PCOS患者子宫内膜白血病抑制因子的表达及意义

目的:探讨多囊卵巢综合征(PCOS)患者不同组织学分期的子宫内膜白血病抑制因子(LIF)的表达与子宫内膜容受性的关系。方法:20例已婚PCOS患者(PCOS组)和26例已婚不孕症患者(对照组)在月经周期第5￣14日及排卵后7￣8 d采集其子宫内膜标本,经HE染色判定内膜组织学分期,采用免疫组织化学法检测内膜LIF的表达。结果:PCOS组间质反应不良和分泌反应欠佳的发生率均高于对照组,差异有统计学意义(χ2=5.000,P<0.05;χ2=7.219,P<0.01)。LIF的表达以腺上皮细胞的胞质为主,其在分泌中期子宫内膜的表达水平均高于增生期(P<0.01)。LIF在PCOS组增生期和分泌中期子宫内膜的表达水平均低于其相应的对照组(P<0.01)。结论:PCOS患者着床窗口期LIF的低表达可能影响着床的多个环节,参与了PCOS患者内分泌紊乱纠正后仍出现妊娠率低、流产率高的发生、发展过程。     

月经周期中不同类型人子宫内膜体外培养的细胞形态学特点

目的:探讨不同类型子宫内膜细胞体外培养的细胞形态学特点。方法:在月经周期的不同时期,通过B超检测判断患者子宫内膜的厚度和类型,取不同形态分型的人子宫内膜进行体外培养,倒置显微镜下观察子宫内膜体外培养的细胞形态学特性,并通过免疫荧光法进行鉴定,采用培养板单层贴壁细胞的原位计数方法,计算子宫内膜间质细胞和腺上皮细胞数量及比例。结果:不同类型子宫内膜经培养后,其中间质细胞形态呈扁平状,胞质透明,核圆、居中,波形蛋白表达阳性;腺上皮细胞呈多角形或蝌蚪形,旋涡状排列,核圆而大,角蛋白表达阳性。A型子宫内膜组织腺细胞贴壁率为85.8±5.7%,贴壁培养后腺上皮细胞的比例占43.3±11.7%,间质细胞比例占56.7±11.7%;B型子宫内膜组织腺细胞贴壁率为8.7±3.9%,贴壁培养后腺上皮细胞的比例占13.3±3.3%,间质细胞比例占86.7±3.3%;C型子宫内膜组织腺细胞贴壁率为6.0±1.9%,贴壁培养后腺上皮细胞的比例占12.3±3.0%,间质细胞比例占87.7±3.0%。A组与B组、C组两组腺上皮细胞贴壁率及贴壁后腺细胞比例有明显统计学差异(P0.05),B、C组之间腺上皮细胞贴壁率及腺细胞比例无明显统计学差异(P0.05)。结论:B、C型子宫内膜体外培养腺上皮细胞贴壁比例低于间质细胞,体外培养后以间质细胞为主;A型子宫内膜细胞培养所得的间质细胞及腺细胞均较多,腺细胞贴壁率及腺细胞比例明显高于B、C型子宫内膜,是用于胚胎着床机制等实验研究较好的标本来源。     

温肾活血汤联合克罗米芬改善促排卵子宫内膜容受性疗效研究

目的:探讨温肾活血汤联合克罗米芬(clomiphene citrate,CC)促排卵治疗后对子宫内膜容受性的影响。方法:45例排卵障碍型不孕患者随机分成A组(CC)、B组(CC+阿司匹林)、C组(CC+温肾活血中药),每组15例。治疗1～3个疗程,观察排卵率、妊娠率及hCG注射日子宫内膜类型及厚度。结果:C组A+B型内膜率(91.18%)显著高于A组(76.92%,P<0.01)及B组(66.67%,P<0.05);C组内膜平均厚度(9.4±2.2mm)显著高于A组(7.8±1.4mm),P<0.05。周期排卵率C组(82.35%)>B组(76.92%)>A组(69.23%),但各组间无统计学差异(P>0.05);未破裂卵泡黄素化综合征(LUFS)发生率C组(5.88%)显著低于A组(23.08%)(P<0.05)。周期妊娠率C组(23.5%)>B组(15.4%)>A组(10.3%)(P<0.05)。结论:温肾活血汤能提高克罗米芬促排卵治疗后的妊娠率,其机制可能与促进排卵、降低LUFS发生及改善子宫内膜容受性有关,其改善内膜容受性的效果好于阿司匹林联合CC。     

