Ureteral reimplantation for the management of pelvic lipomatosis.

Introduction: Pelvic lipomatosis is a rare benign disease characterized by urethral elongation, bladder deformity, and/or hydronephrosis. Conservative management is not effective, and urinary diversion is the most effective treatment option but is usually unacceptable for relatively young patients. Ureteral reimplantation seemed to be an appropriate modality under these conditions. We present one case in which pelvic lipomatosis was managed with ureteral reimplantation. Patient presentation: A 45-year-old, previously healthy man presented with right flank pain. Pelvic CT and CT urography showed excessive pelvic fat, bilateral hydronephrosis, tortuous ureters, and a pear-shaped bladder, all of which indicated a diagnosis of pelvic lipomatosis. We performed laparoscopic bilateral urinary tract infection on this patient. At follow-up, bilateral hydronephrosis and flank pain were greatly relieved. Conclusion: Pelvic lipomatosis can be managed safely and effectively by urinary tract infection, but longer follow-up periods are needed to evaluate the long-term efficacy of this approach.

Does Internet Use Connect Us to a Healthy Diet? Evidence from Rural China.

Dietary patterns in China have changed dramatically over the past few decades as the Internet has become rapidly available. Based on data from the China Health and Nutrition Survey (2006-2011), we use a two-way fixed effects model and an instrumental variable approach to determine the impact of Internet use on the dietary quality of rural residents. The results indicate that Internet use could significantly improve the dietary quality of Chinese rural residents, with an increase of about 10.4% in the China Food Pagoda Score (CFPS), mainly due to the increase in the dietary quality score for five food groups: fruits, meats, eggs, oil, and salt. We also found that Internet use significantly increased the consumption amounts of milk and its products (4 g), fruits (31 g), eggs (8 g), and vegetables (34 g), while also decreasing the intake of salts (2 g) and oil (6 g). A possible mechanism is that Internet use improves the dietary knowledge of rural residents, thus optimizing their dietary structure. Moreover, the effect of the Internet was greater among females and those who prepare food for a family. Rural residents without a college degree enjoyed more benefits. In summary, governments should further promote Internet penetration in rural areas for health purposes.

Glycyrrhizic Acid Inhibits Core Fucosylation Modification Modulated EMT and Attenuates Bleomycin-Induced Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal and incurable chronic interstitial lung disease with an unknown etiology. Recent evidence suggests that epithelial-mesenchymal transition (EMT) is one of the possible factors in the pathogenesis of pulmonary fibrosis. Glycyrrhizic acid (GA) is a natural active ingredient extracted from the root of the traditional Chinese herb licorice, which has been shown in previous studies to have the effect of alleviating lung injury. In this study, our objective was to investigate whether GA could ameliorate pulmonary fibrosis by altering EMT, as well as the therapeutic potential of changing core fucosylation (CF) to target EMT-related pathways. First, we verified that GA partially reverses EMT in a rat model of bleomycin-induced lung interstitial fibrosis, alleviating pulmonary fibrosis, and implying that GA has antifibrotic potential. Next, we discovered that GA attenuated lung interstitial fibrosis by reducing CF modifications to some extent. Interestingly, we found that GA therapy reduced the expression of phosphorylated Smad2/3 (p-Smad2/3) and ß-catenin in the EMT pathway and that GA inhibited the modification of TGF-ßR and WNT receptor proteins by CF, suggesting that GA may interfere with the EMT process by modulating TGF-ßR, WNT core fucosylation modifications to attenuate pulmonary fibrosis. In conclusion, these findings indicate that GA could be a potential therapeutic agent for IPF, and further support the idea that targeting CF alterations could be a novel technique for the treatment of diseases involving EMT.

TFAP2C-Mediated lncRNA PCAT1 Inhibits Ferroptosis in Docetaxel-Resistant Prostate Cancer Through c-Myc/miR-25-3p/SLC7A11 Signaling.

