Castration-resistant prostate cancer (CRPC) has been a major cause of tumor-associated death among men worldwide. The discovery of novel therapeutic medicines for CRPC remains imperative. Atractylenolide I (ATR-I), a prominent bioactive component from Atractylodes macrocephala, exhibits powerful anticancer potentials in various malignancies. Nevertheless, the ATR-I’s activity on CRPC has not been reported. An enzalutamide-resistant (EnzR) cell line was successfully constructed. CCK-8, EdU, wound healing, Transwell assays, flow cytometry, and xenograft tumor models were applied to investigate the antitumor activity of ATR-I against CRPC. The changes in the gene expression profiles after ATR-I treatment were analyzed using RNA sequencing. ATR-I suppressed the proliferative and migratory abilities of AR+ and AR− CRPC cells, while triggering cell cycle arrest and apoptosis. ATR-I also exerted anti-cancer activity on EnzR cell lines. Intriguingly, a combination of ATR-I with enzalutamide synergistically induced more apoptosis of tumor cells. RNA-sequencing identified kinesin family member 15 (KIF15) as a potential target of ATR-I. KIF15 was up-regulated in prostate cancer (PCa), and its higher level was associated with poorer clinical outcomes. Further investigation showed that ATR-I mediated ubiquitin-proteasomal degradation of AR/AR-V7 through targeting KIF15, resulting in CRPC repression. Finally, our in vivo experiment verified that ATR-I alone or in combination with enzalutamide retarded the growth of EnzR xenograft tumors. These findings identified ATR-I as a promising therapeutic drug for overcoming enzalutamide resistance in CRPC patients and increased our understanding about its antitumor mechanisms.

BACKGROUND:Calcitriol has the potential to counteract fibrotic diseases beyond its classical action of maintaining calcium and bone metabolism; however, its functional mechanism remains unknown. Autophagy-related gene 16-like 1 (Atg16l1) is one of the genes related to autophagy and is involved in protecting against fibrotic diseases. The present study aimed to explore the contribution of autophagy to the inhibition of calcitriol-induced hepatic fibrosis, as well as its potential molecular mechanism. METHODS:Carbon tetrachloride (Ccl4)-treated mice were established as hepatic fibrosis models and received calcitriol treatment for 6 weeks. Quantification of Sirius red staining and measurement of key fibrotic markers (collagen-1 and α-SMA) was performed to detect hepatic fibrosis. Chloroquine (CQ) treatment was used to observe autophagic flux, and 3-methyladenine (3-MA) was used to inhibit autophagy. Furthermore, the effects of calcitriol on transforming growth factor β1 (TGFβ1)-stimulated primary hepatic stellate cells (HSCs) were detected. Downregulation of Atg16l1 or vitamin D receptor (VDR) in LX-2 cells was used to explore the mechanism of action of calcitriol in fibrosis and autophagy. Additionally, the electrophoretic mobility shift assay (EMSA) was used to investigate the interactions between VDR and ATG16L1. RESULTS:Calcitriol increased the expression of VDR and ATG16L1, enhanced autophagy and attenuated hepatic fibrosis. 3-MA treatment and VDR silencing abolished the protective effects of calcitriol against fibrosis. Calcitriol-induced anti-fibrosis effects were blocked by ATG16L1 suppression. Furthermore, VDR bound to the ATG16L1 promoter and downregulation of VDR decreased the expression of ATG16L1 in LX-2 cells. CONCLUSION:Calcitriol mitigates hepatic fibrosis partly through ATG16L1-mediated autophagy.

Phosphodiesterase-5 inhibitors (PDE5-i) have been widely used in clinical practice for the treatment of erectile dysfunction (ED). However, due to its suboptimal therapeutic effects and side effects, it is necessary to develop new medicines for ED treatment. Botanical drugs have been widely investigated as potential ED treatment drugs and have shown promising therapeutic effects. This review summarized 34 studies, including five botanical drugs with PDE5 inhibitory activity, seven botanical drugs without PDE5 inhibitory activity, and six mixed botanical drugs. The results of clinical studies regarding the aforementioned botanical drugs and relevant mechanisms are summarized in this study. It is necessary to conduct high-quality clinical trials to verify the dosage, targeted patients and therapeutic effects, and further pharmacology experiments are also needed to identify the active compounds.

