Giant peritoneal loose body and its protein composition: a case report.

Peritoneal loose body (PLB) is a kind of lesions located in the abdominal cavity or pelvic cavity, which is rare and difficult to diagnose. The diameter of PLB is mostly 0.5-2.5 cm. Most PLBS are asymptomatic. Here we reported a case of giant PLB in the pelvis and analyzed its structure and protein composition. Surgical exploration revealed a white oval mass (4.5*4*3 cm) in the pelvic cavity. After the mass was removed, the symptoms of hematuria disappeared and the patient was discharged on the second postoperative day. Histochemical staining showed that PLB was mainly composed of collagen and scattered calcification. The protein components of PLB were detected by proteome analysis, and a variety of proteins related to collagen deposition and calcification were identified in PLB.

Hsa_circ_0003596 enhances the development of cell renal clear cell carcinoma through the miR-502-5p/IGF1/PI3K/AKT axis.

Accumulating research findings have shown that circular RNAs (circRNAs) play an indispensable role in tumorigenesis and tumor progression. The current study aimed to explore the role and modulatory mechanism of hsa_circ_0003596 in clear cell renal cell carcinoma (ccRCC). Quantitative real-time polymerase chain reaction was adopted to detect the expression of hsa_circ_0003596 in ccRCC tissue and cell lines. 5-Ethynyl-2'-deoxyuridine, cell counting kit 8 and the colony formation assay were utilized to assess the proliferation potential of the ccRCC cells. Transwell along with wound healing assays were adopted to quantify infiltration coupled with the migration potential of the cells. The current research study found that the circRNA hsa_circ_0003596 was overexpressed in ccRCC tissue and cell lines. Further, result showed that hsa_circ_0003596 was associated with distant metastasis of renal cancer. Notably, the knockdown of hsa_circ_0003596 can lower the proliferation, infiltration and migration potential of ccRCC cells. The results of in vivo experiments found that the reduction of hsa_circ_0003596 significantly hampered the growth of tumors in mice. In addition, it was evident that hsa_circ_0003596 acts as a "molecular sponge" for miR-502-5p to upregulate the expression of the microRNA-502-5p (miR-502-5p) target insulin-like growth factor 1 (IGF1R). Furthermore, it was found that the phosphatidylinositol 3-kinase (PI3K)/AKT signaling was the downstream cascade of hsa_circ_0003596/miR-502-5p/IGF1R cascade, which is partly responsible for the cancer-promoting effect. Overall, the results of the present study showed that hsa_circ_0003596 facilitated the proliferation, infiltration and migration of ccRCC through the miR-502-5p/IGF1R/PI3K/AKT axis. Therefore, it was evident that hsa_circ_0003596 can serve as a possible biomarker and therapeutic target against ccRCC.

Immune Microenvironment Terms Signature Robustly Predicts the Prognosis and Immunotherapy Response in Bladder Cancer Based on Large Population Cohorts.

Immune microenvironment is implicated in cancer progression. However, the role of immune microenvironment in bladder cancer has not been fully explored. Open-accessed datasets GSE120736, GSE128959, GSE13507, GSE31684, GSE32548, GSE48075, GSE83586, and The Cancer Genome Atlas (TCGA) database were enrolled in our study. Single-sample gene set enrichment analysis (ssGSEA) was used to quantify 53 immune terms in combined BLCA cohorts. The top 10 important immune terms were identified through random forest algorithm for model establishment. Our model showed satisfactory efficacy in prognosis prediction. Furthermore, we explored clinical and genomic feature differences between high- and low-risk groups. The results indicated that the patients in the high-risk group might be associated with worse clinical features. Gene set enrichment analysis showed that epithelial-mesenchymal translational, mTORC1 signaling, mitotic spindle, glycolysis, E2F target, and G2M checkpoint pathways were aberrantly activated in high-risk patients, partially explaining its worse prognosis. Patients in the low-risk group showed better immunotherapy response according to TIDE and TCIA analysis, indicating that our model could effectively predict the immunotherapy response rate. KCNH4, UGT1A1, TPO, SHANK1, PITX3, MYH1, MYH13, KRT3, DEC1, and OBP2A genes were identified as feature genes in the high- and low-risk patients. CMAP analysis was performed to identify potential compounds targeting the riskscore.

