Objective In the testis of Drosophila, spermatogonia transit-amplification (TA) divisions are necessary for germline proliferation and differentiation. Both the germline and the surrounding somatic cyst cells (SCCs) have a significant influence on these processes. However, the underlying mechanism is largely unknown. Methods Flies were used to generate tissue-specific gene knockdown. Immunofluorescence was used to determine protein localization and expression pattern. Small interfering RNAs were used to knockdown genes in S2 cells. qRT-PCR was used to examine the relative mRNA expression level. Results Our findings indicate that spermatogonial RpS13 regulates cyst cell growth through a non-autonomous manner. In terms of mechanism, RpS13 may regulate the adhesion junctions of the soma–germline via the DE-cad and Arm proteins in addition to dpERK, which is found in SCCs. Interestingly, Rho1 and RpS13 mutually inhibit each other in Drosophila S2 cells. Additionally, Rho1 controlled cell adhesions that rely on DE-cad, Arm, and dpERK and imitated the actions of RpS13 in Drosophila testis. Conclusion All of these findings implied that during spermatogonia TA-divisions in the testis of Drosophila, RpS13 regulates the development of cyst cells via Rho1-mediated adhesion junctions. ### Competing Interest Statement The authors have declared no competing interest.

Objective Spermatogenesis is a highly conserved and widespread process in eukaryotes, and Drosophila testes serve as an effective model system for its study. Many well- characterized signaling pathways are crucial for germline differentiation. Wnt proteins play important roles in regulating stem and progenitor cell proliferation and differentiation. In this study, we used the Drosophila model to investigate the function of Wnt6 in germline development. Methods Drosophila strains were maintained under specific conditions. Transgenic RNA interference (RNAi) lines were obtained from relevant sources, and fly crosses were carried out. Immunostaining was performed using specific primary and secondary antibodies, confocal images were acquired and analyzed, and statistical analysis was conducted. Results Knockdown of Wnt6 in early germline cells led to partial loss of germline stem cells (GSCs) and impaired GSC differentiation. Wnt6 regulated the adhesion junctions in the stem cell niche of Drosophila testes, as its knockdown reduced the expression of Arm and Rho1. Wnt6 deficiency in spermatogonia caused Arm- and Rho1- dependent adhesion junction impairment. Rac1 and Cdc42 were essential for GSC maintenance and differentiation, and Wnt6 regulated Rac1- and Cdc42- mediated adhesion junction signals. The loss of Wnt6, Rac1, and Cdc42 in Drosophila testes led to abnormal inactivation of dpERK. Conclusion Wnt6 plays a critical role in regulating GSC differentiation in the stem cell niche of Drosophila testes. Wnt6 regulates GSC self-renewal and differentiation through Rac1- and Cdc42- mediated adhesion junctions, highlighting the crosstalk between Wnt signaling and adhesion junctions. The regulation of germline stem cell self-renewal and differentiation by Wnt6 is closely associated with dpERK signaling. We hypothesize that Wnt6 regulates germ cell differentiation by influencing dpERK signaling through the adhesion junction function mediated by Rac1 and Cdc42.

Background: Mullerian duct anomalies (MDAs) are congenital developmental disorders exhibiting as a variety of malformations of female reproductive tract. The identified etiology of MDAs is limited. The present study aimed to unravel the underlying genetic causes of MDAs. Methods: Rare variants in androgen receptor (AR) were called from the cohort consists of patients with MDAs and underwent whole exome sequencing (WES) at Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China. Sanger sequencing was used to confirm the causative genetic mutations. In silico analysis were used to classify the pathogenicity of each variant. Molecular modeling and simulations were conducted to investigate the conformational changes between the wild-type (WT) and mutant proteins. Results: A total of 3 rare heterozygous variants in AR from the MDAs cohort in our institution were identified, with unknown effects. All variants were missense mutations, including c.173A > T, c.558C > A and c.1208C > T, and were absent or rare in East Asian populations in Genome Aggregation Database and the Exome Aggregation Consortium Database. According to the American College of Medical Genetics and Genomics guidelines, c.1208C > T variant was classified as likely pathogenic, while the other two were variants of uncertain significance. During molecular dynamics simulations, WT and mutant proteins all reached stable status according to rootmean-square variance. Values of radius of gyration showed that Q58L and S186R protein would be more compact than WT, while the structure of A403V became looser. Despite, in comparison with WT, the number of hydrogen bonds increased in Q58L, while decreased in the other two variants. Furthermore, the solventaccessible surface area diminished in Q58L and A403V while enlarged in S186R proteins, when compared with WT. Conclusions: To our knowledge, this is the first report regarding the association of AR mutation and MDAs. The identification of these variants, predicted to damage the structure and function of AR protein, not only expanded the mutational spectrum of causative genes of MDAs, but provide novel molecular genetic reference for future studies.

