ObjectiveAnorectal malformations (ARMs) are one of the commonest anomalies in neonates. Both laparoscopically assisted anorectal pull-through (LAARP) and posterior sagittal anorectoplasty (PSARP) can be used for the treatment of ARMs. The aim of this systematic review and meta-analysis is to compare these two approaches in terms of intraoperative and postoperative outcomes.MethodsMEDLINE, Embase, Web of Science and the Cochrane Library were searched from 2000 to August 2016. Both randomized and non-randomized studies, assessing LAARP and PSARP in pediatric patients with high/intermediate ARMs, were included. The primary outcome measures were operative time, length of hospital stay and total postoperative complications. The second outcome measures were rectal prolapse, anal stenosis, wound infection/dehiscence, anorectal manometry, Kelly's clinical score, and Krickenbeck classification. The quality of the randomized and non-randomized studies was assessed using the Cochrane Collaboration's Risk of Bias tool and Newcastle-Ottawa scale (NOS) respectively. The quality of evidence was assessed by GRADEpro.ResultsFrom 332 retrieved articles, 1, 1, and 8 of randomized control, prospective and retrospective studies, respectively, met the inclusion criteria. The randomized clinical trial was judged to be of low risk of bias, and the nine cohort studies were of moderate to high quality. 191 and 169 pediatric participants had undergone LAARP and PSARP, respectively. Shorter hospital stays, less wound infection/dehiscence, higher anal canal resting pressure, and a lower incidence of grade 2 or 3 constipation were obtained after LAARP compared with PSARP group values. Besides, the LAARP group had marginally less total postoperative complications. However, the result of operative time was inconclusive; meanwhile, there was no significant difference in rectal prolapse, anal stenosis, anorectal manometry, Kelly's clinical score and Krickenbeck classification.ConclusionFor pediatric patients with high/intermediate anorectal malformations, LAARP is a better option compared with PSARP. However, the quality of evidence was very low to moderate.

No abstract

The aim of the present study was to investigate the effect of the serum of patients with secondary hyperparathyroidism (SHPT) on endothelial cells and to examine the protective effect and the possible mechanism of Klotho. A total of three types of mixed serum from 15 patients with SHPT scheduled for parathyroidectomy, 10 chronic kidney disease (CKD) patients at stage 5 without SHPT and 15 healthy volunteers were collected. Initially, human umbilical vein endothelial cells (HUVECs) were incubated in vitro with the three types of serum and levels of proliferation were compared by assessing viable cell numbers with cell counting kit-8 (CCK-8). Subsequently, HUVECs were divided into three groups: Control group (healthy serum medium), SHPT group (SHPT serum) and Klotho treatment group (SHPT serum and Klotho). The proliferative and apoptotic levels of endothelial cells were evaluated by CCK-8 and flow cytometry, respectively. The levels of extracellular signal-regulated kinase (ERK1/2) and phosphorylated forms of ERK1/2 (p-ERK1/2) were detected using western blotting (with or without ERK1/2 inhibitor PD98059). The synthesis of nitric oxide (NO) was measured using the nitrate reduction method. The proliferation of HUVECs was inhibited by the serum from SHPT patients and CKD-5 patients without SHPT and the inhibitory effects of the SHPT serum were the most marked (P<0.05). Inhibition of HUVEC proliferation by SHPT serum occurred in a concentration-dependent manner within a specific range (5-20%; P<0.05) and also in a time-dependent manner within 6-24 h. Proliferation was partly restored and apoptosis was inhibited when 50-100 ng/ml Klotho was added into 10% SHPT serum (P<0.05). At the same time, the expression of p-ERK1/2 was upregulated, which may be inhibited by PD98059. The synthesis of NO was decreased in the SHPT group (P<0.05) and increased following treatment with Klotho (P<0.05). The results of the present study indicated that the proliferation of HUVECs was inhibited by the serum from SHPT patients. Klotho may partly antagonize this effect due to its inhibition of HUVEC apoptosis and upregulation of p-ERK1/2.

Purpose: To determine the role of embryonal transcription factor OCT4 in cisplatin treatment of testicular embryonal carcinoma. Methods: In vitro assays were employed to assess the effect of cisplatin treatment on testicular embryonal carcinoma cell lines under OCT4 silencing. Following treatment with 500 ng/μL cisplatin, MTT assay was used to examine cell proliferation of 2012-EP and 833K-E cells with or without OCT silencing, while wound healing assay was used to examine cell migration ability. Transwell assay and crystal violet staining were employed to measure cell invasive capacity, whereas the distribution pattern of cell cycle was assessed by flow cytometry. The expression levels of several critical components in tumorigenicity related pathways with or without OCT silencing were determined by Western-blot analysis. Results: Cisplatin enhanced OCT4-silenced cell viability at all concentration (p < 0.01) when compared to control cells. Upon treatment with 500 ng/μL cisplatin, OCT4-silenced cells showed 2-to 3-fold enhancement in cell proliferation (p < 0.001), 2-fold increase in cell migration capacity (p < 0.001), and about 1.5-fold enhancement in invasive capacity (p < 0.001) when compared to control cells. In addition, OCT4 silencing upregulated the expression level of the proteins involved in cell proliferation, cell mobility, cancer metastasis and cell cycle control. Conclusion: The results suggest that OCT4 may serve as a therapeutic target for testicular embryonal carcinoma treatment in combination with cisplatin by modulating OCT4 expression level. This physiological evidence indicates that OCT4 downregulation contributes to cisplatin resistance in chemotherapy and subsequent disease relapse.