Insights into homeobox B9: a propeller for metastasis in dormant prostate cancer progenitor cells.

BACKGROUND: Metastasis is the major cause of treatment failure and cancer-related deaths in prostate cancer (PCa) patients. Our previous study demonstrated that a CD44+ subpopulation isolated from PCa cells or tumours possesses both stem cell properties and metastatic potential, serving as metastatic prostate cancer stem cells (mPCSCs) in PCa metastasis. However, the underlying mechanisms remain unknown. METHODS: In this study, we established PCa models via the orthotopic and subcutaneous implantation of different human PCa cancer cell lines, and compared the metastatic efficacy, after which process function analysis of target genes was pinpointed. RESULTS: Several novel differentially expressed genes (DEGs) between orthotopic and ectopic tumours were identified. Among them, human homeobox B9 (HOXB9) transcription factor was found to be essential for PCa metastasis, as evidenced by the diminished number of lung metastatic foci derived from orthotopic implantation with HOXB9-deficient CWR22 cells, compared with the control. In addition, HOXB9 protein expression was upregulated in PCa tissues, compared with paracancer and benign prostate hyperplasia tissues. It was also positively correlated with Gleason scores. Gain- and loss-of-function assays showed that HOXB9 altered the expression of various tumour metastasis- and cancer stem cell (CSC) growth-related genes in a transforming growth factor beta (TGFß)-dependent manner. Moreover, HOXB9 was overexpressed in an ALDH+CD44+CXCR4+CD24+ subpopulation of PCa cells that exhibited enhanced TGFß-dependent tumorigenic and metastatic abilities, compared with other isogenic PCa cells. This suggests that HOXB9 may contribute to PCa tumorigenesis and metastasis via TGFß signalling. Of note, ALDH+CD44+CXCR4+CD24+-PCa cells exhibited resistance to castration and antiandrogen therapy and were present in human PCa tissues. CONCLUSION: Taken together, our study identified HOXB9 as a critical regulator of metastatic mPCSC behaviour. This occurs through altering the expression of a panel of CSC growth- and invasion/metastasis-related genes via TGFß signalling. Thus, targeting HOXB9 is a potential novel therapeutic PCa treatment strategy.

Epidemic investigation of benign prostatic obstruction with coexisting overactive bladder in Shanghai Pudong New Area and its impact on the health-related quality of life.

BACKGROUND: We aimed to investigate the prevalence, relative risk factors, and the impact on the health-related quality of life (HRQoL) of benign prostatic obstruction (BPO) with coexisting overactive bladder (OAB) in men aged over 50 and living in Shanghai Pudong New Area. METHODS: Using a multi-stage sampling and descriptive epidemiological method, 1632 men were selected from among the general population. Participants completed an evaluation of lower urinary tracts symptoms (LUTS), including international prostate symptom score (IPSS) and quality of life (QoL) questionnaires. Erectile function was assessed using the International Index of Erectile Function-5 (IIEF-5) questionnaire. In addition, the Overactive Bladder Symptom Score (OABSS) and King's health questionnaire (KHQ) were used to assess the impact of BPO with coexisting OAB on the HRQoL. Maximum flow rate (Qmax), postvoid residual urine volume (PVR) and prostate-specific antigen (PSA) were also recorded. RESULTS: A total of 1476 men with complete data were analyzed. The overall prevalence of BPO with coexisting OAB was 39.6%. Age and prostate volume were associated risk factors for BPO with coexisting OAB. In addition, BPO with coexisting OAB negatively impacted the HRQoL, with increased IPSS, QoL, OABSS, and KHQ scores and decreased IIEF-5 scores compared to that in patients with BPO without OAB. CONCLUSIONS: Qmax, PVR and serum PSA did not predict whether the patients had a combined BPO + OAB or not. The prostate volume and age were associated risk factors for BPO with coexisting OAB. BPO is a progressive disease and may be one of the risk factors for OAB.