Background and purpose: Castration-resistant prostate cancer (CRPC) has been a major cause of tumor-associated death among men worldwide. The discovery of novel therapeutic approaches for CRPC remains imperative. Atractylenolide I (ATR-I), a prominent bioactive component from Atractylodes macrocephala, exhibits powerful anticancer potentials in various malignancies. Nevertheless, the ATR-I’s activity on CRPC and its underlying mechanism has not been reported. Experimental approach: An enzalutamide-resistant (EnzR) cell line was successfully constructed. The pharmacological effects of ATR-I were assessed in vitro and in vivo. The changes in the gene expression profiles after ATR-I treatment were analyzed using RNA sequencing (RNA-seq). Key results: ATR-I suppressed the proliferative and migratory abilities of CRPC cells, while triggering cell cycle arrest and apoptosis. In constructed EnzR cells, ATR-I also inhibited their proliferation and promoted apoptosis. Intriguingly, a combination of ATR-I with enzalutamide synergistically induced more apoptosis of EnzR cells. Mechanistically, RNA-seq results identified kinesin family member 15 (KIF15) as a potential target of ATR-I. KIF15 was up-regulated in prostate cancer (PCa), and its higher level was associated with poorer clinical outcomes. Further investigation showed that ATR-I inhibited the expression of KIF15 mRNA and protein, thus mediating ubiquitin-proteasomal degradation of AR/AR-V7. Finally, our in vivo experiment verified that ATR-I alone or in combination with enzalutamide retarded the growth of EnzR xenograft tumors. Conclusion and implications: This study elucidated the antitumor mechanism of ATR-I against CRPC. Notably, ATR-I may be a promising therapeutic drug for CPRC patients and enhance the response to enzalutamide in EnzR patients.

Background and purpose: Castration-resistant prostate cancer (CRPC) has been a major cause of tumor-associated death among men worldwide. The discovery of novel therapeutic approaches for CRPC remains imperative. Atractylenolide I (ATR-I), a prominent bioactive component from Atractylodes macrocephala, exhibits powerful anticancer potentials in various malignancies. Nevertheless, the ATR-I’s activity on CRPC and its underlying mechanism has not been reported. Experimental approach: An enzalutamide-resistant (EnzR) cell line was successfully constructed. The pharmacological effects of ATR-I were assessed in vitro and in vivo. The changes in the gene expression profiles after ATR-I treatment were analyzed using RNA sequencing (RNA-seq). Key results: ATR-I suppressed the proliferative and migratory abilities of CRPC cells, while triggering cell cycle arrest and apoptosis. In constructed EnzR cells, ATR-I also inhibited their proliferation and promoted apoptosis. Intriguingly, a combination of ATR-I with enzalutamide synergistically induced more apoptosis of EnzR cells. Mechanistically, RNA-seq results identified kinesin family member 15 (KIF15) as a potential target of ATR-I. KIF15 was up-regulated in prostate cancer (PCa), and its higher level was associated with poorer clinical outcomes. Further investigation showed that ATR-I inhibited the expression of KIF15 mRNA and protein, thus mediating ubiquitin-proteasomal degradation of AR/AR-V7. Finally, our in vivo experiment verified that ATR-I alone or in combination with enzalutamide retarded the growth of EnzR xenograft tumors. Conclusion and implications: This study elucidated the antitumor mechanism of ATR-I against CRPC. Notably, ATR-I may be a promising therapeutic drug for CPRC patients and enhance the response to enzalutamide in EnzR patients.

