SIRT1-mediated deacetylation of FOXO3 enhances mitophagy and drives hormone resistance in endometrial cancer.

BACKGROUND: The complex interplay between Sirtuin 1 (SIRT1) and FOXO3 in endometrial cancer (EC) remains understudied. This research aims to unravel the interactions of deacetylase SIRT1 and transcription factor FOXO3 in EC, focusing on their impact on mitophagy and hormone resistance. METHODS: High-throughput sequencing, cell experiments, and bioinformatics tools were employed to investigate the roles and interactions of SIRT1 and FOXO3 in EC. Co-immunoprecipitation (Co-IP) assay was used to assess the interaction between SIRT1 and FOXO3 in RL95-2 cells. Functional assays were used to assess cell viability, proliferation, migration, invasion, apoptosis, and the expression of related genes and proteins. A mouse model of EC was established to evaluate tumor growth and hormone resistance under different interventions. Immunohistochemistry and TUNEL assays were used to assess protein expression and apoptosis in tumor tissues. RESULTS: High-throughput transcriptome sequencing revealed a close association between SIRT1, FOXO3, and EC development. Co-IP showed a protein-protein interaction between SIRT1 and FOXO3. Overexpression of SIRT1 enhanced FOXO3 deacetylation and activity, promoting BNIP3 transcription and PINK1/Parkin-mediated mitophagy, which in turn promoted cell proliferation, migration, invasion, and inhibited apoptosis in vitro, as well as increased tumor growth and hormone resistance in vivo. These findings highlighted SIRT1 as an upstream regulator and potential therapeutic target in EC. CONCLUSION: This study reveals a novel molecular mechanism underlying the functional relevance of SIRT1 in regulating mitophagy and hormone resistance through the deacetylation of FOXO3 in EC, thereby providing valuable insights for new therapeutic strategies.

An intelligent grasper to provide real-time force feedback to shorten the learning curve in laparoscopic training.

BACKGROUND: A lack of force feedback in laparoscopic surgery often leads to a steep learning curve to the novices and traditional training system equipped with force feedback need a high educational cost. This study aimed to use a laparoscopic grasper providing force feedback in laparoscopic training which can assist in controlling of gripping forces and improve the learning processing of the novices. METHODS: Firstly, we conducted a pre-experiment to verify the role of force feedback in gripping operations and establish the safe gripping force threshold for the tasks. Following this, we proceeded with a four-week training program. Unlike the novices without feedback (Group A2), the novices receiving feedback (Group B2) underwent training that included force feedback. Finally, we completed a follow-up period without providing force feedback to assess the training effect under different conditions. Real-time force parameters were recorded and compared. RESULTS: In the pre-experiment, we set the gripping force threshold for the tasks based on the experienced surgeons' performance. This is reasonable as the experienced surgeons have obtained adequate skill of handling grasper. The thresholds for task 1, 2, and 3 were set as 0.731 N, 1.203 N and 0.938 N, respectively. With force feedback, the gripping force applied by the novices with feedback (Group B1) was lower than that of the novices without feedback (Group A1) (p < 0.005). During the training period, the Group B2 takes 6 trails to achieve gripping force of 0.635 N, which is lower than the threshold line, whereas the Group A2 needs 11 trails, meaning that the learning curve of Group B2 was significantly shorter than that of Group A2. Additionally, during the follow-up period, there was no significant decline in force learning, and Group B2 demonstrated better control of gripping operations. The training with force feedback received positive evaluations. CONCLUSION: Our study shows that using a grasper providing force feedback in laparoscopic training can help to control the gripping force and shorten the learning curve. It is anticipated that the laparoscopic grasper equipped with FBG sensor is promising to provide force feedback during laparoscopic training, which ultimately shows great potential in laparoscopic surgery.

MicroRNA-16 Promotes Ovarian Granulosa Cell Proliferation and Suppresses Apoptosis Through Targeting PDCD4 in Polycystic Ovarian Syndrome.