Recent evidence has shown that the induction of ferroptosis is a new therapeutic strategy for advanced prostate cancer (PCa) when used as a monotherapy or in combination with second-generation antiandrogens. However, whether ferroptosis inducers are effective against docetaxel-resistant PCa remains unclear. In addition, the biological role and intrinsic regulatory mechanisms of long noncoding RNAs (lncRNAs) in ferroptosis and chemoresistance are not well understood. In this study, we established two acquired docetaxel-resistant PCa cell lines and found that docetaxel-resistant PCa cells developed tolerance toward ferroptosis. In addition, dysregulated lncRNAs in drug-resistant and -sensitive PCa cells were identified by RNA sequencing, and we identified that prostate cancer-associated transcript 1 (PCAT1) was highly expressed in the docetaxel-resistant PCa cell lines and clinical samples. Overexpression of PCAT1 inhibited ferroptosis and increased docetaxel resistance, which could be attenuated by PCAT1 knockdown. Furthermore, we revealed that PCAT1 inhibited ferroptosis by activating solute carrier family 7-member 11 (SLC7A11) expression via reducing iron accumulation and subsequent oxidative damage. Mechanistically, we demonstrated that PCAT1 interacted with c-Myc and increased its protein stability using nucleotides 1093-1367 of PCAT1 and 151-202 amino acids of c-Myc protein, thereby transcriptionally promoting SLC7A11 expression. In addition, PCAT1 facilitated SLC7A11 expression by competing for microRNA-25-3p. Finally, transcription factor AP-2 gamma (TFAP2C) activated PCAT1 expression at the transcriptional level to reduce ferroptosis susceptibility and enhance chemoresistance. Collectively, our findings demonstrated that TFAP2C-induced PCAT1 promotes chemoresistance by blocking ferroptotic cell death through c-Myc/miR-25-3p/SLC7A11 signaling.

LncRNA OIP5-AS1 inhibits ferroptosis in prostate cancer with long-term cadmium exposure through miR-128-3p/SLC7A11 signaling.

Previous studies suggest that cadmium (Cd) is one of the causative factors of prostate cancer (PCa), but the effect of chronic Cd exposure on PCa progression remains unclear. Besides, whether long noncoding RNAs (lncRNAs) are involved in the regulation of prolonged exposure to Cd in PCa needs to be elucidated. In the present study, we found that the serum concentration of Cd in PCa patients was positively correlated with the Gleason score and tumor-node-metastasis (TNM) classification. To simulate chronic Cd exposure in PCa, we subjected PC3 and DU145 cells to long-term, low-dose Cd exposure and further examined tumor behavior. Functional studies identified that chronic Cd exposure promoted cell growth and ferroptosis resistance in vitro and in vivo. Furthermore, we found that lncRNA OIP5-AS1 expression was greatly elevated in PC3 and DU145 cells upon chronic Cd exposure. Dysregulation of OIP5-AS1 expression mediated cell growth and Cd-induced ferroptosis. Mechanistically, we demonstrated that OIP5-AS1 served as an endogenous sponge of miR-128-3p to regulate the expression of SLC7A11, a surrogate marker of ferroptosis. Moreover, miR-128-3p decreased cell viability by enhancing ferroptosis. Taken together, our data indicate that lncRNA OIP5-AS1 promotes PCa progression and ferroptosis resistance through miR-128-3p/SLC7A11 signaling.

LncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.

