The advent of chimeric antigen receptor (CAR) T cell therapy has yielded transformative efficacy in hematological malignancies, yet its application in solid tumors remains constrained by the immunosuppressive tumor microenvironment (TME). Characterized by hypoxia, acidosis, and nutrient deprivation, the TME critically compromises CAR-T cell infiltration, persistence, and effector functions. Hypoxia-inducible factor 1α (HIF-1α), a central regulator of cellular adaptation to hypoxia within the TME, modulates T cell metabolism and functionality—presenting a strategic framework for enhancing CAR-T cell efficacy in solid malignancies. This review characterizes the role of HIF-1α in reprogramming the tumor-immune microenvironment, with specific emphasis on its metabolic regulation of T cells and translational implications for CAR-T therapy. Under hypoxic stress, HIF-1α orchestrates a metabolic shift toward glycolysis in effector T cells by suppressing oxidative phosphorylation (OXPHOS) while upregulating key glycolytic enzymes (e.g. GLUT1, HK2, LDHA). This adaptation sustains ATP production while attenuating mitochondrial reactive oxygen species (ROS) accumulation, thereby mitigating T cell exhaustion and augmenting cytotoxic persistence. This HIF-1α-mediated metabolic reprogramming provides critical insights for overcoming barriers to CAR-T cell efficacy in solid tumors.

This study aimed to elucidate the pathological mechanism of Steroid 5 Alpha-Reductase 2 (SRD5A2) in benign prostatic hyperplasia (BPH) using various methods. BPH datasets from the Gene Expression Omnibus (GEO) database were analyzed, and correlations between SRD5A2 and other genes were calculated. Gene Set Enrichment Analysis (GSEA) identified potential functions of SRD5A2, and key pathways were determined by intersecting the enrichment results of differentially expressed genes (DEGs) in BPH and control samples with SRD5A2 enrichment. Single sample gene set enrichment analysis (ssGSEA) and weighted gene co-expression network analysis (WGCNA) identified key pathways-related genes. Candidate genes were defined as overlapping genes among SRD5A2-related genes, key pathways-related genes, and DEGs. Functional similarity analysis identified genes significantly associated with SRD5A2. Support Vector Machine (SVM) analysis based on these genes revealed four key genes (SLIT3, TCF21, MATN2, and PSMG4) with good diagnostic efficacy. Quantitative real-time PCR (qRT-PCR) confirmed statistically significant differential expression of MATN2 and PSMG4. In conclusion, this study explored the potential biological functions of SRD5A2-related genes in BPH, providing insights into its treatment.

Additional file 10: (A) BLCA with lymphovascular invasion expressed more FAP and VCAN than without lymphovascular invasion. In OS (B) and DSS (C) events, FAP, VCAN, N-cadherin, and Vimentin expression in the deceased group is higher than in the alive group. (D) In PFI events, VCAN and N-cadherin are more highly expressed in the deceased group. Immunohistochemistry (E) and dot blot (F) shows that the expression of TGF-β1, FAP, VCAN, N-cadherin, and Vimentin in BLCA tissues is significantly higher than in adjacent normal tissues, while the expression of E-cadherin in BLCA tissues is lower than in adjacent normal tissues. (G) TGF-β1 dominates stromal fibroblast-mediated EMT of bladder cancer cells via the FAP/VCAN axis to promote the invasion and metastasis of BLCA.

