Novel laparoscopic surgery for the repair of cesarean scar defect without processing scar resection.

BACKGROUND: Cesarean scar defect (CSD), especially CSD with residual myometrium less than 3 mm is reported to be the highest risk agent associated with uterine rupture for subsequent pregnancy. Currently, laparoscopic resection and suture was the mainstay therapy method for CSD with a residual myometrium less than 3 mm in women with a desire to conceive. Besides, the women have CSD related symptoms, especially postmenstrual bleeding, should be recommended for CSD treatment. This study is to investigate the efficiency of this novel laparoscopic surgery for the repair of cesarean scar defect (CSD) without scar resection for residual myometrium thickening. METHOD: This retrospective clinical study enrolled 76 women diagnosed with CSD who had a residual myometrium thickness less than 3 mm and also had a desire to conceive, had undergone laparoscopic surgery for the repair of CSD in the time period March 2016 to March 2018. Two study cohorts were created among the 76 patients: 40 patients had undergone the novel laparoscopic repair of CSD without processing scar resection (Group A), whereas 36 patients had undergone the traditional laparoscopic resection and suture of CSD (Group B). RESULTS: Residual myometrium thickening occurred among all the 76 patients and the average residual myometrium thickness was increased to almost 6 mm, presenting no between-group difference. In Group A, all the CSD-related postmenstrual bleeding was resolved or improved, but one patient in Group B has no obvious change to postmenstrual bleeding. After CSD repair, 20 patients got pregnant naturally in Group A, and there was no cesarean scar pregnancy and uterine rupture. While, there were 9 cases of natural pregnancy in Group B. No uterine rupture occurred among these 9 pregnant women of Group B, but 1 case of pregnancy was terminated due to cesarean scar pregnancy. CONCLUSION: Laparoscopic repair without processing scar resection seems to be a feasible, safe and simple operative approach for CSD treatment, which can thicken residual myometrium and improve postmenstrual bleeding.

Endoscopic Treatment of Previous Cesarean Scar Defect in Women with Postmenstrual Bleeding: A Retrospective Cohort Study.

OBJECTIVE: To compare the incidence of postmenstrual bleeding after hysteroscopic resection versus laparoscopic repair of previous cesarean scar defect (PCSD). MATERIALS AND METHODS: Retrospective analysis of computerized patient records. For the diagnosis of PCSD, patients underwent transvaginal ultrasound first without and then with saline-assisted sonohysterography. Hysteroscopic PCSD resection was performed under sonographic guidance, while laparoscopic repair was guided by hysteroscopy for the confirmation of scar margins. RESULTS: Records of 62 patients presenting with PCSD-related postmenstrual bleeding were included in analysis. Hysteroscopic surgery had significantly shorter operative time compared to the laparoscopic approach (Mean =30.9 vs 71.0 minutes; p < 0.001). Blood loss and hospital stay were significantly less (p < 0.001) in hysteroscopic resection (10.4 ± 4.6 ml and 2.1 ± 0.4 days) than in laparoscopic repair (36.6 ± 4 ml, and 4.6 ± 1 days). After surgical interventions, the postmenstrual bleeding was resolved or improved. The effectiveness rates of hysteroscopic resection and laparoscopic repair were 91.4% and 96.3%, respectively. Incidence of post-treatment postmenstrual bleeding was not significantly different between hysteroscopy and laparoscopy (OR= 1.29 [95% confidence interval 0.367, 4.86]; p = 0.662). Pretreatment postmenstrual bleeding was associated with time since cesarean section (B= -0.091 [-0.158, -0.023]; p = 0.01) and PCSD length (B = 0.502 [0.085, 0.919]; p = 0.019). CONCLUSION: Both hysteroscopic resection and laparoscopic repair of PCSD yield comparable efficacy in reducing postmenstrual bleeding. However, hysteoroscopic resection of PCSD is associated with comparatively shorter operative time, less blood loss, and shorter hospital stay.

lncRNA SNHG16 promotes glioma tumorigenicity through miR-373/EGFR axis by activating PI3K/AKT pathway.

Glioma is one of the most common and aggressive malignant primary brain tumor with invariably poor 5-year survival rates. Because of the high recurrence rate and mortality rate, effective therapies for glioma are still weak. Recently, several studies has been proved that long non-coding RNAs (lncRNAs) have been identified to play regulatory mediators in the tumorigenesis of glioma. Nevertheless, the role of lncRNAs and their downstream transcripts are still elusive in the progression of glioma. Small nucleolar RNA host gene 16 (SNHG16), a newly identified lncRNA, has been verified to be up-regulated in human malignant carcinomas. In the present study, we confirmed that lncRNA SNHG16 was highly expressed in glioma and may exert oncogenic function as a competing endogenous RNA (ceRNA) to regulate EGFR by sponging of miR-373-3p through activating PI3K/AKT pathway, which providing a new insight of the regulatory network of lncRNA SNHG16 in the development of glioma.

lncRNA SNHG16 Exerts Oncogenic Functions in Promoting Proliferation of Glioma Through Suppressing p21.

