基质金属蛋白酶-2在子宫腺肌病子宫内膜-肌层界面的表达

目的探讨子宫腺肌病患者子宫内膜-肌层界面（endometrial-myometrial interface,EMI）基质金属蛋白酶-2（matrix metalloproteinases-2,MMP-2）的表达及意义。方法采用免疫组化SP法对40例子宫腺肌病子宫内膜（含部分肌层）和对照组40例子宫肌瘤子宫内膜（含部分肌层）的组织进行标记及分析。结果腺肌病组MMP-2的表达强度EMI处显著高于远肌层（P〈0.05）。EMI处MMP-2表达,腺肌病组显著高于对照组（P〈0.05）。结论子宫腺肌病组EMI处的内膜腺体中MMP-2的高表达,可使子宫内膜的侵蚀能力增强,可能参与子宫腺肌病的发生和发展。     

浅析超声用于子宫腺肌病中的诊断价值

目的 探讨超声用于子宫腺肌病中的诊断价值.方法 回顾分析52例患者的临床资料.结果 弥漫性子宫腺肌病为27例,局限性子宫腺肌病为13例,合并卵巢内膜异位症12例.结论 子宫腺肌病是内膜腺体细胞及间质细胞向肌层侵蚀,伴随着子宫平滑肌细胞增生而引起的一种良性病变.超声诊断子宫腺肌病的符合率较高,且具有无创、安全、可重复检查等优点,对子宫腺肌病的诊断及鉴别诊断有重要的临床价值.     

子宫腺肌病42例超声诊断分析

子宫腺肌病是妇科常见病,属于子宫内膜异位症疾病的一种,由具有功能的子宫内膜腺体细胞及间质细胞向肌层侵蚀,伴随着子宫平滑肌细胞增生而引起的一种良性病变,子宫腺肌病合并症较多,现将我院近5年42例子宫腺肌病的声像图资料分析报告如下.     

超声诊断子宫腺肌病的临床分析

子宫腺肌病是指内膜腺体细胞及间质细胞向肌层侵蚀,伴随着子宫平滑肌细胞增生而引起的一种良性病变。是妇科常见病,多发生于30～50岁经产妇。本文对35例经手术病理证实的子宫腺肌病的声像图进行分析,以体现超声在子宫腺肌病中的诊断价值。     

子宫腺肌病中异位子宫内膜血管发生的研究

目的 探讨子宫腺肌病中异位子宫内膜组织中血管生长因子(VEGF)和肿瘤坏死因子-α(TNF-α)的表达与发病机制的关系.方法 采用免疫组织化学技术检测40例正常子宫内膜和40例子宫腺肌病异位内膜中VEGF和TNF-α的表达.结果 子宫腺肌病异位内膜腺上皮细胞及间质细胞中VEGF和TNF-α的表达明显高于正常内膜腺上皮(P＜0.05).结论 子宫腺肌病异位内膜中VEGF和TNF-α表达的明显增高可能导致局部新生毛细血管的增多,从而促进子宫内膜在子宫肌层内异位种植和生长.     

细胞周期蛋白A与p27蛋白在子宫腺肌病中的表达及其意义

目的检测体外培养子宫腺肌病在位内膜腺上皮细胞中细胞周期蛋白A(CyclinA)与p27蛋白的表达,探讨CyclinA及p27蛋白与子宫腺肌病的发病关系。方法体外培养子宫腺肌病在位内膜腺上皮细胞,用Western-blot法定量检测CyclinA和p27在子宫腺肌病组、对照组(子宫肌瘤组)培养细胞中的表达。结果子宫腺肌病组腺上皮细胞中CyclinA表达高于对照组(P<0.05),p27表达低于对照组(P<0.05)。结论子宫腺肌病的发病也可能与细胞周期调节失控导致细胞不正常生长,增殖活性改变有关。     

宫腔镜下子宫内膜切除联合孕三烯酮治疗子宫肌腺病

目的 探讨保留子宫的子宫肌腺病的治疗方法.方法 2005年1月-2007年12月38例子宫肌腺病患者行子宫内膜切除后行口服孕三烯酮治疗与单纯口服孕三烯酮疗效的比较,随访12个月.结果 两组患者在经量改变、痛经程度及子宫体积差异显著.结论 宫腔镜下子宫内膜切除联合孕三烯酮治疗子宫肌腺病是一种中青年患者乐于接受的、疗效显著的、新的治疗方法.     