Background Bladder cancer is one of the most common malignant tumors of the urinary system and is associated with a poor prognosis once invasion and distant metastases occur. Epithelial-mesenchymal transition (EMT) drives metastasis and invasion in bladder cancer. Transforming growth factor β1 (TGF-β1) and stromal fibroblasts, especially cancer-associated fibroblasts (CAFs), are positive regulators of EMT in bladder cancer. However, it remains unclear how TGF-β1 mediates crosstalk between bladder cancer cells and CAFs and how it induces stromal fibroblast-mediated EMT in bladder cancer. We aimed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells. Methods Primary CAFs with high expression of fibroblast activation protein (FAP) were isolated from bladder cancer tissue samples. Subsequently, different conditioned media were used to stimulate the bladder cancer cell line T24 in a co-culture system. Gene set enrichment analysis, a human cytokine antibody array, and cytological assays were performed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells. Results Among the TGF-β family, TGF-β1 was the most highly expressed factor in bladder cancer tissue and primary stromal fibroblast supernatant. In the tumor microenvironment, TGF-β1 was mainly derived from stromal fibroblasts, especially CAFs. In stimulated bladder cells, stromal fibroblast-derived TGF-β1 promoted bladder cancer cell migration, invasion, and EMT. Furthermore, TGF-β1 promoted the activation of stromal fibroblasts, inducing CAF-like features, by upregulating FAP in primary normal fibroblasts and a normal fibroblast cell line. Stromal fibroblast-mediated EMT was induced in bladder cancer cells by TGF-β1/FAP. Versican (VCAN), a downstream molecule of FAP, plays an essential role in TGF-β1/FAP axis-induced EMT in bladder cancer cells. VCAN may also function through the PI3K/AKT1 signaling pathway. Conclusions TGF-β1 is a critical mediator of crosstalk between stromal fibroblasts and bladder cancer cells. We revealed a new mechanism whereby TGF-β1 dominated stromal fibroblast-mediated EMT of bladder cancer cells via the FAP/VCAN axis and identified potential biomarkers (FAP, VCAN, N-cadherin, and Vimentin) of bladder cancer. These results enhance our understanding of bladder cancer invasion and metastasis and provide potential strategies for diagnosis, treatment, and prognosis.

目的 探讨青蒿素(Artemisinin)调控ENO2 对肾透明细胞癌(clear cell renal cell carcinomas,ccRCC)细胞增殖和有氧糖酵解的作用及具体调控机制.方法 分别将ccRCC细胞系OSRC2 和ACHN暴露于 0、10、20、30、40 µmol/L青蒿素中,OSRC2 和ACHN细胞经 25 µmol/L青蒿素处理或同时转染si-ENO2,CCK-8 检测细胞活力,葡萄糖测试盒和乳酸测试盒检测葡萄糖消耗和乳酸生成量,Western blot检测HK2、LDHA和ENO2的表达,RT-qPCR检测ENO2 mRNA相对表达.结果 OSRC2 和ACHN细胞存活率随青蒿素浓度和暴露时间的增加而降低,OSRC2 细胞的IC50 值为25.47 µmol/L,ACHN细胞的IC50 值为26.31 µmol/L.ENO2 在OSRC2和ACHN细胞中表达升高(P<0.01),青蒿素可下调ENO2 在癌细胞中的表达(P<0.05).暴露于 25 µmol/L青蒿素或敲降ENO2 可抑制OSRC2 和ACHN细胞的存活(P<0.001)、葡萄糖消耗(P<0.05)、乳酸生成(均P<0.05)以及HK2 和LDHA的蛋白表达(P<0.05).同时敲降ENO2 且暴露于 25 µmol/L青蒿素组中OSRC2 和ACHN细胞的存活率(P<0.001)、葡萄糖消耗(P<0.05)、乳酸生成(P<0.05)以及HK2 和LDHA的表达(均P<0.05)低于仅敲降ENO2 组.结论 青蒿素可抑制ccRCC细胞的存活率和有氧糖酵解,并通过下调ENO2 在ccRCC中的表达而发挥作用.