BACKGROUND/AIMS: Several miRNAs have been reported to be involved in the pathogenesis of polycystic ovarian syndrome (PCOS). However, the biological roles of miR-16 and its molecular mechanisms in PCOS development remain to be elucidated. METHODS: qRT-PCR was performed to detect the expression levels of miR-16 and programmed cell death protein 4 (PDCD4). GCs proliferation, cell cycle distribution and apoptosis were examined by MTT assay and flow cytometry analysis. Luciferase reporter assay and RIP assay were applied to confirm the regulatory relationship between miR-16 and PDCD4. Western blot was applied to measure the protein levels of PDCD4, PCNA and caspase-3. ELISA kits were used to determine the serum levels of steroids. RESULTS: miR-16 expression was down-regulated in ovarian cortex tissues and serums of PCOS patients. PDCD4 expression was up-regulated in ovarian cortex tissues of PCOS patients. miR-16 overexpression facilitated cell proliferation, induced cell cycle progression, and inhibited apoptosis in GCs. Moreover, PDCD4 was a direct target of miR-16. Also, enforced expression of PDCD4 abated the effects of miR-16 on GCs growth and apoptosis. Additionally, testosterone resulted in a decrease of miR-16 expression and an increase of PDCD4 expression, thus blocking cell growth and enhanced apoptosis in GCs. Furthermore, miR-16 overexpression alleviated PCOS in vivo by regulating PDCD4. CONCLUSIONS: miR-16 promoted ovarian GCs proliferation and inhibited apoptosis through directly targeting PDCD4 in PCOS, contributing to a better understanding of the molecular mechanism of GCs dysregulation and providing a promising target in PCOS.

Human umbilical cord mesenchymal stem cell transplantation restores damaged ovaries.

Ovarian injury because of chemotherapy can decrease the levels of sexual hormones and potentia generandi of patients, thereby greatly reducing quality of life. The goal of this study was to investigate which transplantation method for human umbilical cord mesenchymal stem cells (HUMSCs) can recover ovarian function that has been damaged by chemotherapy. A rat model of ovarian injury was established using an intraperitoneal injection of cyclophosphamide. Membrane-labelled HUMSCs were subsequently injected directly into ovary tissue or tail vein. The distribution of fluorescently labelled HUMSCs, estrous cycle, sexual hormone levels, and potentia generandi of treated and control rats were then examined. HUMSCs injected into the ovary only distributed to the ovary and uterus, while HUMSCs injected via tail vein were detected in the ovary, uterus, kidney, liver and lung. The estrous cycle, levels of sex hormones and potentia generandi of the treated rats were also recovered to a certain degree. Moreover, in some transplanted rats, fertility was restored and their offspring developed normally. While ovary injection could recover ovarian function faster, both methods produced similar results in the later stages of observation. Therefore, our results suggest that transplantation of HUMSCs by tail vein injection represents a minimally invasive and effective treatment method for ovarian injury.

Comparison of laparoscopy and laparotomy in the surgical management of early-stage ovarian cancer.

OBJECTIVE: The aim of this study is to investigate the safety and efficacy of laparoscopy in the treatment of early-stage ovarian cancer (EOC). METHODS: We retrospectively analyzed the clinical data of patients who underwent laparoscopy (35 patients) or laparotomy (40 patients) for the comprehensive surgical staging of EOC in Zhujiang Hospital during the period of 2002 to 2010 and compared the 2 surgical approaches in operative time, intraoperative blood loss, number of dissected lymph nodes, tumor rupture rate, length of hospital stay, time of gastrointestinal function recovery, wound healing condition, complication rate, upstaging rate, rate of postoperative chemotherapy, and postoperative follow-up condition. RESULTS: The laparoscopy group had significantly shorter hospital stay and time of first postoperative flatus and had significantly lower rate of poor wound healing than the laparotomy group. The 2 groups did not show significant differences in operative time, intraoperative blood loss, number of dissected lymph nodes, tumor rupture rate, complication rate, upstaging rate, and rate of postoperative chemotherapy. CONCLUSIONS: Laparoscopy is safe and effective for the comprehensive surgical staging of EOC and has the advantages of shorter hospital stay, faster recovery of gastrointestinal function, and good wound healing.

[Video endoscopic inguinal lymphadenectomy via hypogastric/limb subcutaneous approach for early-stage vulvar cancer].