患者,男,72岁,因"进行性排尿困难并肉眼血尿半年"就诊于我院泌尿外科.患者于2011年行经腹直肠癌根治术,术后按期化疗.2021年1月因直肠癌复发于我院行腹腔镜下腹会阴联合直肠癌根治术(Miles术)、结肠造口术,术后病理:直肠中-低分化腺癌,侵及直肠周围软组织.患者既往于2018年因冠心病行冠状动脉支架置入术,无家族遗传病史.

Background: Previous studies have shown that oxidative stress contributes to hyperglycemia-induced erectile dysfunction. A preferential direct inhibitor of NOX1 and NOX4, GKT-137831, exhibited a strong anti-oxidative role via blockade of reactive oxygen species (ROS) generation in endothelial cells, but whether GKT-137831 could improve erectile function was not clear. Aim: Our study was designed to investigate the effect of NOX1/4 inhibition on improving diabetic erectile dysfunction (ED) in rats. Methods: We used streptozotocin to induce type 1 diabetes mellitus (DM) in 32 male Sprague Dawley (SD) rats (8 weeks old). Eight weeks later, type 1 diabetes mellitus-induced erectile dysfunction (DMED) in rats was confirmed using an apomorphine test. Our study consisted of 3 groups: (i) nondiabetic control group (n = 8), (ii) DMED + vehicle group (DMED group; n = 8), and (iii) DMED + GKT-137831 group (n = 9); GKT-137831 was given as a once-daily intraperitoneal injection for 4 weeks. Cavernous nerve electrostimulation was used to evaluate erectile function. Western blot, ELISA, immunohistochemistry, and immunofluorescence were used to measure expression of specific proteins, and DHE fluorescent probe was performed to detect ROS level. Outcomes: Intracavernous pressure (ICP), nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway, oxidative stress level, inflammatory response, corporal autophagy, and apoptosis were measured. Results: Erectile function in the DMED group was significantly impaired compared to the nondiabetic control group, whereas this impairment was improved with GKT-137831 treatment by 70%. Similarly, endothelial function and overactivated oxidative stress in the corpus cavernosum (CC) of the DMED + GKT-137831 group were improved. The DMED group showed serious inflammatory responses and excessive autophagy, which were inhibited by GKT-137831 treatment in the DMED + GKT-137831 group. Clinical Translation: Our study showed improvement in erectile function with GKT-137831 in a diabetic rat ED model. Strength and Limitations: This study suggested for the first time that GKT-137831, an NOX1/4 inhibitor undergoing clinical trials, is effective in improving erectile function in rats with type 1 DMED. However, we only investigated GKT-137831 treatment of streptozotocin-induced type 1 diabetic rats, and therapeutic evidence in other types of diabetes is lacking. Conclusion: GKT-137831 improves erectile function by 70% in type 1 DMED rats and constitutes a promising compound for the treatment of type 1 DMED, likely by inhibition of overactivated oxidative stress, down-regulation of proinflammatory factors, and amelioration of excessive autophagy and endothelial function. Copyright (C) 2021, International Society of Sexual Medicine. Published by Elsevier Inc. All rights reserved.

目的 通过生物信息学方法筛选良性前列腺增生(BPH)的关键基因和相关通路,探究BPH发生、发展可能的病理、生理机制.方法 利用基因表达汇编(GEO)数据库下载BPH与正常前列腺组织的两个芯片数据(GSE7307与GSE119195),通过Rstudio软件对数据集进行差异基因(DEGs)筛选及京都基因与基因组百科全书(KEGG)分析及可视化;运用Cytoscape软件中的ClueGO插件进行基因本体论(GO)富集分析与可视化.利用STRING数据库构建蛋白质-蛋白质相互作用(PPI)网络,在Cytoscape中可视化,并通过Cytoscape中的cytoHubba插件得到关键基因.通过NetworkAnalyst预测调控关键基因的转录因子和miRNA.结果 本分析共得到36个上调DEGs,45个下调DEGs.GO分析发现DEGs主要富集于干细胞负性增殖调控、乙醇初步代谢、维生素效应等生物学过程,KEGG主要富集于Hippo信号通路、PPAR信号通路、肾素分泌等信号通路;最终得到CCL2、LPL、VCAN、IGF1、WNT2这5个关键基因.结论 本研究通过生物信息学方法筛选获得可能参与BPH发生、发展的关键基因及其相关通路,为阐明BPH的发病机制提供了一定的理论基础.

