目的 分享经膀胱路径机器人辅助腹腔镜根治性前列腺切除术(TvRARP)的技术要点及体会.方法 收集2021年11月-2022年5月于西安交通大学第二附属医院行TvRARP的13例患者的临床资料.评估该术式手术时间、术中估计出血量、术中输血量、术后拔除尿管时间、术后住院时间、术后即刻尿控率、术后国际勃起功能指数-5问卷(IIEF-5)评分及围手术期并发症等.结果 13例患者手术时间为(142±39)min.术中估计出血量为(76±40)mL,无患者输血.术后中位ⅡEF-5评分16(12～22)分,术后中位住院时间3(2～5)d.术后中位拔除尿管时间7(5～14)d,其中12例(92.3％)患者拔除尿管后实现即刻尿控.无ClavienⅢ级及以上并发症发生,ClavienⅠ～Ⅱ级并发症4例(30.8％).结论 TvRARP有较高的即刻控尿率和较佳的性功能保护作用,无严重并发症发生,适合经严格筛选的早期局限性前列腺癌患者.

Objective:To explore the effects of flutamide(FLU) on the mitochondrial respiratory chain in prostate cancer cells LNCaP, and to investigate its mechanisms.Methods:Androgen-dependent cell lines(LNCaP) were obtained for cell culture to obtain stable growth and passage of cell lines Changes in mitochondrial protein, enzyme changes, the androgen receptor antagonist FLU roles in the culture prostate cancer cell line of androgen at different concentrations drugs. Mitochondria at different time points of LNCaP under the interventions were extracte. Mitochondrial respiratory changes and differences at different time points and under the action of different drug concentration in LNCaP were measured and compared.Results:The morphological activity of LNCaP cells was gradually decreased after treated with FLU, After FLU acts on LNCaP cells, The content of mitochondrial protein increased significantly( P<0.05), but the content of SDH、NADH、COX decreased significantly( P<0.05), The decreasing degree of each index is difference in different time points. Conclusions:FLU can cause expression of mitochondrial protein decreased in LNCaP, and control cell proliferation.

目的 探讨腹腔镜筋膜内前列腺根治术对不同年龄前列腺癌患者控尿及性功能恢复的影响.方法 将62例前列腺癌患者根据患者年龄分为A组(≤60岁)及B组(＞ 60岁),2组患者均行腹腔镜筋膜内前列腺根治术.对比2组患者的围术期指标,术后并发症发生情况,术后3、6、12个月的控尿能力以及术前、术后3、6及12个月的IIEF-5评分.结果 2组患者的手术时间、术中出血量和留置尿管时间对比,无统计学差异(P＞0.05);术后A组患者并发症发生率为7.14％,B组患者术后并发症发生率为11.76％,2组差异无统计学意义(P＞0.05).术后3、6个月时,A组控尿正常率显著高于B组(P＜0.05);术后12个月时,2组的控尿能力对比差异无统计学意义(P＞0.05).A组术后3、6个月时的IIEF-5评分显著低于术前(P＜0.05),术后12个月时与术前对比差异无统计学意义(P＞0.05);B组术后3、6、12个月的IIEF-5评分均明显低于术前;术前、术后3个月2组的IIEF-5评分对比差异无统计学意义(P＞0.05),术后6、12个月时A组的IIEF-5评分明显高于B组(P＜0.05).结论 腹腔镜筋膜内前列腺根治术对前列腺癌患者均安全有效,术后年轻患者的控尿能力及性功能恢复较快,该手术对年轻患者的治疗效果更佳.

