[Double-channel expansion of the subcutaneous lower abdominal tunnel for sequential inguinal lymph node dissection in penile cancer - Report of six cases].

OBJECTIVE: To investigate the safety and efficacy of the two-channel dilatation procedure for subcutaneous tunneling in the lower abdomen during pelvic lymph node dissection for penile cancer. METHODS: A retrospective analysis was conducted on the clinical data of 6 patients treated from January 2020 to December 2022 using the dual-channel expansion technique for penile cancer lymph node dissection. RESULTS: All 6 cases ( 12 sides) successfully underwent prophylactic inguinal lymph node dissection. The average laparoscopic dissection time was ( 82.50 ± 12.08) minutes per side, with an average blood loss of （28.33 ± 10.95） ml. The number of lymph nodes dissected was （11.16 ± 1.02） for the superficial group and ( 0.67 ± 0.74 ) for the deep group. Postoperative pathology was negative in all cases. The average postoperative hospital stay was （7.33 ± 1.60 ） days, with a catheter removal time of （12.00 ± 2.06）days. Postoperative complications included abnormal skin sensations in 5 sides, lower limb edema in 3 sides, lymphedema in 3 sides, and cellulitis in 1 side. During a follow-up period of （20.60 ± 12.51）months, there were no instances of tumor recurrence or metastasis in the inguinal region among the patients. CONCLUSION: The dual-channel expansion technique for inguinal lymph node dissection via a subcutaneous tunnel is a safe and feasible treatment for penile cancer. It has a low complication rate, allows for thorough dissection of inguinal lymph nodes, and offers advantages in terms of surgical time.

Renal phenotypes correlate with genotypes in unrelated individuals with tuberous sclerosis complex in China.

PURPOSE: To explore the relationship between the genotype and renal phenotype in a Chinese cohort and guide clinical decision-making for treating tuberous sclerosis complex (TSC). MATERIALS AND METHODS: We reviewed 173 patients with definite TSC at three centers in China from September 2014 to September 2020. All the patients underwent TSC1 and TSC2 genetic testing as well as renal phenotypic evaluation. All analyses were performed using the SPSS software, version 19.0, with a cut-off P value of 0.05 considered statistically significant. RESULTS: We identified variants in 93% (161/173) cases, including 16% TSC1 and 77% TSC2 variants. Analysis of the relationship between the genotype and renal phenotype, revealed that those with TSC2 variants were more likely to develop severe renal AML (> 4) (P = 0.044). In terms of treatment, TSC2 variants were more likely to undergo nephrectomy/partial nephrectomy (P = 0.036) and receive mTOR medication such as everolimus (P < 0.001). However, there was no significant difference between the two groups in terms of their response to the everolimus treatment. CONCLUSION: Patients with TSC2 variants exhibit more severe renal phenotypes, especially those associated with renal angiomyolipomas (AML), and they often require nephrectomy/partial nephrectomy or mTOR medication. Detection of the genotype is helpful in TSC management.

Dual-tracer PET/CT-targeted, mpMRI-targeted, systematic biopsy, and combined biopsy for the diagnosis of prostate cancer: a pilot study.