Intrauterine adhesions(IUAs)are a form of uterine fibrotic scar tissue that develops in response to traumatic injury to the endometrial basal layer.Patients with IUAs can suffer from menstrual abnormalities and various obstetric complications[1].

Cervical cancer is the fourth most common malignancy tumor worldwide with high incidence and mortality. Accumulating evidence indicated that through an m6A-dependent or m6A-independent mechanism, fat mass and obesity associated gene (FTO) exhibits the tumor-promoting and suppressive roles of FTO involved in various cancers, including cervical cancer. This study aims to verify the biological function and potential mechanisms of FTO in cervical cancer cell proliferation, colony formation, migration, and invasion in vitro as well as tumor growth in vivo. Herein, we confirmed that knockdown of FTO inhibits cell proliferation, colony formation, migration, and invasion of cervical cancer cells in vitro via cell counting kit-8 (CCK8) assay, colony formation assay, and transwell migration and invasion assay. The demethylase activity of FTO is required for cell proliferation, colony formation, migration, and invasion of cervical cancer cells in vitro. RNA sequencing, online database analysis, and western blotting revealed that FTO regulated the BMP4/Hippo/YAP1/TAZ pathway. In addition, FTO upregulates the expression of BMP4 in an m6A-dependent manner and binds to the N-terminal of BMP4 to form a dimer at the C-terminal in cervical cancer cells through protein-protein interaction. We further discovered that BMP4 treatment promoted cell proliferation, colony formation, migration, and invasion of cervical cancer cells, and rescue experiments validated that BMP4 treatment reversed the inhibition of FTO knockdown on the Hippo/YAP1/TAZ pathway and the progression of cervical cancer cells in vitro. Notably, the knockdown of FTO significantly suppressed xenograft tumor growth and the protein level of BMP4 in vivo. Collectively, our results demonstrate that the FTO promotes cervical cancer progression in vitro and in vivo via the regulation of the BMP4/Hippo/YAP1/TAZ pathway, suggesting that FTO acts as an oncogenic molecule and the FTO/BMP4 Hippo/YAP1/TAZ axis may serve as valuable targets for cervical cancer treatment.

Background Endometriosis, a common gynaecological disease in women, affects 10% of women of childbearing age. Among infertile women, this proportion is as high as 30–50%. Despite the high prevalence of endometriosis, the pathogenesis of endometriosis is still unclear. Methods In the present study, bioinformatics analysis and molecular and animal experiments were employed to explore the functions of PCGEM1 in the pathogenesis of endometriosis. We established an endometriosis rat model and isolated endometrial stromal cells (ESCs) and primary normal ESCs (NESCs). Bioinformatics analysis was adopted to study the roles of PCGEM1 in promoting the pathogenesis of endometriosis. Luciferase reporter assays and RNA pull-down assays were carried out to study the mechanism by which PCGEM1 regulates ANTXR2. Results Our results indicated that PCGEM1 promoted the motility and proliferation of ectopic endometrial cells, and the underlying mechanism was due to the direct binding of PCGEM1 to miR-124-3p to modulate ANTXR2 expression. Conclusion PCGEM1 can influence endometrial stromal cell proliferation and motility and may be a novel therapeutic target for endometriosis.