Background— Neurogenic erectile dysfunction (ED) is often refractory to treatment due to insufficient functional nerve recovery after injury or insult. Noninvasive mechano-biological intervention, such as microenergy acoustic pulse (MAP), low-intensity pulsed ultrasound (LIPUS), and low-intensity extracorporeal shockwave treatment (Li-ESWT), is an optimal approach to stimulate nerve regeneration. Aim— To establish a new model in vitro to simulate nerve injury in neurogenic ED and to explore the mechanisms of MAP in vitro. Methods— Sprague-Dawley rats were used to isolate Schwann cells (SCs), major pelvic ganglion (MPG), and cavernous nerve with MPG (CN/MPG). SCs were then treated with MAP (0.033 mJ/mm 2 , 1Hz, 100 pulses), and SC exosomes were isolated. The MPG and CN/MPG were treated with MAP (0.033 mJ/mm 2 , 1 Hz) at different dosages (25, 50, 100, 200, or 300 pulses) or exosomes derived from MAP-treated SCs in vitro. Outcomes— Neurite growth from the MPG fragments and CN was photographed and measured. Expression of neurotropic factors (BDNF, NGF, and NT-3) was checked. Results— Neurite outgrowth from MPG and CN/MPG was enhanced by MAP in a dosage response manner, peaking at 100 pulses. MAP promoted SC proliferation, neurotropic factor (BDNF, NGF and NT-3) expression, and exosome secretion. SC-derived exosomes significantly enhanced neurite outgrowth from MPG in vitro. Strength & Limitations— We confirmed that MAP enhance penile nerve regeneration through exsomes. Limitations of this study include that our study did not explore the exact mechanisms of how MAP increases SC exosome secretion nor whether MAP modulates the content of exosomes. Conclusion— This study revealed that neurite outgrowth from MPG was enhanced by MAP and by SC-derived exosomes which were isolated after MAP treatment. Our findings indicate that one mechanism by which MAP induces nerve regeneration is by stimulation of SCs to secrete exosomes.

Overweight females are prone to obesity-associated stress urinary incontinence (OA-SUI), and there are no definitive medical therapies for this common urologic condition. This study was designed to test the hypothesis that regenerative therapy to restore urethral striated muscle (stM) and pelvic floor muscles might represent a valuable therapeutic approach. For the in vitro experiment, single-guide RNAs targeting myostatin (MSTN) were used for CRISPRi/dCas9-Kruppel associated box (KRAB)-mediated gene silencing. For the in vivo experiment, a total of 14 female lean ZUC-Leprfa 186 and 14 fatty ZUC-Leprfa 185 rats were used as control and CRISPRi-MSTN treated groups, respectively. The results indicated that lentivirus-mediated expression of MSTN CRISPRi/dCas9-KRAB caused sustained downregulation of MSTN in rat L6 myoblast cells and significantly enhanced myogenesis in vitro. In vivo, the urethral sphincter injection of lentiviral-MSTN sgRNA and lentiviral-dCas9-KRAB significantly increased the leak point pressure, the thickness of the stM layer, the ratio of stM to smooth muscle, and the number of neuromuscular junctions. Downregulation of MSTN with CRISPRi/dCas9-KRAB-mediated gene silencing significantly enhanced myogenesis in vitro and in vivo. It also improved urethral continence in the OA-SUI rat model.