膀胱癌是我国泌尿生殖系统肿瘤中最常见的恶性肿瘤,发病率占第一位[1] ,其中男性病人居多,且发病率随着年龄的增长呈现逐年上升的趋势[2] ,约一半以上的病人为75岁以上老年人[3].根治性膀胱切除术( radical cystectomy, RC)是肌层浸润性膀胱癌及复发的高级别非肌层浸润性膀胱癌的标准治疗措施.尽管外科微创技术在不断提高,但病人术后不良结局的发生常有报道[4].老年病人因身体机能衰退和应激能力下降,术后更易发生不良结局.衰弱( frailty)是机体生理功能减退和抵抗力下降的一个指标,用于描述老年人虚弱、平衡感差、低体质量等情况[5].衰弱可累及身体多个器官功能,使机体能量储备和应激抵抗能力下降,引发机体功能恶化.衰弱也可因一次轻微的身体伤害,如使用新的药物或轻度感染等,导致不良后果的发生[6] ,增加术后早期再入院率或使病人入住长期照护中心等[7].本文将探讨老年RC病人衰弱风险的研究现状,以评价该类人群的衰弱风险,提高医护人员对病人术前衰弱风险评估的认识.

Clear cell renal cell carcinoma (ccRCC) preferentially invades into perinephric adipose tissue (PAT), a process associated with poor prognosis. However, the detailed mechanisms underlying this interaction remain elusive. Here, we describe a bi-directional communication between ccRCC cells and the PAT. We found that ccRCC cells secrete parathyroid-hormone-related protein (PTHrP) to promote the browning of PAT by PKA activation, while PAT-mediated thermogenesis results in the release of excess lactate to enhance ccRCC growth, invasion, and metastasis. Further, tyrosine kinase inhibitors (TKIs) extensively used in the treatment of ccRCC enhanced this vicious cycle of ccRCC-PAT communication by promoting the browning of PAT. However, if this cross-communication was short circuited by the pharmacological suppression of adipocyte browning via H89 or KT5720, the anti-tumor efficacy of the TKI, sunitinib, was enhanced. These results suggest that ccRCC-PAT cross-communication has important clinical relevance, and use of combined therapy holds great promise in enhancing the efficacy of TKIs.

BACKGROUND:Increasing evidences have proved that long noncoding RNAs (lncRNAs) regulate the occurrence of bladder cancer (BC) and participate in various pathophysiology processes. However, little is unknown about the role of lncRNAs in drug resistance of BC cells. In this study, we explored the role of non-coding RNA activated by DNA damage (NORAD) in the gemcitabine (GEM) resistant of BC cells and explored its potential mechanism.METHODS:Real-time quantitative PCR (RT-qPCR) was used to detect the expression of NORAD and miR-155-5p of BC cells. Cell counting kit-8 (CCK-8) and Western blot were used to detect cell inhibition rate and the expression of WEE1 G2 checkpoint kinase (WEE1), P-glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP1). Flow cytometry detected cell cycle and apoptosis. Dual luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to confirm the targeting relationship between miR-155-5p, NORAD and WEE1. The xenograft model was used to observe the function of NORAD in vivo. immunohistochemistry (IHC) assay was used to detect the expression of WEE1, caspase-3 and Ki67 in tumor tissues.RESULTS:NORAD highly expressed in GEM-resistant BC cell lines. Knockdown of NORAD significantly inhibited the proliferation of T24/GEM cells, the expression of drug-resistant proteins P-gp and MRP1, inhibit the G0/G1 phase of cells, and induce cell apoptosis. Knockdown of NORAD reversed the promotion effect of miR-155-5p on WEE1 expression and promoted the sensitivity of T24/GEM cells to GEM. In vivo, knockdown of NORAD inhibited the tumor growth, and enhanced the GEM-sensitivity in mice.CONCLUSION:These data highlight the potential of NORAD acts as a therapeutic target for BC GEM resistance. It revealed the vital roles of NORAD/miR-155-5p/WEE1 axis in GEM resistant BC cells, providing a novel therapeutic strategy for BC.