Antimony is a common environmental contaminant that causes biological toxicity in exposed populations worldwide. Previous studies have revealed that antimony promotes prostate cancer growth by stabilizing the c-Myc protein and mimicking androgen activity. However, the role of lncRNAs in the regulation of antimony-induced carcinogenesis remains unknown, and the precise mechanisms need to be explored. In the present study, we found that chronic exposure to antimony promoted cell growth and lipid metabolic disequilibrium in prostate cancer. Mechanistically, we identified a long noncoding RNA molecule, PCA3, that was substantially upregulated in LNCaP cells in response to long-term antimony exposure. Functional studies indicated that abnormal PCA3 expression modulated antimony-induced proliferation and cellular triglyceride and cholesterol levels. In addition, PCA3 levels were found to be inversely correlated with MIR-132-3 P levels by acting as a decoy for MIR-132-3P. Besides, SREBP1 directly interacted with MIR-132-3 P to increase cell growth and disrupt lipid metabolism by targeting its 3'UTR regions. Taken together, our results revealed that lncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.

Astragalus Polysaccharides Inhibits Tumorigenesis and Lipid Metabolism Through miR-138-5p/SIRT1/SREBP1 Pathway in Prostate Cancer.

Astragalus polysaccharides (APS) is a traditional Chinese medicine and have been proved to involve in multiple biological processes, including inflammation, metabolism, and carcinogenics. However, the specific mechanisms by which APS on prostate cancer (PCa) remains largely unknown. In the current study, we found APS greatly inhibited the proliferation and invasion of PCa cells in a dose-dependent and time-dependent manner in vitro and in vivo. In addition, cellular triglyceride and cholesterol levels were also decreased significantly under APS treatment. Microarray data revealed the SIRT1 expression was markably suppressed under APS exposure. Mechanistic studies demonstrated that over-expression of SIRT1 inhibits the expression and nuclear translocation of SREBP1 via activating AMPK phosphorylation to suppress lipid metabolism. Otherwise, knockdown of SIRT1 significantly promotes AMPK/SREBP1 signaling and its associated target genes. Besides, we also found miR-138-5p was greatly inhibited the SIRT1 expression to regulating cell metabolism by targeting its 3'UTR region. To summarize, our findings suggested that APS inhibits tumorigenesis and lipid metabolism through miR-138-5p/SIRT1/SREBP1 pathways in PCa.

LncRNA NEAT1 promotes docetaxel resistance in prostate cancer by regulating ACSL4 via sponging miR-34a-5p and miR-204-5p.

Docetaxel resistance remains one of the main problems in clinical treatment of metastatic prostate cancer (PCa). Previous studies identified differently expressed lncRNAs in docetaxel-resistant PCa cell lines, while the potential mechanisms were still unknown. In the present study, we found NEAT1 was expressed at high levels in docetaxel-resistant PCa clinical samples and related cell lines. When knockdown NEAT1, cell proliferation and invasion in docetaxel-resistant PCa cells in vitro and in vivo were downregulated. Our further researches explained that NEAT1 exerts oncogenic function in PCa by competitively 'sponging' both miR-34a-5p and miR-204-5p. Inhibition of miR-34a-5p or miR-204-5p expression mimics the docetaxel-resistant activity of NEAT1, whereas ectopic expression of miR-34a-5p or miR-204-5p attenuates the anti-drug function of NEAT1 in PCa cells. Besides, we also found ACSL4 is a target of both miR-34a-5p and miR-204-5p, and ACSL4 was also inhibited by miR-34a-5p and miR-204-5p. Moreover, suppression of miR-34a-5p or/and miR-204-5p greatly restrained the expression of ACSL4 upon NEAT1 overexpression. Joint expression of miR-34a-5p and miR-204a-5p synergistically decreased the expression of ASCL4, indicating miR-34a-5p and miR-204a-5p collaboratively inhibit the expression of ACSL4. Innovatively, we concluded that NEAT1 contributes to the docetaxel resistance by increasing ACSL4 via sponging miR-34a-5p and miR-204-5p in PCa cells.

Radical cystectomy for pT1 urothelial carcinoma of bladder not amenable to TURBT: Long-term results.