Glioma is a malignant brain tumor that accounts for 30% of all brain tumors and 80% of malignant brain tumors. This poor clinical outcome makes the study of molecular mechanisms in glioma as an urgent subject. However, the certain mechanism remains unclear. Long non-coding RNAs (lncRNAs) plays a key role in glioma development and progression. In the present study, we aimed to explore the potential mechanisms of lncRNA SNHG16 in glioma. The levels of lncRNA SNHG16 were qualified in both glioma tissues and cell lines using qRT-PCR assay. The ability of cell proliferation was tested via CCK-8 and colony formation assays. Transfections were performed to knockdown SNHG16 and its target gene p21. The cell cycles and cell apoptosis were evaluated using flow cytometry, and the expression of SNHG16, p21 and apoptosis biomarkers were qualified with qRT-PCR and western blot assays. The expression of SNHG16 were up-regulated in both glioma tissues and cell lines. Knockdown of SNHG16 was associated with poor proliferation, decreased monoclonal formation rates, but increased apoptosis rates, which also caused the high expression of p21. Moreover, p21 could mediate cell proliferation and monoclonal formation, promote cell apoptosis in glioma, which was negatively correlated with lncRNA SNHG16. The molecule mechanism experiments revealed that SNHG16 could not only inhibit the expression of p21 but also suppressed the level of caspase 3 and 9, while promoted cyclinD1 and cyclinB1 expression. lncRNA SNHG16 could promote the cell proliferation and inhibit the apoptosis of glioma through suppressing p21, indicating that lncRNA SNHG16 might be quite vital for the diagnosis and progression of glioma and could even be a novel therapeutic target for glioma.

miR­483­3p regulates osteogenic differentiation of bone marrow mesenchymal stem cells by targeting STAT1.

Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is regulated by a variety of intracellular regulatory factors including osterix, runt­related transcription factor 2 (RUNX2), bone morphogenetic proteins and transforming growth factorß. Recent studies have shown that microRNAs (miRs) serve a crucial role in this process. In the present study, miR­483­3p levels were significantly increased during osteogenic differentiation of mouse and human BMSCs. Overexpression of miR­483­3p promoted osteogenic differentiation, whereas inhibition of miR­483­3p reversed these effects. miR­483­3p regulated osteogenic differentiation of BMSCs by targeting STAT1, and thus enhancing RUNX2 transcriptional activity and RUNX2 nuclear translocation. In vivo, overexpression of miR­483­3p using a BMSC­specific aptamer delivery system stimulated bone formation in aged mice. Therefore, the present study suggested that miR­483­3p promoted osteogenic differentiation of BMSCs by targeting STAT1, and miR­483­3 prepresent a potential therapeutic target for age­related bone loss.

miR-125a inhibits the migration and invasion of liver cancer cells via suppression of the PI3K/AKT/mTOR signaling pathway.

In order to explore the regulation of the invasive ability of hepatocellular carcinoma cells and the underlying mechanism, mimics sequences of microRNA (miR)-125a (miR-125a-3p/5p) and scramble sequences (miR-125a-3p-s/5p-s) were transfected into human hepatocellular carcinoma cell lines, HCC-LM3 and HepG2, and the non-malignant epithelioid hepatic cell line QZG. To inhibit and upregulate the expression of miR-125a individually. Protein expression was detected by western blotting, and the cell proliferation and migration abilities were evaluated by soft agar colony formation and Transwell assay, respectively. It was revealed that the expression of miR-125a was downregulated in HepG2 and HCC-LM3 cells compared with that of QZG cells, and expression was markedly lower in HCC-LM3 cells than that in HepG2 cells (P<0.01). The colony formation and migration rates of the cells transfected with miR-125a-3p/5p were decreased compared with negative controls, but were increased in cells transfected with miR-125a-3p-3/5p-s (P<0.01). The protein and messenger RNA expression of phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) was decreased following transfection with miR-125a-5p, whereas expression was increased compared with negative controls following transfection with miR-125a-5p-s (P<0.01). Furthermore, the proliferation and migration abilities of cells were attenuated following inhibition of the PI3K/AKT/mTOR pathway by LY294002. The results of the present study indicated that miR-125a inhibits the invasive ability of hepatocellular carcinoma cells via regulation of the PI3K/AKT/mTOR pathway.

[Clinical analysis of hysteroscopic surgery for cesarean scar pregnancy in 64 cases].

OBJECTIVE: To explore the rationale therapy method of hysteroscopic surgery for cesarean scar pregnancy. METHODS: A retrospective review of medical records of 64 patients with cesarean scar pregnancy admitted in Shengjing Hospital of China Medical University from January 2006 to April 2009 was performed, 27 cases out of them were referred from other institutions, and received various interventions before admission, while 37 cases were admitted to our hospital without prior treatments. RESULTS: The diagnosis was confirmed by serum human chorionic gonadotropin-beta subunit (beta-hCG) and ultrasound. Sixty-three patients were removed of conceptive tissues underwent hysteroscopy assisted by ultrasonic guidance, while 1 patient underwent hysteroscopic removal of conceptive tissues assisted by laparoscopic surveillance. Seven cases of sixty-four were experienced second salvage operation. Pathological examinations were performed for all cases and 1 case was diagnosed to be choriocarcinoma. CONCLUSION: Hysteroscopic removal of conceptive tissues implanted in the cesarean section scar seems to be a feasible and safe procedure that might be considered as a treatment option and it should be monitor the levels of beta-hCG and the residual lesions after surgery.