[A simplified technique for reconstruction of vesicourethral support in laparoscopic radical prostatectomy improves immediate continence].

OBJECTIVE: To investigate the application of a simplified technique for reconstruction of vesicourethral support (RVUS) in laparoscopic radical prostatectomy (LRP). METHODS: From January 2017 to August 2019, 122 patients with localized prostate cancer underwent extraperitoneal LRP, 65 with RVUS (the RVUS group) and 57 without RVUS (the non-RVUS group). We compared the operation time, intraoperative blood loss, rate of pelvic lymph node dissection, neurovascular bundle sparing, incidence of urethrovesical anastomotic urinary leakage (UVAUL), postoperative urinary continence, postoperative hospital stay, intraperitoneal drainage tube removal time, and urethral catheter removal time between the two groups of patients. RESULTS: No statistically significant differences were observed between the two groups in the operation time, intraoperative blood loss, rate of pelvic lymph node dissection, neurovascular bundle sparing, or urethral catheter removal time (P > 0.05). The incidence rate of UVAUL was lower in the non-RVUS than in the RVUS group (8.8% vs 0%, P < 0.05), and so were the rates of postoperative urinary continence immediate after (0% vs 32.3%, P < 0.05) and at 1 month (38.6% vs 56.9%, P < 0.05), 3 months (59.6% vs 80%, P < 0.05), 6 months (78.9% vs 84.6%, P > 0.05) and 12 months after catheter removal (87.7% vs 92.3%, P > 0.05). The postoperative hospital stay was dramatically longer in the non-RVUS than in the RVUS group (ï¼»9.1 ± 4.3ï¼½ vs ï¼»6.7 ± 1.8ï¼½ d, P < 0.01) and so was the intraperitoneal drainage tube removal time (ï¼»6.9 ± 4.5ï¼½ vs ï¼»4.8 ± 1.5ï¼½ d, P < 0.01). CONCLUSIONS: The simplified technique for reconstruction of vesicourethral support in laparoscopic radical prostatectomy improves early urinary continence, especially immediate continence, decreases the incidence rate of urethrovesical anastomotic urinary leakage, and shortens the intraperitoneal drainage tube removal time and postoperative hospital stay.?

[Hydrogen-rich water improves progressive sperm motility in rats by reducing oxidative stress and upregulating CLDN3 and SRD5A2 expressions].

Objective: To investigate the protective effect of long-term consumption of hydrogen-rich water (HRW) on the percentage of progressively motile sperm (PMS) in male rats. METHODS: Twenty normal healthy male SD rats were equally randomized into an HRW and a control group, the former given HRW (1.2 ppm) and the latter normal saline, both intragastrically at 2 ml/d for 9 months. Then, the bilateral epididymides of the rats were harvested for preparation of sperm suspension and detection of the percentage of PMS. The testis tissue was isolated for HE staining and determination of the expressions of the Ki67, CYBB, eNOS, CLDN3 and SRD5A2 proteins using the streptavidin-peroxidase (SP) immunohistochemical method. RESULTS: The percentage of PMS was significantly higher in the HRW than in the control group (ï¼»64.3 ± 4.7ï¼½% vs ï¼»55.3 ± 9.5ï¼½%, P < 0.05), and so was the expression of Ki67 in the testicular tissue (P < 0.01). Compared with the controls, the rats in the HRW group showed markedly decreased oxidative stress-related index CYBB (P < 0.01), increased eNOS level (P < 0.01), and upregulated expressions of sperm development-related proteins CLDN3 and SRD5A2 (P < 0.01 and P < 0.05). CONCLUSIONS: Hydrogen not only regulates the expressions of some oxidative stress-related indicators, but also increases the expressions of the molecules promoting sperm maturation and motility, which provides a theoretical basis and experimental support for the application and studies of hydrogen in asthenospermia.

Correction: Epalrestat, an Aldose Reductase Inhibitor, Restores Erectile Function in Streptozocin-induced Diabetic Rats.

This Article was originally published under Nature Research's License to Publish, but has now been made available under a CC BY 4.0 license. The PDF and HTML versions of the Article have been modified accordingly.

Epalrestat, an Aldose Reductase Inhibitor, Restores Erectile Function in Streptozocin-induced Diabetic Rats.

Epalrestat, an aldose reductase inhibitor (ARI), was adopted to improve the function of peripheral nerves in diabetic patients. The aim of this study was to investigate whether epalrestat could restore the erectile function of diabetic erectile dysfunction using a rat model. From June 2016, 24 rats were given streptozocin (STZ) to induce the diabetic rat model, and epalrestat was administered to ten diabetic erectile dysfunction (DED) rats. Intracavernous pressure (ICP) and mean systemic arterial pressure (MAP), levels of aldose reductase (AR), nerve growth factor (NGF), neuronal nitric oxide synthase (nNOS), α-smooth muscle antigen (α-SMA), and von Willebrand factor (vWF) in the corpus cavernosum were analyzed. We discovered that epalrestat acted on cavernous tissue and partly restored erectile function. NGF and nNOS levels in the corpora were increased after treatment with epalrestat. We also found that the content of α-SMA-positive smooth muscle cells and vWF-positive endothelial cells in the corpora cavernosum were declined. Accordingly, epalrestat might improve erectile function by increasing the upregulation of NGF and nNOS to restore the function of the dorsal nerve of the penis.