PURPOSE: Growing evidence proved the efficacy of multi-parametric MRI (mpMRI) and prostate-specific membrane antigen (PSMA) positron emission tomography/computed tomography (PET/CT)-guided targeted biopsy (TB) in prostate cancer (PCa) diagnosis, but there is no direct comparison between mpMRI-TB and PSMA PET/CT-TB. Gastrin-releasing peptide receptor (GRPR) is highly expressed in PCa, which can compensate for the unstable expression of PSMA in PCa. Therefore, we designed a study to compare the efficiency of mpMRI-TB, dual-tracer (GRPR and PSMA) PET/CT-TB, systematic biopsy, and combined biopsy for the diagnosis of prostate cancer. METHODS: One hundred twelve suspicious PCa patients were enrolled from September 2020 to June 2021. Patients with anyone of positive dual-tracer PET/CT or mpMRI underwent TB, and all enrolled patients underwent systematic biopsy (SB) after TB. The primary outcome was the detection rates of PCa in different biopsy strategies. Secondary outcomes were the performance of three imaging methods, omission diagnostic rates, and upgrading and downgrading of biopsy samples relative to those of prostatectomy specimens in different biopsy strategies. McNemar's tests and Bonferroni correction in multiple comparisons were used to compare the primary and secondary outcomes. RESULTS: In 112 men, clinically significant PCa (grade group[GG] ≥ 2) accounted for 34.82% (39/112), and nonclinically significant PCa (GG = 1) accounted for 4.46% (5/112). 68 Ga-PSMA PET/CT-TB achieved higher PCa detection rate (69.77%) and positive ratio of biopsy cores (0.44) compared with SB (39.29% and 0.12) and mpMRI-TB (36.14% and 0.23), respectively (P < 0.005). Dual-tracer PET/CT screen out patients for avoiding 52.67% (59/112) unnecessary biopsy, whereas dual-tracer PET/CT-TB plus SB achieved high detection rate (77.36%) without misdiagnosis of csPCa. CONCLUSION: Dual-tracer PET/CT might screen patients for avoiding unnecessary biopsy. Dual-tracer PET/CT-TB plus SB might be a more effective and promising strategy for the definite diagnosis of clinically significant PCa than mpMRI-TB.

Development of a prognostic signature for bladder cancer based on immune-related genes.

BACKGROUND: Although the prognosis of patients with bladder cancer (BC) has improved significantly with the use of multimodal therapy, reliable prognostic biomarkers are still urgently needed due to the heterogeneity of tumors. Our aim was to develop an individualized immune-related gene pair (IRGP) signature that could precisely predict prognosis in BC patients. METHODS: Gene expression profiles and corresponding clinical information were collected from eight microarray data sets and one RNA-Seq data set. RESULTS: Among 1,811 immune genes, a 30-IRGP signature consisting of 52 unique genes was generated in the training cohort, which significantly stratified patients into low- and high-risk groups in terms of overall survival. In the testing and validation cohorts, the IRGP signature was also associated with patient prognosis in the univariate and multivariate Cox regression analyses. Several biological processes, including the immune response, chemotaxis, and the inflammatory response, were enriched among genes in the IRGP signature. When the signature was integrated with the TNM stage, an IRGP nomogram was developed and showed improved prognostic accuracy relative to the IRGP signature alone. CONCLUSIONS: In short, we identified a robust IRGP signature for estimating overall survival in BC patients that could also be used as a promising biomarker for identifying high-risk patients for individualized therapy.

Circular RNA circKIF4A Sponges miR-375/1231 to Promote Bladder Cancer Progression by Upregulating NOTCH2 Expression.

Circular RNAs (circRNAs) have been found to be important mediators of many biological processes in the growth and metastasis of various cancers. However, the potential roles of most circRNAs in the progression of bladder cancer remain unclear. In this research, we investigate the role of circKIF4A (hsa_circ_0007255) in the development and progression of bladder cancer. Detected by qRT-PCR analysis, circKIF4A was significantly upregulated in bladder cancer tissues and cell lines. We conducted CCK-8, colony-formation, transwell and mouse xenograft assays to explore the function of circKIF4A in bladder cancer. Functionally, knockdown of circKIF4A inhibited the proliferation and colony-formation ability of bladder cancer cells. Migration and metastatic ability were dramatically decreased after transfection with small interfering RNA targeting circKIF4A in both in vitro and in vivo assays. Mechanically, luciferase reporter assays and RNA immunoprecipitation assays were carried out to elucidate the underlying molecular mechanism of circKIF4A. The results revealed that circKIF4A sponges miR-375/1231 to promote bladder cancer progression by upregulating NOTCH2. Generally, our research unveils the essential role of circKIF4A-miR-375/1231-NOTCH2 axis in bladder cancer progression possibly via the competing endogenous RNA mechanism.

