Ovarian cancer (OC) is a highly aggressive malignancy with poor prognosis and limited response to immunotherapy. Ribosomal stress, a cellular response to disrupted ribosome biogenesis, has been increasingly implicated in tumorigenesis and immune regulation, yet its contribution to OC remains unclear. We integrated four GEO transcriptomic datasets and identified ribosomal stress related signature genes (RSRGs) through differential expression and functional enrichment analyses. To construct a robust diagnostic model, three machine learning algorithms: LASSO regression, support vector machine recursive feature elimination (SVM-RFE), and random forest were combined. Immune infiltration patterns were evaluated using CIBERSORT, and interpretability analysis was performed using SHAP to determine feature importance. Functional validation of BMP6 was performed in ovarian cancer cell lines by RT-qPCR, Western blot, CCK-8, colony formation, and Transwell assays to evaluate its effects on proliferation, migration, and invasion. A total of 117 differentially expressed RSRGs were identified, mainly enriched in cytoskeletal regulation, lipid metabolism, proteoglycan signaling, and IL-17 mediated inflammatory pathways. The integrated machine learning approach identified six feature genes (SPP1, MAPK13, LCN2, JUP, DSP, and BMP6). SHAP analysis revealed that SPP1 and DSP had the greatest contributions to the predictive model. Immune profiling revealed increased macrophage M0/M2 and decreased CD8 + T cell infiltration in high-risk samples, with SPP1, MAPK13, and DSP positively correlated with macrophage abundance. Functional assays demonstrated that BMP6 was downregulated in ovarian cancer cells and that its overexpression significantly inhibited proliferation, migration, and invasion. This study identifies a six-gene ribosomal stress signature linking tumor intrinsic pathways and immune remodeling in OC. BMP6 exerts tumor-suppressive effects, supporting the potential of targeting ribosomal stress and its immune axis as a therapeutic strategy in ovarian cancer. Machine learning, based integration of multi-dataset analysis identified six ribosomal stress related genes (SPP1, MAPK13, LCN2, JUP, DSP, and BMP6) as diagnostic biomarkers for ovarian cancer. Functional validation of BMP6 demonstrates its tumor-suppressive role by inhibiting ovarian cancer cell proliferation, migration, and invasion. Ribosomal stress pathways intersect with IL-17 signaling and metabolic remodeling, linking nucleolar dysfunction to immune evasion and tumor progression in ovarian cancer.

Granulosa Cell Tumors (GCT) of ovary is a malignant tumor originating from sex cord stromal cells.

Objective: The aim of this study was to investigate the role of metformin in reversing the chemoresistance of ovarian cancer and the underlying mechanism. Material and Methods: The expression of E-cadherin、 vimentin and p-Akt in A2780 and A2780/DDP cells was determined by Western blot. The regulatory effects of metformin on proliferative and apoptosis in A2780/DDP cells were evaluated by the Cell Counting Kit 8 (CCK-8) and the Annexin V-FITC Kit. The expression of E-cadherin、vimentin and p-Akt in different groups of A2780/DDP cells was determined by Western blot. Results: The expression levels of E-cadherin were significantly lower in A2780/DDP cells than in A2780 cells (p<0.05); in contrast, the expression levels of vimentin and p-Akt were significantly higher (p<0.05). The combination of metformin and cisplatin reduced cell viability compared with cisplatin treatment only. However, the combination of cisplatin and metformin had no effect on apoptosis in A2780/DDP cells. In addition, cisplatin was shown to induce EMT in A2780/DDP cells (p<0.05), while the combination of metformin and cisplatin reversed EMT. Cisplatin was also shown to increase the expression levels of p-Akt in A2780/DDP cells (p<0.05), while the combination of metformin and cisplatin reversed the expression of p-Akt. Conclusion: Metformin can sensitize A2780/DDP cells to cisplatin by inhibiting EMT. We hypothesize that the mechanism responsible for this effect involves the inhibition of the Akt signaling pathway

目的 探讨无举宫的腹腔镜下广泛子宫切除术在早期宫颈癌的临床应用价值.方法 选取确诊早期宫颈癌的患者32例,其中IA2期18例,IB1期14例.采用无举宫器的腹腔镜下子宫广泛切除及盆腔淋巴切除术.结果 手术均获成功,术中无血管、输尿管、膀胱及肠管损伤,手术时间130 ～ 190 min,平均150 min;出血量为30～200 mL,平均120 mL;术后拔除尿管时间10 ～21 d,平均13 d.所有患者术后随访9 ～24个月,平均14.8个月,复查未发现肿瘤复发转移.结论 无举宫的腹腔镜下广泛子宫切除术及盆腔淋巴切除治疗早期宫颈癌安全可行,为临床应用无举宫的腹腔镜手术提供了一定参考价值.