Pancreatic kininogenase improves erectile function in streptozotocin-induced type 2 diabetic rats with erectile dysfunction.

Erectile dysfunction (ED) associated with type 2 diabetes is a severe problem that requires effective treatment. Pancreatic kininogenase (PK) has the potential to improve the erectile function of ED patients. This study aims to investigate the effect of PK on erectile function in streptozotocin-induced type 2 diabetic ED rats. To achieve this goal, we divided male Sprague-Dawley rats into five groups. One group was not treated, and the other four groups were treated with saline, sildenafil, PK or sildenafil, and PK, respectively, for 4 weeks after the induction of type 2 diabetic ED. Then, intracavernous pressure under cavernous nerve stimulation was measured, and penile tissue was collected for further study. Endothelial nitric oxide synthase levels, smooth muscle content, endothelium content, cyclic guanosine monophosphate (cGMP) levels in the corpus cavernosum, and neuronal nitric oxide synthase levels in the dorsal penile nerve were measured. Improved erectile function and endothelium and smooth muscle content in the corpus cavernosum were observed in diabetic ED rats. When treating diabetic ED rats with PK and sildenafil at the same time, a better therapeutic effect was achieved. These data demonstrate that intraperitoneal injection of PK can improve erectile function in a rat model of type 2 diabetic ED. With further research on specific mechanisms of erectile function improvement, PK may become a novel treatment for diabetic ED.

[Correlation of abnormal topological properties of the white matter fibers connecting the left amygdale with psychogenic erectile dysfunction].

OBJECTIVE: To explore the topological properties of the degree and strength of nodes in the binary and weighted brain white matter networks of the patients with psychogenic erectile dysfunction (pED) and analyze the changes of myelin integrity, number and length of the white matter fibers in the topological space. METHODS: Diffusion tensor imaging data were obtained from 21 patients with pED and 24 healthy controls matched in sex, age, and years of education and subjected to preprocessing. The whole cerebral cortex was divided into 90 regions, followed by fiber tracking, construction of the binary and weighted white matter networks, and calculation of the node degrees and connectivity strengths in different brain regions. The property values were compared between the two groups using the two-sample t-test, the results were corrected by multiple testing correction, and the correlation of the property values with the erectile function of the patients was subjected to Pearson's correlation analysis. RESULTS: Compared with the healthy controls, the pED patients showed significantly decreased node degree of the left triangular part of inferior frontal gyrus (IFG) (7.54±1.44 vs 5.95±1.28, t = －3.88, corrected P = 0.02), medial orbital part of superior frontal gyrus (SFG) (10.08±3.60 vs 6.29±3.30, t = －3.67, corrected P = 0.02), and amygdala (6.50±2.11 vs 4.29±1.31, t = －4.16, corrected P = 0.01) in the binary networks, as well as the connectivity strength of the left triangular part of IFG (2.50±0.68 vs 1.72±0.50, t = －4.35, corrected P = 0.01), medial orbital part of SFG (3.17±0.97 vs 2.08±1.10, t = －3.53, corrected P = 0.03), and amygdala (1.80±0.69 vs 1.11±0.39, t = －4.03, corrected P = 0.01) in the fractional anisotropy (FA) weighted networks. The node degree of the left amygdala was negatively correlated with the total score (r = －0.47,P = 0.04), second item score (r = －0.46, P = 0.03), and third item score of IIEF-5 (r = －0.45, P = 0.04) in the pED patients. CONCLUSIONS: The myelin integrity of the white matter fibers in the left frontal lobe and amygdale is impaired in pED patients, which leads to the aberrant generation, processing and regulation of their emotions. The decreased pivotal role and importance of the white matter fibers connecting the left amygdale may be associated with pED.

Augmenter of liver regeneration inhibits TGF-ß1-induced renal tubular epithelial-to-mesenchymal transition via suppressing TßR II expression in vitro.

Tubular epithelial-to-mesenchymal transition (EMT) plays a crucial role in the progression of renal tubular interstitial fibrosis (TIF), which subsequently leads to chronic kidney disease (CKD) and eventually, end-stage renal disease (ESRD). We propose that augmenter of liver regeneration (ALR), a member of the newly discovered ALR/Erv1 protein family shown to ameliorate hepatic fibrosis, plays a similar protective role in renal tubular cells and has potential as a new treatment option for CKD. Here, we showed that recombinant human ALR (rhALR) inhibits EMT in renal tubular cells by antagonizing activation of the transforming growth factor-ß1 (TGF-ß1) signaling pathway. Further investigation revealed that rhALR suppresses the expression of TGF-ß receptor type II (TßR II) and significantly alleviates TGF-ß1-induced phosphorylation of Smad2 and nuclear factor-κB (NF-κB). No apparent adverse effects were observed upon the addition of rhALR alone to cells. These findings collectively suggest that ALR plays a role in inhibiting progression of renal tubular EMT, supporting its potential utility as an effective antifibrotic strategy to reverse TIF in CKD.