KIFC1 (kinesin family member C1) plays a critical role in clustering of extra centrosomes in various cancer cells and thus could be considered as a promising therapeutic target. However, whether KIFC1 is involved in the procession of renal cell carcinoma (RCC) still remains unclear. In this study, we found that KIFC1 was upregulated in RCC tissues and is responsible for RCC tumorigenesis (p < 0.001). The high expression of KIFC1 correlates with aggressive clinicopathologic parameters. Kaplan-Meier analysis suggested that KIFC1 was associated with poor survival prognosis in RCC. Silencing KIFC1 dramatically resulted in inhibition of proliferation, delayed the cell cycle at G₂/M phase, and suppressed cell invasion and migration in vitro. The antiproliferative effect of KIFC1 silencing was also observed in xenografted tumors in vivo. miR-338-3p could directly bind to the 3'-untranslated region (3'-UTR) of KIFC1, and ectopic miR-338-3p expression mimicked the inhibitory functions of KIFC1 silencing on RCC cells through inactivation of the PI3K/AKT signaling pathway. Therefore, these results revealed that KIFC1 may be a novel biomarker and an effective therapeutic target for the treatment of RCC.

目的 探讨在泌尿外科临床规培医师的教学中应用PBL联合MDT模式的教学效果.方法 以2016年1月—2018年3月在西安交通大学第二附属医院泌尿外科进行临床医师规范化培训的70名医师为研究对象,所有医师均为外科学非泌尿外科专业.随机将其分为对照组35名(采用传统教学法)和实验组35名(采用PBL联合MDT模式),分别按照各组规培方式进行泌尿外科临床规培,比较两组教学效果(出科理论考试和临床操作考试成绩)及教学满意度的差别.结果 实验组基础理论成绩与对照组比较,差异无统计学意义(P>0.05),但病例分析成绩和临床操作成绩实验组高于对照组(P<0.01);同时,实验组对本组的教学满意度高于对照组(P<0.05).结论 PBL联合MDT模式在泌尿外科临床医师规范化培训中效果明显,符合现代新型教学理念,值得推广.

Purpose: To evaluate whether low energy shock wave preconditioning could reduce renal ischemic reperfusion injury caused by renal artery occlusion. Methods: The right kidneys of 64 male Sprague Dawley rats were removed to establish an isolated kidney model. The rats were then divided into four treatment groups: Group 1 was the sham treatment group; Group 2, received only low-energy (12 kv, 1 Hz, 200 times) shock wave preconditioning; Group 3 received the same low-energy shock wave preconditioning as Group 2, and then the left renal artery was occluded for 45 minutes; and Group 4 had the left renal artery occluded for 45 minutes. At 24 hours and one-week time points after reperfusion, serum inducible nitric oxide synthase (iNOS), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), creatinine (Cr), and cystatin C (Cys C) levels were measured, malondialdehyde (MDA) in kidney tissue was detected, and changes in nephric morphology were evaluated by light and electron microscopy. Results: Twenty-four hours after reperfusion, serum iNOS, NGAL, Cr, Cys C, and MDA levels in Group 3 were significantly lower than those in Group 4; light and electron microscopy showed that the renal tissue injury in Group 3 was significantly lighter than that in Group 4. One week after reperfusion, serum NGAL, KIM-1, and Cys C levels in Group 3 were significantly lower than those in Group 4. Conclusion: Low-energy shock wave preconditioning can reduce renal ischemic reperfusion injury caused by renal artery occlusion in an isolated kidney rat model.

Inositol polyphosphate 4-phosphatase B (INPP4B) has been identified as a tumour suppressor in different human cancers. However, the role of INPP4B in the angiogenesis of human prostate cancer cells remains unclear. In this study, we first compared the expression of INPP4B between prostate cancer tissues and tumour-adjacent normal prostate tissues using immunohistochemistry. Then, we explored the role of INPP4B in prostate cancer progression via transfection of a Flag-INPP4B plasmid into PC3 and DU145 cells in vitro and in vivo. Our results showed that reduced INPP4B staining was significantly correlated with the tumour-node-metastasis stage. Moreover, transfection with Flag-INPP4B plasmid suppressed the migration and invasion of prostate cancer cells through inactivating the PI3K/Akt signalling pathway, at the same time decreased vascular endothelial growth factor secretion and suppressed human umbilical vein endothelial cells proliferation and tube formation. Futhermore, it was also found that INPP4B could inhibit tumour growth and angiogenesis in vivo. Altogether, our results supported that INPP4B acted as a tumour suppressor in human prostate cancer, and provided insights into development of a targeted therapy for this disease.