目的 对比自体组织修补(native tissue repair,NTR)与经阴道植入网片(transvaginal mesh,TVM)盆底重建治疗盆腔器官脱垂(pelvic organ prolapse,POP)的效果.方法 回顾性分析2018 年1 月～2021 年 10 月症状性重度阴道前壁膨出为主的POP行NTR 32 例和 TVM 47 例的临床资料.NTR 组行阴道前壁修补联合高位骶韧带悬吊术(high uterosacral ligament suspension,HUS),TVM组采用TiLOOP Total 6 套盒网片进行盆底重建.比较2 组手术时间、出血量、围手术期并发症及术后远期并发症.采用盆底不适调查表简表(PFDI-20)评估生活质量,患者整体印象改善评分量表(PGI-I)评估主观满意率.采用复合标准定义手术成功:①脱垂最远端不超过处女膜;②无脱垂症状;③无脱垂再治疗意愿.结果 NTR组较TVM组手术时间更长[(165.5±41.0)min vs.(138.5±28.4)min,t =3.239,P =0.002],2 组出血量及围手术期并发症差异无统计学意义(P>0.05).79 例术后随访12～51 个月,(29.7±11.8)月.NTR组19 例(59.4％)、TVM组41 例(87.2％)完成术后24 个月随访.2 组术后PFDI-20 评分较术前均显著下降(P<0.05),2 组间差异无统计学意义(P>0.05).2 组术后远期并发症包括新发下尿路症状、新发便秘、新发疼痛、缝线暴露发生率均无统计学差异(P>0.05).NTR组术后 9、16 个月前盆腔复发各1 例,TVM组无复发(P =0.161).TVM组术后网片暴露率2.1％(1/47).NTR组与TVM组术后主观满意率无统计学差异[94.7％(18/19)vs.95.1％(39/41),P =1.000],手术成功率无统计学差异[89.5％(17/19)vs 100％(41/41),P = 0.097].2 组均无因并发症导致二次手术.结论 在症状性重度阴道前壁膨出的治疗中,NTR疗效不劣于TVM,在手术并发症方面二者同样安全.

Endometriosis (EMs) is a common gynecological disease with an increasing incidence in recent years. Because of the lack of specific molecular biological indicators in clinical practice, diagnosis is often delayed and the quality of life of patients is seriously reduced. Therefore, the discovery of effective molecular biomarkers is crucial for the early diagnosis and treatment of EMs patients. With the development of high-throughput sequencing technology, the mechanism of lncRNAs in EMs has been increasingly confirmed experimentally. This article summarizes the biological characteristics and functions of EMs-related lncRNAs, and introduces the mechanisms of EMs-related lncRNAs in the context of ceRNAs, in exosomes, under hypoxic conditions, and related antisense RNAs. The mechanism of the most popular imprinted gene H19 and metastasis-associated lung adenocarcinoma transcript 1 in EMs is then introduced. Finally, we explore the challenges of molecular biomarker EMs-related lncRNAs in the diagnosis and treatment of EMs, anticipating their potential value in clinical applications.

目的 探讨改良电刺激模式结合手法按摩治疗产后盆底肌高张的临床疗效.方法 选取2021年2—11月首都医科大学附属北京妇产医院产后盆底肌高张患者60例,采用随机数字表法分为治疗组和对照组,各30例.对照组予盆底肌镇痛解痉电流结合手法按摩治疗;治疗组在此基础上加用脉管平滑肌电刺激及骨盆带肌筋膜触发点镇痛电流治疗.使用盆底表面肌电图检测盆底肌前后静息阶段肌电平均值,视觉模拟评分法评估盆底肌压痛及骨盆带主观疼痛程度.结果 治疗后两组盆底肌前后静息电位、盆底肌筋膜压痛视觉模拟评分、骨盆带主观疼痛视觉模拟评分均较治疗前下降(P<0.05);治疗后治疗组前后静息电位、骨盆带主观疼痛视觉模拟评分低于对照组(P<0.05).结论 改良电刺激模式结合手法按摩治疗盆底肌高张、缓解骨盆带疼痛较传统方案具有优势.