目的 探讨外周血CTCs与前列腺癌临床特征的相关性,及其在前列腺癌筛查、监测中的应用价值.方法 回顾性分析2016年1月至2018年12月期间昆明市延安医院泌尿外科收治的110例前列腺疾病(前列腺增生或前列腺癌)患者的临床资料.按诊断不同分为两组,其中57例前列腺癌患者作为研究组,53例前列腺增生患者作为对照组.利用免疫磁球分离及荧光染色法对外周血中的CTC进行计数.统计并分析研究组与对照组CTCs阳性率的差异.根据CTCs计数结果 ,将研究组57例进一步分为CTCs阳性组和CTCs阴性组,对比2组PSA、Gleason评分、病理分期≥T3a发生率、骨转移发生率等指标的差异.CTCs阳性标准:外周血中CTCs≥5个/3.75 mL.结果 研究组CTCs平均数量(7.4±1.5)个显著高于对照组(2.1±0.9)个,差异具有统计学意义(t=22.2616,P<0.0001).研究组CTCs阳性率61.4％(35/57)显著高于对照组5.7％(3/53),差异具有统计学意义(χ2=35.3157,P<0.0001).CTCs阳性组患者PSA值[(35.4±15.7)ng/mL与(17.5±10.6)ng/mL]、Gleason评分[(8.1±1.3)与(7.2±1.1)]和骨转移发生率[34.3％(12/35)与9.1％(2/22)]均显著高于CTCs阴性组,差异具有统计学意义(P<0.05).CTCs阳性组的病理分期≥T3a发生率[29.2％(7/24)与30.3％(10/33)]大于CTCs阴性组,但差异不具有显著性(P>0.05).结论 CTCs与前列腺癌的发病风险呈正相关性,CTCs阳性与前列腺癌PSA值、Gleason评分和骨转移发生率有明显相关性,CTCs检测可作为一项辅助诊断技术应用于前列腺癌的筛查和病情监测、预后风险评估,具有较好的潜在临床应用价值.

BACKGROUND:Cisplatin could result in a wide range of kidney injuries. During the pathogenetic process, the excessive generation of reactive oxygen species (ROS) induced by cisplatin has been regarded as the initial and critical role, by which DNA damage and cell death could subsequently come up. Therefore the elimination of ROS has long been considered as effective mean to prevent cisplatin-induced kidney injury. Myricitrin is a newfound natural polyphenol hydroxy flavonoid glycoside compound, whose forceful anti-oxidative properties had been confirmed. Thus, we aim to investigate if myricitrin could protect against cisplatin-induced kidney injury.METHODS:A cisplatin-induced kidney injury model was established in mice by intraperitoneal injection of cisplatin. The protective effect of myricitrin on kidney injury was evaluated by serum BUN and Cre level. The Kidney pathology was observed with H&E and TUNEL staining. Then cell viability and apoptosis rate were measured using MMT assay and flow cytometry to assess if myricitrin could protect KH-2 cells against cisplatin-induced injury. The intracellular ROS was detected by ROS fluorogenic probe and quantitatively analyzed by flow cytometry. Finally, the expression of Bcl-2 and Bax was investigated by western blotting to indicate the influence in apoptosis pathway.RESULTS:Myricitrin could significantly remit kidney injury induced by cisplatin and inhibit apoptosis of KH-2 cells. In mechanism, myricitrin could eliminate ROS and subsequently block activation of apoptosis pathway.CONCLUSION:Myricitrin protects against cisplatin-induced kidney injury by eliminating excessive ROS.