目的 探讨米非司酮对人早孕绒毛组织中人类白细胞抗原G(HLA-G)表达的影响以及与终止妊娠之间的关系.方法 用免疫组化法和RT-PCR方法分别检测药物流产组和人工流产组绒毛组织中HLA-G的表达水平,结果用平均光密度和光度比值半定量方法进行分析.结果 ①免疫组化结果药物流产组(18例)绒毛组织中HLA-G的免疫组化结果的平均光密度为(0.286 957±0.108 249),人工流产组(15例)绒毛组织中该指标的平均光密度为(0.443 333±0.170 178),两组之间差别有统计学意义(P＜0.01);②RT-PCR结果药物流产组(18例)绒毛组织中HLA-G的平均光度度比值为(0.282 209±0.353 621),人工流产组(15例)该指标的平均光度比值为(1.112 719±0.724 514),两组之间差异有统计学意义(P＜0.01).结论 米非司酮药物可降低早孕绒毛组织中HLA-G的表达,从而抑制妊娠时母胎界面的免疫功能,破坏母体对胎儿组织的阶段性容受,可能是该药物致早孕流产的机制之一.

目的 探讨宁夏地区围绝经期妇女激素替代治疗状况.方法 选取2016年10月-2018年9月宁夏回族自治区人民医院收治的围绝经期综合征患者196例为研究对象,统计记录所有患者基本资料,包括年龄、受教育程度、医疗保险、婚姻、收入水平、职业、月经情况及患有慢性病情况等资料,随访依据患者接受治疗方式分为激素替代治疗组和非激素替代治疗组,分析是否接受激素替代治疗的影响因素.并采用改良Kupperman更年期评分标准评估两组患者治疗前、治疗后病情程度,量表包括失眠、潮热出汗、眩晕、性交痛、感觉异常、皮肤蚁走感、焦虑烦躁、抑郁、骨关节痛、泌尿系统感染、心悸、头痛及疲乏等内容,各项评分越低表明病情越轻.结果 196例患者中,有124例患者接受激素替代治疗,占63.27％;72例患者接受非激素替代治疗,占36.73％.治疗后,激素替代治疗组失眠、潮热出汗、眩晕、性交痛、感觉异常、皮肤蚁走感、焦虑烦躁、抑郁、骨关节痛、泌尿系统感染、心悸、头痛、疲乏评分及总分均较低于非激素替代治疗组(P＜0.05).单因素分析结果显示,激素替代治疗组患者在受教育程度、是否参与医疗保险、婚姻状况、家庭收入水平及职业等方面与非激素替代治疗组比较,差异无统计学意义(P＞0.05);激素替代治疗组患者在年龄、月经情况及患有慢性病情况与非激素替代治疗组比较(P＜0.05).多因素Logistic回归分析结果显示,年龄≤60岁、患有慢性病≥2种、绝经及月经不规律是女性接受激素替代治疗的影响因素(OR＞1,P＜0.05).结论 激素替代治疗围绝经期综合征效果确切,患者是否接受激素替代治疗受当前月经状况、自身患有慢性病情况及患者年龄等因素影响.

The rates of caesarean scar pregnancy have increased. An increasing incidence has been considered most likely related to much higher rates of cesarean section. It is a rare and potentially life-threatening complication of pregnancy because of misdiagnosis. Therefore, it is important to train gynecologists and sonographers in timely diagnosis of CSP and management. Here we present one cases of CSP that were treated in our department by uterine artery embolization with methotrexate infusion combined curettage. She was treated successfully by laparotomy because of profuse bleeding 21 days after UAE.

目的 检测子痫前期(PE)孕妇血清及尿液中胎盘生长因子(PIGF)及可溶性血管内皮生长因子受体l,探讨此指标与疾病的关系及对子痫前期的预测价值.方法 将妊娠32～37周的60例PE孕妇为研究组,60例正常妊娠孕妇为对照组,采用酶联免疫吸附法检测各组孕妇血清及尿液中PLGF、可容性酷氨酸激酶(Flt-1)及计算sFlt-1/PLGF值.结果 PE组血清中PLGF(20.6±17.50与151.4±162.3)pg/mL、sFlt-1(930.1±783.9与188.2±60.5) pg/mL及slit-1/PLGF值(46.6±38.0与2.1±1.1)pg/mL,与对照组比较差异有统计学意义(P＜0.05);PE组尿液中PLGF(24.6±10.4与37.2±10.0)pg/mL、sFlt-1(241.6±16.9与188.2±31.6)pg/mL及slit-1/PLGF值(23.0±38.0与5.8±1.8)pg/mL,与对照组比较PLGF及sFlt-1差异均有统计学意义(P＜0.05),但sFlt-1/PLGF值差异无统计学意义(P＞0.05);PE组中血清sFlt-1 (930.1±783.9) pg/mL高于尿液水平(241.6±16.9) pg/mL,差别有统计学意义(P＜0.05).结论 子痫前期孕妇血清中PIGF、sFlt-1水平及sFlt-1/PLGF值与对照组存在差异,尿液中PIGF、sFlt-1水平与对照组存在差异,通过检测孕妇血尿液中的PLGF及sFlt-1水平有望成为预测PE发生的指标,指导治疗并预防疾病的发生.