Ovarian endometriosis is a frequently occurring gynecological disease with large socioeconomic impact. Accumulating evidence has suggested that aberrant miRNA-mRNA interactions are involved in the pathogenesis and progression of ovarian endometriosis. This study aims to identify key miRNAs in ovarian endometriosis by using integrated bioinformatic analysis of a dysregulated miRNA-mRNA co-expression network. Expression profiling of miRNA and mRNA in three normal endometria and five pairs of ectopic/eutopic endometria from patients with ovarian endometriosis was determined by high-throughput sequencing techniques. The data were then integrated with the public sequencing datasets (GSE105764 and GSE105765) using a non-biased approach and a miRNA-mRNA co-expression regulatory network was constructed by in-depth bioinformatic analysis. The constructed miRNA-mRNA network included 87 functionally DEMs, 482 target mRNAs and 1850 paired miRNA-mRNA regulatory interactions. Specifically, five miRNAs (miR-141-3p, miR-363-3p, miR-577, miR-767-5p, miR-96-5p) were gradually decreased and two miRNAs (miR-493-5p, miR-592) were gradually increased from normal endometria to eutopic endometria, and then ectopic endometria tissues. Importantly, miR-141-3p, miR-363-3p and miR-96-5p belonged to the miR-200 family, miR-106a-363 cluster and miR-183/96/182 cluster, respectively. Their target mRNAs were mainly associated with cell adhesion, locomotion and binding, which are suggested to play vital regulatory roles in the pathogenesis of ovarian endometriosis. Integrated bioinformatic analysis of the miRNA-mRNA co-expression network defines the crucial roles of the miR-200 family, miR-106a-363 cluster and miR-183/96/182 cluster in the pathogenesis of ovarian endometriosis. Further in-depth functional studies are needed to unveil the molecular mechanisms of these miRNAs, and may provide clues for the optimization of therapeutic strategies for ovarian endometriosis.

INTRODUCTION:Ovarian endometriosis is a frequently occurring gynecological disease with large socioeconomic impact. Accumulating evidence has suggested that aberrant miRNA-mRNA interactions are involved in the pathogenesis and progression of ovarian endometriosis. This study aims to identify key miRNAs in ovarian endometriosis by using integrated bioinformatic analysis of a dysregulated miRNA-mRNA co-expression network.MATERIAL AND METHODS:Expression profiling of miRNA and mRNA in three normal endometria and five pairs of ectopic/eutopic endometria from patients with ovarian endometriosis was determined by high-throughput sequencing techniques. The data were then integrated with the public sequencing datasets (GSE105764 and GSE105765) using a non-biased approach and a miRNA-mRNA co-expression regulatory network was constructed by in-depth bioinformatic analysis.RESULTS:The constructed miRNA-mRNA network included 87 functionally DEMs, 482 target mRNAs and 1850 paired miRNA-mRNA regulatory interactions. Specifically, five miRNAs (miR-141-3p, miR-363-3p, miR-577, miR-767-5p, miR-96-5p) were gradually decreased and two miRNAs (miR-493-5p, miR-592) were gradually increased from normal endometria to eutopic endometria, and then ectopic endometria tissues. Importantly, miR-141-3p, miR-363-3p and miR-96-5p belonged to the miR-200 family, miR-106a-363 cluster and miR-183/96/182 cluster, respectively. Their target mRNAs were mainly associated with cell adhesion, locomotion and binding, which are suggested to play vital regulatory roles in the pathogenesis of ovarian endometriosis.CONCLUSIONS:Integrated bioinformatic analysis of the miRNA-mRNA co-expression network defines the crucial roles of the miR-200 family, miR-106a-363 cluster and miR-183/96/182 cluster in the pathogenesis of ovarian endometriosis. Further in-depth functional studies are needed to unveil the molecular mechanisms of these miRNAs, and may provide clues for the optimization of therapeutic strategies for ovarian endometriosis.