ISYNA1 is overexpressed in bladder carcinoma and regulates cell proliferation and apoptosis.

BACKGROUND: Bladder cancer (BCa) is one of the most common urological malignancies. While Inositol-3-phosphate synthase 1 (ISYNA1) expression and function were largely unknown in BCa. We aimed to study the expression and role of ISYNA1 in bladder cancer and investigate its potential mechanisms via ingenuity pathway analysis (IPA). METHODS: ISYNA1 expression was quantified by qRT-PCR in bladder cancer cell lines as well as normal urothelial cell line. Knocking down ISYNA1 gene in BCa T24 cells was achieved by shRNA lentivirus transfection. MTT and Celigo assay were used to assess cell proliferation. Flow cytometry was applied to test cell cycle and apoptosis. In addition, IPA was performed using PrimeView™ Human Gene Expression Array. Imunohistochemistry (IHC) was performed in BCa patient tissue microarray to verify the association between ISYNA1 expression and patients' clinicopathological features. RESULTS: ISYNA1 was significantly upregulated in BCa samples vs. para-tumor tissues. Higher expression were significantly associated with tumor T stage and lymph node metastasis of bladder cancer patients. Similarly, it was elevated in BCa cell lines (5637 and T24) compared with SVHUC cells. Knocking down ISYNA1 significantly decreased proliferation, induced apoptosis and cell cycle arrest in T24 cells. Furthermore, IPA indicated that ISYNA1 was an important regulatory factors and related networks were involved in multiple functional processes. CONCLUSION: Taken together, current study suggest ISYNA1 promotes proliferation and inhibit apoptosis in bladder cancer cells, and its expression correlated with BCa patients' clinicopathological features. Thus, ISYNA1 may serve as a potential biomarker and therapeutic target for BCa patients.

Glucocorticoid-Inducible Kinase 2 Promotes Bladder Cancer Cell Proliferation, Migration and Invasion by Enhancing ß-catenin/c-Myc Signaling Pathway.

Background: Bladder cancer is one of the most common malignancies in urologic system. The glucocorticoid-inducible kinase 2 (SGK2) expression and function were largely unknown in cancers. Current study was aimed to investigate the role of SGK2 in bladder cancer and its potential mechanisms. Methods: SGK2 expression was quantified by western blot (WB) in multiple bladder cancer cell lines (T24, 5637, J82 and UMUC3) compared with normal urothelial cell line (SVHUC). SGK2 knocking down and overexpression model were established by lentivirus transfection. MTT, colony formation, wound healing and transwell assay were used to assess the tumor cell proliferation, migration and invasion abilities, respectively. In addition, molecular function analysis was performed using FunRich software V3. Immunoprecipitation (IP) assay was applied to investigate the interaction between SGK2 and ß-catenin at protein level. TCGA database was retrieved to verify the association between these genes and clinical tumor stage as well as prognosis among bladder cancer patients. Results: SGK2 expression was significantly upregulated in multiple bladder cancer cell lines compared with SVHUC at protein level. Cell proliferation, migration and invasion abilities were significantly decreased after knocking down SGK2 in J82 and UMUC3 cell lines. Inversely, cell aggressive phenotypes were significantly increased after overexpressing SGK2 in T24 cell line. Furthermore, functional analyses of SGK2 based on TCGA database showed that SGK2 related genes were involved in receptor activity, ATP binding, DNA repair protein, trans-membrane receptor activity and lipid binding. In addition, protein interaction analysis identified c-Myc was significantly enriched in SGK2 positively associated genes. The prediction was validated by WB and IP assay that SGK2 could directly bind with ß-catenin at protein level to regulate their downstream gene c-Myc expression in bladder cancer to influence tumor progression. And clinical data generated from TCGA database also identified these downstream genes were significantly associated with tumor stage and survival status of bladder cancer patients. Conclusion: Taken together, our findings suggest SGK2 promotes bladder cancer progression via mediating ß-catenin/c-Myc signaling pathway, which may serve as a potential therapeutic target for bladder cancer patients.

