脱氢表雄酮抑制血管平滑肌细胞增殖的体外研究

目的研究脱氢表雄酮(DHEA)在血管紧张素Ⅱ(AngⅡ)诱导的血管平滑肌细胞(VSMC)增殖过程中的作用及机制。方法 AngⅡ处理体外培养的VSMC,再用DHEA处理VSMC,MTS、细胞计数检测DHEA对AngⅡ诱导的VSMC增殖的影响。定量实时聚合酶链反应(qRT-PCR)、Western blot检测DHEA对AngⅡ诱导的VSMC中增殖细胞核抗原(PCNA)、Krüppel样因子5(KLF5)和诱导型一氧化氮合酶(iNOS)表达的影响。酶联免疫吸附法(ELISA)检测DHEA对AngⅡ诱导的VSMC的培养基中过氧亚硝基阴离子(ONOO~-)浓度的影响。用小干扰RNA(siRNA)内源性敲低iNOS,Western blot检测VSMC中PCNA的表达。结果 MTS和细胞计数结果显示,DHEA能显著抑制AngⅡ诱导的VSMC增殖(P0.05)。qRT-PCR和Western blot结果显示,在mRNA和蛋白质水平,DHEA显著抑制AngⅡ诱导的VSMC中PCNA、KLF5和iNOS表达(P0.05)。ELISA结果显示,DHEA显著减少AngⅡ处理的VSMC培养基中ONOO~-的浓度(P0.05)。内源性敲低iNOS后,Western blot结果显示,DHEA对AngⅡ诱导的PCNA蛋白表达无影响(P0.05)。结论 DHEA可能通过抑制iNOS产生的ONOO~-,使KLF5的表达下调,进而发挥抑制AngⅡ诱导的VSMC增殖的作用。     

Zweymüller系统在Crowe-Ⅲ、Ⅳ型髋臼发育不良全髋置换中的应用☆

选择2004-01/2006-12河南中医学院第二附属医院骨科收治的髋臼发育不良患者13例13髋，使用Zweymüller系统的非骨水泥双锥面螺旋臼及SL股骨柄，采用软组织彻底松解、原位髋臼、股骨不截骨的全髋置换治疗。其中男5例5髋，女8例8髋；年龄28~62岁，平均51岁；按Crowe分型，Ⅲ型9例9髋，Ⅳ型4例4髋。术前下肢短缩3~6 cm。13例患者全部获得随访，随访时间12~36个月，平均24个月。术后下肢延长2~6 cm，基本恢复双下肢平衡。未出现关节脱位、股骨干骨折、股神经及坐骨神经损伤等并发症，无假体松动的临床和X射线征象。术后髋关节疼痛和功能障碍得到明显缓解。     

Analysis of TGFBI gene mutation in a Chinese family with atypical Reis-Bückler corneal dystrophy

Objective To identify the TGFBI gene mutation and the relationship between genotype and phenotype of a Chinese family with atypical Reis-Bückler corneal dystrophy (RBCD). Methods Four patients, two non-carrier relatives of the family were enrolled in the present study. In addition to ophthalmologic examinations, PCR amplification and DNA sequencing of exons 4, 11, 12, and 14 of the TGFBI gene were carried out. Exon 14 was also sequenced in 100 healthy controls. Results A G to A transition at eodon 623 in all affected members was identified. This mutation resulted in a substitution of glyeine (GGC) to aspartic acid (GAC) at the protein level. None of the healthy family members, or any of the 100 control subjects carried this mutation. Conclusion The G623D mutation of the TGFBI gene caused an atypical Reis-Buckler corneal dystrophy in this family. This mutation is reported in Chinese for the first time.     

Analysis of TGFBI gene mutation in a Chinese family with atypical Reis-Bückler corneal dystrophy

Objective To identify the TGFBI gene mutation and the relationship between genotype and phenotype of a Chinese family with atypical Reis-Bückler corneal dystrophy (RBCD). Methods Four patients, two non-carrier relatives of the family were enrolled in the present study. In addition to ophthalmologic examinations, PCR amplification and DNA sequencing of exons 4, 11, 12, and 14 of the TGFBI gene were carried out. Exon 14 was also sequenced in 100 healthy controls. Results A G to A transition at eodon 623 in all affected members was identified. This mutation resulted in a substitution of glyeine (GGC) to aspartic acid (GAC) at the protein level. None of the healthy family members, or any of the 100 control subjects carried this mutation. Conclusion The G623D mutation of the TGFBI gene caused an atypical Reis-Buckler corneal dystrophy in this family. This mutation is reported in Chinese for the first time.     

带囊施源器中子源治疗食管癌的临床应用

带囊施源器是在中子源治疗管的外周加一个扩充囊，该囊可注入显影剂，在治疗时把该施源器插入所需要治疗的食管病变处，通过影像设备显示出显影液充盈情况，使高剂量点位于治疗管或囊腔内。以前使用的施源器不带囊，无法控制治疗管在食管中的位置，导致剂量分布不均匀，从而影响治疗效果。我们拟观察使用带囊施源器后施以中子源治疗后剂量分布的均匀程度，治疗后放射性食管炎的变化及与不带囊的区别。     

外照射结合252cf腔内照射放疗中晚期食管癌护理

食管癌是我国三大难治恶性肿瘤之一,当食管癌确诊时,中晚期病例占80%以上。在这些病例的治疗中,外照射加252cf腔内照射治疗食管癌,能明显提高放疗的有效率和生存率。但在实     