OBJECTIVE:(1) To characterize the cytokine expression profiles of endometriosis related infertile women in comparison to fertile women with endometriosis; (2) to investigate the correlation of the cytokine levels from different tissues. METHODS:100 stage IV endometriosis patients were recruited and grouped by infertility status (n = 50, separately). Concentrations of TNF-α, TGF-β1, IL-10, and IL-17A from the serum, peritoneal fluid (PF), eutopic, and ectopic endometrium samples were measured. RESULTS:(1) In the infertile group, the concentrations of IL-10 within serum, PF and eutopic endometrium were all significantly higher (p = .022 and <.01, .013, respectively), the levels of TGF-β1 in serum and eutopic endometrium samples were both higher (p = .025 and p < .01), the levels of IL-17A in the PF, eutopic, and ectopic endometrium were all lower (p < .01, all). (2) Significant positive correlation was observed between IL-17A from PF and the ectopic endometrium (p = .014), IL-17A from PF and eutopic endometrium (p < .01). The PF IL-10 levels positively correlated with those in the serum (p = .007). CONCLUSIONS:This is the first study comparing the levels of cytokines within four different tissues of endometriosis women with or without infertility. The study revealed that endometriosis-related infertile women possess significant differences in cytokine levels in comparison to fertile women with endometriosis. The levels of inflammatory factors from different tissues had certain positive correlations. Infertility may indicate the progress of the disease.

Objective:To construct a risk nomogram early prediction model for myasthenia gravis (MG) after thymoma resection and to verify the predictive performance of the model.Methods:Using the convenient sampling method, a total of 477 patients undergoing thymoma resection who were admitted to Department of Thoracic Surgery in Beijing Tongren Hospital Affiliated to Capital Medical University from March 2018 to February 2021 were selected as the training set. A total of 62 patients who underwent thymoma resection from March 2017 to February 2018 were set as the validation set for retrospective analysis. The clinical data of the included patients were analyzed. Logistic regression analysis was used to explore the independent risk factors of MG after thymoma resection and a risk nomogram prediction model was constructed.Results:The incidence of postoperative MG in 477 patients who underwent thymoma resection was confirmed by chest X-ray, CT and related tests, which was 14.05% (67/477) . There were statistical differences between the two groups of patients with MG and those without MG in terms of combination of immune diseases, preoperative course of disease, surgical route, complete tumor resection, WHO pathological classification, postoperative pulmonary infection, postoperative radiotherapy and chemotherapy and other data ( P<0.05) . Logistic regression analysis showed that combined immune disease, thoracotomy, incomplete tumor resection, WHO pathological classification of A+AB, postoperative pulmonary infection and no postoperative chemoradiotherapy were independent risk factors for MG after thymoma resection ( P<0.05) . Based on 6 independent risk factors, a risk nomogram prediction model of MG after thymoma resection was established. The results showed that the C- index of the training set and the validation set were 0.837 (95% CI: 0.807-0.867) and 0.817 (95% CI: 0.807-0.867) , respectively. The calibration curves for both sets showed good fit to the ideal curve, with areas under the receiver operating characteristic curves of 0.834 (95% CI: 0.794-0.874) and 0.825 (95% CI: 0.789-0.861) , respectively. Conclusions:Combination of immune diseases, surgical approach of thoracotomy, incomplete tumor resection, WHO pathological classification of A+AB, postoperative pulmonary infection and no postoperative radiotherapy and chemotherapy are independent risk factors for MG after thymoma resection. The risk nomogram prediction model established based on the above risk factors can accurately assess and quantify the risk of MG after thymoma resection, which has good predictive ability.

