子宫角妊娠18例临床分析

目的　提高对子宫角妊娠的早期诊断水平。方法　回顾性分析我院二十年间收治的 18例子宫角妊娠病例 ,总结其临床表现、诊断、处理。结果　子宫角妊娠占同期异位妊娠的 1.5 6%,术前确诊率为 44 .44 %,易误诊为流产、输卵管妊娠。结论　认为血 β -HCG、B超及腹腔镜检查对本病的早期诊断有重要意义 ,避免了如子宫破裂、胎盘滞留等严重并发症     

Dual repressive effect of angiotensin II-type 1 receptor blocker telmisartan on angiotensin II-induced and estradiol-induced uterine leiomyoma cell proliferation

BACKGROUND: Although uterine leiomyomas or fibroids are the most common gynecological benign tumor and greatly affect reproductive health and well-being, the pathophysiology and epidemiology of uterine leiomyomas are poorly understood. Elevated blood pressure has an independent, positive association with risk for clinically detected uterine leiomyoma. Angiotensin II (Ang II) is a key biological peptide in the renin-angiotensin system that regulates blood pressure. METHODS: In this study, we investigated the potential role of Ang II (1-1000 nM) in the proliferation of rat ELT-3 leiomyoma cells in vitro. RT-PCR and western blot analysis with cell proliferation and DNA transfection assays were performed to determine the mechanism of action of Ang II. RESULTS: Ang II induced ELT-3 leiomyoma cell proliferation (P < 0.01) and the expression of Ang II type 1 receptor (AT(1)R) and AT(2)R mRNA and protein was confirmed. Regarding the intracellular signaling pathway, the Ang II-induced cell proliferation was AT(1)R-, epidermal growth factor receptor-, extracellular-regulated kinase- and protein kinase C-dependent but was not dependent on the AT(2)R or phosphatidylinositol-3 kinase or JAK kinase. The AT(1)R blocker telmisartan, effectively repressed Ang II-induced and estradiol-induced cell proliferation (P < 0.01). AT(1)R, but not AT(2)R, plays a role in Ang II-induced ELT-3 cell proliferation. CONCLUSIONS: These experimental findings in vitro highlight the potential role of Ang II in the proliferation of leiomyoma cells.     

Correlations between reduced expression of the metastasis suppressor gene KAI-1 and accumulation of p53 in uterine carcinomas and sarcomas

Kangai (KAI)-1 (CD82) is a metastasis suppressor gene, which belongs to the family of tetraspanin proteins. A loss of KAI-1 expression is associated with the advanced stages of many human malignancies. The present study was designed to investigate the expression pattern of KAI-1 in the normal endometrium and uterine tumors and to correlate it with the expression of tumor suppressor protein p53. KAI-1 could be found in the normal endometrium throughout the menstrual cycle. Thirteen of 42 endometrial carcinomas demonstrated moderate KAI-1 expression, but low expression of p53. Twenty-nine of 42 endometrial carcinomas showed reduced or absent KAI-1 expression, which correlated with strong expression of p53 (p < 0.001). There were significant correlations between KAI-1 expression and histological type, e.g., 93% of endometrioid carcinomas displayed a low or moderate immunostaining for KAI-1, whereas nearly all of the serous/clear cell carcinomas were KAI-1 negative (p < 0.001); tumor grading, e.g., 73% of high grade tumors showed no KAI-1 expression (p < 0.001). Most of the investigated uterine sarcomas were negative for KAI-1, whereas they displayed a strong immunostaining for p53. In conclusion, KAI-1 and p53 show inverse expression. The reduced KAI-1 expression may be the result of dysregulated p53 function and could be an important step in the endometrial carcinogenesis.     

