2型 糖尿病患者和正常对照组的血小板4项临床参数；应用免疫荧光技术观察血小板形态结构的变化；应用流式细胞术测定两 组血小板内线粒体O2·-、胞浆O2·- 和H2O2水平；用NADH/PMS和H2O2分别处理正常对照组血小板，流式细胞术检测血小板 的活化阳性百分率；应用Western Blot 检测两组血小板内过氧化氢酶（Catalase）、超氧化物歧化酶2 型（Mn-SOD）的表达差 异。【结果】2型糖尿病组平均血小板体积（MPV）明显高于正常对照组（P < 0.001），而血小板数量（PLT）、血小板分布宽度 （PDW）、血小板比积（PCT）差异均无统计学意义；免疫荧光显示2型糖尿病组血小板形态结构较正常对照组发生改变，流式 细胞术检测血小板的线粒体O2·- 、H2O2水平明显高于正常对照组（P < 0.05），而胞浆O2·- 水平差异无统计学意义。通过流 式分析H2O2和NADH/PMS体系明显促进血小板的活化（P < 0.01）。Western Blot结果显示2型糖尿病组血小板Catalase的表 达下调，而Mn-SOD的表达及活性无差异。【结论】糖尿病血小板内Catalase表达下调可能是导致线粒体O2·-、H2O2水平升高 的原因，从而调控糖尿病血小板的异常活化。

【目的】 降低成本，增大产出，提高K5突变体（mK5）在原核系统的单位表达量。 【方法】 调整可能影响表达的参数：抗生素浓度、pH、A600值、IPTG终浓度、诱导时间、诱导温度，同时固定其它参数。通过电泳分析，获得mK5在原核系统pET22b-BL21的最优表达条件；组氨酸结合柱亲和层析、纯化获得mK5蛋白，SDS-PAGE和Western-blot方法鉴定mK5蛋白；MTT法分析mK5对人视网膜毛细血管内皮细胞（HRCEC）增殖的影响。【结果】 优化后的表达条件为：最适细菌培养温度为37℃，最佳抗生素浓度为50μg/mL羧苄青霉素，最适pH值为7.0，在A600为0.9～1.0时加入终浓度为1.0 mmol/L的IPTG为最佳诱导条件，37℃诱导10 h为最佳诱导时间；优化条件后mK5纯化蛋白得率为21 mg/L，产量较优化前(15 mg/L)提高近30％；mK5特异性地抑制HRCEC的增殖，IC50=40 nmol/L。【结论】 本研究确定了mK5蛋白诱导表达的最适参数，并获得具有生物活性的高纯度、高表达量的重组蛋白，为工业化大规模发酵生产提供了基本参数。

【目的】探讨前列腺增生（BPH）和前列腺癌（PCa）组织中血管增生抑制因子，如视网膜色素上皮细胞源因子（PEDF）、血管抑素（angiostatin）、内皮抑素endostatin的表达情况及其血管依赖性生长的分子机制。【方法】收集正常前列腺、前列腺增生和前列腺癌组织标本，RT—PCR技术检测样品中PEDF、angiostatin、endostatin的mRNA表达量，Western blot技术检测样品中PEDF蛋白的表达量。【结果】和正常前列腺组织相比，PEDF表达量在BPH中无明显变化（P〉0．05），在前列腺癌中普遍显著下降（P〈0．05）；良性前列腺增生组织中endostatin表达量较正常前列腺组织显著升高（P〈0．05），前列腺癌比正常前列腺显著升高（P〈0．05），而且前列腺癌组织较良性前列腺增生进一步显著增高（P〈0．05）；三种组织中均未检测到angiostatin的表达。【结论】良性前列腺增生及前列腺癌组织抑制因子表达变化可能和其血管依赖性生长相关；PEDF可能是前列腺组织最主要的血管增生内源性抑制因子。

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