The radiation resistance of renal cell carcinoma (RCC) remains the primary obstacle to improve patient survival. This study aimed to investigate the effects of curcumin on the radiosensitivity of RCC cells. Human RCC cell (ACHN) was exposed to irradiation (IR) and/or curcumin treatment. Cell viability, DNA repair, cell cycle, and apoptosis, were evaluated by MTT, immunofluoresence staining and flow cytometry. Moreover, ACHN cells were xenografted into nude mice and subjected to IR and/or curcumin treatment. The expression of NF-κB signaling related proteins in ACHN cells and xenografts was detected by western blot analysis. The results showed that curcumin significantly increased radiosensitivity of ACHN cells by inhibiting the cell proliferation and DNA damage repair, causing cell cycle arrest at G2/M phase, inducing apoptosis in vitro, and suppressing the growth of xenografts in vivo. In addition, curcumin enhanced radiosensitivity was through markedly inhibiting IR-induced NF-κB signaling by modulating the related protein expressions including NF-κBP65, I-κB, VEGF, COX2, and Bcl-2 in ACHN cells, which was further strengthened by NF-κB inhibitor PDTC treatment. Thus, curcumin may confer radiosensitivity on RCC via inhibition of NF-κB activation and its downstream regulars, suggesting the potential application of curcumin as an adjuvant in radiotherapy of RCC.

Objectives To investigate the change of double hydrogen testosterone(DHT)and flutamide(FLU)on the mitochondrion in prostate cancer cells LNCaP.Methods Drogen-dependent(LNCaP)prostate cancer cell lines and cell lines with stable growth and transmission were acquired by cell culture.the androgen receptor agonist DHT and the androgen receptor antagonist FLU applied to the culture prostate cancer cell line of androgen at different concentrations drugs.Mitochondria at different time points of LNCaP under the interventions were extracted.Mitochondrial radidal and differences at different time points and under the action of different drug concentration in LNCaP were measured and compared.Results After DHT acted on LNCaP cells, the GSH of mitochondron decreased significantly(P﹤0.05), but the difference of the decreasing degree of each index in different time points was found.After FLU acted on LNCaP cells, the content of GSH increased significantly on the middle dose group(P﹤0.05),the other groups was not significantly(P>0.05).Conclusions DHT can cause decreasing of GSH on the mitochondrion,and promote cell proliferation.FLU can not remove the GSH on LNCaP cells,and cause the accumulation of free radicals, can inhibit the proliferation of LNCaP cells effectively.

Our previous work has shown that depletion of recombination signal-binding protein J (RBPJ) results in reduced cell growth in prostate cancer cells. In this study, we aimed to investigate the function of RBPJ in the chemoresistance of prostate cancer. The expression of RBPJ was quantified in docetaxel-resistant and parental prostate cancer cells. Loss- and gain-of-function experiments were conducted to explore the regulatory role of RBPJ in prostate cancer sensitivity to docetaxel. The pro-apoptotic effect of RBPJ silencing was checked in docetaxel-resistant prostate cancer cells. We found that docetaxel-resistant PC3-DR and DU145-DR cells expressed 3–5-fold high levels of RBPJ than parental PC3 and DU145 cells. Short hairpin RNA-mediated knockdown of RBPJ inhibited cell proliferation and colony formation and reversed docetaxel resistance in docetaxel-resistant prostate cancer cells. In contrast, overexpression of RBPJ promoted cell growth, colony formation, and docetaxel resistance in parental prostate cancer cells. Downregulation of RBPJ induced apoptosis in docetaxel-resistant cells, which was accompanied by enhanced cleavage of caspase-3. In addition, RBPJ silencing or overexpression markedly modulated the expression of the Bcl-2 family members including Bcl-2, Bcl-xL, Mcl-1, Bax, and Bak. Altogether, RBPJ contributes to acquisition of docetaxel resistance in prostate cancer cells and may thus represent a potential target for overcoming chemotherapeutic resistance in this malignancy.