病灶切除治疗子宫腺肌病疼痛73例分析

子宫腺肌病是指子宫内膜向子宫肌层良性浸润并在其中弥漫性生长，如果侵入子宫内膜腺体及间质周围的肌纤维聚合成结节称为子宫肌腺瘤，其特征是子宫肌层中出现了异位的内膜和腺体，伴有其周同的肌层细胞肥大和增生，有子宫内子宫内膜异位症之称。早在1908年已经描述过此病，但至今仍缺乏好的治疗方法。我院在2005年5月～2006年8月共为73例患者行子宫腺肌病病灶部分切除，术后进行随访，以探讨这种手术能否改善该病的症状。     

突变型P53在子宫腺肌病中的表达及意义

子宫腺肌病是指子宫内膜组织存在于子宫肌层中,并伴有不同程度的肌层平滑肌细胞增生和肥大。该病虽然属于妇科良性疾病,但具有恶性肿瘤的某些生物学行为,其确切的发病机理至今仍不十分清楚。近几年来子宫腺肌病的发病机理多从恶性肿瘤发生的角度来探讨已成为该疾病研究的突破点。P53基因的突变或失活均与多种肿瘤的发生发展有着密切的关系。本实验应用免疫组化SP法来检测突变型P53在子宫腺肌病患者的在位内膜、异位内膜的表达及意义。     

子宫腺肌瘤切除术38例临床分析

子宫腺肌症是指子宫内膜向肌层良性浸润并在其中弥漫性生长,其特征是在子宫肌层中出现了异位的内膜和腺体,伴有其周围的肌层细胞肥大和增生[1].子宫腺肌瘤是子宫腺肌症的一种形式,累及局部,并有局部增大的平滑肌所环绕,特称为子宫腺肌瘤.近年发病有增多趋势,在妇科较为常见,日益受到人们的重视.本院自2001年1月至2005年1月行子宫腺肌瘤切除术38例,效果满意,报告如下.     

泛素在子宫腺肌病在位及异位子宫内膜的表达

目的：探讨泛素在子宫腺肌病发病机制中的作用及对细胞凋亡的影响.方法：利用免疫组化SP法测定子宫腺肌病患者在位、异位内膜腺体和间质细胞中泛素的表达,通过HE染色计数凋亡细胞数,并与正常子宫内膜进行比较.结果：异位内膜的泛素表达高于在位及正常内膜,细胞凋亡减少,尤其以间质细胞表现明显;在位内膜的泛素表达高于正常内膜（P＜0.05）.结论：在位内膜的异常可能有利于子宫内膜的移位,泛素具有抑制异位内膜细胞凋亡的作用,与子宫腺肌病的发生密切相关.     

The expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and its regulation by ovarian steroids in rat uterine stromal cells

The effects of ovarian steroids on the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in rat uterus were examined. Intense expression of GM-CSF mRNA was dispersedly located in the endometrial-myometrial junction and stroma of the uterus. GM-CSF was immunohistochemically localized in stromal cells and luminal epithelium. Ovariectomy significantly reduced the appearance of GM-CSF-mRNA-positive cells and the levels of expression for GM-CSF mRNA in the whole uterus, whereas treatment with 17beta-estradiol (E2) or a combination of E2 and progesterone (P4) for 5 days on ovariectomized animals recruited GM-CSF-mRNA-positive cells and stimulated its expression. The combined treatment with E2 and P4 also stimulates the expression for GM-CSF mRNA and the production of immunoreactive GM-CSF in the stromal tissues. These data suggest that the expression of GM-CSF in uterine stromal cells is partially regulated by ovarian steroids.     