Upregulation of TRPV1 in spinal dorsal root ganglion by activating NGF-TrkA pathway contributes to pelvic organ cross-sensitisation in rats with experimental autoimmune prostatitis.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is the prostate gland inflammation characterised as genitourinary pain in the pelvic region. The rat experimental autoimmune prostatitis (EAP) was achieved to mimic CP/CPPS. The expressions of transient receptor potential vanilloid 1 (TRPV1) in the prostate, bladder and spinal dorsal root ganglion (DRG) were analysed by Western blotting. Tropomyosin receptor kinase A (TrkA) and nerve growth factor (NGF) in the DRG were also analysed by Western blotting. Measurements of inflammatory cytokines were carried out according to the instructions of the corresponding kits. The expressions of TRPV1 in the prostate, bladder and DRG in the EAP group were significantly higher than those in the control group. The expressions of NGF and TrkA in the DRG in the EAP group were significantly higher than those in the control group. The levels of serum TNF-α and IL-1ß in the EAP group were significantly higher than those in the control group. We conclude that CP/CPPS may participate in the pathological activation of neurons in the L5-S1 segment of DRG by activating NGF-TrkA pathway and cause pelvic organ cross-sensitisation by upregulating the expression of TRPV1 in the prostate, bladder and DRG.

Tetracycline attenuates calcifying nanoparticles-induced renal epithelial injury through suppression of inflammation, oxidative stress, and apoptosis in rat models.

BACKGROUND: Calcifying nanoparticles (CNPs) has been associated with the occurrence and development of kidney stones, but the exact mechanism is not clear. This study aimed to establish a rat model of CNP-induced renal epithelial injury and assess the efficacy of tetracycline in preventing this injury. METHODS: Kidney stones from patients after percutaneous nephrolithotomy (PCNL) were collected to isolate and culture CNPs. Thirty Sprague-Dawley rats were divided into three groups: the sham group (G1), the CNP group (G2), and the CNP + tetracycline group (G3). Rats in G2 and G3 were given an intravenous injection of CNPs via the tail vein, while rats in G1 were given saline. Meanwhile, rats in G3 were given tetracycline by gavage twice a day at a dose of 25 mg/kg. After 8 weeks, the 24-h urine of all rats was collected, and all rats were sacrificed to obtain blood and kidneys. RESULTS: The results revealed that in G2, activities of antioxidant enzymes such as superoxide dismutase and catalase were significantly lower than those in G1, while malondialdehyde activity in G2 was significantly higher than that in G1 and both of them were inhibited by tetracycline co-treatment in G3. CNPs significantly increased expression of inflammatory cytokines, including monocyte chemotactic protein 1 and interleukin 6, which were largely alleviated in G3. CNPs significantly increased TUNEL-positive cells and the apoptosis activity of Bcl2-associated X protein but decreased B-cell lymphoma-2 level compared with that in G1, and was limited by tetracycline co-treatment in G3. Furthermore, CNPs led to notable renal tubular epithelial cell damage, hyaline cast formation, desquamation, swelling, vacuolization in histology, all of which were alleviated by tetracycline. CONCLUSIONS: Tetracycline can attenuate CNP-induced renal epithelial injury through suppression of inflammation, oxidative stress, and apoptosis.

Role of leptin and the leptin receptor in the pathogenesis of varicocele-induced testicular dysfunction.

The present study investigated the expression of leptin and its receptor in the left testis and hypothalamus of rats with varicocele and clarified their roles in the pathogenesis of varicocele­induced testicular dysfunction. A total of 40 male rats were divided randomly into four groups. Groups 1 (G1) and 3 (G3) underwent a sham operation. Groups 2 (G2) and 4 (G4) underwent operations to form a varicocele created by partial ligation of the left renal vein. G1 and G2 rats were euthanized 4 weeks after the operation while G3 and G4 rats were euthanized at 8 weeks. The expression of leptin and its receptor was analyzed by immunohistochemistry. The mRNA levels of leptin, its receptor, kisspeptin (KiSS­1), G­protein coupled receptor 54 (GPR54), gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), and follicle­stimulating hormone (FSH) were measured by reverse transcription­quantitative polymerase chain reaction. Testicular spermatogenesis function and gonadal hormone levels were measured. Compared with G1 and G3, the expression of leptin and its receptor in rat testis was significantly higher in G2 and G4, respectively. Leptin expression was inversely associated with the number of sperm in the left epididymis, thickness of the seminiferous epithelium and the diameter of seminiferous tubules. The expression of leptin receptors in the hypothalamus of G2 and G4 was significantly increased compared with that in G1 and G3, respectively. The mRNA levels of KiSS­1, GPR54, GnRH, LH and FSH in G2 and G4 were significantly increased compared with that in G1 and G3, respectively. Serum testosterone levels in G2 and G4 rats were significantly lower than those in G1 and G3 rats, respectively. There was no significant difference between the serum levels of FSH, LH and leptin. These results suggest that leptin and its receptor may serve significant roles in the pathogenesis of varicocele-induced testicular dysfunction.

