Overexpression of DUSP26 gene suppressed the proliferation, migration, and invasion of human prostate cancer cells.

Prostate cancer (PCa) is threatening the health of millions of people, the pathological mechanism of prostate cancer has not been fully elaborated, and needs to be further explored. Here, we found that the expression of DUSP26 is dramatically suppressed, and a positive connection of its expression with PCa prognosis was also observed. In vitro, overexpression of DUSP26 significantly inhibited the proliferative, migrative, and invasive capacities of PC3 cells, DUSP26 silencing presented opposite results. Tumor formation experiments in subcutaneous nude mice demonstrated that DUSP26 overexpression could significantly suppress PC3 growth in vivo. Moreover, the mechanism of DUSP26 gene and PCa was discovered by RNA-Seq analysis. We found that DUSP26 significantly inhibited MAPK signaling pathway activation, and further experiments displayed that DUSP26 could impair TAK1, p38, and JNK phosphorylation. Interestingly, treatment with the TAK1 inhibitor (iTAK1) attenuated the effect of DUSP26 on PC3 cells. Together, these results suggested that DUSP26 may serve as a novel therapeutic target for PC3 cell type PCa, the underlying mechanism may be through TAK1-JNK/p38 signaling.

Abnormal expression of FOXM1 in carcinogenesis of renal cell carcinoma: From experimental findings to clinical applications.

Renal cell carcinoma (RCC) is a prevalent malignancy within the genitourinary system. At present, patients with high-grade or advanced RCC continue to have a bleak prognosis. Mounting research have emphasized the significant involvement of Forkhead box M1 (FOXM1) in RCC development and progression. Therefore, it is imperative to consolidate the existing evidence regarding the contributions of FOXM1 to RCC tumorigenesis through a comprehensive review. This study elucidated the essential functions of FOXM1 in promoting RCC growth, invasion, and metastasis by regulating cell cycle progression, DNA repair, angiogenesis, and epithelial-mesenchymal transition (EMT). Also, FOXM1 might serve as a novel diagnostic and prognostic biomarker as well as a therapeutic target for RCC. Clinical findings demonstrated that the expression of FOXM1 was markedly upregulated in RCC samples, while a high level of FOXM1 was found to be associated with a poor overall survival rate of RCC. Furthermore, it is worth noting that FOXM1 may have a significant impact on the resistance of renal cell carcinoma (RCC) to radiotherapy. This observation suggests that inhibiting FOXM1 could be a promising strategy to impede the progression of RCC and enhance its sensitivity to radiotherapy. The present review highlighted the pivotal role of FOXM1 in RCC development. FOXM1 has the capacity to emerge as not only a valuable diagnostic and prognostic tool but also a viable therapeutic option for unresectable RCC.

Causal relationship between prostatic diseases and prostate cancer: a mendelian randomization study.

BACKGROUND: Although it is thought that prostatitis or benign prostatic hyperplasia (BPH) is related to prostate cancer (PCa), the underlying causal effects of these diseases are unclear. METHODS: We assessed the causal relationship between prostatitis or BPH and PCa using a two-sample Mendelian randomization (MR) approach. The data utilized in this study were sourced from genome-wide association study. The association of genetic variants from cohorts of prostatitis or BPH and PCa patients was determined using inverse-variance weighted and MR Egger regression techniques. The direction of chance was determined using independent genetic variants with genome-wide significance (P < 5 × 10-6). The accuracy of the results was confirmed using sensitivity analyses. RESULTS: MR analysis showed that BPH had a significant causal effect on PCa (Odds Ratio = 1.209, 95% Confidence Interval: 0.098-0.281, P = 5.079 × 10- 5) while prostatitis had no significant causal effect on PCa (P > 0.05). Additionally, the pleiotropic test and leave-one-out analysis showed the two-sample MR analyses were valid and reliable. CONCLUSIONS: This MR study supports that BPH has a positive causal effect on PCa, while genetically predicted prostatitis has no causal effect on PCa. Nonetheless, further studies should explore the underlying biochemical mechanism and potential therapeutic targets for the prevention of these diseases.

Comparison of traditional and novel tip-flexible suctioning ureteral access sheath combined with flexible ureteroscope to treat unilateral renal calculi.