Association of metformin intake with bladder cancer risk and oncologic outcomes in type 2 diabetes mellitus patients: A systematic review and meta-analysis.

BACKGROUND: Recent clinical trials indicated that metformin intake might play a protective role in the incidence and oncologic outcomes of various cancers. However, its protective effect on bladder cancer remains uncertain. METHODS: We performed a meta-analysis to investigate the association between metformin intake and bladder cancer risk as well as oncologic outcomes in diabetes mellitus (DM) patients. A comprehensive literature search was performed using PubMed, Embase, and the Cochrane Central Search Library in December 2017. Hazard ratio (HR) with 95% confidence interval (CI) was pooled. RESULTS: A total of 9 retrospective cohort studies with 1,270,179 patients were included. A meta-analysis revealed that metformin intake was associated with an increased recurrence-free survival (HR = 0.55, 95% confidence interval [CI] = 0.35-0.88; P = .01; I = 64%), improved progression-free survival (HR = 0.70, 95% CI = 0.51-0.96; P = .03; I = 33%), and prolonged cancer-specific survival (HR = 0.57, 95% CI = 0.40-0.81; P = .002; I = 0%). However, results demonstrated that metformin intake was not associated with a decreased incidence of bladder cancer (HR = 0.82, 95% CI = 0.61-1.09; P = .17; I = 85%) or an increased overall survival in bladder cancer patients (HR = 0.83, 95% CI = 0.47-1.44; P = .50; I = 64%). CONCLUSION: The present meta-analysis indicated that metformin intake could improve the prognosis of bladder cancer patients. Further prospective cohort studies and mechanistic studies are still required to determine the precise role of metformin in the initiation and progression of bladder cancer.

Association Between 12 Polymorphisms of VEGF/Hypoxia/Angiogenesis Pathway Genes and Risk of Urogenital Carcinomas: A Meta-Analysis Based on Case-Control Studies.

Objective: Previous studies indicated potential associations between polymorphisms in genes of VEGF/hypoxia/angiogenesis pathway and risk of urogenital carcinomas However, the results were controversial and inconclusive. Here, we conducted an in-depth meta-analysis to investigate the precise associations between polymorphisms in VEGF/hypoxia/angiogenesis related genes and risk of urogenital carcinomas. Methods: We searched PubMed, Web of Science, EMBASE, and Cochrane Library to identify all eligible publications. Pooled odds ratios (ORs) corresponding with the 95% confidence intervals (CIs) were calculated to evaluate their associations. Subgroup analysis was conducted to further ascertain such relationship and investigate sources of heterogeneity. Results: In the end, a total of 96 case-control studies fulfilled the inclusion criteria were enrolled for 12 polymorphisms in 4 VEGF/hypoxia/angiogenesis related genes. The pooled results showed eNOS-rs2070744 polymorphism conferred a significantly increased overall risk of urogenital carcinomas in allele, homozygote, and recessive models, respectively. In addition, eNOS-Intron 4a/b VNTR polymorphism was identified related to an increased risk of urogenital carcinomas in recessive model. And VEGF-rs699947 polymorphism was also identified an increased risk of renal cell carcinoma (RCC) in allelic, heterozygote, dominant, homozygote, and recessive models. Conclusion: To conclude, eNOS-rs2070744 and eNOS-Intron 4a/b VNTR polymorphisms are risk factors for urogenital carcinomas. VEGF-rs699947 polymorphism was also identified as an increased risk factor for renal carcinoma.

High Expression of Long Noncoding RNA MALAT1 Indicates a Poor Prognosis and Promotes Clinical Progression and Metastasis in Bladder Cancer.