PURPOSE:NTrap® stone entrapment and extraction device (NTrap®) is a device used to extract and remove stones from the urinary tract and to minimize retrograde stone migration during ureterolithotripsy (URS). This study aimed to evaluate the efficacy and safety of NTrap® in URS. METHODS:From Jan 2014 to June 2017, 148 patients underwent URS with the aid of NTrap® (Group A), and 209 patients underwent standard URS without any anti-retropulsion device (Group B). Their demographics, operation time, complications, stone migration rate, and stone-free rate (SFR) were recorded for comparison. RESULTS:Compared with group B, Group A had a significantly shorter operative and lasering time (P = 0.003, P<0.001, respectively). There was no significant difference between the 2 groups in overall complications, a decrease in mean hemoglobin, and length of stay (LOS) (P = 0.426, P = 0.097, P = 0.058, respectively). The incidence of stone migration was significantly lower in Group A than Group B (P = 0.035). The postoperative auxiliary procedure rate (in patients with stones retropulsion during the operation) was significantly lower in Group A compared to Group B (P = 0.024). The SFR was considerably higher in Group A than Group B (P = 0.009). CONCLUSION:URS, with the aid of NTrap®, is an effective and safe method for treating ureteric stones. It may prevent stones from retropulsion and shorten the operative time.

Background: Neurogenic erectile dysfunction (ED) is often refractory to treatment because of insufficient functional nerve recovery after injury or insult. Noninvasive mechano-biological intervention, such as micro-energy acoustic pulse (MAP), low-intensity pulsed ultrasound, and low-intensity extracorporeal shockwave treatment, is an optimal approach to stimulate nerve regeneration. Aim: To establish a new model in vitro to simulate nerve injury in neurogenic ED and to explore the mechanisms of MAP in vitro. Methods: Sprague-Dawley rats were used to isolate Schwann cells (SCs), major pelvic ganglion (MPG), and cavernous nerve with MPG (CN/MPG). SCs were then treated with MAP (0.033 mJ/mm(2), 1 Hz, 100 pulses), and SC exosomes were isolated. The MPG and CN/MPG were treated with MAP (0.033 mJ/mm2, 1 Hz) at different dosages (25, 50, 100, 200, or 300 pulses) or exosomes derived from MAP-treated SCs in vitro. Outcomes: Neurite growth from the MPG fragments and CN was photographed and measured. Expression of neurotropic factors (brain-derived neurotrophic factor, nerve growth factor, and neurotrophin-3) was checked. Results: Neurite outgrowth from MPG and CN/MPG was enhanced by MAP in a dosage response manner, peaking at 100 pulses. MAP promoted SC proliferation, neurotropic factor (brain-derived neurotrophic factor, nerve growth factor, and neurotrophin-3) expression, and exosome secretion. SC-derived exosomes significantly enhanced neurite outgrowth from MPG in vitro. Clinical Implications: MAP may have utility in the treatment of neurogenic ED by SC-derived exosomes. Strength & Limitations: We confirmed that MAP enhances penile nerve regeneration through exsomes. Limitations of this study include that our study did not explore the exact mechanisms of how MAP increases SC exosome secretion nor whether MAP modulates the content of exosomes. Conclusion: This study revealed that neurite outgrowth from MPG was enhanced by MAP and by SC-derived exosomes which were isolated after MAP treatment. Our findings indicate that one mechanism by which MAP induces nerve regeneration is by stimulation of SCs to secrete exosomes. Copyright (C) 2020, International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.