兔眼视网膜铁锈症中Müller氏细胞的变化

在电镜下观察了兔眼视网膜铁锈症中Müller氏细胞的变化。其变化有:(1)细胞变形,极性特征消失;(2)胞突扩张,填补细胞变性的空隙;(3)胞浆内出现大量线粒体;(4)并见色素颗粒及感光细胞的残片;(5)在视网膜不同层次,Müller氏细胞之间形成排列紊乱的粘着小带。证实Müller氏细胞具有相当活跃的吞噬及修补功能。推测含铁物质的毒性可能通过Müller氏细胞传递,影响视网膜色素上皮细胞及感光细胞。     

金纳多对高糖所致视网膜Müller细胞合成谷胱甘肽减少的保护作用

目的研究高浓度葡萄糖对体外培养兔视网膜Müller细胞合成谷胱甘肽（GSH）的影响及自由基清除剂金纳多（EGb761）的作用。方法采用比色法测定不同浓度葡萄糖（5.5、30、40、50mmol/L）下,兔Müller细胞合成GSH的质量分数。在50mmol/L葡萄糖培养液中加入不同质量浓度EGb761（0、5、10、15、20、25、30、45、90μg/mL）培养3d后测定兔视网膜Müller合成GSH的质量分数。结果各浓度葡萄糖均使兔视网膜Müller细胞合成GSH的质量分数减少。加入各质量浓度EGb761后GSH合成增加,质量浓度为10μg/mL时增加最高。结论EGb761对高浓度葡萄糖致兔视网膜Müller细胞合成GSH质量分数减少起保护作用。     

Clinical Report on Californium-252 Neutron Intraluminal Brachylherapy Combined with External Irradiation for Cervical Carcinoma Treatment

OBJECTIVE To observe the curative effects and complications of californium-252 （^252Cf） neutron intraluminal brachytherapy （IBT） combined with external irradiation （El） for treatment of cervical carcinoma. METHODS From December 2000 to December 2004, 128 cases of cer vical carcinoma staged into IIA-IIIB according to the International Federation of Gynecology and Obstetrics （FIGO） standards were treated with ^252Cf neutron IBT using 8-10 Gy per fraction, once a week. The total dose at reference A point was 36-40 Gy in 4-5 fractions. From the second day after ^252Cf neutron IBT treatment, the whole pelvic cavity was treated with ^60Co y-ray El, applying 2 Gy per fraction, 4 times per week. After 20-25Gy of El, the center of the whole pelvic field was blocked with 4 cm of lead in width. The total dose of El was 45-50 Gy. RESULTS The short-term therapeutic effects were CR 95.3% and PR 4.7%. The 3 and 5-year local control rates were 93.5% and 87.9%. The overall 3-year survival rate was 87.5% and for Stages Ⅱ and Ⅲ , 90.9% and 81.5% respectively; the overall 5-year survival rate was 70% and for Stages II and III, 76.2% and 61% respectively. The rate of radiation complications was 4.7% for radiation cystitis, 7.8% for radiation proctitis, 6.3% for vagina contracture and adhesion and 5.5% for protracted radiation proctitis. CONCLUSION An combination of ^252Cf neutron IBT with El for treatment of cervical carcinoma can be well-tolerated by cervical carcinoma patients. The rate of local tumor control is high and radiation complications are few.     

微小 RNA?34a调控儿童急性淋巴细胞白血病细胞 CEM/C1生长和迁移的分子机制研究

目的研究微小 RNA?34a(miR?34a)对儿童急性淋巴细胞白血病(ALL)细胞 CEM/C1增殖、迁移的影响以及可能作用机制。方法选取重庆市第十三人民医院血液科 2017年 10月至 2018年 12月住院 32例 ALL病儿骨髓样本。另选取该院同期 25例原发性血小板减少症病儿的骨髓样本作为对照组。实时荧光定量多聚核苷酸链式反应(qPCR)检测 miR?34a在 ALL骨髓样本的表达量; CEM/C1细胞按随机数字表法分为对照组、阴性对照(NC)组、 miR?34a组;对照组细胞常规培养, NC组和 miR?34a组 CEM/C1细胞分别在 Lipofectamine 2000介导下转染阴性对照质粒以及 miR?34a模拟物, qPCR检测转染效率;细胞计数试剂盒 8(CCK?8)实验检测 CEM/C1细胞的增殖, Transwell检测细胞迁移;在线软件 TargetScan预测 miR?34a与 Krüppel样因子 4(KLF4)的靶向关系,双荧光素酶报告基因进一步进行验证。结果与对照组相比, ALL骨髓样本中 miR?34a的表达量下调［(0.33±0.05)比(1.00±0.08)t＝15.680,P＜0.001］。与对照组(1.00±0.08)相比, NC组 miR?34a的表达量(0.99±0.08)无明显变化, miR?34a组 CEM/C1细胞中,miR?34a的表达量(3.21±0.23)上调(F＝423.135,P＜0.05)。对照组、 NC组、 miR?34a组细胞培养 48 h后细胞活性分别为(0.65±0.05)、(0.69±0.06)、(0.42±0.04)F＝40.818,P＜0.001;迁移细胞数分别为(142.36±12.47)个、(137.45±13.49)个、(79.89±6.23)个, F＝57.683,P＜0.001,差异计学意义。与 NC与 KLF4?wt共转染的细胞相比, miR?34a有统,与 KLF4?wt共转染的细胞荧光素酶活性［(0.45±0.03)比(1.00±0.06)t＝20.083,P＜0.001］降低;与 NC与 KLF4?mut共转染的细胞相比, miR?34a与 KLF4?mut共转染的细胞荧光素酶活性差异无统计学,意义［(1.03±0.07)比(1.01±0.07),t＝0.495,P＞0.05)］。结论 miR?34a在 ALL中表达量下调,其可通过对靶基因 KLF4的调控影响 CEM/C1细胞增殖、迁移。