Purpose of investigation: Leiomyomatosis peritonealis disseminata (LPD) is a special type of leiomyomatosis with an unclear pathogenesis. Materials and Methods: The authors investigated five LPD patients who were treated at the Fudan University Shanghai Cancer Center (Shanghai. China) from 2012 to 2016. They reviewed the medical history, preoperative examination, intraoperative manifestation, and postoperative pathologic results. Results: The five LPD patients were all in reproductive age and four of them had a medical history of laparoscopy for uterine fibroids. Two of them had pathologic results of mitotically active leiomyoma. All the conditions may have contributed to the development of LPD. Conclusion: The use of laparoscopic power morcellation, active proliferative status of the uterine fibroids, and hormone in female patients may help cause LPD. The present study may improve our understanding of the disease.

Rab25, a member of the Rab family of small guanosine triphosphatase, was reported to have an essential role in the development of human epithelial ovarian cancer. The present study demonstrated that Rab25 mediated the sensitivity of ovarian cancer to cisplatin, a first‑line chemotherapeutic agent for the treatment of ovarian cancer in the clinic. Overexpression of Rab25 and increased phosphoinositide 3‑kinase (PI3K)/AKT signaling were detected in cisplatin‑resistant SKOV‑3 cells compared with those in cisplatin‑sensitive ES‑2 cells. The results of the present study indicated that cisplatin resistance was primarily due to reduced G1 cell cycle arrest following cisplatin treatment in SKOV‑3 cells. By contrast, the corresponding phenomenon was not observed following treatment with a Rab25‑specific small interfering RNA or treatment with the PI3K/AKT inhibitor LY294002. Of note, inhibition of the PI3K/AKT pathway reduced Rab25 gene expression and sensitized SKOV‑3 cells to cisplatin. Furthermore, knockdown of Rab25 showed an effect comparable with blocking the PI3K/AKT pathway. In conclusion, the results of the present study demonstrated that PI3K/AKT and Rab25 significantly contributed to cisplatin resistance in human epithelial ovarian cancer; in addition, silencing Rab25 or inhibiting the PI3K/AKT pathway markedly increased the sensitivity of these cells to cisplatin.

This study was to investigate the role of Fas in the development of Cisplatin-resistant ovarian cancer. On the cellular level, Fas expression was significantly reduced in Cisplatin resistant A2780 (A2780/CP) cells compared with A2780 cells. Fas silence with siRNA would promote tumor cell lines proliferation, facilitate tumor cell cycle transition of G1/S, prevent cell apoptosis, and promote cell migration. Expression of drug resistance gene was negatively correlated to Fas. In nude mice metastasis model of human ovarian carcinoma by subcutaneous transplantation, after Ad-Fas injected intratumorly, we found that upregulation of Fas could inhibit transplantation tumor tissue growth and reduce the expression of drug resistance gene. Our results indicated that upregulation of Fas in epithelial ovarian cancer reversed the development of resistance to Cisplatin. In conclusion, our findings suggested that Fas might act as a promising therapeutic target for improvement of the sensibility to Cisplatin in ovarian cancer.

HELLP occurs in 0.5%–0.9% of all pregnancies. About 30% of the cases happen within 48 hours after delivery. Women with postpartum HELLP syndrome have significantly higher incidences of complications. Because of the absence of classical signs of preeclampsia, it can confuse physicians and lead to delay in diagnosis. Therefore, it is associated with serious maternal morbidity. We present two cases of acute postpartum HELLP syndrome after caesarean section following severe preeclampsia. Our cases were successfully managed with the timely diagnosis and therapy.

目的 探讨脂肪酸合成酶(FAS)在卵巢上皮性肿瘤组织中的表达及临床病理意义.方法 免疫组化方法检测38例卵巢浆液性腺癌、32例非卵巢浆液性腺癌(15例卵巢黏液性腺癌,17例子宫内膜样腺癌)、14例卵巢交界性肿瘤、16例卵巢良性组织、20例正常卵巢组织中FAS的表达情况,结合临床病理特征进行统计学分析.结果 FAS在卵巢癌组织中呈高表达,而在卵巢良性肿瘤及正常卵巢组织中仅少量表达或无表达,差异有统计学意义(P＜0.05).与临床分期,组织分化及淋巴结转移之间存在相关性.结论 FAS的表达可能与卵巢上皮性癌的发生、发展密切相关,FAS可望作为卵巢上皮癌治疗的一个新靶点.