整合素α~6和β_4亚单位在人类月经周期和早孕时子宫内膜中的表达

目前认为,整合素在子宫内膜中参与调节细胞与细胞之间及细胞与间质之间的相互反应。本研究通过单克隆抗体免疫组化法,了解整合素α~6和β~4亚单位在月经周期和早孕子宫内膜表面和腺上皮表达。32例妇女(平均年龄34.14±3.4岁)分成两组,A组13例,孕6周～孕9周自愿要求人工流产时取子宫内膜;B组19例非妊娠者因妇科疾患需行宫腔镜下活检、子宫内膜诊刮或子宫切除时取子宫内膜。B组子宫内膜分为三期,植入前期(7例):病理学检查表现为增生期至排卵后3天之间;植入期(6例):病理学枪查表现为排卵后4天至排卵后9天之间;植入后期(6例):病理学检查表现为排卵后10天至排卵后14天之间。所有子宫内膜切片行单克隆抗体免疫组化染色。     

多囊卵巢综合征临床内分泌代谢对子宫内膜病变的影响

目的　探讨多囊卵巢综合征 (PCOS)患者临床内分泌代谢改变对子宫内膜病变的影响。方法　用组织学方法检测 94例PCOS患者子宫内膜病理改变 ,用放射免疫学方法测定血清泌乳素、黄体生成激素、卵泡刺激素、雌二醇、睾酮、雄烯二酮水平 ,82例同时行糖耐量及胰岛素释放实验。结果　① 70例PCOS患者子宫内膜为无排卵型 ,其中增殖期内膜 45例 ,增殖症 2 5例 (单纯增生 2 3例、不典型增生 2例 ) ;2 4例为排卵型子宫内膜 ,其中13例分泌反应不佳 ,11例分泌反应良好。②无排卵型子宫内膜组与排卵型子宫内膜组比较 ,前者血清空腹及糖负荷后 6 0min、12 0min的胰岛素水平和胰岛素曲线下面积明显增高 (P均 <0 0 5 )。③子宫内膜增殖症患者与增殖期内膜患者比较 ,前者胰岛素曲线下面积明显增高 (P <0 0 5 ) ,其中单纯增生患者糖负荷后 6 0min、12 0min的胰岛素水平和胰岛素曲线下面积比增殖期内膜患者明显增高 (P均 <0 0 5 )。结论　PCOS患者高胰岛素血症是导致无排卵型子宫内膜的重要因素之一 ,增高的胰岛素对子宫内膜的异常增生也可能起促进作用。     

宫腔镜下不同手术方式治疗子宫内膜息肉的临床疗效观察

目的探讨宫腔镜下不同手术方式治疗子宫内膜息肉的疗效。方法对不同年龄和不同生育要求的子宫内膜息肉患者327例,分别行子宫内膜息肉切除+子宫内膜汽化电切术(A组,53例);子宫内膜息肉切除+子宫内膜电切术(B组,175例);子宫内膜息肉切除+息肉旁浅层内膜切除术(C组,54例,要求保留生育功能者);子宫内膜息肉切除+子宫内膜电凝术(D组,45例,绝经后患者)。结果手术时间:A组(15·1±0·8)s,B组(19·7±0·7)s,C组(20·9±0·7)s,D组(22·1±0·8)s,A组平均手术时间与其他3组比较,差异有统计学意义(P<0·01);术后子宫内膜息肉复发率:A、D组为0,B组为1·7%(3/175),C组为7·4%(4/54),C组术后复发率与其他3组分别比较,差异均有统计学意义(P<0·05);C组术后无闭经者,但术后息肉复发率高于其他3组,C组中有14例术后5~23个月妊娠。结论宫腔镜下不同手术方式治疗子宫内膜息肉的临床疗效无明显差异,但子宫内膜息肉切除+息肉旁浅层内膜切除术后复发率高;应根据患者年龄、生育要求等选择适宜的宫腔镜下手术方式。     