Effect of Interventions for Premature Ejaculation in the Treatment of Chronic Prostatitis with Secondary Premature Ejaculation.

Objective To evaluate the effect of interventions for premature ejaculation (PE) in the management of patients with chronic prostatitis and secondary premature ejaculation. Methods Totally 90 patients diagnosed as chronic prostatitis with PE were randomly divided into control group (n=45) and interventional group (n=45). Control group received a conventional therapy consisted of oral administration of antibiotics,α-receptor blocker,and proprietary Chinese medicine for clearing away heat and promoting diuresis. Interventional group received a conventional therapy combined with treatment for ameliorating the PE symptom (oral dapoxetine on-demand and ejaculation control exercise).National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI),Chinese Index of Sexual Function for Premature Ejaculation (CIPE)-5 questionnaires,intravaginal ejaculatory latency time,and the number of coituses per week were applied for evaluating the treatment outcomes. Results Follow-up was accomplished in 35 and 38 patients in the control and interventional group.The CIPE-5 score,intravaginal ejaculatory latency time,and the number of coituses per week were significantly improved in both two groups but more significantly in interventional group (all P<0.05). The NIH-CPSI pain,urination,and quality of life subscores and total score were improved significantly in both two groups after treatment,but the NIH-CPSI pain and quality of life subscores had been improved more significantly in the interventional group (all P<0.05). The variation of NIH-CPSI was negatively correlated with that of CIPE-5 in both two groups (r=-0.362,P=0.016;r=-0.330,P=0.021). Conclusions For CP with secondary PE patients,the interventions for PE can not only improve the quality of sexual life but also help improve the NIH-CPSI pain and quality of life subscores. PE should be routinely screened and treated during the management of CP.p.

Association between NQO1 C609T polymorphism and bladder cancer susceptibility: a systemic review and meta-analysis.

There is growing evidence for the important roles of genetic factors in the host's susceptibility to bladder cancer. NAD(P)H:quinone oxidoreductase 1 (NQO1) is a cytosolic enzyme that catalyzes the two-electron reduction of quinoid compounds into hydroquinones. Since the NQO1 C609T polymorphism is linked to enzymatic activity of NQO1, it has also been hypothesized that NQO1 C609T polymorphism may affect the host's susceptibility to bladder cancer by modifying the exposure to carcinogens. There were many studies carried out to assess the association between NQO1 C609T polymorphism and bladder cancer risk, but they reported contradictory results. We conducted a meta-analysis to examine the hypotheses that the NQO1 C609T polymorphism modifies the risk of bladder cancer. Eleven case-control studies with 2,937 bladder cancer cases and 3,008 controls were included in the meta-analysis. Overall, there was no obvious association between NQO1 C609T polymorphism and bladder cancer susceptibility (for T versus C: odds ratio (OR) = 1.12, 95 % confidence interval (95 %CI) 0.99-1.26, P OR = 0.069; for TT versus CC: OR = 1.31, 95 %CI 0.95-1.81, P OR = 0.100; for TT/CT versus CC: OR = 1.06, 95 %CI 0.95-1.18, P OR = 0.304; for TT versus CT/CC: OR = 1.29, 95 %CI 0.94-1.77, P OR = 0.112). After adjusting for heterogeneity, meta-analysis of those left 10 studies showed that there was an obvious association between NQO1 C609T polymorphism and bladder cancer susceptibility (for T versus C: OR = 1.18, 95 %CI 1.06-1.31, P OR = 0.003; for TT versus CC: OR = 1.47, 95 %CI 1.14-1.90, P OR = 0.003; for TT/CT versus CC: OR = 1.16, 95 %CI 1.01-1.34, P OR = 0.036; for TT versus CT/CC: OR = 1.39, 95 %CI 1.10-1.75, P OR = 0.006). There was low risk of publication bias. Therefore, our meta-analysis suggests that NQO1 C609T polymorphism is associated with bladder cancer susceptibility.