PURPOSE: This study sought to identify factors associated with survival of pT1 urothelial carcinoma of bladder (UCB) after radical cystectomy (RC). METHODS: This study consists of 114 pT1 UCB [primary 83, recurrent 31, none were amenable to transurethral resection (TUR)] treated by radical cystectomy. Survival analysis using Cox regression tests were performed to identify factors associated with survival of pT1 UCB after RC. RESULTS: Pelvic lymph node (LN) status, age and lymphovascular invasion (LVI) are associated with survival of pT1 UCB after RC; recurrent pT1 UCB of high grade origin (HGO) tends to have poorer CSS than primary pT1 UCB or recurrent pT1 UCB of low grade origin (LGO) (5-year and 10-year CSS rates was 75% and 73% for primary cases; 77% and 77% for recurrent pT1 UCB of LGO; and 56% and 37% for recurrent pT1 UCB of HGO, p = 0.078). CONCLUSIONS: LN status, age and LVI were significantly associated with survival of pT1 UCB after RC. Recurrent pT1 UCB of HGO should be managed with radical cystectomy in a timely fashion given that these cases tend to have poorer CSS than primary pT1 UCB after RC, even if they did not progress to muscle-invasive bladder cancer (MIBC).

CtBP2 overexpression is associated with tumorigenesis and poor clinical outcome of prostate cancer.

INTRODUCTION: The aim of the study was to evaluate the expression of CtBP2 in prostate cancer and to determine its relationship with clinicopathologic parameters. MATERIAL AND METHODS: The expression of CtBP2 in 119 prostate cancer tissues and 41 normal tissues was examined by qPCR and Western blot analysis, and the results were correlated with clinicopathologic parameters. RESULTS: CtBP2 expression in prostate cancer tissues was higher than that in normal samples. CtBP2 overexpression was closely correlated with serum prostatic specific antigen (PSA) (p = 0.018), advanced tumor stage (T3) (p = 0.025), higher Gleason scores (p = 0.019), positive extraprostatic extension (p = 0.012), positive vascular invasion (p = 0.011) and perineural invasion (p = 0.035). However, no significant association was found between CtBP2 abnormal expression and other parameters, including age (p = 0.776), positive lymph node (p = 0.872) and positive surgical margin (p = 0.37). Moreover, CtBP2 overexpression was significantly associated with poor clinical outcome of prostate cancer (p = 0.0168). CONCLUSIONS: CtBP2 is overexpressed in prostate cancer, and its increased expression is closely associated with tumor progression and the outcome of prostate cancer.

New retractor facilitates exposure of the vascular pedicles in Chinese men with complex pelvis during radical cystectomy.

OBJECTIVE: To evaluate the surgical instrument, the double-slice retractor of pelvis (DBR), for the division of the vascular pedicles from the bladder and prostate in male patients with complex pelvis during radical cystectomy. METHODS: Radical cystectomy was performed on 140 male patients (all cases body mass index >28 kg/m(2), 29 cases having undergone partial cystectomy) with bladder cancer. With the aid of the double-slice retractor to expose vascular pedicles from the bladder and prostate, 80 radical cystectomies were performed. The others were treated as the control. RESULTS: The double-slice retractor provided excellent exposure for the division of vascular pedicles from the bladder and prostate. The handling of the vascular pedicles from the bladder and prostate became easier and safer without unnecessary bleeding and injury in the rectum. In double-slice retractor and control groups, the operative time to handle the vascular pedicles during radical cystectomy in the double-slice retractor group was 12.2 ± 1.4 min compared with 22.6 ± 3.4 min for the control group (P < 0.05), and the blood loss was 30.3 ± 2.2 ml compared with 50.2 ± 4.5 ml (P < 0.05). For the whole radical cystectomy procedure, the operative time lasted 72.1 ± 9.2 min in the double-slice retractor group compared with 85.7 ± 6.8 min for the control group (P < 0.05), the whole blood loss was reduced to 340.3 ± 12.7 ml from 410.1 ± 11.4 ml in the control group (P < 0.05). And the rate of transfusion was geared down to 10% in the double-slice retractor group from 25% in the control (P < 0.05). CONCLUSIONS: The use of the double-slice retractor for the exposure of vascular pedicles from the bladder and prostate is simple and effective in male patients with complex pelvis during radical cystectomy. We have devised a promising surgical instrument for the exposure of vascular pedicles.