BACKGROUND: Recent studies have demonstrated that the expression of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) promotes cancer cell proliferation, invasion, and metastasis in many tumor types, but the association between bladder cancer and MALAT1 remains unknown. MATERIALS: The expression of MALAT1 was tested by in situ hybridization (ISH) in 120 bladder cancer specimens. The association between MALAT1 expression and clinicopathological features and prognosis of the patients with bladder cancer was analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to verify the relationship between the expression of MALAT1 and progression and metastasis of bladder cancer. RESULTS: ISH showed that high MALAT1 expression was associated with advanced histological grade, high tumor stage, and positive lymph nodes. Kaplan-Meier survival analysis and Cox regression analysis indicated that high tumor stage, positive lymph nodes, and high MALAT1 expression were independent prognostic indicators for overall survival (OS) of patients with bladder cancer. qRT-PCR showed that the expression of MALAT1 in bladder cancer tissues was 2.85 times higher than those measured in adjacent normal tissues (P < .001). The expression of MALAT1 was 2.673 ± 0.254 in non-muscle-invasive bladder cancer and 2.987 ± 0.381 in muscle-invasive bladder cancer (P = .018). In bladder cancer specimens with positive lymph nodes, MALAT1 expression was 3.167 ± 0.297 versus 2.896 ± 0.329 in bladder cancer specimens with negative lymph nodes (P = .020). CONCLUSION: High MALAT1 expression could serve as an independent prognostic factor for OS of patients with bladder cancer and could be considered as a potential therapeutic target of bladder cancer.

Expression and clinical significance of microRNA-21, maspin and vascular endothelial growth factor-C in bladder cancer.

The present study aimed to explore the expression and clinical significance of microRNA-21 (miR-21), maspin and vascular endothelial growth factor C (VEGF-C) in bladder cancer (BC). A total of 53 BC samples and 12 normal bladder tissue samples were collected. Total messenger RNA (mRNA) was extracted, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to evaluate the expression of miR-21 and maspin in BC and normal bladder tissues. Immunohistochemistry was used for the detection of maspin and VEGF-C protein expression. Furthermore, the correlations between these molecules and certain clinicopathological parameters were investigated, and survival analysis was performed to assess their prognostic significance. miR-21 mRNA expression and VEGF-C protein expression were increased in BC tissues compared with those in normal bladder tissues, whereas maspin mRNA and protein expression levels in BC tissues were significantly decreased (P<0.01). miR-21, maspin and VEGF-C expression were significantly associated with the stage, grade and lymph node metastasis of BC (P<0.05), but not the other clinicopathological features evaluated. There was a marked inverse correlation between the mRNA expression of miR-21 and maspin, with a coefficient of -0.978 (P<0.001). Similarly, there was a significant inverse correlation between the protein expression of maspin and VEGF-C, with a coefficient of -0.589 (P<0.001). Overexpression of miR-21 and VEGF-C, as well as decreased maspin expression, were associated with a poorer prognosis. These results suggested that upregulation of miR-21, decreased maspin expression and enhanced VEGF-C in BC may promote tumor progression. miR-21, maspin and VEGF-C may therefore have significant roles as biomarkers for prognosis and as therapeutic targets of BC.

CCL21/CCR7 enhances the proliferation, migration, and invasion of human bladder cancer T24 cells.