瘦素及瘦素长受体在多囊卵巢综合征患者子宫内膜的表达

目的　探讨瘦素 (leptin)和瘦素长受体 (Ob RL)mRNA及蛋白在多囊卵巢综合征(PCOS)患者着床期子宫内膜的表达及意义。方法　应用免疫组织化学技术及原位杂交技术 ,分别对15例正常妇女 (对照组 )、14例无排卵PCOS患者 (PCOS组 )促排卵治疗后着床期子宫内膜的leptin、Ob RL mRNA及蛋白进行测定。结果　对照组中 ,子宫内膜 10例呈分泌期中期改变 ,5例呈分泌期早期改变。PCOS组中 ,子宫内膜 3例呈分泌期中期改变 ,6例呈分泌期早期改变 ,1例呈增殖期改变 ,4例呈增殖期并分泌期早期改变 ;子宫内膜发育不良发生率 79% (11/ 14 ) ,与对照组比较 ,差异有显著性 (P <0 .0 5 )。Ob RL mRNA和蛋白在PCOS患者子宫内膜腺体呈阴性到强阳性表达 ,但多呈弱阳性和阳性表达 ,对照组则呈弱阳性到强阳性表达 ,两组比较 ,差异有显著性 (P <0 .0 5 ) ;leptinmRNA和蛋白在PCOS患者子宫内膜的表达与对照组相似 ,两组比较 ,差异无显著性 (P >0 .0 5 )。结论　促排卵周期中 ,Ob RL 在PCOS患者着床期子宫内膜腺体表达减弱 ,可能与PCOS患者妊娠率低有关     

近排卵期高回声子宫内膜及干预对子宫内膜异位症患者体外受精结局的影响

目的:评价近排卵期高回声子宫内膜及干预对子宫内膜异位症(内异症)患者体外受精(IVF)结局的影响。方法:内异症性不孕患者142例(147个周期),IVF前阴道B超监测自然周期子宫内膜,以近排卵期出现高回声子宫内膜患者为研究组,根据是否干预内膜再分成干预组(39例,42个周期)和未干预组(19例,19个周期);以内膜形态正常患者为对照组(84例,86个周期)。分析3组IVF结局。结果:干预组种植率及临床妊娠率高于未干预组及对照组(P<0.05);未干预组种植率低于对照组(P<0.05),临床妊娠率低于对照组(分别为15.8%及36.0%),但差异无统计学意义;干预组与未干预相比,HCG日内膜异常形态比率显著降低(P<0.05);干预组与对照组相比,HCG日内膜异常比率高,A型内膜比率低,B型内膜比率显著升高(P<0.05);未干预组与对照组相比,HCG日异常内膜比率高,A型及B型内膜比率低(P<0.05)。结论:内异症患者自然周期近排卵期出现高回声子宫内膜可降低IVF种植率及临床妊娠率,干预后可改善内膜形态及IVF结局。     