膀胱平滑肌瘤是一种罕见的间叶组织来源良性肿瘤,华中科技大学同济医学院附属同济医院泌尿外科于2018年8月收治1例巨大膀胱平滑肌瘤患者,采用经尿道激光剜除术治疗,取得满意疗效,现报告如下. 患者,男,70岁,排尿中断伴下腹部胀痛3月余,伴有尿频、尿急症状,偶有肉眼血尿,血尿症状能自行缓解,无发热及腰痛.既往2年前因前列腺增生症行前列腺激光剜除术,术后恢复良好.入院体格检查及 PSA未见明显异常.全腹部增强CT提示膀胱尿道内口处见不规则团块状软组织密度影,突向膀胱腔内,边界可见散在高密度钙化灶,增强不均匀强化,大小约55 mm×46 mm ×62 mm ,腹膜后及盆壁未见肿大淋巴结影(图1). MRI平扫+DWI提示膀胱左前壁可见菜花样稍长T1 稍长 T2 信号,可见低信号"蒂"影,DWI弥散明显受限,肌层未见明显侵及,盆腔内未见肿大淋巴结(图2) .经尿道膀胱镜检查提示膀胱颈口可见巨大新生物,类圆形,表面光滑,基底部位于膀胱颈左上方,因肿瘤遮挡,双侧输尿管口无法窥及.膀胱镜病理活检:梭形细胞肿瘤,结合免疫组化,考虑平滑肌来源;免疫组化:EM A (+) ,DES (+) ,CaLdesmon(+) ,SDHB (+) ,SMA (弱+) ,ALK (散在+) ,CD117(－) ,CD34 (－) ,DOG1 (－) ,S‐100 (－) ,SOX10 (－) ,ST A T6 (－) ,PCK (－) ,GAT A‐3 (－) ,HMB45 (－) , MeLanA (－) ,Ki‐67 LI约5%.

Introduction: Modulating tissue-resident stem and progenitor cells with a non-invasive, mechanobiological intervention is an optimal approach for tissue regeneration. Stem cell antigen-1 (Sca-1) has been identified as a stem cell marker within many organs but never within the penis. Aim: To localize and isolate penile stem/progenitor cells (PSPCs) and to evaluate cellular differentiation after exposure to induction medium and microenergy acoustic pulse (MAP) therapy. Methods: Six male Sprague-Dawley rats were used to isolate PSPCs. Isolation was followed by stem cell characterization and differentiation assays. The PSPCs were then treated with MAP (0.033 mJ/mm(2), 1 Hz) at various dosages (25, 50, 100, and 200 pulses) and for different durations (1, 2, 4, 6, or 8 hours) in vitro. Main Outcome Measure: The PSPCs (Sca-1-positive cells) were isolated using the magnetic-activated cell sorting system. PSPC cellular differentiation was assessed after induction with induction medium and with MAP in vitro. Wnt/beta-catenin signaling was also assayed. Results: The PSPCs were successfully localized within the penile subtunic and perisinusoidal spaces, and they were successfully isolated using magnetic-activated cell sorting. The stemness of the cells was confirmed by stem cell marker characterization and by multiple differentiation into smooth muscle cells, endothelial cells, adipocytes, and neurons. MAP-induced PSPCs differentiated into smooth muscle cells by activating the Wnt/beta-catenin signaling pathway in a time- and dosage-dependent manner. Clinical Implications: By modulating resident PSPCs, MAP may have utility in the treatment of erectile dysfunction (ED). Strengths & Limitations: This study provides solid evidence in support of microenergy therapies, including both MAP and low-intensity extracorporeal shock wave therapy, for the treatment of ED. Additional studies are needed and should include additional stem cells markers. Furthermore, studies exploring the underling mechanisms for PSPC activation and differentiation are required. Conclusion: PSPCs were successfully identified, localized, and isolated. Additionally, MAP provoked PSPCs to differentiate into smooth muscle cells via the Wnt/beta-catenin signaling pathway. As such, MAP provides a novel method for activating endogenous tissue-resident stem/progenitor cells and might facilitate stem cell regenerative therapy targeting ED. Copyright (C) 2019, International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.

