Different Surgical Approaches to 313 Cesarean Scar Pregnancies.

STUDY OBJECTIVE: To evaluate the efficacy of different surgical treatments for cesarean scar pregnancy (CSP). DESIGN: Retrospective study (Canadian Task Force classification II-3). SETTING: Affiliated university hospitals. PATIENTS: Women (n = 313) with CSP. INTERVENTIONS: Dilation and curettage under ultrasound guidance (DCUS, n = 124), dilation and curettage with hysteroscopic guidance (DCH, n = 103), vaginal excision (n = 55), laparotomy (n = 12), and laparoscopy (n = 19). MEASUREMENTS AND MAIN RESULTS: Undetectable serum human chorionic gonadotropin (hCG) levels and thickness of the uterine scar were measured before and after surgery. Success rates of the 5 surgical treatments of CSP (DCUS, DCH, vaginal excision, laparotomy, and laparoscopy) ranged between 89% and 100%. Postoperative treatment was not needed in the vaginal and laparotomy groups, and vaginal treatment was associated with shorter operative time than laparotomy and laparoscopy and shorter time to undetectable hCG levels than DCUS and DCH. Serum hCG levels on day 3 after surgery were significantly lower than baseline levels in all groups of patients, but there was no significant difference between levels on days 3 and 5 postoperatively. Median scar thickness after surgery in the vaginal surgery, laparotomy, and laparoscopy groups was thicker than that in the DCUS and DCH groups. CONCLUSION: In certain circumstances, CSP can be treated simply by DCH or DCUS. However, time to undetectable hCG levels is prolonged compared with more invasive techniques.

Endoscopy-assisted inguinal lymphadenectomy in vulvar cancer.

OBJECTIVE: To explore the feasibility and efficiency of video endoscopic inguinal lymphadenectomy (VEIL) for vulvar cancer. METHODS: We evaluated 46 patients with vulvar cancer. Treatment included VEIL using the hypogastric subcutaneous approach (VEIL-H, 17 patients), VEIL with the limb subcutaneous surgical approach (VEIL-L, 8 patients), and open inguinal lymphadenectomy (OIL, 21 patients). All patients underwent radical vulvectomy; we evaluated operative time, the amount of bleeding, SF score, recurrence rate, etc. RESULTS: The durations of VEIL-H and VEIL-L were 170.79 ± 18.92 and 180.12 ± 17.88 min, respectively, which were longer than that of OIL (100.68 ± 11.37 min; P = 0.028). Bleeding volumes in the VEIL-H and VEIL-L groups were 15.23 ± 2.17 and 17.16 ± 2.35 ml, respectively; there were significantly lower than that of the OIL group (36.68 ± 3.48 ml; P = 0.021). The numbers of unilateral lymph nodes harvested were similar in all groups. The duration of hospitalization in VEIL group was shorter than that of the OIL group. There were less skin and lymphatic complications after VEIL than after OIL. Total SF-36 scores were significantly higher in the VEIL group than that in the OIL group (P = 0.032). There were no statistically significant differences in local recurrence, distant metastasis, and mortality among the three groups. CONCLUSION: VEIL for vulvar cancer treatment is effective, with the advantages of short hospitalization stay, less bleeding, and reduced postoperative complications comparing the OIL.

Icaritin inhibits decidualization of endometrial stromal cells.

The aim of the present study was to investigate the effects of Icaritin on the proliferation and decidualization of endometrial stromal cells (ESCs). A total of 20 specimens of endometrium were collected during hysterectomy at the Gynecology Department of Shenzhen Nanshan People's Hospital (Shenzhen, China) between August 2014 and December 2015. The endometrium was digested with high concentrations of collagenase and DNase and filtered with meshes, and then the glandular epithelial and stromal cells were separated by the adhesion purification method. The purity of stromal cells was identified by vimetin and cytokeratin 7 immunostaining. The estradiol + progesterone (E2+P4) and/or cyclic adenosine monophosphate (cAMP) were added to induce an in vitro decidualization model, which was used to analyze the effect of Icaritin on the decidualization ability of the human ESCs. The decidualization markers of human ESCs, prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP-1), was analyzed by reverse-transcription quantitative polymerase chain reaction measurements of the mRNA levels, PRL immunostaining and ELISA analysis of the IGFBP-1 protein levels in the cells or cell culture supernatant separately. The results demonstrated that treatment with E2+P4 and/or cAMP for 96 h was able to induce decidualization in ESCs, and that the cells demonstrated polygon-shaped epithelioid changes. The cell nuclei revealed multinuclear changes, and the cells were also observed to be large and round in shape. The PRL expression and upregulated IGFBP-1 mRNA and protein levels in the E2+P4+cAMP treatment group indicated successful decidualization of the in vitro model. However, the addition of Icaritin inhibited the expression of PRL and IGFBP-1 mRNA, as well as IGFBP-1 protein in the induced ESCs compared with groups without Icaritin. These results suggest that Icaritin was able to inhibit the expression of decidualization-related genes in ESCs in vitro. However, the exact mechanisms require further investigation.

Endostar combined with cisplatin inhibits tumor growth and lymphatic metastasis of lewis lung carcinoma xenografts in mice.

OBJECTIVE: To investigate the effects of endostar, a recombined humanized endostatin, plus cisplatin on the growth, lymphangiogenesis and lymphatic metastasis of the Lewis lung carcinoma (LLC) in mice. METHODS: A tumor model were established in C57BL/6 mice by intravenious transplantation of LLC cells. Then the mice were randomized to receive administration with NS, endostar, cisplatin, or endostar plus cisplatin. After the mice were sacrificed, tumor multiplicity, tumor size and lymph node metastasis were assessed. Then the expression of vascular endothelial growth factor-c (VEGF-C) and podoplanin were determined by immunohistochemical staining. RESULTS: Endostar plus cisplatin significantly suppressed tumor growth. lymphatic metastasis and prolonged survival time of the mice without obvious toxicity. The inhibition of lymphatic metastasis was associated with decreased microlymphatic vessel density (MLVD) and expression of VEGF-C. CONCLUSIONS: Endostar combined with cisplatin was more effective to suppress tumor growth and lymphatic metastasis than either agent alone. Thus this may provide a rational alternative for lung carcinoma treatment.

[Effects of endostatin on the growth and lymphangiogenesis of Lewis lung carcinoma xenograft in mice].

OBJECTIVE: to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice. METHODS: lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0.2 ml of 0.9% sodium chloride for 15 days, and treatment group received 500 µg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density (MLVD) were observed by immunohistochemical staining. RESULTS: tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7.8 ± 1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group. CONCLUSION: endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.