目的 探讨病灶切除术在妊娠滋养细胞肿瘤(GTN)治疗中的价值及适应证.方法 对因GTN化疗效果不佳而行局部及转移病灶切除术的5例病例进行回顾性分析.结果 5例病例手术前均经正规、足量化疗治疗达到临床治愈,治疗后6~12个月的随访期间,血HCG再次增高并发现转移性病灶;3例患者行子宫局部病灶切除,2例行肺部转移病灶切除,术后均再次给于2~3疗程的化疗,随访未见复发,效果良好.结论 GTN的治疗对化疗效果不佳者,局部病灶或孤立进行手术切除是一个必要的辅助治疗.

胎儿宫内生长受限( FGR)的发生率为4％～7％,明显增加新生儿在围生期的死亡率(4～6倍)[1].目前胎儿宫内生长受限的发病机理尚不清楚,近年来,胰岛素或胰岛素样生长因子(IGF)及其受体(IGF-R)分泌和功能的失调成为目前研究的重点[2].胰岛素样生长因子在细胞的分化、增殖、个体的生长发育中具有重要的促进作用.并且在妊娠过程中,该类分子水平的异常及其下游信号通路的异常可能导致胎儿宫内生长停滞[3].本研究通过测定分娩正常儿、FGR的产妇胎盘组织中胰岛素样生长因子/丝裂原活化蛋白激酶(IGF/MAPK)信号通路中多种分子蛋白的表达,探讨其与胎儿生长发育之间的关系.

Chemotherapy resistance is a great obstacle for effective treatment of ovarian cancer.Drug resistance of ovarian cancer is the results of combined action of multi- factors.Further study of drug resistancerelated genes can provide new ideas for reversing drug resistance fundamentally. Key words: Ovarian neoplasm, Drug therapy,Cisplatin

The immune tolerance or immune escape plays important roles in the genesis and progression of malignant gynecological neoplasms.Human leukocyte antigen G(HLA-G)is an important member of major histocompatiblity complex class Ⅰ.HLA-G seems to affect almost every aspect of human immunity.It can inhibit immunological function,and play an important role in immune escape of malignant gynecological neoplasms.

Objective To investigate the effect of mifepristone on the function of transforming growth factor β signal transduction in chorionic villi and the molecular mechanism of mifepristone inducing abortion.Methods Early pregnant chorionic villi were obtained from the surgical aspiration group(n=13) and the mifepristone inducing abortion group(n=20).Expression of smad7 which was the targeting gene of the TGF-β/smads signal transduction pathway in chorionic villi was determined by immunohistochemical staining with specific antibody and RT-PCR.Mean opec density and density scale were anzlyzed.Results Mean optic density of Smad7 in chorionic villi in the mifepristone inducing abortion group(0.346 6±0.046 9)was statistically higher than that in the surgical aspiration group(0.2337±0.0657)(P＜0.01).Also,density scale of smad7mRNA in chorionic villi in the mifepristone inducing abortion group(0.561 7±0.410 3) was statistically higher than that in the surgical aspiration group (0.2222±0.2441)(P＜0.02).Conclusion Mifepristone can up-regulate the function of the TGF-β/smads signal transduction pathway and expression of targeted genes,such as plasminogen activator inhibitor 1,affect migration and evasion of tropholast cells,which may be one of the molecular mechanisms for termination of early pregnancy by this drug.

Objective To investigate the relationship between the status of the TGFβR/Smads signal pathway in cancer cells and in its stromal cells,and if this may affect the development of endometrioid adenocarcinoma.Methods TGFβRⅠ,TGFβRⅡ,Smad2,Smad3,Smad4 and Smad7 were determined in hysteromyoma(12 cases) and endometrioid adenocarcinoma(18 cases) by the SP immunohistochemical method.Results TGFβRⅠ,TGFβRⅡ,Smad2,Smad3,Smad4 and Smad7 were found in hysteromyoma.TGFβR expression which was in positive correlation with Smads expression in normal endometrium cells(r=0.86,r=0.78).TGFβR/Smads expression disagreed in endometrial cancer cells and stromal cells and it was not found in stromal cells of endometrial adenocarcinoma per se.Conclusions TGFβR/Smads signals exist in cells of normal endometrial proliferative /secretory phase but its pathway is defected in tumor stroma.To get the information about TGFβR/Smads signal way in stroma probably provides a neotarget for gene therapy of endometrioid carcinoma.