OBJECTIVE: To investigate the effects of CCL21/CCR7 on the proliferation, migration, and invasion of T24 cells and the possible associated mechanisms: expression of MMP-2 and MMP-9, and regulation of BCL-2 and BAX proteins. METHODS: T24 cells received corresponding treatments including vehicle control, antibody (20 ng/mL CCR7 antibody and 50 ng/ml CCL21), and 50, 100, and 200 ng/ml CCL21. Proliferation was evaluated by MTT assay; cell migration and invasion were assayed using a transwell chamber. Cell apoptosis was induced by Adriamycin (ADM). The rate of cell apoptosis was examined by flow cytometry using annexin V-FITC/PI staining. Western-blot was used to analyze MMP-2 and MMP-9 and BCL-2 and BAX proteins. RESULTS: CCL21 promoted T24 cell proliferation in concentration-dependent manner with that 200 ng/mL induced the largest amount of proliferation. Significant differences of cell migration were found between CCL21treatment groups and the control group in both the migration and invasion studies (P < 0.001 for all). The expressions of MMP-2 and MMP-9 proteins were significantly increased after CCL21 treatment (p < 0.05 for all). Protein expression of Bcl-21 follows an ascending trend while the expression of Bax follows a descending trend as the concentration of CCL21 increases. No difference was found between the control group and antibody group for all assessments. CONCLUSION: CCL21/CCR7 promoted T24 cell proliferation and enhanced its migration and invasion via the increased expression of MMP-2 and MMP-9. CCL21/CCR7 had antiapoptotic activities on T24 cells via regulation of Bcl-2 and Bax proteins. CCL21/CCR7 may promote bladder cancer development and metastasis.

Hyperbaric Oxygen Therapy as an Adjuvant Therapy for Comprehensive Treatment of Fournier's Gangrene.

OBJECTIVES: To compare simple conventional treatment with the addition of hyperbaric oxygen therapy (HBOT) to conventional therapies in the treatment of Fournier's gangrene (FG). METHODS: A retrospective study of clinical data was performed by reviewing 28 cases of FG from January 2004 to December 2013 at Xiangya Hospital, Central South University. Among them, 12 patients were treated with the conventional therapy (non-HBOT group) and the other 16 cases were combined with hyperbaric oxygen therapy besides conventional therapy (HBOT group). All patients were followed up for 2 months to assess the therapeutic effect. The analyzed data included age, Fournier gangrene severity index (FGSI) score, number of surgical debridement, indwelling drainage tube time, length of stay (LOS), effective time, and curative time. RESULTS: The mortality rate was lower in the HBOT group at 12.5% (2/16) compared to the non-HBOT group, which was 33.3% (4/12). The difference in the number of surgical debridement, indwelling drainage tube time, and curative time between were significantly lower in the HBOT group compared to the non-HBOT group. CONCLUSIONS: Our preliminary research suggests that the effect of combining hyperbaric oxygen therapy with conventional therapy offers considerable advantage in the management of Fournier's gangrene. Multicenter studies with a larger sample size are required to confirm these observations.

miR-128 downregulation promotes growth and metastasis of bladder cancer cells and involves VEGF-C upregulation.

MicroRNA-128 (miR-128) serves an important role in regulating growth, invasiveness, stem cell-like traits, differentiation and apoptosis of different types of tumor cells. Vascular endothelial growth factor-C (VEGF-C) has been associated with angiogenesis, lymphangiogenesis and regional lymph node metastasis and has previously been reported to have an anti-apoptotic and proliferative role in bladder cancer (BC). To investigate the regulation of miR-128 on VEGF-C expression and their effects on proliferation and metastasis of bladder cancer, T24 and 5637 BC cells were transfected with pre-miR-128, anti-miR-128 and their respective negative control. miR-128 was downregulated in BC tissues and cell lines, while the expression levels of VEGF-C were upregulated. The present results indicated that miR-128 negatively regulated VEGF-C expression in BC T24 and 5637 BC cells. VEGF-C is a direct target of miR-128 in BC cells. Overexpression of miR-128 inhibited cell proliferation, migration and invasion. Knockdown of miR-128 promoted proliferation, migration and invasion in BC cells. Therefore, downregulation mediated malignant progression of BC may be partly attributed to increased VEGF-C expression. Consequently, the findings of the present study provide a molecular basis for the role of miR-128/VEGF-C in the progression of human BC and indicate a novel target for treatment of BC.

Preservation of the saphenous vein during laparoendoscopic single-site inguinal lymphadenectomy: comparison with the conventional laparoscopic technique.