子宫内膜异位症好发于生育活跃期患者,其发病率高、病变广泛.因腹腔镜操作受限,子宫内膜异位症的临床诊断常具有延迟性,导致患者错失最佳诊治时机,所以迫切需要寻找一种非侵入性、高特异性和敏感性的诊断方法.微RNA(miRNA/miR)是生物体内重要的转录后调控因子,可参与多种疾病的发生发展过程,具有敏感性高、不易降解等特点,极易在组织中被检出.在子宫内膜异位症患者的血液中,miR-125b、miR-17、miR-122、miR-199a和miR-200家族表达水平明显升高,且与子宫内膜异位症发病具有相关性,有望成为诊断子宫内膜异位症的生物标志物.

日间宫腔镜手术是指患者一日内且不过夜入、出院完成的宫腔镜手术，设置日间宫腔镜手术中心是适应现代医院发展模式的重大转变。全国有资质的各级医疗机构以不同形式和规模在开展日间宫腔镜手术，但尚缺乏统一的制度流程和规范。本共识以国际日间手术学会和中国日间手术合作联盟发布的相关文献为参考，结合中国开展日间手术成熟的医疗机构的制度流程，从日间宫腔镜手术中心的设置、管理制度、管理流程到质量控制以及并发症的处理及转运给予了共识性建议，同时，对医疗、护理和麻醉三个维度的评估和相关问题处理制定了规范化流程。

Mayer–Rokitansky–Küster–Hauser (MRKH) syndrome, also known as Müllerian agenesis, is characterized by uterovaginal aplasia in an otherwise phenotypically normal female with a normal 46,XX karyotype. Previous studies have associated sequence variants of PAX8, TBX6, GEN1, WNT4, WNT9B, BMP4, BMP7, HOXA10, EMX2, LHX1, GREB1L, LAMC1, and other genes with MRKH syndrome. The purpose of this study was to identify the novel genetic causes of MRKH syndrome. Ten patients with MRKH syndrome were recruited at Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China. Whole-exome sequencing was performed for each patient. Sanger sequencing confirmed the potential causative genetic variants in each patient. In silico analysis and American College of Medical Genetics and Genomics (ACMG) guidelines helped to classify the pathogenicity of each variant. The Robetta online protein structure prediction tool determined whether the variants affected protein structures. Eleven variants were identified in 90% (9/10) of the patients and were considered a molecular genetic diagnosis of MRKH syndrome. These 11 variants were related to nine genes: TBC1D1, KMT2D, HOXD3, DLG5, GLI3, HIRA, GATA3, LIFR, and CLIP1. Sequence variants of TBC1D1 were found in two unrelated patients. All variants were heterozygous. These changes included one frameshift variant, one stop-codon variant, and nine missense variants. All identified variants were absent or rare in gnomAD East Asian populations. Two of the 11 variants (18.2%) were classified as pathogenic according to the ACMG guidelines, and the remaining nine (81.8%) were classified as variants of uncertain significance. Robetta online protein structure prediction analysis suggested that missense variants in TBC1D1 (p.E357Q), HOXD3 (p.P192R), and GLI3 (p.L299V) proteins caused significant structural changes compared to those in wild-type proteins, which in turn may lead to changes in protein function. This study identified many novel genes, especially TBC1D1, related to the pathogenesis of MRKH syndrome. The identification of these variants provides new insights into the etiology of MRKH syndrome and a new molecular genetic reference for the development of the reproductive tract.

This phase 3, randomized, open-label, active-controlled, multicenter study investigated the efficacy of triptorelin pamoate prolonged-release (PR) 3-month in Chinese patients with endometriosis by demonstrating the noninferiority of the 3-month formulation to the standard of care, triptorelin acetate PR 1-month. The trial was conducted in 24 clinical centers in China, and included 300 Chinese women (18–45 years) with endometriosis and regular menstrual cycles who required treatment with a gonadotropin-releasing hormone agonist for 6 months. One group of patients (n = 150) was treated with triptorelin pamoate PR 3-month (15 mg per injection, once every 12 weeks), and the other (n = 150) with triptorelin acetate PR 1-month (3.75 mg per injection, once every 4 weeks). The primary outcome measure was the proportion of patients with estradiol (E2) concentrations suppressed to castration levels (≤ 184 pmol/L, or 50 pg/mL) after 12 weeks of treatment. Triptorelin pamoate PR 3-month was noninferior to triptorelin acetate PR 1-month for the treatment of endometriosis: over 98% of patients in both groups were chemically castrated at week 12. Both formulations were also equally efficacious in reducing endometriosis-associated pelvic pain, and reducing serum concentrations of E2, luteinizing hormone, and follicle-stimulating hormone over time. No new safety concerns were identified. Triptorelin pamoate PR 3-month is a valid alternative to triptorelin acetate PR 1-month for the treatment of Chinese women with endometriosis, with fewer injections and a potentially lower burden of care. NCT03232281.