NGF及其受体trkA及p75NTR在子宫内膜异位症患者在位内膜中的表达及其与内异症疼痛的关系

目的:研究子宫内膜异位症(内异症)患者在位内膜神经生长因子(NGF)及其受体trkA、p75NTR的表达,探讨上述因子与内异症疼痛的关系。方法:选择就诊于北京协和医院并进行了腹腔镜手术的28例子宫内膜异位症患者作为研究组,非子宫内膜异位症患者10例作为对照组(B组),收集上述患者分泌期在位子宫内膜。根据患者有无痛经,分为内异症疼痛组(A1组,18例)及内异症非疼痛组(A2组,10例)。采用免疫组化比较各组病灶中NGF及其受体trkA、p75NTR的表达,并分析其与痛经的关系。结果:各组在位内膜腺上皮中NGF的表达显著高于间质(P<0.05);内异症疼痛组腺上皮NGF表达较非疼痛组明显升高(359.9±18.7 vs 201.3±34.3,P<0.05)。p75NTR主要在子宫内膜间质细胞中表达;内异症组明显高于非内异症组(58.8±21.1、22.5±16.1 vs 0,P<0.05);内异症疼痛组较非疼痛组p75NTR表达明显升高(58.8±21.1 vs 22.5±16.1,P<0.05)。trkA在非内异症组子宫内膜间质中表达明显高于腺上皮(P<0.05);在内异症组腺上皮中,trkA的表达较非内异症组明显增高(P<0.05);trkA的表达量与内异症患者疼痛无关。结论:p75NTR可能参与内异症的发病,NGF及其受体p75NTR在在位内膜中的表达与患者疼痛相关,表明其可能参与了内异症疼痛发病机制。     

不同雄激素水平PCOS患者诱导排卵临床结局分析

目的:探讨多囊卵巢综合征(PCOS)患者在不同雄激素水平下诱导排卵的临床妊娠结局。方法:PCOS合并不孕患者352例,根据诱导排卵前基础睾酮(T)水平分为4组:A组60例,基础T正常,直接诱导排卵;B组64例,基础T正常,但仍给予达英-35治疗3个周期后诱导排卵;C组120例,基础T升高,给予达英-35治疗3个周期,复查T正常后诱导排卵;D组108例,基础T升高,给予达英-35治疗3个周期,复查T仍高于正常水平,经患者知情同意后,诱导排卵。比较4组子宫内膜厚度、尿促性素(HMG)用量、周期排卵率、临床妊娠率、流产率的差异。结果:4组子宫内膜厚度、排卵周期临床妊娠率组间比较差异无统计学意义(P>0.05);A组HMG用量最多,周期排卵率、总临床妊娠率最低,与其它3组的差异均有统计学意义(P<0.01,P<0.01,P<0.05);B、C、D组间周期排卵率、总妊娠率比较差异无统计学意义(P>0.05)。A组早期流产率最高,但4组间比较差异无统计学意义(P>0.05)。结论:基础T水平正常的PCOS患者,诱导排卵前应用口服避孕药治疗可改善临床妊娠结局;口服避孕药治疗后T未降至正常水平,且有生育要求的PCOS患者可试行诱导排卵治疗。     

多囊卵巢综合征患者子宫内膜病理改变及雌,孕激素受体测定

目的观察多囊卵巢卵巢综合征（ＰＣＯＳ）患者子宫内膜病理改变及雌激素受体（ＥＲ）、孕激素受体（ＰＲ）改变。方法对３９例ＰＣＯＳ患者进行子宫内膜病理检查,采用免疫组化方法测定子宫内膜ＥＲ及ＰＲ,并以正常妇女作为对照。结果３４例（８７．２％）ＰＣＯＳ患者子宫内膜呈无排卵型,内膜增殖症发生率为５１．３％（２０／３９）,内膜腺体发育不同步为３５．９％（１４／３９）,内膜间质反应不良为４６．２％（１８／３９）。ＰＣＯＳ患者子宫内膜增殖期ＥＲ、ＰＲ较正常妇女增多（Ｐ＜０．０５）,内膜增殖症者间质ＰＲ减少（Ｐ＜０．０５）且分布不均匀。结论ＰＣＯＳ患者子宫内膜的病理改变和局部ＥＲ、ＰＲ减少或缺乏,可能是不孕的原因之一。     