Objective To investigate the clinical efficacy of dorsal mosaic surgery with penis free flap for the treatment of anterior urethral stricture after TURP.Methods We analyzed the clinical data of the patients with anterior urethral stricture after TURP from January 2010 to December 2017 in Yan'an hospital affiliated to Kunming medical university retrospectively.The patients' age ranged from 58 to 75 years,with an average of 64.3 years.The time from TURP to the diagnosis of anterior urethral stricture was 1-12 month,with an average of 3.5 months.5 cases were urethral stricture at penis segment,11 cases were urethral stricture at the junction of penis and scrotum,and the length of the narrow urethra was 2-5 cm,with an average of 3.4cm.The average maximum uroflowmetry in preoperative was (5.3 ± 2.7) ml/s.11 cases were treated with regular urethral dilatation and the treatment durable time was more than 6 months,5 cases were treated with intraurethral incision combined with urethral dilatation (1 or 2 times).16 cases were not effective after receiving the above treatment,so that all cases were treated with dorsal mosaic surgery with penis free flap.Subarachnoid anesthesia combined with epidural anesthesia,the patient took the supine position.The distal end of urethral stricture was defined by urethral dilator.Incision from the ventral side of the urethra.The length of the incision was extended 0.5 cm based on the length of urethral stricture in urethral angiography.Anatomize the left and right sides of the urethral stricture and longitudinally incision the ventral side of the urethral cavernous body.The length of the incision was extended 0.5 cm to the normal urethral mucosa.The traction line retracts the ventral urethral edge along both sides.The corresponding medial line of the dorsal urethra was incised to the tunica albuginea,and the urethral edge of the dorsal side was separated from the tunica albuginea to form an elliptical region on the tunica albuginea.According to the size of the ellipse,the full thickness of the penis flap was taken,and the size of the flap was beyond the edge of the elliptical area about 0.3 cm.The free flap was covered with the 6-0 absorbable suture on the elliptical area (the skin surface was on the inner side of the urethra),the edge of the free flap was intermittently sutured with the urethral edge of the dorsal side,Multi-needle intermittent sutured flap surface on the corpus cavernosum bed.Using a silicone catheter as the stent tube of the new urethra,the 6-0 absorbable suture closes the ventral side of the incisional urethral sponge.The multi-layered meat film was sutured to prevent leakage of urine,and the fascia and skin were sutured layer by layer.The 5-0 absorbable thread sutures the wound after the foreskin was taken.Results The operations were successfully completed.The operation time was 90-120 min,with an average of 102.3 min.The intraoperative blood loss was 10-30 ml.The symptoms of dysuria were relieved in all patients after removal of the catheter at 3 weeks postoperative.4 weeks after surgery,no signs of urethral stricture were observed in urethrography.And the maximum flow rate was ＞ 15 ml/s in 13 cases,while 3 cases was 10-15 ml/s.The mean maximum flow rate in postoperative was [(20.4 ± 7.3) ml/s],which was significantly higher than that in preoperative (t =7.7602,P ＜ 0.05).B-ultrasound showed 13 cases without residual urine and 3 cases of residual urine volume ＜ 30 ml.All patients had no serious complications such as urinary fistula,urethral diverticulum and extravasation of urine.After 1 year of follow-up,1 patient was lost to follow up,and none of the remaining15 cases had urethral obstruction due to re-stricture.Conclusion Dorsal mosaic surgery with penis free flap could be an effective method and had no obvious complications for the treatment of anterior urethral stricture after TURP.

Long non-coding RNAs (lncRNAs) were playing critical roles in tumorigenesis. However, in prostate cancer, the roles and mechanisms of lncRNAs especially ANRIL were largely unknown. We investigated the effects of ANRIL on the proliferation and migration of prostate cancer cells using CCK-8 assay and Transwell migration assay. Real-time PCR and western blotting assays were used to analyze the levels of ANRIL, let-7a, TGF-β1, p-Smad2 and p-Smad7. Our results showed that ANRIL was significantly overexpressed in prostate cancer tissues compared with corresponding normal tissues. Knockdown of ANRIL significantly inhibited the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. Knockdown of ANRIL significantly decreased the levels of TGF-β1 and p-Smad2, and increased the level of p-Smad7 in prostate cancer LNCap cells. We further found that knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. And let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the activity of TGF-β1/Smad signaling pathway in prostate cancer LNCap cells. Taken together, our findings indicated that overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-β1/Smad signaling pathway.