目的:探究人脐带间充质干细胞来源的外泌体(MSC-exosomes)对盆腔器官脱垂(POP)患者阴道壁成纤维细胞的调节作用.方法:采用超速离心法提取MSC-exo-somes,应用透射电镜观察外泌体形态,Western blot法检测特异分子HSP90、CD63和TSG101表达,对外泌体进行综合鉴定.采用组织爬块和胶原酶消化法从POP患者阴道壁组织中分离培养成纤维细胞.采用PKH-67绿色荧光染料标记外泌体,添加PKH-67标记的MSC-exosomes,观察成纤维细胞对外泌体的摄取情况.分别将终浓度为50μg/mL、100μg/mL的MSC-exosomes加入成纤维细胞中,对照组加等体积PBS.MTS法检测3组细胞在12、24、36、48、60h和72h的增殖情况.收集成纤维细胞蛋白,Western blot法检测成纤维细胞胞外基质代谢相关基因CollagenⅠ、CollagenⅢ、LOXL-2、Fibronectin和MMP-2等表达,并进行相对定量统计分析.结果:分离到的外泌体特异表达标志蛋白HSP90和CD63,不表达内质网蛋白TSG101,透射电镜观察到具有双层脂膜结构的圆形囊泡小体,表明分离得到了外泌体.从脱垂患者阴道壁组织中成功培养得到成纤维细胞,其形态呈长梭型或纺锤形,细胞排列成簇状.PKH-67标记的MSC-exosomes添加24 h后,细胞内可见丰富的绿色荧光信号,表明MSC-exosomes可被阴道壁成纤维细胞有效大量摄取.50、100μg/mL MSC-exosomes均可促进阴道壁成纤维细胞的增殖.50、100μg/mL exosome作用24h后,CollagenⅠ、CollagenⅢ、LOXL-2、Fibronectin表达增加,其中Fibronectin表达升高最显著,100μg/mL exosome组较50μg/mL exosomes组促进作用更明显,Collagen I在48 h时较24 h升高作用更明显,而MMP-2在MSC-exosomes添加后均出现蛋白表达下降,表明细胞外基质分解降低.结论:MSC-exosomes可有效促进POP阴道壁成纤维细胞的增殖,并促进成纤维细胞胞外基质的合成,减少细胞外基质的降解.

Ultrasonography and magnetic resonance imaging (MRI) are used more commonly in diagnosing obstetrics disorders as non-invasive and non-ionizing methods. Ultrasonography is a safe and available modality that provides real-time images in multiple planes. MRI can perform as a subsequent evaluation for cases in which ultrasonography is doubtful. This systematic study aimed to identify the current knowledge regarding the use of ultrasonography and MRI in diagnosing obstetrics cardiac disorders, their medical applications, safety issues, limitations, and future applications.

女性生育力保护技术的需求急剧增长.全球每年新增恶性肿瘤患者超过1400万例 [1],抗癌治疗在显著降低患者死亡率的同时,其性腺毒性却对患者的卵巢功能造成严重损伤,尤其在造血干细胞移植后,卵巢早衰的发生率可达100％[2].随着发病年龄的年轻化与生育年龄的推迟,78.3％的年轻恶性肿瘤患者有强烈的生育需求 [3].