Fhit和ki-67在子宫内膜异位症的表达及意义

目的:通过观察脆性组氨酸三联体Fhit和细胞核增殖抗原ki-67在子宫内膜异位症的表达,探讨Fhit和ki-67在子宫内膜异位症发病中的作用。方法:用免疫组化SP法检测58例子宫内膜异位症(EMS)患者的异位内膜和在位内膜及15例子宫肌瘤患者子宫内膜(对照组)Fhit和ki-67的表达。结果:Fhit主要在腺上皮细胞的胞浆和胞膜表达,其表达强弱顺序为:对照组子宫内膜>EMS组在位内膜>EMS组异位内膜,EMS在位和异位内膜Fhit表达在增生期和分泌期无统计学差异(P>0.05);EMS组在位内膜的Fhit表达在临床r-AFS不同分期中无统计学差异(P>0.05),但异位内膜的Fhit表达在临床r-AFS不同分期中差异显著。ki-67主要在腺上皮细胞的胞核和胞膜表达,EMS在位内膜和对照组子宫内膜增生期ki-67表达均显著强于分泌期,EMS异位内膜腺体中ki-67表达在增生期和分泌期无统计学差异(P>0.05);EMS组异位内膜腺体ki-67表达在增生期弱于自身在位内膜(P<0.01),但分泌期强于其自身在位内膜(P<0.01)。EMS异位内膜腺体Ⅰ~Ⅱ期的ki-67表达高于Ⅲ、Ⅳ期,但在位内膜ki-67表达在不同临床分期中无统计学差异(P>0.05)。结论:Fhit和ki-67可能与子宫内膜异位症有关。     

Deregulation of tissue homeostasis in endometria from patients with polycystic ovarian syndrome with and without endometrial hyperplasia

OBJECTIVE: To study the proteins involved in endometrial homeostasis in PCOS women. METHODS: Protein expression of Ki67, Bcl-2, Bax, Pro-Caspase-3 and Caspase-3 by immunohistochemistry and/or Western blot, and DNA fragmentation using in situ 3'-end labeling of apoptotic cells, was measured in 9 samples of normal endometrium (NE), 12 PCOS endometria without treatment (PCOSE), 7 endometria from PCOS women with endometrial hyperplasia (HPCOSE) and 9 endometria from patients with endometrial hyperplasia (HE). RESULTS: Cell proliferation was higher in epithelium from PCOSE (P<0.05), HPCOSE and HE vs NE. A higher Bcl-2/Bax relative ratio in PCOSE and HPCOSE was observed, in absence of active Caspase-3 and scarce DNA fragmentation in the four groups of endometria studied. CONCLUSION: As the apoptosis was scarce in all of the groups studied, endometrial homeostasis deregulation in PCOS could be a result of increased proliferation. Therefore, the onset of endometrial hyperplasia in PCOS endometrium could be linked to inadequate cell proliferation, and concomitantly to inadequate cell survival.     

Apoptosis and Ki-67 expression in adenomyotic lesions and in the corresponding eutopic endometrium.

OBJECTIVE: To examine biologic and proliferative properties of adenomyotic lesions and to determine whether adenomyotic lesions originate in the basal layer of the eutopic endometrium. METHODS: We examined eutopic and ectopic endometria from 23 patients with adenomyosis. To obtain evidence for the induction of programmed cell death, apoptotic cells were identified using a modified terminal deoxynucleotidyltransferase-biotin nick end-labeling method. To evaluate cell death repressor activity, bcl-2 gene expression was examined using immunohistochemical staining. As a proliferative marker, Ki-67 expression was also examined immunohistochemically. RESULTS: In the eutopic endometrium, apoptosis was most frequently observed in epithelial cells during mid- to late secretory phases, although it was rarely found during early proliferative through early secretory phases (P<.01). In contrast, bcl-2 gene expression inversely correlated with the appearance of apoptosis. A similar tendency was observed in stromal cells. In the ectopic endometrium of adenomyosis, endometrial dating revealed that secretory change was rare, even in the secretory phase, and that induction of apoptotic cells as well as bcl-2 gene expression showed no cyclic change. In stromal cells of the ectopic endometrium, apoptosis was more frequent than was seen in the eutopic endometrium, in all menstrual phases (P<.05). Ki-67 was constantly expressed in the glandular epithelium of the ectopic endometrium, irrespective of the menstrual phases, whereas in the secretory phase it was less expressed in the eutopic endometrium of functional and basal layers (P<.01). CONCLUSION: The induction of apoptosis seems to be regulated by hormonal changes in the eutopic endometrium and has an inverse correlation with bcl-2 gene expression. The ectopic endometrium in adenomyosis is rarely influenced by hormonal change and has different biologic and proliferative properties than events observed in the eutopic endometrium findings, which strongly suggest that the adenomyotic lesion does not originate in the basal endometrium.     