OBJECTIVE: To describe and compare video endoscopic inguinal lymphadenectomy via hypogastric and limb approach (VEIL-H vs VEIL-L) in patients with invasive vulvar cancer. METHODS: From March 2011 to August 2013, 7 women with early-stage vulvar cancer were selected for this integrated procedure with a combination of VEIL-H and VEIL-L in bilateral groins.VEIL-L was performed on limb with old surgical scar in ipsilateral hypogastric area of 3 patients and VEIL-H in contralateral limb. Both novel procedures were performed with triple trocars respectively. The boundaries of inguinal lymph node dissection were the same template of open inguinal lymphadenectomy. Preoperative data, surgical techniques and follow-up outcomes were compared.Standard statistical tests were used. RESULTS: The combination of VEIL-H and VEIL-L was successfully completed in 7 patients without conversion into open surgery. The great saphenous vein was spared in 13 limbs.No difference existed in mean operative duration, average blood loss volume and median total regional lymph nodes removed in two groups. All nodes were confirmed tumor-free. Mean drain duration was (4.7 ± 1.4) days in the VEIL-H group and (2.7 ± 0.9) days in VEIL-L group respectively (P < 0.01). Mean drain volume was (123 ± 55) ml in VEIL-H group and (62 ± 32) ml respectively (P < 0.05). Mean postoperative hospital stay was (8.6 ± 2.2) days.No major intraoperative complications occurred. However, hypercarbia in one patient 1 was completely reversible with hyperventilation.Unilateral great saphenous vein was injured in another one.Regarding postoperative complications, one patient suffered lymphocele in VEIL-H side and another had lymphorrhea through drain orifice in VEIL-L side. During a follow-up period of (19 ± 7) months, there was no disease recurrence so far. CONCLUSION: The combination of VEIL-H and VEIL-L has the reproducibility and therapeutic potentials in the treatment for patients with vulvar cancer. Both minimal invasive techniques are viable. Although short-term results are encouraging, larger series with a longer follow-up are required to fully evaluate the therapeutic efficacy of VEIL-H and VEIL-L.

Smart laparoscopic grasper integrated with fiber Bragg grating based tactile sensor for real-time force feedback.

Minimally invasive surgery, such as laparoscopic surgery, has developed rapidly due to its small wound, less bleeding and quick recovery. However, a lack of force feedback, which leads to tissue damage, is still unsolved. Many sensors have been used to offer force feedback but still limited by their large size, low security and high complexity. Based on the advantages of small size, high sensitivity and immunity to electromagnetic interferences, we propose a tactile sensor integrated with fiber Bragg gratings (FBGs) at the tip of laparoscopic grasper to offer real-time force feedback in the laparoscopic surgery. The tactile sensor shows a force sensitivity of 0.076 nm/N with a repeatable accuracy of 0.118 N. A bench test is conducted in a laparoscopic training box to verify its feasibility. Test results illustrate that gripping force exerted on the laparoscopic grasper in terms of peak and standard deviation values reduce significantly for the novice subjects with force feedback compared to those without force feedback. The proposed sensor integrated at the tip of the laparoscopic grasper demonstrates a better control of the gripping force among the novice surgeons and indicates that the smart grasper can help surgeons achieve precise gripping force to reduce unnecessary tissue trauma.

microRNA-671-5p reduces tumorigenicity of ovarian cancer via suppressing HDAC5 and HIF-1α expression.

OBJECTIVE: microRNA (miR)-based therapeutic reference has been established and expanded in the treatment of cancers. For this reason, we explored how miR-671-5p regulated tumorigenicity of ovarian cancer (OC) through regulating histone deacetylase 5 (HDAC5) and hypoxia-inducible factor-1α (HIF-1α). METHODS: miR-671-5p, HDAC5 and HIF-1α expression levels were determined in OC clinical tissues. The OC cell line H8910 was screened and transfected with the vectors that altered miR-671-5p, HDAC5 and HIF-1α levels. Finally, the proliferation, migration, invasion and apoptosis of the transfected H8910 cells were determined and the role of miR-671-5p and HDAC5 in vivo tumor growth was further discussed. RESULTS: Low expression miR-671-5p and high expression HDAC5 and HIF-1α levels were tested in OC tissues. Up-regulating miR-671-5p or down-regulating HDAC5 or HIF-1α suppressed proliferation, migration, invasion and augmented apoptosis of H8910 cells while silenced miR-671-5p or enhanced HDAC5 caused the opposite consequences. Overexpression of HDAC5 reduced while depletion of HDAC5 enhanced the influence of up-regulated miR-671-5p on OC cell growth. In animal models, suppressing miR-671-5p or promoting HDAC5 encouraged OC tumor growth. CONCLUSION: A summary delineates that miR-671-5p reduces tumorigenicity of OC via suppressing HDAC5 and HIF-1α expression levels.

Gut Microbiota Exceeds Cervical Microbiota for Early Diagnosis of Endometriosis.