体外培养子宫腺肌病在位内膜腺上皮中Kiss-1和乙酰肝素酶的表达及意义

目的探讨Kiss-1和乙酰肝素酶(Hpa)在子宫腺肌病发生、发展中的作用。方法选择10例子宫腺肌病患者作为研究组,8例宫颈上皮内瘤变(CIN)Ⅲ级患者作为对照组,通过对子宫内膜腺上皮细胞的体外培养,用反转录-聚合酶链反应半定量分析Kiss-1和Hpa mRNA在研究组、对照组子宫内膜腺上皮细胞的表达。结果研究组腺上皮细胞Kiss-1 mRNA的表达在增殖期与分泌期均较对照组降低,差异有统计学意义(P<0.05),而同一组中增殖期腺上皮细胞Kiss-1 mRNA的表达与分泌期相比差异无统计学意义(P>0.05)。研究组腺上皮细胞Hpa mRNA的表达在增殖期与分泌期均较对照组升高,差异有统计学意义(P<0.05),而同一组中增殖期腺上皮细胞Hpa mRNA的表达与分泌期相比差异无统计学意义(P>0.05)。结论Kiss-1 mRNA表达减弱和Hpa mRNA表达增强可能与子宫腺肌病的侵袭过程有关,两者在腺肌病的发生发展中发挥重要作用。     

Corneal edema induced by bis (tributyltin) oxide

Comeal edema induced by bis (tributyltin) oxide (TBTO) was studied with an electron microscope and the accumulation sites of tin were determined with an X-ray microanalyzer. Male Wistar rats received an intramuscular injection of 0.5 ml/kg TBTO. After time intervals of 2,4, 6, 8, 10, 12 h after injection, corneas were isolated and provided for electron microscopy. Corneas from untreated rats served as controls. Marked swelling of mitochondria in the corneal endothelial cells occurred at 4 h after TBTO injection. The corneal edema appeared in the endothelial layer and the stroma at 6 h after injection. By X-ray microanalysis, Sn peaks were obtained from swollen mitochondria in the endothelial cells. At 12 h after TBTO injection, edematous swelling of the corneal tissue became more advanced. These results indicated that parenterally administered TBTO accumulated in the mitochondria of corneal endothelial cells. The direct toxic effects of TBTO on the mitochondria might cause the interference with active pump function of endothelial cells and induced the corneal edema.     

以siRNA表达载体稳定抑制缝隙连接蛋白43表达的睾丸间质细胞和睾丸支持细胞系的建立

目的构建Cx43-siRNA真核表达载体,获得连接蛋白43(connexin43,Cx43)被长期稳定抑制的睾丸间质细胞(TM3细胞)系和睾丸支持细胞(TM4细胞)系,为研究Cx43及其形成的细胞缝隙连接(gap junction,GJ)在睾丸组织中的作用提供有用模型。方法设计合成3对针对Cx43的短发夹样siRNA的DNA模板序列,定向连接到siRNA真核表达载体pSilencerTM2.1-U6neo上,通过测序鉴定后以脂质体法瞬时转染睾丸支持细胞,以Western blot方法检测Cx43蛋白表达水平,筛选出最有效的干扰序列,再将之分别转染睾丸间质细胞和睾丸支持细胞,G418筛选出能稳定表达siRNA的细胞系,以"Parachute"荧光传递示踪法检测细胞缝隙连接功能。结果 Western blot结果显示,第3对干扰序列对Cx43表达抑制效果最佳,以表达该序列的质粒稳定转染的TM3细胞和TM4细胞上Cx43蛋白表达水平均明显降低;荧光传递示踪法检测表明,两种细胞系的GJ功能均被明显抑制。结论以Cx43-siRNA真核表达载体稳定转染的方法能长期干扰TM3和TM4细胞上Cx43的表达,并抑制由其形成的GJ功能。     

VEGF MVD在子宫腺肌病中的表达

目的 探讨子宫腺肌病异位内膜组织中血管内皮生长因子(VEGF)和微血管密度(MVD)的表达.方法 采用免疫组织化学方法检测子宫腺肌病异位内膜与正常子宫内膜中VEGF和MVD的表达.结果 子宫腺肌病异位内膜组织中VEGF和MVD在增生期和分泌期的表达均明显高于正常内膜(P＜0.05).结论 异位内膜组织中VEGF和MVD的高表达可能对子宫腺肌病的发生发展起重要作用.     