[Expression of PIM-1 in prostate cancer tissue and its relationship with PSA recurrence].

OBJECTIVE: To explore the expression of the PIM-1 protein in prostate cancer tissue and its relationship with PSA recurrence. METHODS: We used the immunohistochemical SP method to detect the expression of the PIM-1 protein in the prostate tissues of 68 cases of prostate cancer (PCa) and 37 cases of benign prostatic hyperplasia (BPH). RESULTS: The positive rate of the PIM-1 protein expression was 67.65% (46/68) in the PCa tissue, significantly higher than 40.54% (15/37) in the BPH tissue (P<0.05). Its positive rates in PCa Gleason scores 6, 7 and 8-10 were 33.33% (7/21), 77.5% (21/28) and 94.74% (18/19), respectively, with significant between-group differences (P<0.05), and those in stages I , II, III and IV of PCa were 47.62%, 53.85%, 73.33% and 94.74%, respectively. Kaplan-Meier analysis of the results of a 36-month follow-up showed the ratios of PIM-1 expression to PSA recurrence and non-recurrence were 10/22 (45.45%) and 36/46 (78.26%), respectively, with statistically significant differences (P<0.05). CONCLUSION: PIM-1 protein expression in PCa tissue is closely related to the Gleason score and clinical stage of PCa and PSA recurrence, which suggests that the PIM-1 gene plays an important role in PCa evolution and progression, and may be an indicator for the prognosis of PCa.

The interleukin-6 -174G/C polymorphism and prostate cancer risk: a systematic review and meta-analysis.

OBJECTIVE: This systematic review and meta-analysis was undertaken to integrate previous findings and summarize the effect size of the association of interleukin-6 (IL-6) genetic polymorphism -174G/C with susceptibility to prostate cancer (PCa). METHODS: All eligible studies of IL-6 -174G/C polymorphism and PCa risk were collected from the following electronic databases: PubMed and the Cochrane Library, with the last report up to June 1, 2011. Statistical analyses were performed by Review Manage version 5.0 and Stata 10.0. RESULTS: A total of 7 independent studies, including 9,959 cases and 12,361 controls, were identified. When all studies were pooled, we did not detect a significant association of -174G/C polymorphism with PCa risk. When stratifying for race, similar results were obtained; evidence of a significant relation was absent in both Caucasians and the mixed population. After stratifying the studies by study types, -174G/C polymorphism was significantly associated with PCa risk when examining the contrast of CC + GC versus GG (OR = 1.44, 95% CI = 1.05-1.98, p = 0.03) in cohort studies but not in case-control studies. CONCLUSIONS: Our review suggest that -174G/C polymorphism is associated with an increased PCa risk in two cohort studies from one article. Additional well-designed studies are warranted to validate these findings.

[Correlation of histological prostatitis with PSA, prostate volume, PSAD, IPSS, Qmax and PVR in BPH patients].

OBJECTIVE: To explore the correlation of histologically proven prostatitis with the level of prostate specific antigen (PSA), prostate volume, PSA density (PSAD), international prostate symptom score (IPSS), maximum flow rate (Qmax) and post-void residual volume (PVR) in men with symptoms of benign prostate hyperplasia (BPH). METHODS: Totally 673 patients surgically treated for BPH were divided into Groups A and B in accordance with histological findings, the former including those with histological prostatitis, and the latter without it. Comparisons were made between the two groups in the PSA level, prostate volume, PSAD, IPSS, Qmax and PVR. RESULTS: The PSA level, prostate volume, IPSS and PVR were significantly higher in Group A ([5.64 +/- 2.48] microg/L, [43.66 +/- 13.11] ml, 24.72 +/- 5.39 and [124.90 +/- 49.80] ml) than in B ([4.97 +/- 1.99] microg/L, [40.41 +/- 11.44] ml, 23.40 +/- 6.21 and [112.73 +/- 50.03] ml) (P<0.05), while Qmax markedly lower in the former ([6.94 +/- 3.23] ml/s) than in the latter ([7.75 +/- 3.52] ml/s) (P<0.05), but PSAD showed no statistically significant difference between the two groups (0.129 +/- 0.048 vs 0.123 +/- 0.034, P>0.05). CONCLUSION: Histological prostatitis can significantly increase the PSA level, prostate volume, IPSS and PVR, and reduce the Qmax of the patient, but is not correlated with PSAD. It is an important factor influencing the clinical progression of BPH.