The diagnosis of endometriosis is typically delayed by years for the unexclusive symptom and the traumatic diagnostic method. Several studies have demonstrated that gut microbiota and cervical mucus potentially can be used as auxiliary diagnostic biomarkers. However, none of the previous studies has compared the robustness of endometriosis classifiers based on microbiota of different body sites or demonstrated the correlation among microbiota of gut, cervical mucus, and peritoneal fluid of endometriosis, searching for alternative diagnostic approaches. Herein, we enrolled 41 women (control, n = 20; endometriosis, n = 21) and collected 122 well-matched samples, derived from feces, cervical mucus, and peritoneal fluid, to explore the nature of microbiome of endometriosis patients. Our results indicated that microbial composition is remarkably distinguished between three body sites, with 19 overlapped taxa. Moreover, endometriosis patients harbor distinct microbial communities versus control group especially in feces and peritoneal fluid, with increased abundance of pathogens in peritoneal fluid and depletion of protective microbes in feces. Particularly, genera of Ruminococcus and Pseudomonas were identified as potential biomarkers in gut and peritoneal fluid, respectively. Furthermore, novel endometriosis classifiers were constructed based on taxa selected by a robust machine learning method. These results demonstrated that gut microbiota exceeds cervical microbiota in diagnosing endometriosis. Collectively, this study reveals important insights into the microbial profiling in different body sites of endometriosis, which warrant future exploration into the role of microbiota in endometriosis and highlighted values on gut microbiota in early diagnosis of endometriosis.

Association between DNA damage repair gene somatic mutations and immune-related gene expression in ovarian cancer.

BACKGROUND: Defects in DNA damage repair (DDR) system may lead to genomic instability and manifest as increased immunogenicity. DDR deficiency is prevalent in ovarian cancer (OvCa); however, the association of DDR mutation with immune profiles in OvCa remains largely unknown. This knowledge will provide an essential basis to the rational design of biomarker-guided immune combination therapy of OvCa in the future. METHODS: Whole-exome sequencing data of 587 OvCa from The Cancer Genome Atlas (TCGA) were used to determine the expression profiles of 47 immune-related genes and the abundance of tumor-infiltrating immune cells. A Chinese OvCa cohort (n = 220) tested by next-generation sequencing (NGS) was used to validate the association between DDR status and tumor mutation burden (TMB). RESULTS: A total of 19.3% in TCGA cohort and 25.9% in Chinese cohort harbored at least one DDR somatic mutation. DDR deficiency exhibited a distinct immune profile with significant higher expression levels of PTPRCAP, CCL5, IFI16, LAG3, IL15RA, and GBP1 in OvCa in the TCGA cohort. Different DDR pathway deficiency displayed various immune profiles. Increased levels of Th1 cells, TMB, and neoantigen were also observed in DDR-deficient tumors. CONCLUSIONS: DDR deficiency was associated with specific immune signatures in OvCa. Our findings emphasize the urgent need for biomarker-guided rational immune combination therapy to maximize the OvCa patients who could benefit from immunotherapy.

Correction to: miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

An amendment to this paper has been published and can be accessed via the original article.

miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

BACKGROUND: miRNA expression profiles in ectopic endometrium (EC) serving as pathophysiologic genetic fingerprints contribute to determining endometriosis progression; however, the underlying molecular mechanisms remain unknown. METHODS: miRNA microarray analysis was used to determine the expression profiling of EC fresh tissues. qRT-PCR was performed to screen miR-205-5p expression in EC tissues. The roles of miR-205-5p and its candidate target gene, angiopoietin-2 (ANGPT2), in endometriosis progression were confirmed on the basis of both in vitro and in vivo systems. miR-205-5p and ANGPT2 expression were measured by in situ hybridization and immunochemistry, and their clinical significance was statistically analysed. RESULTS: miR-205-5p was screened as a novel suppressor of endometriosis through primary ectopic endometrial stromal cell migration, invasion, and apoptosis assay in vitro, along with endometrial-like xenograft growth and apoptosis in vivo. In addition, ANGPT2 was identified as a direct target of miR-205-5p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of ANGPT2 could respectively rescue and simulate the effects induced by miR-205-5p. Importantly, the miR-205-5p-ANGPT2 axis was found to activate the ERK/AKT pathway in endometriosis. Finally, miR-205-5p and ANGPT2 expression were closely correlated with the endometriosis severity. CONCLUSION: The newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.

Overexpression of miR-21 in stem cells improves ovarian structure and function in rats with chemotherapy-induced ovarian damage by targeting PDCD4 and PTEN to inhibit granulosa cell apoptosis.