Stress urinary incontinence (SUI) after prostate surgery is primarily caused by urethral sphincter damage. There are few effective therapeutic approaches for male SUI due to both insufficient study of the structure of the external urethral sphincter (EUS) and incomplete understanding of the resident EUS stem/progenitor cells. The goals of this study were to localize and to determine the distribution of tissue-resident stem/progenitor cells in the male EUS throughout EUS development and to understand the anatomic temporal patterns of the EUS. Newborn Sprague Dawley rats were intraperitoneally injected with the thymidine analogue, 5-ethynyl-2-deoxyuridine (EdU), and the EUS was harvested at five time points (1, 2, 3, 4, and 8 weeks postinjection). The tissue was then processed for EdU staining and immunofluorescence staining for stem cell markers Ki67 and proliferating cell nuclear antigen. We counted the EdU+ label-retaining cells (LRCs) at each time point and colocalized with each stem cell marker, also we isolated and cultured the cells in vitro. The results revealed that the number of EdU+ LRCs in each EUS cross-section decreased over time and that the LRCs were located immediately under the basal membrane of laminin, densely adherent to the muscle fibers. In addition, the thickness of the striated muscle layer developed much faster than the smooth muscle layer during EUS development. By 4 weeks, the structure of the EUS layers was well differentiated. The EUS resident stem/progenitor cells were isolated with MACS® MicroBeads system, and myogenesis was confirmed. In this study, we defined both the time-course development of the EUS and the distribution of resident stem/progenitor cells. This information is crucial for forthcoming studies regarding male micturition and for development of novel therapeutic approaches for postoperative male SUI.

Objective Nephron﹣sparing nephrectomy has gradually become the preferred treat﹣ment for patients with small renal tumors. Controlling the warm ischemic time is vital for the pro﹣tection of renal function. T his article will discuss the feasibility ,safety and prospect of retroperitone﹣al laparoscopic thulium laser zero ischemia partial nephrectomy for small renal tumors. Methods T wo patients with small renal tumors treated by thulium laser zero ischemia resection were reported in our center ,including the effects of surgeries and 5﹣year follow﹣up data ,and then related literature was reviewed. Results T wo cases of renal tumors were successfully resected by thulium laser without ischemia. T here were no massive hemorrhage during operations and no significant decrease in renal function after operations. Pathological examination showed that one case was renal clear cell carcinoma (Fuhrman grade 1) ,and another was papillary renal cell carcinoma (type I). Both of ca﹣ses showed negative margins ,and there was no recurrence within 5 years. Conclusions Retroper﹣itoneal laparoscopic thulium laser nephron﹣sparing nephrectomy is a safe , feasible and promising method for the treatment of small renal tumor.

Objective: To evaluate the safety and effectiveness of ultrasound-guided percutaneous nephrolithotomy (PCNL) accessed by SVOF-principle and two-step puncture techniques. Methods: A total of 838 cases with upper urinary stones underwent percutaneous nephrolithotomy successfully accessed by ultrasound-guided between June 2007 and December 2015 at Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. Of all cases were divided in two groups: hydronephrosis calyces puncture group include 425 cases and SVOF-principle puncture group include 413 cases. The access establishment time, operation time, stone free rate (SFR), postoperative complications, and postoperative hospitalization time between the two groups we compared by t test or χ2 test. Results: Statistically significant differences were observed between hydronephrosis calyces puncture group and SVOF-principle puncturegroup in the first access establishment time ((16.5±8.4) minutes vs. (11.2±5.9) minutes, t=3.931, P=0.013), one-stage SFR (74.3% vs. 85.7%, χ2=16.868, P=0.000), postoperative hospitalization time ((6.4±2.1) days vs. (4.8±1.8)days, t=4.574, P=0.000), transfusion rate (7.1% vs. 2.9%, χ2=8.027, P=0.006), and embolization rate (3.3% vs. 1.0%, χ2=5.390, P=0.020). There were no statistically significant differences in operation time, total SFR, postoperative fever and sever infection between these two groups (all P>0.05). In both two groups, no serious complications such as peripheral organ injury and death occurred. Conclusions: PCNL accessed guided by ultrasound with SVOF-principle and two-step puncture techniques has advantages of quick puncture location, high stone free rate, fewer complications and fast recovery. This technique is an effective and safe treatment option for upper urinary stones and deserved promotion and application in clinic.