Ectopic activation of the canonical Hedgehog signaling pathway is involved in the development and progression of prostate cancer, which is one of the leading causes of cancer-associated mortality in males worldwide. However, the role of the non-canonical Hedgehog signaling pathway in prostate cancer remains generally unexplored. In the present study, it was identified that Gli (glioma-associated oncogene)1 and Gli2 were highly expressed at the protein level in the androgen-independent prostate cancer cell lines PC3 and DU145, but not in the androgen-dependent cancer cell line LNCaP. Silencing of Gli1 using small interfering RNA markedly decreased PC3 cell viability and liquid colony formation in vitro. The Gli1/2-specific inhibitor GANT61 markedly decreased cell viability by inducing cell apoptosis in PC3 and DU145 cells. GANT61 also alleviated liquid colony formation efficiency in PC3 and DU145 cells, suggesting that the activity of Gli1 is required for prostate cancer cell survival. To explore further the upstream signaling pathway involved in the regulation of Gli1 expression, it was identified that tumor necrosis factor α-triggered mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase 1 (S6K1) activation was required for Gli1 expression. Pharmacological and genetic inhibition of S6K1 activation markedly decreased Gli1 and its downstream target gene mRNA expression. In addition, the phosphoinositide 3-kinase/mTOR inhibitor BEZ235 markedly decreased in vitro PC3 cell proliferation. The results of the present study indicate that the non-canonical Hedgehog pathway (mTOR/S6K1/Gli1) contributes to the development and progression of prostate cancer and that Gli1 is a potential therapeutic target in the treatment of prostate cancer.

Resveratrol is a polyphenolic compound, which has been revealed to induce apoptosis in numerous human cancer cells; however, the effects of resveratrol on the migration and invasion of human bladder cancer cells have not been reported. The present study aimed to evaluate the anti‑metastatic potential of resveratrol against bladder cancer and its mechanism of action. The results indicated that resveratrol inhibits the adhesion, migration and invasion of bladder cancer cells in a dose‑dependent manner. Resveratrol was shown to significantly inhibit the expression and secretion of matrix metalloproteinase (MMP)‑2 and MMP‑9 in bladder cancer cells. Furthermore, resveratrol suppressed the phosphorylation of c‑Jun N‑terminal kinase and extracellular signal‑regulated protein kinase. In conclusion, the present study is the first, to the best of our knowledge, to demonstrate that resveratrol may be considered a novel anticancer agent for the treatment of bladder cancer via the inhibition of migration and invasion.

PBL教学模式在医学实习教育中运用日渐增多.随着移动网络覆盖医学院校和医院,各种手持设备在教师和学生中普及,在线学习逐渐被移动学习代替.通过传统在线学习和移动网络PBL教学在临床实习中的对照研究,发现移动网络PBL教学新颖且能激发学习兴趣,提高沟通能力,活跃课堂气氛,获得良好的教学效果.

OBJECTIVE:To investigate the factors influencing life-threatening complications during perioperative period in patients undergoing traditional cystectomy with orthotopic neobladder.METHODS:To retrospectively analyze the clinical data of 206 cases who underwent radical cystectomy with orthotopic neobladder. Logistic regression analysis was used to analyze the significance of the factors such as age, amount of bleeding, pathological stage, effective supplement of albumin, cardiovascular disease, diabetes mellitus, operation duration, intestinal preparation, etc., on the occurrence of severe complications.RESULTS:Among the 206 patients who underwent radical cystectomy with orthotopic neobladder, 22 cases (10.7%) had life-threatening complications (intestinal fistula, hemorrhagic shock, severe infection) during the perioperative period, and 9 cases died (mortality rate 4.4%). Logistic regression analysis showed that the elderly age, long operation duration, lack of effective supplement of albumin, diabetes mellitus are independent factors influencing the occurrence of life-threatening complications during the perioperative period of radical cystectomy with orthotopic ileal neobladder (P<0.05 for all), and are risk factors positively correlated with the severe complications.CONCLUSION:The elderly age, long operation duration, lack of effective supplement of albumin, and diabetes mellitus are risk factors of the occurrence of life-threatening complications during the perioperative period in patients undergoing radical cystectomy with orthotopic ileal neobladder, therefore, attention should be paid to this issue.