Expression of steroid receptors, Ki-67, and epidermal growth factor receptor in tamoxifen-treated endometrium.

Endometrial specimens of 34 (25 premenopausal and 9 postmenopausal) breast cancer patients receiving tamoxifen were immunohistochemically examined using estrogen receptor (ER), progesterone receptor (PR), Ki-67, and epidermal growth factor receptor (EGFR) antibodies. Proliferative (n = 6), secretory (n = 9), and postmenopausal (n = 6) endometria served as controls. The ER and PR expressions of the glandular cells in tamoxifen-treated patients did not differ from those of the glandular cells in the control women regardless of menopausal status. The Ki-67 index of glandular cells in tamoxifen-induced amenorrheic women was found to be lower than that of the proliferative glandular cells in the control women (p < 0.03), whereas the Ki-67 index of glandular cells in the tamoxifen-treated postmenopausal patients was higher than that of the glandular cells in the control women (p < 0.02). No EGFR overexpression was found in the glandular cells of the tamoxifen-treated premenopausal patients, but expression of EGFR was high in glandular cells of the tamoxifen-treated postmenopausal patients associated with a high Ki-67 index. In competition with ovarian estrogen secretion, tamoxifen may have an antiestrogenic effect on the endometrium, but tamoxifen probably has an estrogenic effect in the absence of ovarian estrogen secretion. This estrogenic effect of tamoxifen may be associated with an EGFR autocrine system.     

育龄期功能失调性子宫出血患者子宫内膜组织中雌、孕激素及其受体的变化与意义

目的:研究育龄期功能失调性子宫出血患者子宫内膜组织中雌、孕激素及其受体的变化。方法:随机采集2005年8月至2006年11月北方学院附属第一医院妇产科门诊育龄期功血35例患者的静脉血及子宫内膜功能层组织为研究组,以20例月经正常健康女性排卵后期标本为对照组。(1)采用放免法测定研究组及对照组血清及子宫内膜组织中雌二醇(E2)、孕激素(P)的含量;(2)HE染色后对子宫内膜进行组织学诊断;(3)用TUNEL原位标记技术精确测定子宫内膜功能层细胞凋亡指数;(4)用免疫组化法检测子宫内膜中雌、孕激素受体(ER、PR)的表达。结果:育龄期功血患者以排卵型为主(30/35),其子宫内膜组织中E2含量高于对照组(P<0.05),而P含量低于对照组(排卵后期的子宫内膜),二者差异有统计学意义(P<0.05);两组血清中E2、P差异无统计学意义(P>0.05),但血清、子宫内膜中E2和P呈正相关(rE2=0.74,PE2<0.01;rP=0.65PP<0.01);育龄期功血患者子宫内膜中ER、PR表达及凋亡指数较对照组显著增高,差异有统计学意义(P<0.01)。结论:育龄期功血绝大多数可能系体内作用于子宫内膜的雌、孕激素产生的时间、数量及其受体比例失衡所致,细胞凋亡也参与了功血的发生。     