OBJECTIVE: To prospectively study the surgical strategies and clinical efficacy of laparoendoscopic single-site (LESS) inguinal lymphadenectomy compared with conventional endoscopic inguinal lymphadenectomy for the management of inguinal nodes. PATIENTS AND METHODS: A total of 12 patients with squamous cell carcinoma of the penis who underwent penectomy between February and July 2013 were enrolled in the study. All 12 patients underwent bilateral inguinal lymphadenectomy (LESS inguinal lymphadenectomy in one limb and conventional endoscopic inguinal lymphadenectomy in the other) with preservation of the saphenous vein. All lymphatic tissue in the boundaries of the adductor longus muscle (medially), the sartorius muscle (laterally), 2 cm above the inguinal ligament (superiorly), the Scarpa fascia (superficially) and femoral vessels (deeply) was removed in both surgical techniques. All 24 procedures were performed by one experienced surgeon. RESULTS: All 24 procedures (12 LESS and 12 conventional endoscopic inguinal lymphadenectomies) were completed successfully without conversion to open surgery. For LESS inguinal lymphadenectomy and conventional endoscopic inguinal lymphadenectomy groups, the mean ± sd operating time was 94.6 ± 14.8 min and 90.8 ± 10.6 min, respectively (P = 0.145). No significant differences in the incidence of postoperative complications (skin-related problems, hecatomb, lower extremity oedema, lymphatic complications and overall complications) were noted between the two groups (P > 0.05). No lower extremity oedema occurred in any limbs of the two groups. No significant differences were observed in either lymph node clearance rate or detection rate of histologically positive lymph nodes (P > 0.05). The patient satisfaction rate with scar appearance and cosmetic results was significantly better in the LESS inguinal lymphadenectomy group than in the conventional endoscopic inguinal lymphadenectomy group of (75 vs 25%; P = 0.039). CONCLUSIONS: This preliminary study suggests that both LESS inguinal lymphadenectomy and conventional endoscopic inguinal lymphadenectomy are safe and feasible procedures for inguinal lymphadenectomy. Preservation of the saphenous vein during LESS inguinal lymphadenectomy/conventional endoscopic inguinal lymphadenectomy can effectively reduce the incidence of postoperative lower extremity oedema. LESS inguinal lymphadenectomy seems to provide better cosmetic results than conventional endoscopic inguinal lymphadenectomy.

Retroperitoneoscopic dismembered pyeloplasty for ureteropelvic junction obstruction: modification of the procedure and our experience.

PURPOSE: To report a modified retroperitoneoscopic dismembered pyeloplasty technique and its application in the treatment of ureteropelvic junction obstruction (UPJO). MATERIALS AND METHODS: From June 2010 to March 2012, retroperitoneoscopic dismembered pyeloplasty was performed in 46 patients with UPJO. Briefly, the renal pelvis was incised in the anterior aspect instead of the lateral aspect, and proximal ureter was spatulated with incision on its posterior wall. After adequately trim­ming, two layers of ureteropelvic anastomosis respectively lay on left and right side of one laparoscopic plane other than two different planes. In our refined procedure, the difficulty of intracorporeal suturing was greatly decreased. Data from 19 months mean follow-up were analyzed to evaluate the surgical outcomes. RESULTS: All operations were completed without open conversion. The mean operative time, estimated blood loss, and postoperative hospitalization stay were 108 min (75 to 155 min), 30 mL (15 to 60 mL) and 4 days (2 to 9 days), respectively. No intraoperative complications were occurred. Postoperative complications included 2 cases of minor abdominal wall hematoma and 1 case of transient postoperative anastomotic leakage for 8 days, which all were successfully treated by conservative management. A mean follow-up of 19 months (12 to 36 months) was performed which showed a success rate of 97.8%. One case (2.2%) underwent open surgery for persistence UPJO two months later. CONCLUSION: Our modification to the retroperitoneoscopic dismembered pyeloplasty procedure is technically feasible and reliable with low complications. It could be implemented as a useful alternative technique to great­ly decrease the difficulty of this procedure.