Laparoscopic simple enucleation and coagulation on tumor bed using argon beam coagulator for treating small renal cell carcinomas: an animal study followed by clinical application.

MATERIAL/METHODS: The animal experiments of coagulation therapy on the wound tissue bed during partial nephrectomy with an argon beam coagulator were performed on 16 rabbits, which were randomly divided into 4 groups. Groups A and B had renal artery occlusion; the treatment time of coagulation was 4 seconds and 6 seconds, respectively. Groups C and D did not have renal artery occlusion; the treatment time of coagulation was 2 seconds and 4 seconds, respectively. Then 30 clinical operations of laparoscopic simple enucleation and coagulation on tumor bed using an argon beam coagulator were performed. RESULTS: All 16 rabbits successfully underwent the operation. By the histological examination, the scab depth of the wound tissue bed in groups A, B, C, and D were 2.76 ± 0.17 mm, 3.15 ± 0.15 mm, 2.28 ± 0.16 mm and 2.75 ± 0.06 mm, respectively. Group A differed significantly from groups B and C (P=0.012, 0.007), and group D differed significantly from groups B and C (P=0.002, 0.002). In the clinical study, all 30 patients successfully underwent the operation. The mean operative time was 182 minutes, and the mean blood loss was 280 ml. With a median follow-up time of 37 months, neither local recurrence nor distant metastasis was found by computerized tomography scan. CONCLUSIONS: Laparoscopic simple enucleation and coagulation on tumor bed using an argon beam coagulator can be considered for treating small renal cell carcinomas. However, the indication of this procedure should be highly selected.

Association between COX-2 rs2745557 polymorphism and prostate cancer risk: a systematic review and meta-analysis.

BACKGROUND: Evidence is accumulating that chronic inflammation may have an important role in prostate cancer (PCa). The COX-2 polymorphism rs2745557 (+202 C/T) has been extensively investigated as a potential risk factor for PCa, but the results have thus far been inconclusive. This meta-analysis was performed to derive a more precise estimation of the association. METHODS: A comprehensive search was conducted to identify all case-control studies of COX-2 rs2745557 polymorphism and PCa risk. We used odds ratios (ORs) to assess the strength of the association, and 95% confidence intervals (CIs) give a sense of the precision of the estimate. Statistical analyses were performed by Review Manage, version 5.0 and Stata 10.0. RESULTS: A total of 8 available studies were considered in the present meta-analysis, with 11356 patients and 11641 controls for rs2745557. When all groups were pooled, there was no evidence that rs2745557 had significant association with PCa under co-dominant, recessive, over-dominant, and allelic models. However, our analysis suggested that rs2745557 was associated with a lower PCa risk under dominant model in overall population (OR=0.85, 95%CI=0.74-0.97, P=0.02). When stratifying for race, there was a significant association between rs2745557 polymorphism and lower PCa risk in dominant model comparison in the subgroup of Caucasians (OR=0.86, 95%CI=0.75-0.99, P=0.04), but not in co-dominant, recessive, over-dominant and allelic comparisons. CONCLUSION: Based on our meta-analysis, COX-2 rs2745557 was associated with a lower PCa risk under dominant model in Caucasians.