多囊卵巢综合征患者并发子宫内膜增生症的临床研究

目的:探讨多囊卵巢综合征(polycystic ovary syndrome,PCOS)患者并发子宫内膜增生症(endometrial hyperplasia,EH)的患病率、病理类型、高危因素及超声检查在筛查该并发症的作用和临床转归。方法:根据是否合并EH将440例PCOS患者分为组1(合并EH组,n=18)和组2(非EH组,n=422),比较2组的一般特征、月经失调的类型、超声指标、生殖内分泌激素和糖代谢,随访治疗后子宫内膜的病理改变。结果:PCOS患者并发EH的发病率为4.1%,简单型和复杂型17例(94.44%),不典型1例(5.45%);月经失调类型中,表现为功血者发生EH的风险大于其它类型月经失调(P<0.01,拟然比为21.47),表现为月经稀发继发闭经者发生EH的风险小于其它类型月经失调(P<0.05,拟然比6.282)。组1的年龄及相应病程大于组2(28.82±6.80岁vs23.05±5.32岁,12.42±7.13年vs7.28±5.65年,P<0.01);组1的子宫内膜厚度大于组2(11.75±4.77mmvs7.72±3.14mm,P<0.01),组1子宫内膜异常回声高于组2(100%vs0.47%,P<0.01),子宫动脉的搏动指数和阻力指数低于组2(1.68±0.54vs2.85±1.98,0.77±0.08vs0.88±0.27,P<0.01);两组FSH、LH、LH/FSH、总睾酮和游离雄激素指数的差别没有统计学意义,但组1的性激素结合蛋白低于组2(82.94±41.80mmol/Lvs128.17±117.21mmol/L,P<0.01);两组空腹胰岛素、胰岛素释放试验的曲线下面积、空腹血糖、葡萄糖耐量试验的曲线下面积和稳态模型的胰岛素抵抗指数的差异无统计学意义(P>0.05);治疗后子宫内膜均转化为正常。结论:PCOS患者合并EH的临床转归良好,超声检查在PCOS患者并发EH筛查中有重要作用。     

Expression of replication-licensing factors MCM2 and MCM3 in normal, hyperplastic, and carcinomatous endometrium: correlation with expression of Ki-67 and estrogen and progesterone receptors.

Minichromosome maintenance (MCM) proteins are essential for cell cycling due to their function as replication-licensing factors. The aim of the present study was to investigate the clinicopathologic implications of the MCM2 and MCM3 in endometrial carcinogenesis. The authors investigated the immunohistochemical expression of MCM2 and MCM3, Ki-67, estrogen receptor, and progesterone receptor in 23 normal endometria, 9 endometrial hyperplasias, and 60 endometrial carcinomas. In the normal endometrial glands, the expression of MCM2 and MCM3 was significantly higher in the proliferative phase than in the secretory phase and was strongly correlated with Ki-67 expression. Similar correlation between the expression of MCMs and Ki-67 was also found in endometrial hyperplasia. In endometrial carcinomas, however, the expression of MCM2 and MCM3 was significantly lower than that in the normal proliferative endometrium. There was only a weak correlation between MCM2 and Ki-67, and no significant correlation between MCM3 and Ki-67 expression. These findings suggest that the expression of MCM2 and MCM3 directly reflects cell proliferation in normal and hyperplastic endometria. In endometrial carcinomas, however, there is a discrepancy between the expression of MCMs and cell proliferation, suggesting that the replication-licensing system may be aberrant in endometrial carcinomas.     

曼月乐对子宫内膜异位症患者在位内膜增殖与凋亡的影响

目的:从增殖与凋亡的角度探讨左炔诺孕酮宫内节育系统(曼月乐)防治子宫内膜异位症的作用机理。方法:采集中、重度子宫内膜异位症患者放置曼月乐前后的在位内膜,以透射电镜观察细胞形态,TUNEL法检测细胞凋亡率,免疫组化法检测Ki-67的表达。结果:放置曼月乐后,在位内膜腺体细胞Ki-67表达为阴性,凋亡率由24.4±35.0%升高至51.0±37.8%(P=0.027);间质细胞Ki-67的免疫组化HSCROE评分由2.0±1.2降至1.5±0.9(P=0.001),凋亡率由35.3±30.2%升高至76.4±11.2%(P=0.008)。结论:曼月乐能显著抑制内异症患者在位内膜的增殖并诱导凋亡,从而减少通过经血逆流进入腹腔的活性细胞数量,达到防止异位种植的效果。