Benign prostatic hyperplasia (BPH) is highly prevalent among older men, impacting on their quality of life, sexual function, and genitourinary health, and has become an important global burden of disease. Transurethral plasmakinetic resection of prostate (TUPKP) is one of the foremost surgical procedures for the treatment of BPH. It has become well established in clinical practice with good efficacy and safety. In 2018, we issued the guideline “2018 Standard Edition”. However much new direct evidence has now emerged and this may change some of previous recommendations. The time is ripe to develop new evidence-based guidelines, so we formed a working group of clinical experts and methodologists. The steering group members posed 31 questions relevant to the management of TUPKP for BPH covering the following areas: questions relevant to the perioperative period (preoperative, intraoperative, and postoperative) of TUPKP in the treatment of BPH, postoperative complications and the level of surgeons’ surgical skill. We searched the literature for direct evidence on the management of TUPKP for BPH, and assessed its certainty generated recommendations using the grade criteria by the European Association of Urology. Recommendations were either strong or weak, or in the form of an ungraded consensus-based statement. Finally, we issued 36 statements. Among them, 23 carried strong recommendations, and 13 carried weak recommendations for the stated procedure. They covered questions relevant to the aforementioned three areas. The preoperative period for TUPKP in the treatment of BPH included indications and contraindications for TUPKP, precautions for preoperative preparation in patients with renal impairment and urinary tract infection due to urinary retention, and preoperative prophylactic use of antibiotics. Questions relevant to the intraoperative period incorporated surgical operation techniques and prevention and management of bladder explosion. The application to different populations incorporating the efficacy and safety of TUPKP in the treatment of normal volume (< 80 ml) and large-volume (≥ 80 ml) BPH compared with transurethral urethral resection prostate, transurethral plasmakinetic enucleation of prostate and open prostatectomy; the efficacy and safety of TUPKP in high-risk populations and among people taking anticoagulant (antithrombotic) drugs. Questions relevant to the postoperative period incorporated the time and speed of flushing, the time indwelling catheters are needed, principles of postoperative therapeutic use of antibiotics, follow-up time and follow-up content. Questions related to complications incorporated types of complications and their incidence, postoperative leukocyturia, the treatment measures for the perforation and extravasation of the capsule, transurethral resection syndrome, postoperative bleeding, urinary catheter blockage, bladder spasm, overactive bladder, urinary incontinence, urethral stricture, rectal injury during surgery, postoperative erectile dysfunction and retrograde ejaculation. Final questions were related to surgeons’ skills when performing TUPKP for the treatment of BPH. We hope these recommendations can help support healthcare workers caring for patients having TUPKP for the treatment of BPH.

Oxidative stress and inflammatory response are closely related to nephrolithiasis. This study is aimed at exploring whether rosiglitazone (ROSI), a regulator of macrophage (Mp) polarization, could reduce renal calcium oxalate (CaOx) deposition by ameliorating oxidative stress and inflammatory response. Male C57 mice were equally and randomly divided into 7 groups. Kidney sections were collected on day 5 or day 8 after treatment. Pizzolato staining and polarized light optical microscopy were used to detect crystal deposition. PAS staining and TUNEL assay were performed to assess the tubular injury and cell apoptosis, respectively. Gene expression was assessed by immunohistochemistry, immunofluorescence, ELISA, qRT‐PCR, and Western blot. The reactive oxygen species (ROS) level was assessed using a fluorescence microplate and fluorescence microscope. Hydrogen peroxide (H₂O₂), malonaldehyde (MDA), and glutathione (GSH) were evaluated to determine oxidative stress. Lactic dehydrogenase (LDH) activity was examined to detect cell injury. Adhesion of CaOx monohydrate (COM) crystals to HK‐2 cells was detected by crystal adhesion assay. HK‐2 cell death or renal macrophage polarization was assessed by flow cytometry. In vivo, renal crystal deposition, tubular injury, crystal adhesion, cell apoptosis, oxidative stress, and inflammatory response were significantly increased in the 7‐day glyoxylic acid‐ (Gly‐) treated group but were decreased in the ROSI‐treated groups, especially in the groups pretreated with ROSI. Moreover, ROSI significantly reduced renal Mp aggregation and M1Mp polarization but significantly enhanced renal M2Mp polarization. In vitro, ROSI significantly suppressed renal injury, apoptosis, and crystal adhesion of HK‐2 cells and markedly shifted COM‐stimulated M1Mps to M2Mps, presenting an anti‐inflammatory effect. Furthermore, ROSI significantly suppressed oxidative stress by promoting the Nrf2/HO‐1 pathway in HK‐2 cells. These findings indicate that ROSI could ameliorate renal tubular injury that resulted from oxidative stress and inflammatory response by suppressing M1Mp polarization and promoting M2Mp polarization. Therefore, ROSI is a potential therapeutic and preventive drug for CaOx nephrolithiasis.