Inositol polyphosphate 4-phosphatase type II emerges as a tumor suppressor in prostate cancer, and its loss of expression is associated with poor prognosis for prostate cancer. However, the mechanism of downregulation of inositol polyphosphate 4-phosphatase type II in prostate cancer development has not yet been fully clarified. In this study, microRNA-590-3p was found to be upregulated in both prostate cancer tissues and cell lines. Overexpression of microRNA-590-3p by microRNA-590-3p mimics promoted prostate cancer cell proliferation and invasion and accelerated the growth of xenografted tumors, while microRNA-590-3p inhibitors contributed to inhibition of cellular proliferation and invasion as well as tumor growth. A dual-luciferase reporter assay and expression analysis further confirmed that inositol polyphosphate 4-phosphatase type II was a direct target of microRNA-590-3p. Enforced expression of microRNA-590-3p led to repression of inositol polyphosphate 4-phosphatase type II messenger RNA and protein expression, as well as upregulation of p-Akt, p-FoxO3a, and cyclin D1 and downregulation of p21 expression in prostate cancer cell lines. Overexpression of inositol polyphosphate 4-phosphatase type II could reduce microRNA-590-3p-induced cell proliferation and invasion as well as tumor growth, and decrease microRNA-590-3p-mediated upregulation of cyclin D1 and downregulation of p21 expression in prostate cancer cells. Taken together, our findings reveal that microRNA-590-3p is a potential onco-microRNA that participates in carcinogenesis of human prostate cancer by suppressing inositol polyphosphate 4-phosphatase type II expression and involving the Akt/FoxO3a pathway. MicroRNA-590-3p may represent a potential therapeutic target for prostate cancer patients.

Objective:To investigate the change of Ca2+and discuss the mechanism of Ca2+changes in LNCaP cells by DHT and FLU.Methods:To abtain drogen-dependent(LNCaP)prostate cancer cell lines,by cell culture,to abtain stable cell strains.The androgen receptor agonist DHT and the androgen receptor antagonist FLU acted on the culture prostate cancer cell line of androgen at different concentrations drugs.We extracted cells at different time points of LNCaP under the interventions.By fluorescent dye load measured,to compare the Ca2+differences at differ-ent time points and under the action of different drug concentrations in LNCaP by flow cytometry.Results:After DHT acts on LNCaP cells,the Ca2+of LNCaP increased significantly(P<0.05),but the difference of the increasing degree of each index in different time points.After FLU acts on LNCaP cells,the content of Ca2+increased significantly(P<0.05).Conclusion:The content of Ca2+is not obvious decreased in LNCaP cell by DHT,showed the low effect on signal transduction and the apoptosis.However,the concentration of Ca2+in LNCaP cells could be increased obviously by FLU,which leads to calcium overload and promotes cell apoptosis.

Chemoresistance is a serious problem for the treatment of androgen-independent prostate cancer (PC). The underlying molecular mechanisms by which androgen-independent PC cells acquire the capacity to proliferate remain largely unclear. The aim of this study was to investigate the biological role of prostaglandin reductase 1 (PTGR1) in prostate cancer. Data from the Oncomine database showed that PTGR1 is commonly upregulated in PC tissue in comparison to corresponding normal controls. Two PTGR1-specific short hairpin RNA (shRNA) sequences were used to block the expression of PTGR1 via a lentivirus-mediated system in the androgen-independent PC cell lines DU145 and PC 3. Functional analysis revealed that knockdown of PTGR1 significantly inhibited proliferation and colony formation by PC cells. The inhibition of cell proliferation was related to arrest of the cell cycle in the G0/G1 phase and increased apoptosis in response to PTGR1 knockdown as indicated by flow cytometry. PTGR1 silencing was found to mechanically enhance the expression of p21, caspase 3, and cleaved PARP and to decrease the level of cyclin D1. In conclusion, PTGR1 plays an essential role in PC cells and may be a potential therapeutic target for PC.