随着智能手机、平板电脑等手持设备的普及，移动网络技术在学校和医院的广覆盖，使移动网络下PBL教学在临床实习教学成为可能。通过移动网络下PBL教学的实施，能有效地推广PBL教学方式的普及，提高临床实习教学效率，提高临床实习生的学习兴趣和主动性。

Objective To explore the effects of parthenolide on growth inhibition, cell apoptosis and corresponding molecular mechanism of human T24 bladder cancer cells. Methods The inhibitory effect of parthenolide on human T24 cells was determined by MTT assay. The cell apoptosis and the cell cycle were analyzed by flow cytometry. Alterations in signal pathway of NF-κB and Bcl-2 family proteins were analyzed by Western blot.Results Parthenolide inhibited the proliferation of T24 cells in a dose-dependent and time-dependent manner. As showed by flow cytometry, parthenolide treatment of the T24 cells led to significant G1-phase cell cycle arrest in a dose-dependent manner and a decrease in cell population in the S-phase, whereas the population of cells in G2/M phase did not chang significantly. Flow cytometry also showed a dose dependent increase in T24 cells apoptosis by parthenolide treatment. Western blot analysis indicated a down-regulation of phosphorylated IκBα in a dose-dependent manner without an effect on IκBα expression in T24 cells by parthenolide treatment. Parthenolide treatment to T24 cell lines resulted a significant reduction in Bcl-2 protein expression but an increase in Bax protein expression in a dose-dependent manner. Conclusions Parthenolide treatment could lead to a significant dose-dependent and time-dependent inhibition in the growth and an increase in apoptosis of human T24 bladder cancer cells. The mechanism of action of parthenolide may be related to inhibition of NF-κB activation and regulation of Bcl-2 family proteins expression in human T24 bladder cancer cells.

目的：探讨参芪扶正注射液联合化疗前列腺癌的临床疗效。方法：选择前列腺癌患者80例，分为两组，各40例，对照组实施多西紫杉醇75mg／m2，静滴每天，每3周重复，治疗组则在对照组的基础上使用参芪扶正注射液连续治疗12周后，比较两组治疗前后自然杀灭细胞数量，并统计两组治疗期间发生的不良反应。结果：治疗后治疗组自然杀灭细胞数量高于治疗前（P＜0．05），对照组自然杀灭细胞数量低于治疗组（P＜0．05），治疗组治疗后自然杀灭细胞数量高于治疗后对照组（P＜0．05），治疗组发生肝、肾功能损伤，白细胞减少，红细胞减少和恶心呕吐的比例显著低于对照组（P＜0．05）。结论：前列腺癌实施化疗患者，联合使用参芪扶正注射液，能显著提高自然杀灭细胞数量，减少治疗不良反应，值得临床应用。

目的:评价逆行性膀胱颈保护(BNP)技术在开放性前列腺癌根治术中的应用效果.方法:回顾性分析2011年12月～2013年6月采用逆行性BNP技术所开展的前列腺癌根治术26例患者的临床资料,观察患者手术时间、术中出血量、围手术期输血量、术后患者并发症的发生情况、术后住院时间、拔除尿管时间及随访情况等.结果:26例患者手术均采用开放性耻骨后前列腺癌根治术,手术时间130～210min,平均156min;出血量50～400ml,平均出血量210ml,无患者在围手术期输血;术后住院时间7～12天,平均8.9天;术后病理分期为T2期23例,Tsa期3例;所有患者术后病理检查均未发现盆腔淋巴结阳性,无手术切缘阳性;围手术期未发生膀胱-尿道吻合口漏;拔除尿管后,患者排尿均通畅,无吻合口狭窄发生.本组26例患者均在术后7天拔除尿管,其中5例患者在术后1周内恢复尿控功能,12例患者在术后4周内恢复尿控功能,其余9例患者在术后3个月内恢复尿控功能.所有患者在3个月后均能正常排尿,无排尿困难和尿失禁表现;3个月后复查血PSA,其中23例患者均达到0.02 μg/L以下水平,其余3例患者PSA下降未达到以上标准,随后进行了辅助盆腔外放射治疗.结论:同国内外相关研究结果相比较,逆行性BNP技术可以提高前列腺癌根治术后患者的尿控能力,降低手术并发症,提高患者术后生活质量,是一种安全有效的手术方法.