Protective effect of pioglitazone on kidney injury in diabetic rats.

OBJECTIVES: To investigate the protective effect of pioglitazone on kidney injury in diabetic rat model and its mechanisms. METHODS: Forty healthy Sprague Dawley rats were selected and randomly divided into five groups, with 8 rats in each group. Group A served as control group and were administered with sterile citrate buffer (i.p.) as placebo. Groups B, C, D and E rats were injected (i.p.) with streptozotocin to induce type I diabetes. Diabetic rats in Group B were intragastrically administered with sterile saline solution alone. Groups C, D and E rats were intragastrically given pioglitazone hydrochloride suspension at doses of 10, 20, 30 mg/kg per day, respectively. After eight weeks of treatment, all rats were anesthetized and blood was withdrawn from the abdominal aortic for detection of hemoglobin A1c, serum creatinine (SCr) and blood urea nitrogen (BUN) levels. Rats were then sacrificed and the left kidney was excised for calculation of kidney hypertrophy index (KHI), observation of renal pathological changes using light microscope and electron microscope. Mean glomerular cross-sectional areas (MGA), mean glomerular volume (MGV), glomerular basement membrane thickness and foot process fusion ratio were calculated. RT-PCR was employed for detection of podocalyxin (PCX) protein expression. RESULTS: Results showed that levels of hemoglobin A1c, BUN, SCr in Groups B, C, D and E rats were significantly higher than those in Group A (P<0.05), while BUN and SCr levels in rats of Groups C, D and E were significantly lower than those in Group B (P<0.05). KHI, MGA and MGV levels were significantly higher in Groups B, C, D and E rats than those in Group A (P<0.05); KHI and MGA levels in Group B rats were significantly higher than those in Groups C, D and E (P<0.05) and MGV in Groups D and E was significantly lower than that in Groups B and C (P<0.05). Histology study showed normal glomerulus structure, morphology, volume, endothelial cells and mesangial cells as well as clear glomerular capillary in Group A rats. Renal mesangial matrix proliferation and expansion of glomerulus cavities in Groups B, C, D and E were observed. However, damage degree in Groups C, D and E were more moderate than that in Group B. CONCLUSIONS: Pioglitazone can reduce kidney damage in diabetic rats, which may be attributed to its role in increasing glomerular PCX protein expression and inhibiting urinary excretion of PCX, and its effect is dose dependent.

Transforming growth factor­ß1 induces epithelial­mesenchymal transition and increased expression of matrix metalloproteinase­16 via miR­200b downregulation in bladder cancer cells.

Transforming growth factor­ß1 (TGF­ß1) is involved in the migration and metastases of bladder cancer. The present study was designed to investigate whether TGF­ß1 is able to induce epithelial­mesenchymal transition (EMT) and the upregulation of matrix metalloproteinase­16 (MMP­16), and to identify an association between EMT and MMP­16 in bladder cancer. Following TGF­ß1 treatment, samples of HTB9 and T24 bladder cancer cells were collected at various time points. Western blotting and quantitative polymerase chain reaction (qPCR) confirmed that TGF­ß1 induced EMT in HTB9 and T24 cells at the protein and mRNA levels. The expression levels of the miR­200 family were determined by qPCR, which indicated that TGF­ß1 treatment significantly reduced the expression of miR­200b. Bioinformatic analysis indicated that MMP­16 may be the target of miR­200b. Reporter luciferase assay confirmed that MMP­16 is a direct downstream functional target of miR­200b. A Matrigel migration assay demonstrated that miR­200b overexpression inhibited the migration of bladder cancer cells. In summary, the current study demonstrated that exogenous TGF­ß1 leads to the induction of EMT and the downregulation of miR­200b in bladder cancer cells. To the best of our knowledge, this is the first evidence that MMP­16 is a direct target of miR­200b.