Peutz–Jeghers syndrome-associated atypical mucinous proliferation of the uterine cervix: A case of minimal deviation adenocarcinoma (‘adenoma malignum’) in situ

We describe a case of a non-invasive precursor of minimal deviation adenocarcinoma (MDA) of the uterine cervix, associated with Peutz–Jeghers syndrome (PJS). A 27-year-old woman, who had been followed for PJS, was referred to the gynecology clinic. Colposcopic examination demonstrated a small polypoid lesion in the transformation zone. Microscopic examination of the biopsy specimen demonstrated papillary proliferation of the mucinous epithelium with bland nuclear morphology. Conization revealed lobular endocervical glandular hyperplasia (LEGH) with distinct nuclear anaplasia, as well as papillary proliferation of the mucinous epithelium with mild to moderate nuclear abnormalities. This case suggests that the incipient phase of PJS-associated MDA is related to atypical LEGH (“MDA in situ”), and indicates the importance of early screening and surveillance by gynecologists in cases of PJS to detect cervical adenocarcinomas.     

Gestrinone inhibits growth of human uterine leiomyoma may relate to activity regulation of ERα, Src and P38 MAPK

The study was to investigate the effect of gestrinone on the growth of human uterine leiomyoma cells and on the levels and activity of p38, Src and estrogen receptor alpha (ERα). Human uterine leiomyoma cells were cultured and treated with dimethylsulfoxide (DMSO) or a gestrinone concentration gradient. Morphological changes were observed and apoptosis was evaluated. Levels of p38 and phosphorylated-p38 (pp38) were assayed by enzyme-linked immunosorbent assay (ELISA). Levels of ERα and Src were analyzed using real-time RT-PCR and Western blotting. The result showed that gestrinone significantly inhibited the growth of cultured human uterine leiomyoma cells in a concentration- and time-dependent manner, with a 50% inhibitory concentration (IC₅₀) value and corresponding 95% confidence intervals (CI) of 43.67 (23.46∼81.32), 27.78 (12.51∼61.68) and 15.25 (7.17∼32.43) μmol/L at 20, 40 and 60 h, respectively. Compared with control-treated leiomyoma cells, gestrinone significantly reduced both the expression of ERα (P < 0.05) and the levels of phospho-Ser167-ERα (P < 0.05). Gestrinone also markedly suppressed the level of phospho-Tyr416-Src (P < 0.05). Moreover, gestrinone significantly increased the ratio of phospho-p38/p38 mitogen-activated protein kinase (MAPK) (P < 0.05). However, no significant increase in apoptosis or cell cycle arrest was observed (P > 0.05) in response to the tested concentrations of 0.1 to 3.0 μmol/L. As a conclusion, gestrinone suppresses the proliferation of uterine leiomyoma cells mainly by regulating the activity of ERα/Src/p38 MAPK in a concentration-dependent manner at a low concentration of 0.1∼3.0 μM, but not significantly regulating apoptosis. Gestrinone opposes the growth of uterine leiomyoma through multiple genes.     

Role of the purinergic system in patients with cervical intraepithelial neoplasia and uterine cancer

Introduction

Cervical cancer remains the second leading cause of death among women. Intraepithelial neoplasias and uterine invasive cancer are frequently associated with disturbances in coagulation and changes in the concentrations of adenine nucleotides. This work intended to analyze changes in extracellular adenine nucleotide hydrolysis and blood platelet aggregation in patients diagnosed for cervical intraepithelial neoplasia in different stages as well as uterine invasive cancer.

Patients and methods

NTPDase, E-NPP, 5′-nucleotidase, total ADA and its isoforms (ADA1 and ADA2), as well as the platelet aggregation from patients with different stages of cervical intraepithelial neoplasia (NICs I, NIC II, NIC III) and uterine invasive cancer were verified.

Results

Neither ATP hydrolysis nor E-NPP activity was changed by the neoplasia stage. On the other hand, ADP and AMP hydrolysis as well as ADA activity were enhanced in NIC I group. AMP hydrolysis was also increased in the cancer group. ADA 1 was the ADA isoform found in platelets from both control and patient groups.

Conclusion

Our results showed for the first time that NTPDase, 5′-nucleotidase, E-NPP and ADA are not sensible regarding the grade of neoplasia development, since no significant difference was found between the groups studied. Only ADP hydrolysis and ADA activity showed a significant enhancement in NIC I group related to the other stages possibly as a result of the beginning of the neoplasic transformation. This increase could be reflecting a body's reaction against the probable high adenosine levels. We propose for the first time that the ADA isoform present in platelets is ADA 1.     