目的 研究青年男性勃起功能障碍(ED)患者精神心理状态特点并分析与勃起功能国际问卷(IIEF-5)评分的相关性.方法 选择自2013年1月至2014年12月期间到我院泌尿外科就诊的青年ED患者60例,明确诊断后采用精神症状自评量表(SCL-90)评估患者精神心理状态,采用IIEF-5评定患者勃起功能.结果 ED患者量表中敌对、恐怖评分及阳性项目数较常模有显著升高(P＜0.05),躯体化、抑郁、焦虑、精神病性评分较常模有极显著性差异(P＜0.01),强迫、人际关系、偏执评分较常模虽有升高但未见显著统计学差异(P＞0.05).60例ED患者中轻度35例,中度15例,重度10例.相关性分析表明,IIEF-5评分与SCL-90总分未见显著相关性(r＝0.017,P＞0.05),IIEF-5评分与SCL-90阳性项目数呈显著负相关(r＝-0.276,P＜0.05).结论 SCL-90量表阳性项目总数与勃起功能显著相关,精神心理状态异常是导致青年人群发生ED的重要因素.

在开展泌尿外科腹腔镜手术的长期实践过程中,我们建立了泌尿外科腹腔镜手术实践教学体系.该体系依据各类泌尿外科腹腔镜手术特点及一般教学科学规律,将目前已成熟的培训内容和临床已开展的各类泌尿外科腹腔镜手术分解成5个教学阶段13个标准化教学模块,制定每一个教学模块的学习内容与目标并建议相应的学习训练方法.该体系同时配套全程责任管理制度与成就激励制度,为最终实现教学目标奠定了坚实基础.该实践教学体系设计具有宏观性、系统性和可延伸性,在泌尿外科腹腔镜手术实践教学中应用效果显著,具有较高的推广应用价值.

Hypoxia is a hallmark of solid tumor growth microenvironment and appropriates the major contributor for the failure and poor prognosis of clinical tumor treatment, including prostate cancer (PCa). Ectopic expression of netrin-1 is reportedly associated with the progression of several carcinomas. Here, we aimed to investigate the role of netrin-1 in hypoxic metastasis potential of prostate carcinoma. Here, hypoxia induced the up-regulation of netrin-1 mRNA and protein expression in prostate cancer cell lines PC3 and DU145. Importantly, knockdown of netrin-1 dramatically suppressed cell invasion, migration and epithelial-to-mesenchymal transition (EMT) of PC3 and DU145 cells under hypoxia. Furthermore, hypoxia treatment increased the activity of Yes-associated protein (YAP) by increasing YAP expression in the nucleus and inhibiting p-YAP levels. However, YAP activation was notably restrained following netrin-1 down-regulation. Interestingly, interrupting YAP expression attenuated hypoxia-triggered cell invasion, migration and EMT of DU145 cells. More importantly, restoring YAP expression strikingly antagonized the inhibitory effects of netrin-1 decrease on the metastatic potential of prostate cancer cells. Together, these results indicate that netrin-1 may function as a positive regulator of hypoxia-triggered malignant behavior in PCa by activating the YAP signaling. Accordingly, netrin-1 could be a promising therapeutic agent against prostate carcinoma.