The objectives of the study are to compare the safety and efficacy of "all-seeing needle" optical puncture system micro-percutaneous nephrolithotomy (micro-PCNL) and flexible ureterorenoscopy (FURS) for the treatment of lower calyceal stones of ≤ 2 cm and to determine the advantages and disadvantages of each. 116 patients in total with lower calyceal stones of ≤ 2 cm were randomly divided into two equal groups, "all-seeing needle" optical puncture system micro-PCNL and FURS. In both groups, holmium laser was utilized for lithotripsy. The perioperative parameters were compared between the two groups. Compared to the "all-seeing needle" micro-PCNL group, the mean operative time was significantly longer in the FURS group (P = 0.000). However, there was no significant difference between the two groups with respect to mean hemoglobin reduction (P = 0.087), complications (P = 0.731) and LOS (P = 0.856). The overall SFR of the "all-seeing needle" micro-PCNL group and FURS group was 84.5% (49/58) and 79.3% (46/58), respectively, without any significant difference between the groups (P = 0.469). For treating lower calyceal stones of ≤ 2 cm, the "all-seeing needle" micro-PCNL group had shorter operative time than FURS, while no significant differences between the two groups with respect to mean hemoglobin reduction, complications, LOS and SFR were found.

目的 研究代谢综合征导致勃起功能障碍大鼠阴茎海绵体组织中氧化应激变化,探讨氧化应激导致代谢综合征大鼠勃起功能障碍的机制.方法 将40只3周龄雄性SD大鼠随机分为实验组30只(高脂高糖饲料喂养6个月)和正常对照组10只(普通饲料喂养6个月).喂养6个月后检测实验组和正常对照组大鼠体质量、血脂、空腹血糖、血压和胰岛素水平,筛选出代谢综合征大鼠,随后阿扑吗啡试验筛选出代谢综合征相关的勃起功能障碍(MED)大鼠.检测喂养后MED组和正常对照组大鼠阴茎海绵体内压(ICP)/平均动脉压(MAP)变化,应用Western blot检测两组大鼠阴茎海绵体组织中NADPH氧化酶各亚基和eNOS表达,DHE染色检测阴茎海绵体组织活性氧水平,ELISA检测阴茎海绵体组织中cGMP浓度.结果 (1)喂养后MED组大鼠体质量、空腹血糖、血浆中胰岛素和胆固醇水平较正常对照组明显升高(均P<0.05);(2)喂养后MED组大鼠Max ICP/MAP较正常对照组明显降低(P<0.05);(3)喂养后MED组大鼠阴茎海绵体组织中gp91phox蛋白表达和活性氧水平较正常对照组明显升高(均P<0.05);(4)喂养后MED组大鼠阴茎海绵体组织中eNOS蛋白表达和cGMP浓度较正常对照组明显降低(均P<0.05).结论 氧化应激可能通过引起阴茎海绵体内皮细胞功能障碍从而导致代谢综合征大鼠勃起功能障碍的发生.

Objective To discuss diagnosis and treatments of prostatic cysts. Methods We diagnosed a patient with lower urinary tract obstruction associated with prostatic cyst by B-ultra-sonography and MRI,then the patient was treated with transurethral plasmakinetic vaporization re-section. Results The operation lasted 20 minutes and the amount of intraoperative blood loss was 30 ml.After surgery,the urinary catheter was indwelt for 5 days.During the follow-up period of 2 months,the patient experienced smooth urination,no dysuria or residual urine was found.Moreo-ver,the patient's erectile function and ejaculatory function were also normal. Conclusions B-ultra-sonography and MRI are important methods for the diagnosis of prostatic cysts.For patients with lower urinary tract obstruction,urodynamic and cystoscopy can help with further diagnosis,and the transurethral plasmakinetic vaporization resection is an effective and safe method.