Augmenter of liver regeneration ameliorates renal fibrosis in rats with obstructive nephropathy.

Renal fibrosis is a hallmark in CKD (chronic kidney disease) and is strongly correlated to the deterioration of renal function that is characterized by tubulointerstitial fibrosis, tubular atrophy, glomerulosclerosis and disruption of the normal architecture of the kidney. ALR (augmenter of liver regeneration) is a growth factor with biological functions similar to those of HGF (hepatocyte growth factor). In this study, our results indicate that endogenous ALR is involved in the pathological progression of renal fibrosis in UUO (unilateral ureteral obstruction) rat model. Moreover, we find that administration of rhALR (recombinant human ALR) significantly alleviates renal interstitial fibrosis and reduces renal-fibrosis-related proteins in UUO rats. Further investigation reveals that rhALR suppresses the up-regulated expression of TGF-ß1 (transforming growth factor ß1) induced by UUO operation in the obstructed kidney, and inhibits Smad2 and Smad3 phosphorylation activated by the UUO-induced injury in the animal model. Therefore we suggest that ALR is involved in the progression of renal fibrosis and administration of rhALR protects the kidney against renal fibrosis by inhibition of TGF-ß/Smad activity.

Exogenous augmenter of liver regeneration (ALR) attenuates inflammatory response in renal hypoxia re-oxygenation injury.

Recent studies have highlighted the role of the innate immune system in initiating the inflammatory cascade which leads to detrimental changes in renal ischemia reperfusion (I/R) injury. The augmenter of liver regeneration (ALR) is an anti-apoptosis factor which is highly expressed in renal tubulars of renal cortex and medulla after inducing renal I/R injury in rats. It has been shown that exogenous ALR can enhance renal tubular regeneration. However, whether ALR's protective effect against renal I/R injury results from its immune regulatory function remains unknown. Using rat renal tubular epithelial cell (NRK-52E), we investigate the effect of recombinant rat ALR (rrALR) on immune inflammatory response in hypoxia re-oxygenation (H/R) injury in vitro, and further discuss the possible mechanisms. Cultured NRK-52E cells subjected to hypoxia for 6 h followed by re-oxygenation for 12, 24 and 72 h are administered with different doses of rrALR. Expression of Toll-like receptor 4 (TLR4) and transcription nuclear factor-κB (NF-κB) is assessed by reverse-transcriptase polymerase chain reaction (RT-PCR) and western blot. Expression of interleukin (IL)-6 and IL-1ß are determined by enzyme-linked immunosorbent assay (ELISA). In rrALR intervened H/R cells, TLR4 and NF-κB are down regulated at both mRNA and protein levels compare with those in control cells. Also, rrALR appears to downregulate IL-6 and IL-1ß expression in concentration-dependent manners. In conclusion, rrALR protects NRK-52E cells from H/R injury possibly by relieving the inflammatory response through regulation of TLR4-NF-κB signaling pathway.

Augmenter of liver regeneration attenuates tubular cell apoptosis in acute kidney injury in rats: the possible mechanisms.

Augmenter of liver regeneration (ALR), the expression of which increased in rat kidneys after renal ischemia/reperfusion (I/R) injury, enhances renal tubular cell regeneration in vivo and in vitro. We aimed to investigate the effects of ALR on apoptosis of renal tubular cells after renal I/R injury in vivo and consider the possible mechanisms. Rats that were subjected to bilateral renal ischemia for 60 min followed by reperfusion were administered with either vehicle or recombinant human ALR (rhALR). Renal dysfunction and histologic injury were assessed by the measurement of serum biochemical markers and histological grading. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL). Caspase-3 activity was measured using a colorimetric protease assay. Expression of Bcl-2, Bax Fas, phosphorylated-Akt (p-Akt), and phosphorylated-p53 (p-p53) was determined by western blotting. Compared with vehicle-treated rats, renal dysfunction and histologic injury were significantly attenuated by administration of rhALR. The number of TUNEL-positive tubular cells and caspase-3 activity were decreased, Bcl-2 and p-Akt expression was up-regulated, and Bax and p-p53 expression was down-regulated by administration of rhALR. However, administration of rhALR had no effect on Fas protein expression. These results indicate that the protective effect of rhALR on renal I/R injury is associated with its anti-apoptotic action in renal tubular cells. RhALR inhibits apoptosis by increasing the ratio of Bcl-2 to Bax and by decreasing the activity of caspase-3. The activation of Akt and inactivation of p53 are involved in the rhALR anti-apoptosis process.