OBJECTIVES: To compare the safety and efficacy of novel tip-flexible suctioning ureteral access sheath (NTFS-UAS) and traditional ureteral access sheath (T-UAS) combined with flexible ureteroscope for treating unilateral renal calculi. MATERIALS AND METHODS: The clinical data of 214 patients with unilateral renal calculi treated by NTFS-UAS (n = 102) and T-UAS (n = 112) combined with flexible ureteroscope from August 2021 to April 2022 were analyzed retrospectively. Demographic characteristics, stone-related parameters, operative time, stone-free rates (SFR), hospitalization time and complication rate (CR) were analyzed. RESULT: No significant difference was observed between the two groups in terms of demographic characteristics, stone-related parameters, intraoperative CR, and hospitalization time. The operative time of NTFS-UAS group was significantly shorter than T-UAS group (55.25 ± 11.42 min vs. 59.36 ± 15.59 min; P = 0.028). The NTFS-UAS group obtained significantly higher SFR on 1 day postoperatively (86.3% vs. 75.0%; P = 0.038), and higher SFR on 30 days postoperatively than T-UAS group (91.2% vs. 81.3%; P = 0.037). The hemoglobin loss of NTFS-UAS group (- 0.54 ± 0.69 g/dl) was significantly lower than T-UAS group (- 0.83 ± 0.66 g/dl; P = 0.002). There was a significantly lower incidence of overall CR (11.8% vs. 22.3%; P = 0.041), and infectious CR (8.8% vs. 18.8%; P = 0.037) in the NTFS-UAS group. CONCLUSION: Compared to T-UAS combined with flexible ureteroscope for treating unilateral renal calculi, NTFS-UAS had superiority in higher SFR on 1 day and 30 days postoperatively. Shorter operation time, lower hemoglobin loss, lower incidences of overall and infectious CR were observed in NTFS-UAS group. REGISTRATION NUMBER AND DATE: ChiCTR2300070210; April 5, 2023.

Inhibition of gap junction communication between cells can induce apoptosis of corpus cavernosum smooth muscle in guinea pigs.

In this study, we aimed to investigate the effect of gap junction (GJ) on apoptosis of smooth muscle. Forty adult male guinea pigs were randomly divided into four groups with 10 guinea pigs in each group. Adeno-associated virus (AAV) and Gap27 were injected at the root of the corpus cavernosum. Two weeks later, the corpus cavernosum tissue was taken to be tested. The expression of Cx43 and α-SMC protein was detected by immunofluorescence and Western blotting. The content of corpus cavernosum smooth muscle was detected by Masson trichrome staining. Apoptosis was detected by TUNEL staining and Western blotting. The results showed that Gap27 did not affect Cx43 but decreased the expression of smooth muscle. The results of TUNEL staining and detection of apoptosis-related proteins showed that apoptosis was induced by Gap27. In addition, we found that corpus cavernosum injection of AAV could induce obvious apoptosis. In this study, we examined the effect of inhibition of gap junction on smooth muscle, and suggested that the decrease of gap junction function may be a potential mechanism of smooth muscle apoptosis.

Roles of ferroptosis in urologic malignancies.

Ferroptosis, an iron-dependent form of non-apoptotic cell death, is believed to strongly contribute to the pathogenesis of multiple cancers. Recently, the positive association between ferroptosis and urologic malignancies has drawn considerable attention, while a comprehensive review focused on this issue is absent. Based on this review, ferroptosis has been implicated in the development and therapeutic responses of prostate cancer, kidney cancer, and bladder cancer. Mechanistically, a large number of biomolecules and tumor-associated signaling pathways, including DECR1, PANX2, HSPB1, ACOT8, SUV39H1, NCOA4, PI3K-AKT-mTOR signaling, VHL/HIF-2α pathway, and Hippo/TAZ signaling pathway, have been reported to regulate ferroptosis in urologic cancers. Ferroptosis inducers, such as erastin, ART, CPNPs, and quinazolinyl-arylurea derivatives, exert potential therapeutic effects per se and/or enhance the anticancer response of other anticancer drugs in urologic oncology. A better understanding of ferroptosis may provide a promising way to treat therapy-resistant urologic cancers.

[Effect of recombinant lentivirus of SCL gene on expression of c-kit protein in interstitial cells of Cajal under high glucose condition].

