The new device can be applied to an overwhelming majority of patients with phimosis and excess foreskin. This technique is relatively simple to perform, and patients who underwent this surgery had very few complications. Antibiotics were not required and patients reported less pain than those who were circumcised using conventional methods. Circumcision with this device requires minimal tissue manipulation, and is quicker and safer than circumcision using conventional techniques.

MicroRNA (miRNA or miR)‑485 is a functional miRNA which has received much attention in recent years. However, little is known about the expression of miR‑485 or the role it plays in bladder cancer [namely in metastasis and epithelial‑mesenchymal transition (EMT)]. Thus, in the present study, we aimed to detect the expression of miR‑485 in human bladder cancer tissues and bladder cancer cell lines, and to examine the effects of miR‑485‑5p on bladder cancer cell metastasis and EMT. We found that the expression of miR‑485‑5p was downregulated in the human bladder cancer tissues and different bladder cancer cell lines compared with the normal tissues and cell lines, as demonstrated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). We enforced the expression of miR‑485‑5p in T24 cells and inhibited the expression of miR‑485‑5p in SW780 cells by transfection with miR‑485‑5p mimic or miR‑485‑5p inhibitor, respectively. The ectopic expression of miR‑485‑5p was shown to inhibit cell metastasis and EMT, whereas the inhibition of miR‑485‑5p expression promoted cell metastasis and EMT, as shown by transwell‑matrigel assay, cell adhesion assay and western blot analysis. Furthermore, a luciferase reporter assay revealed that high mobility group AT‑hook 2 (HMGA2) was a direct target of miR‑485‑5p and that the overexpression of HMGA2 reversed the effects of miR‑485‑5p on cell metastasis and EMT. In conclusion and to the very best of our knowledge, the present study, for the first time, identified miR‑485‑5p as a suppressive miRNA in human bladder cancer, and demonstrated that miR‑485‑5p inhibits cell metastasis and EMT at least partly through the suppression of HMGA2 expression.

ObjectiveMicroRNA-100 (miR-100) has been demonstrated to be downregulated in bladder cancer tissues, and enforced expression of this miRNA may inhibit cell growth and colony formation of human bladder cancer 5637 cells in vitro. However, the clinical significance of miR-100 in human bladder cancer has not yet been elucidated. Thus, the aim of this study was to investigate the diagnostic and prognostic values of miR-100 in this disease.MethodsExpression levels of miR-100 in 126 pairs of bladder cancer and adjacent normal tissues were detected by TaqMan real-time quantitative RT-PCR assay. In order to determine its prognostic value, overall survival (OS) and progression-free survival (PFS) were evaluated using the Kaplan-Meier method, and multivariate analysis was performed using the Cox proportional hazard analysis.ResultsExpression levels of miR-100 in bladder cancer tissues were significantly lower than those in adjacent normal tissues (mean expression level: 2.6 ± 1.2 vs. 3.9 ± 1.5, P < 0.001). When categorized into low vs. high expression, low miR-100 expression was negatively associated with the stage (P = 0.01), the recurrence (P = 0.008), the progression (P = 0.01), and the death (P < 0.001) of patients with bladder cancer. Moreover, low miR-100 expression clearly predicted poorer PFS (P = 0.001) and OS (P < 0.001). In the multivariate analysis, low miR-100 expression was an independent prognostic factor for both PFS (P = 0.01) and OS (P = 0.008).ConclusionOur data offer the convincing evidence that miR-100 may play an important role in the progression of bladder cancer and that the reduced expression of this miRNA may be independently associated with shorter PFS and OS of patients, suggesting that miR-100 might be a potential marker for further risk stratification in the treatment of this cancer.Virtual slidesThe virtual slides’ for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1105483419841671

BackgroundBRAF-activated long non-coding RNA (BANCR) has been associated with various types of cancer. Nevertheless, the role of BANCR in clear cell renal cell carcinoma (ccRCC) is still not fully understood. This study aims to investigate the relationship between ccRCC and BANCR.MethodsExpression of BANCR in TCGA renal cancer data sets was analyzed. The expression pattern of BANCR in Immortalized normal human proximal tubule epithelial cell line HK-2 and ccRCC cell lines (ACHN, CAKI-1, A498 and 786-O) was detected by real-time quantitative RT-PCR (qRT-PCR). ccRCC tissues with adjacent normal renal tissues diagnosed by pathological methods from 62 patients were used to detect the expression of BANCR, and its correlation with prognosis of ccRCC patients was assessed by Kaplan-Meier method. The LV-BANCR vector was used to examine the influence of BANCR on the proliferation, migration, invasion, apoptosis and cell cycle distribution of ccRCC cells in vitro.ResultsBANCR was downregulated in renal cancer according to TCGA data sets. Compared with adjacent normal renal tissues and normal human proximal tubule epithelial cell line HK-2, BANCR expression was significantly decreased in ccRCC tissues and ccRCC cell lines, and its low expression was associated with poor prognosis. Moreover, in the condition of BANCR overexpression by LV-BANCR vector, the proliferation, migration, invasion capacity of ccRCC cells was inhibited, while the apoptosis was increased and the G1 cell cycle arrest was induced in vitro.ConclusionsBANCR is downregulated in ccRCC tissues and cell lines, and is associated with ccRCC progression. Thus, BANCR may represent a novel prognostic biomarker and a potential therapeutic target for ccRCC patients.