Background: Clinical studies assessing the feasibility and accuracy of three stone scoring systems’s (SSSs: Guy’s stone score, CROES nomogram and S.T.O.N.E nephrolithometry scoring system) have reported contradictory outcomes. This systematic evaluation was performed to obtain comprehensive evidence with regard to the feasibility and accuracy of three SSSs. Methods: A systematic search of Embase, Pubmed, Medline, and the Cochrane Library was conducted to identify studies that compared three SSSs up to Mar 2018. Patients were categorized according to stone free (SF) and no-stone free (NSF), Outcomes of interest included perioperative variables, stone-free rate (SFR), and complications. Results: Ten studies estimating three SSSs were included for meta-analysis. The results showed that SF patients had a significantly lower proportion of male (OR = 1.48, P = 0.0007), lower stone burden (WMD = -504.28, P < 0.0001), fewer No of involved calyces (OR = -1.23, P = 0.0007) and lower proportion of staghorn stone (OR = 0.33, P < 0.0001). Moreover, SF patients had significantly lower score of Guy score (WMD = -0.64, P < 0.0001), but, S.T.O.N.E. score (WMD = -1.23, P < 0.0001) and a higher score of CROES nomogram (WMD = 29.48, P = 0.003). However, the comparison of area under curves (AUC) of predicting SFR indicated that there was no remarkable difference between three SSSs. Nonetheless, Guy score was the only stone scoring system that predicted complications after PCNL (WMD = -0.29, 95% CI: − 0.57 to − 0.02, P = 0.03). Conclusions: Our meta-analysis indicated that the three SSSs were equally, feasible and accurate for predicting SFR after PCNL. However, Guy score was the only stone scoring system that predicted complications after PCNL.

Oxalate and calcium are the major risk factors for calcium oxalate (CaOx) stone formation. However, the exact mechanism remains unclear. This study was designed to confirm the potential function of miR-155-5p in the formation of CaOx induced by oxalate and calcium oxalate monohydrate (COM). The HK-2 cells were treated by the different concentrations of oxalate and COM for 48 h. We found that oxalate and COM treatment significantly increased ROS generation, LDH release, cellular MDA levels, and H₂O₂ concentration in HK-2 cells. The results of qRT-PCR and western blot showed that expression of NOX2 was upregulated, while that of SOD-2 was downregulated following the treatment with oxalate and COM in HK-2 cells. Moreover, the results of miRNA microarray analysis showed that miR-155-5p was significantly upregulated after oxalate and COM treated in HK-2 cells, but miR-155-5p inhibitor treatment significantly decreased ROS generation, LDH release, cellular MDA levels, and H₂O₂ concentration in HK-2 cells incubated with oxalate and COM. miR-155-5p negatively regulated the expression level of MGP via directly targeting its 3′-UTR, verified by the Dual-Luciferase Reporter System. In vivo, polarized light optical microphotography showed that CaOx crystal significantly increased in the high-dose oxalate and Ca²⁺ groups compared to the control group. Furthermore, IHC analyses showed strong positive staining intensity for the NOX-2 protein in the high-dose oxalate and Ca²⁺-treated mouse kidneys, and miR-155-5p overexpression can further enhance its expression. However, the expression of SOD-2 protein was weakly stained. In conclusion, our study indicates that miR-155-5p promotes oxalate- and COM-induced kidney oxidative stress injury by suppressing MGP expression.

A circadian rhythm is an internalized timing system that synchronizes the cellular, behavioral, and physiological processes of organisms to the Earth’s rotation. Because all physiological activities occur at a specific time, circadian rhythm disturbances can lead to various pathological disorders and diseases. Growing evidence has shown that the circadian clock is tightly connected to male fertility, and circadian perturbations contribute to infertility. The night shiftwork, insufficient sleep, and poor sleep quality are common causes of circadian disturbances, and many studies have reported that they impair sperm quality and increase the risk of male infertility. However, research on the impacts of light, body temperature, and circadian/circannual rhythms is relatively lacking, although some correlations have been demonstrated. Moreover, as the index of sperm quality was diverse and study designs were non-uniform, the conclusions were temporarily inconsistent and underlying mechanisms remain unclear. A better understanding of whether and how circadian disturbances regulate male fertility will be meaningful, as more scientific work schedules and rational lifestyles might help improve infertility.

Background: MicroRNA‐33a (miR‐33a) plays the role of the tumor suppressor gene by regulating the expression level of downstream genes. However, the effects of miR‐33a in renal cell cancer (RCC) remain unknown. Our study was designed to investigate the expression level and potential function of miR‐33a in RCC.Methods: RT‐qPCR was applied to measure the levels of miR‐33a in RCC tissues and cell lines. Western blotting and luciferase reporter assay were used to detect the relationship between miR‐33a and Mouse double minute 4 (MDM4) in RCC cells. CCK‐8 and flow cytometry were applied to detected cell viability and cell cycle. Animal models and TUNEL assay were applied to detect the effect of miR‐33a on the growth of RCC and cell apoptosis.Results: We found that the levels of miR‐33a were significantly decreased in RCC tissues and cell lines. Moreover, the low expression of miR‐33a in RCC patients indicated a shorter overall survival (OS). Notably, MDM4 as a direct target of miR‐33a in RCC, the expression level of MDM4 was significantly increased in RCC cells group than the control group. Furthermore, miR‐33a overexpression significantly inhibited RCC cells growth than the control group, while the inhibitory effects of miR‐33a were reversed upon the overexpression of MDM4. Luciferase reporter assays showed that there was a direct interaction between miR‐33a and 3′ UTR of MDM4 mRNA. In vivo, tumor volumes and weight were significantly decreased in the transfected miR‐33a mimics group than the control group.Conclusion: Taken together, our study indicates that miR‐33a inhibits RCC cell growth by targeting MDM4.