BACKGROUND: Chemotherapy-induced premature ovarian failure (POF) is a severe complication affecting tumor patients at a childbearing age. Mesenchymal stem cells (MSCs) can partially restore the ovarian structure and function damaged by chemotherapy. miR-21 is a microRNA that can regulate cell apoptosis. This study discusses the repair effect and mechanism of MSCs overexpressing miR-21 on chemotherapy-induced POF. METHODS: Rat MSCs and granulosa cells (GCs) were isolated in vitro. MSCs were transfected with miR-21 lentiviral vector (LV-miR-21) to obtain MSCs stably expressing miR-21 (miR-21-MSCs). The microenvironment of an ovary receiving chemotherapy was mimicked by adding phosphamide mustard (PM) into the cellular culture medium. The apoptosis rate and the mRNA and protein expression of target genes PTEN and PDCD4 were detected in MSCs. Apoptosis was induced by adding PM into the culture medium for GCs, which were cocultured with miR-21-MSCs. The apoptosis rate and the mRNA and protein expression of PTEN and PDCD4 were detected. The chemotherapy-induced POF model was built into rats by intraperitoneal cyclophosphamide injection. miR-21-MSCs were transplanted into the bilateral ovary. The rats were sacrificed at 15, 30, 45, and 60 days after the last injection. The ovarian weights, follicle count, estrous cycle, and sex hormone levels (estradiol (E2) and follicle-stimulating hormone (FSH)) were detected. Apoptosis of GCs was determined by TUNEL assay. The miR-21 and mRNA and protein expression of PTEN and PDCD4 were determined. RESULTS: The apoptosis decreased in MSCs transfected with miR-21. The mRNA and protein expression of target genes PTEN and PDCD4 was downregulated. GCs cocultured with miR-21-MSCs showed a decreased apoptosis, an upregulation of miR-21, and a downregulation of PTEN and PDCD4. Following the injection of miR-21-MSCs, the ovarian weight and follicle counts increased; E2 levels increased while FSH levels decreased, with less severe apoptosis of GCs. The miR-21 expression in the ovaries was upregulated, while the mRNA expression and protein expression of PTEN and PDCD4 were downregulated. CONCLUSIONS: Overexpression of miR-21 in MSCs promoted efficacy against chemotherapy-induced POF and its improvement of the repair effect was related to the inhibition of GC apoptosis by targeting PTEN and PDCD4.

miR-100 resensitizes resistant epithelial ovarian cancer to cisplatin.

Epithelial ovarian cancer (EOC) is one of the malignant tumors that seriously affects women's health and chemotherapy resistance is an important reason for the poor prognosis. The present study was conducted to investigate whether microRNA-100 (miR-100) can be used to modulate the tolerance to cisplatin in EOC. Expression of miR-100 was compared between ovarian cancer cells tolerant and not tolerant to cisplatin. Mimic and antisense were used to study the roles and related mechanisms of miR-100 in cisplatin sensitivity in EOC. The alternation in the cisplatin sensitivity was investigated using grafted tumors derived from SKOV3/DDP cells with upregulated or downregulated miR-100 expression. miR-100 was lower in cisplatin resistant cell line SKOV3/DDP than in cisplatin sensitive cell line SKOV3. miR-100 might increase cisplatin sensitivity by inhibiting cell proliferation and conversion from G1 to S phase and increasing apoptosis. We showed that mTOR and PLK1 are targets of miR-100 and the cells were resensitized probably due to targeted downregulation of mTOR and PLK1 by miR-100. In vivo study with nude mice showed that tumors derived from miR-100 mimic-transfected cells were more sensitive to cisplatin and had reduced expression of mTOR and PLK1. miR-100 resensitizes resistant epithelial ovarian cancer to cisplatin probably by inhibiting cell proliferation, inducing apoptosis and arresting cell cycle and by targeted downregulation of mTOR and PLK1 expression.

[Changes of serum epithelial neutrophil-activating peptide-78 in patients with endometriosis].

OBJECTIVE: To investigate the role of serum epithelial neutrophil-activating peptide-78 (ENA-78) in the pathogenesis of endometriosis. METHODS: Serum concentrations of ENA-78 were measured by means of enzyme-linked immunosorbent assay (ELISA) in 42 patients with endometriosis (20 in stages I and II and 22 in stages III and IV) in comparison with 25 women without endometriosis (control group). RESULTS: Serum concentrations of ENA-78 were significantly higher in endometriosis group than in the control group (2.97+/-1.91 ng/ml vs 0.72+/-0.24 ng/ml, P>0.001), and ENA-78 levels in stages III and IV were significantly higher than those in stages I and II (4.48+/-1.25 ng/ml vs 1.30+/-0.74 ng/ml, P>0.001). Significant difference in ENA-78 levels between follicular phase and luteal phase was found in neither of the groups. CONCLUSION: Patients with endometriosis have elevated serum ENA-78 levels, which might be a pathogenic factor of endometriosis.