To investigate the role of centromere protein U (CENPU) in human bladder cancer (BCa), CENPU gene expression was evaluated in human BCa tissues. We used real-time quantitative PCR (qPCR) and found that CENPU gene expression in human BCa tissues was higher compared to that observed in cancer-adjacent normal tissues. High CENPU expression was found to be strongly correlated with tumor size and TNM stage. Kaplan-Meier survival analysis indicated that high CENPU levels were associated with reduced survival. We used a lentivirus to silence endogenous CENPU gene expression in the BCa T24 cell line. CENPU knockdown was confirmed by qPCR. Cellomic imaging and BrdU assays showed that cell proliferation was significantly reduced in the CENPU-silenced cells compared to that noted in the control cells. Flow cytometry revealed that in the CENPU-silenced cells the cell cycle was arrested at the G1 phase relative to that in the control cells. In addition, apoptosis was significantly increased in the CENPU-silenced cells. Giemsa staining showed that CENPU-silenced cells, compared to control cells, displayed a significantly lower number of cell colonies. The genome-wide effect of CENPU knockdown showed that a total of 1,274 differentially expressed genes was found, including 809 downregulated genes and 465 upregulated genes. Network analysis by Ingenuity Pathway Analysis (IPA) resulted in 25 distinct signaling pathways, including the top-ranked network: ‘Cellular compromise, organismal injury and abnormalities, skeletal and muscular disorders’. In-depth IPA analysis revealed that CENPU was associated with the HMGB1 signaling pathway. qPCR and western blot analysis demonstrated that in the HMGB1 signaling pathway, CENPU knockdown downregulated expression levels of ILB, CXCL8, RAC1 and IL1A. In conclusion, our data may provide a potential pathway signature for therapeutic targets with which to treat BCa.

Background: This study aimed to determine the potential utility of plasma fibrinogen as a prognostic factor in patients with bladder cancer (BCa) after radical cystectomy (RC). Methods: Patients with BCa who underwent RC from 2014 to 2019 were analyzed retrospectively. The indexes of plasma coagulation and fibrinolysis system factors were collected. Kaplan-Meier survival curves were used to calculate the overall survival (OS) and diseasefree survival (DFS). The prognostic value of plasma fibrinogen was analyzed by using Cox regression model, and a nomogram of BCa based on plasma fibrinogen was generated by R software. Results: Among 145 patients, the optimal cutoff value of plasma fibrinogen was 3.14g/L. High level of plasma fibrinogen was related to the poor prognosis of patients with BCa, and plasma fibrinogen has a more accurate prognostic ability than other plasma coagulation and fibrinolysis system factors. Multivariate Cox regression analysis showed that plasma fibrinogen was an independent predictor of OS (>3.14 vs ≤3.14 HR, 2.58, 95% CI = 1.28-5.23; p = 0.008) and DFS (>3.14 vs ≤3.14 HR, 2.60, 95% CI = 1.20-5.65; p = 0.016), and the nomogram based on plasma fibrinogen had better accuracy and discrimination (area under the curve (AUC): OS = 0.741, DFS = 0.733). Conclusion: Plasma fibrinogen can be used as an independent predictor of OS and DFS for RC patients, and the nomogram based on plasma fibrinogen was a reliable model for predicting the prognosis after RC.

Object: In order to promote the functional recovery of median nerve rupture patients, this paper proposes an ultrasound-guided percutaneous nerve stimulation regimen based on finite element modeling. Method: First, according to anatomy feature, a multi-layer human forearm model is constructed. What’s more, taking current density and activate function as optimization indicators, the percutaneous nerve stimulation regimen is designed with finite element modeling, including electrical needle angel, distance and position. Finally, to test the performance of designed regimen, a total of 22 patients with median nerve rupture participate in the clinical randomized controlled trial. And the clinical treatment effect is evaluated with BMRC, grip strength, functional score of median nerve and DASH scores. Results: The designed percutaneous nerve stimulation regimen is that, parallel to each other, electrical needles are located at both ends of the injury nerve with a distance of 3 cm. Besides, clinical trial results show that, after treatment the difference in sensory function was statistically significant. In terms of motor function, the BMRC of motor and grip strength are improved in both groups after treatment and there are significant differences between groups. Besides the grip strength improvement of experimental group is 4 times higher than that of control group. On global function, the DASH scores are reduced by 29% with experimental group but only 8% with control group; functional score of median nerve improved by 24% in the experimental group and by 22% in the control group, but the difference between groups is statistically significant after treatment. Conclusion: Clinical trial results demonstrate that the designed percutaneous nerve stimulation regimen can significantly improve the sensory, motor and global function of median nerve rupture, which is a potential clinical treatment regimen. Trial registration: ChiCTR, ChiCTR2000030790. Registered14 march 2020, http://www.chictr.org.cn/ChiCTR2000030790

Purpose To investigate the role of PI3k/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion(I/R). Methods Male Sprague-Dawley rats were subjected to 45 min of ischemia by occluding the superior mesenteric artery and to 2h of reperfusion to establish the model of I/R. Twenty four rats were randomly divided into four groups: Sham, intestinal I/R (II/R), propofol (P), wortmannin (W). In groups P, W, propofol was injected intravenously and continuously at the onset of reperfusion via infusion pump. PI3K inhibitor (wortmannin) was administered intravenously in group W 25 min before ischemia. Intestinal tissues and lung tissues were obtained for determination of histologic injury, wet/dry weight ratio, malondialdehyde (MDA) levels, superoxide dismutase (SOD) and myeloperoxidase (MPO) activities. Meanwhile, the expressions of caspase-3 and phosphorylated Akt (p-Akt) in intestines and lungs were detected by western blot. Results Propofol treatment alleviated intestinal and lung morphological changes which were observed in II/R group , Moreover, wet/dry weight ratio, the MDA level, MPO activity and expression of caspase-3 were significantly decreased whereas the SOD activity and p-Akt expression were significantly increased. Notably, the protections were significantly reversed by pretreatment of wortmannin. Conclusion: PI3K/Akt pathway activation play a critical role in the protective effects of propofol on intestinal and lung injury induced by ischemia/reperfusion.