米非司酮对体外培养子宫腺肌病在位内膜腺上皮细胞Ki-67 mRNA和Caspase-3 mRNA表达的影响和意义

目的探讨米非司酮对体外培养子宫腺肌病在位内膜中腺上皮细胞的增殖及凋亡的影响。方法用反转录聚合酶链反应半定量分析Ki-67 mRNA和Caspase-3 mRNA在病例组、药物干预组、对照组(肌瘤组)子宫内膜腺上皮细胞的表达。结果病例组增生期和分泌期腺上皮细胞均较对照组表达Ki-67 mRNA增强(P<0.05)。用米非司酮药物干预后Ki-67 mRNA表达下降。病例组增生期腺上皮细胞Caspase-3 mRNA表达较对照组明显下降(P<0.05),而病例组分泌期腺上皮细胞Caspase-3 mRNA表达与对照组差异无统计学意义(P>0.05)。用米非司酮药物干预后,病例组增生期腺上皮细胞Caspase-3 mRNA表达增强(P<0.05),而分泌期腺上皮细胞Caspase-3 mRNA表达没有明显增强(P>0.05)。结论子宫内膜腺上皮细胞凋亡与增殖失衡可能是子宫腺肌病的发病机制之一,米非司酮可诱导子宫内膜腺上皮细胞凋亡,抑制内膜腺上皮细胞增殖,从而控制子宫腺肌病的发展。     

Induction of uterine adenomyosis by pituitary grafting and retardation of its development by bromocriptine-mesilate (CB-154) in BALB/c mice.

Development of uterine adenomyosis was examined in BALB/c mice. Anterior pituitary (AP) isografting at 8 weeks of age significantly increased the incidence of adenomyosis in mice by 36 weeks of age as compared to that in control mice bearing no AP isograft. However, in mice with AP grafting, daily administration of 0.2 mg bromocriptine-mesilate (CB-154) between 4 and 8 weeks of age decreased the incidence of adenomyosis at 36 weeks of age to the level of control mice. These results suggest that in mice AP grafting stimulates the development of adenomyosis and that pretreatment with CB-154 during youth can suppress the development.     

体外培养子宫腺肌病在位内膜腺细胞ki-67mRNA的表达

目的探讨体外培养子宫腺肌病在位内膜中腺细胞增殖对疾病的影响。方法用反转录-聚合酶链反应半定量分析ki-67mRNA在病例组与肌瘤组子宫内膜腺细胞的表达。结果病例组增生期和分泌期腺细胞均较肌瘤组表达ki-67mRNA增强(P<0.05)。结论子宫内膜腺细胞增殖能力增强可能是子宫腺肌病的发病机制之一。     

Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43

Rictor is a key component of the mammalian target of rapamycin complex 2 (mTORC2) and is required for Akt phosphorylation (Ser473). Our previous study shows that knockdown of Rictor prevents cardiomyocyte differentiation from mouse embryonic stem (ES) cells and induces abnormal electrophysiology of ES cell-derived cardiomyocytes (ESC-CMs). Besides, knockdown of Rictor causes down-expression of connexin 43 (Cx43), the predominant gap junction protein, that is located in both the sarcolemma and mitochondria in cardiomyocytes. Mitochondrial Cx43 (mtCx43) plays a crucial role in mitochondrial function. In this study, we used the model of cardiomyocyte differentiation from mouse ES cells to elucidate the mechanisms for the mitochondrial damage in ESC-CMs after knockdown of Rictor. We showed swollen and ruptured mitochondria were observed after knockdown of Rictor under transmission electron microscope. ATP production and mitochondrial transmembrane potential were significantly decreased in Rictor-knockdown cells. Furthermore, knockdown of Rictor inhibited the activities of mitochondrial respiratory chain complex. The above-mentioned changes were linked to inhibiting the translocation of Cx43 into mitochondria by knockdown of Rictor. We revealed that knockdown of Rictor inactivated the mTOR/Akt signalling pathway and subsequently decreased HDAC6 expression, resulted in Hsp90 hyper-acetylation caused by HDAC6 inhibition, thus, inhibited the formation of Hsp90-Cx43-TOM20 complex. In conclusion, the mitochondrial Cx43 participates in shRNA-Rictor-induced mitochondrial function damage in the ESC-CMs.