[Expressions of nuclear factor-kappaB and intercellular adhesion molecule-1 in endometriosis].

OBJECTIVE: To investigate the association of nuclear factor-kappaB (NF-kappaB) and intercellular adhesion molecule-1 (ICAM-1) with endometriosis. METHODS: Immunohistochemistry was used to examine the NF-kappaB and VEGF protein expression in 35 specimens of normal endometrium, 48 eutopic endometrium of endometriosis and 76 ectopic endometrium, and the results were analyzed statistically. RESULTS: The expressions of NF-kappaB and ICAM-1 were found mainly in the glandular epithelial cells of the three endometrium specimens, with the ectopic endometriotic tissues showing the highest and normal endometrium the lowest expressions (P<0.001). NF-kappaB and ICAM-1 expressions were positively correlated to normal, eutopic and ectopic endometrium (r=0.688, 0.773 and 0.777, respectively, P<0.01). CONCLUSION: NF-kappaB and ICAM-1 may participate in the process of the pathogenesis in endometriosis.

[Cloning, expression, purification and characterization of human endostatin gene].

OBJECTIVE: To procure biologically active human endostatin. METHODS: Human endostatin gene was acquired by means of reverse transcriptase (RT)-PCR and cloned into PGEM-T vector with subsequent sequence identification. The gene fragment was inserted into the prokaryotic expression vector pBV220 and transformed into E.coli DH5alpha strain. Endostatin expression in the E.coli was identified and the inclusion body isolated, purified and its activity analyzed. RESULTS: The obtained gene fragment 552 bp in length was identified as the functional section of human endostatin gene by sequence analysis, and SDS-PAGE analysis showed that the expressed product was the target protein with biological activity. CONCLUSION: Human endostatin gene was expressed in E.coli and the protein obtained can inhibit the proliferation of ECV 304 cells.

[Evaluation of tumor necrosis factor-alpha and tumor necrosis factor-beta in serum of patients with endometriosis].

OBJECTIVE: To evaluate the levels of tumor necrosis factor-alpha (TNF-alpha) and tumor necrosis factor-beta (TNF-beta) before and after conservative laparoscopic surgery in patients with endometriosis. METHODS: The levels of TNF-alpha and TNF-beta in the serum of both 82 patients with EMS and 68 controls were determined by ELISA. RESULTS: The levels of TNF-alpha and TNF-beta in the serum of patients with EMS were significantly higher than those of the controls (P < 0.01), and they increased with the clinical terms ( P < 0.05). After clearance of endometrosis foci with laparoscopic conservative surgery, the TNF-alpha levels decreased significantly in EMS III - IV, and TNF-beta levels decreased significantly in EMS I - IV. CONCLUSION: Measuring TNF-alpha and TNF-beta levels in the serum of patients with EMS may have important value in postoperative follow-up, surveillance and evaluation of the effectiveness of the surgery.

[Lentiviral vector-mediated short hairpin RNA targeting survivin inhibits abdominal growth of human endometrium xenograft in nude mice].

OBJEVTIVE: To investigate the inhibitory effect of lentiviral vector-mediated short hairpin RNA targeting survivin (LV-survivin shRNA) on the growth of human endometrium xenograft in the abdominal cavity of nude mice. METHODS: The endometrium xenografts from 8 women with endometriosis were injected into the peritoneal cavities of 45 nude mice. The mice were then randomly assigned to receive intraperitoneal injection of LV-survivin shRNA, pGCL-NC-GFP (negative control) or PBS (blank control). Two weeks later, the number and morphometry of endometriotic lesions were quantified and the expression of survivin protein were detected by immunohistochemistry. RESULTS: The formation of endometriotic lesions was significantly suppressed in mice receiving LV-survivin shRNA injection as compared with those in the two control groups (P/0.001). The mice in LV-survivin-shRNA group showed significantly down-regulated expression levels of survivin protein compared with those in the negative and blank control groups, presenting also necrosis in the endometriosis-like lesions in microscopic observation. CONCLUSION: Lentiviral vector-mediated shRNA can effectively inhibit the expression of survivin in human endometrium xengrafts and suppress the formation and growth of endometriotic lesions in the abdominal cavities of nude mice.