Objectives To explore the effects of DHT on the mitochondrial respiratory chain enzyme in prostate cancer cells LNCaP,and to investigate its mechanisms.Methods Drogen-dependent(LNCaP) prostate cancer cell lines was obtained by cell culture.The androgen receptor agonist DHT roles in the culture prostate cancer cell line of androgen at different concentrations drugs and mitochondria at different time points of LNCaP under the interventions were extracted,and mitochondrial respiratory changes and differences at different time points and under the action of different drug concentration in LNCaP were measured and compared.Results After DHT acts on LNCaP cells,the content of mitochondrial protein increased significantly(P ＜ 0.05),but the content of SDH、NADH、COX decreased significantly(P ＜ 0.05).The difference of the decreasing degree of each index in different time points has different.Conclusions DHT can increase expression of mitochondrial protein in LNCaP,and promote cell proliferation.

Docetaxel efficiency in the therapy of prostate cancer (PCa) patients is limited due to the development of chemoresistance. Recent studies have implied a role of INPP4B in tumor chemoresistance, while the effects of INPP4B on docetaxel resistance in PCa have not been elucidated. In the present study, the docetaxel-resistant human PCa cell lines PC3-DR and DU-145-DR were established from the parental cell lines PC3 and DU-145, and the expression and role of INPP4B in docetaxel-resistant PCa cells were investigated. The results demonstrated that INPP4B expression was significantly downregulated in docetaxel-resistant cells. Overexpression of INPP4B increased the sensitivity to docetaxel and promoted cell apoptosis in PC3-DR and DU-145-DR cells. In addition, INPP4B overexpression downregulated the expression of the mesenchymal markers fibronectin, N-cadherin, and vimentin, and upregulated the expression level of the epithelial maker E-cadherin. Furthermore, INPP4B overexpression markedly inhibited the PI3K/Akt pathway. We also found that IGF-1, the inhibitor of PI3K/Akt, markedly blocked the change in EMT markers induced by overexpression of INPP4B, and reversed the resistance of PC3-DR and DU-145-DR cells to docetaxel, which is sensitized by Flag-INPP4B. In summary, the presented data indicate that INPP4B is crucial for docetaxel-resistant PCa cell survival, potentially by regulating EMT through the PI3K/Akt signaling pathway.

In the paper ,we introduced the method of home‐made laparoscopic simulation training sys‐tem by using goods sorting boxes ,adjustable focal length camera ,the market retail training module , universal video capture software and personal computer .With a commercially available laparoscopic training device as a control ,68 trainees participated in a course including studying of laparoscopic bas‐ic theory ,operation observing and simulation box operation training .Training and satisfaction survey results showed that all the 68 trainees were satisfied with the training curriculum .Compared to the commercially available laparoscopic training device ,the home‐made laparoscopic simulation training system had analogous image clarity ,flexibility of operation ,simulation training effect and conven‐ience except slightly unsatisfactory imaging field .The home‐made laparoscopic simulation training system proved to be economic ,effective and convenient with the ability of shorten the learning curve of laparoscopic surgery .

Background/Aims: Notch signaling pathway regulates cancer cell growth. RBPJ is a key transcription factor downstream of Notch receptor activation, whereas the role of RBPJ in carcinogenesis of prostate cancer is ill-defined. Methods: Here, we evaluated the effects of RBPJ inhibition on the growth of prostate cancer cells. We knocked down RBPJ in prostate cancer cells by a short hairpin interfering RNA (shRNA). We measured cell growth by an MTT assay. We analyzed the levels of cell-cycle-associated proteins by Western blot. Results: We found that shRNA for RBPJ efficiently inhibited RBPJ expression in prostate cancer cells, resulting in a significant decrease in the cell growth. Further, RBPJ-mediated cell-growth inhibition appeared to be resulting from alteration of cell-cycle inhibitors p21 and p27, cell-cycle activators CDK2, CDK4 and CyclinD1, and apoptosis-suppressor Bcl-2. Conclusion: Our data suggest that shRNA intervention of RBPJ expression could be a promising therapeutic approach for treating human prostate cancer.