血卟啉单甲醚对人宫颈癌Hela细胞体外影响的研究

目的:初步探讨血卟啉单甲醚(hematoporphyrin monomethyl ether,HMME)介导的光动力疗法(HMME-PDT)对体外培养的人宫颈癌Hela细胞的杀伤效应及影响宫颈癌细胞光动力疗法(photodynamic therapy,PDT)杀伤效应的主要因素。方法:通过采用不同光敏剂浓度、光照能量密度及细胞孵育时间介导的光动力作用于人宫颈癌Hela细胞,MTT法检测24h后的细胞生长抑制率。结果:光敏剂浓度<2.5μg/mL的不同组细胞生长抑制率有明显差异,光照能量密度≥1.5J/cm2及孵育时间≥4h的细胞之间生长抑制率差异无统计学意义。HMME 2.5μg/mL、光照能量密度1.5J/cm2和孵育时间≥4h可能是PDT对Hela细胞杀伤作用的最佳参数。结论:特定光源下,光敏剂的浓度、光照剂量及孵育时间是影响HMME-PDT效应的主要因素。     

一例瘢痕妊娠行子宫动脉栓塞术后即行清宫术的护理

剖宫产子宫瘢痕妊娠(CSP)是指胚胎种植于子宫下段剖宫产复旧后子宫峡部瘢痕处的一种特殊而罕见的异位妊娠.一旦明确诊断,应立即选择适当的方法终止妊娠,以避免出现难以控制的阴道大出血.子宫动脉栓塞术( UAE)治疗子宫切口瘢痕妊娠具有安全性高、并发症少、止血迅速、恢复快且微创等优点,既保留了子宫的完整性,又保留其生育功能[1].我院于2011年9月对1例剖宫产后瘢痕妊娠患者,行子宫动脉栓塞术后即行清宫术治疗,经精心护理,效果满意.现将围术期护理体会报告如下.     

子宫动脉介入栓塞术治疗子宫动静脉瘘的观察及护理

目的 讨论子宫动脉介入栓塞术治疗子宫动静脉瘘的护理.方法 回顾分析2005年12月～2010年3月我院妇产科6例子宫动静脉瘘患者的临床资料(6例患者全部接受选择性子宫动脉介入栓塞术),包括患者首诊症状、婚育史、确诊依据、手术过程、术前术后护理及随访情况.结果 选择性子宫动脉介入栓塞术治疗子宫动静脉瘘,可以保留患者的子宫,优于传统的子宫切除术.结论 正确了解子宫静脉瘘并提供及时有效的护理,对促进病人的康复具有重要的临床意义.     

探讨高强度聚焦超声消融后残余子宫肌瘤组织转归的机制

目的分析超声消融对靶区外不同位点子宫肌瘤组织雌、孕激素受体以及芳香化酶的表达情况,探讨残余子宫肌瘤的转归的可能机制。方法采用MR引导下高强度聚焦超声(HIFU)肿瘤治疗系统消融8个子宫肌瘤,声功率400W,辐照时间60s,以MR检测靶区外子宫肌瘤组织的升温情况。治疗前取1cm×1cm子宫肌瘤组织为对照组。辐照完毕后取靶区外0.5cm、1.0cm、1.5cm处子宫肌瘤组织。以免疫组化法检测超声消融靶区边缘雌、孕激素受体及芳香化酶(P450酶)的表达,以Western-blot半定量检测P450酶蛋白表达水平。结果靶区周围肌瘤组织温度也有不同程度升高,并且靶区外位点的温度逐渐降低。与对照组比较,靶区外肌瘤组织雌、孕激素受体表达均无明显改变。免疫组化及Western-blot半定量结果显示P450酶蛋白在靶区外0.5cm、1.0cm的表达明显低于对照组(P<0.05)。结论超声消融部分子宫肌瘤后,在一定范围内的残余子宫肌瘤的生长会被抑制,其机制与温度影响P450酶的蛋白表达有关。