OBJECTIVE: To determine the effect of a recombinant lentivirus containing human stem cell leukemia (SCL) gene on the expression of c-kit protein in damaged interstitial cells of Cajal (ICC) under high glucose condition.
 Methods: After isolation of ICC, the cells were cultured for 24 hours until the cells were adherent. After identification by inverted microscope and immunofluorescence, ICC cells were divided into two groups: A control group and a high glucose group. The control group was added with a medium containing 5 mmol/L of glucose. The high glucose group was added with a medium containing 20 mmol/L of glucose. After 48 h of continuous cultivation, the high glucose group was divided into 3 subgroups: A blank group, an empty lentivirus group, and an experimental group. The blank group, the empty lentivirus group, and the experimental group were added a medium containing PBS solution, empty lentivirus, and a recombinant lentivirus containing the SCL gene with a glucose concentration of 5 mmol/L, respectively. The cultures were incubated for 24 and 48 h. The expression of c-kit protein in ICC in each group was detected by Western blot.
 Results: After 24 or 48 h, the expression of c-kit protein in ICC was significantly lower in the blank group and the lentivirus group than that in the control group, and the expression of c-kit protein in ICC was significantly higher in the experimental group than that in the blank group and the empty lentivirus group, but it was still lower than that in the control group (all P<0.05).
 Conclusion: The recombinant lentivirus of SCL gene can up-regulate the expression of c-kit protein in functionally impaired ICC under high glucose condition.

Involvement of prostatic interstitial cells of Cajal in inflammatory cytokines-elicited catecholamines production: Implications for the pathophysiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).

In a previous work using guinea pig prostate, we have identified a novel interstitial cells of Cajal (ICCs) which possess close contacts between sympathetic nerve bundles and smooth muscle cells. The ability of prostatic ICCs in mediating excitatory neural inputs was therefore studied using isolated murine prostate ICCs by collagenase digestion combined with FACS method. RT-PCR and Western blotting analyses revealed that prostatic ICCs under a quiescent state expressed abundantly the rate-limiting enzymes essential for catecholamine synthesis. Moreover, distinct proinflammatory cytokines (e.g. IL-1ß, IL-8, ICAM-1 and TNF-α) could significantly stimulate the expression levels of the rate-limiting enzymes of catecholamine production in prostate ICCs. Mechanistically, the above-mentioned stimulatory effects of proinflammatory cytokines appeared to be mediated via activation of NF-κB, HIF-1α and HDACs signaling pathways. Considering that prostatic catecholamine overactivity serves as an essential etiology of pelvic pain by indirectly stimulating the smooth muscle cell proliferation, or by directly causing muscular spasm, our results collectively suggest that targeting the NF-κB, HIF-1α and HDACs pathways in prostate ICCs be considered as a new strategy for treatment of chronic pelvic pain syndrome (CPPS) induced by chronic prostatitis (CP). Overall, the current study should shed novel light on the biology of this unique prostate ICCs.

Unpacking the Gap Box Against Data-Free Knowledge Distillation.

Data-free knowledge distillation (DFKD) improves the student model (S) by mimicking the class probability from a pre-trained teacher model (T) without training data. Under such setting, an ideal scenario is that T can help generate "good" samples from a generator (G) to maximally benefit S. However, existing arts suffer from the non-ideal generated samples under the disturbance of the gap (i.e., either too large or small) between the class probabilities of T and S; for example, the generated samples with too large gap may exhibit excessive information for S, while too small gap leads to the limited knowledge in the samples, resulting into the poor generalization. Meanwhile, they fail to judge the "goodness" of the generated samples for S since the fixed T is not necessarily ideal. In this paper, we aim to answer what is inside the gap box; together with how to yield "good" generated samples for DFKD? To this end, we propose a Gap-Sensitive Sample Generation (GapSSG) approach, by revisiting the empirical distilled risk from a data-free perspective, which confirms the existence of an ideal teacher (T *), while theoretically implying: (1) the gap disturbance originates from the mismatch between T and T *, hence the class probabilities of T enable the approximation to those of T *; and (2) "good" samples should maximally benefit S via T's class probabilities, owing to unknown T *. To this end, we unpack the gap box between T and S as two findings: inherent gap to perceive T and T *; derived gap to monitor S and T *. Benefiting from the derived gap that focuses on the adaptability of generated sample to S, we attempt to track student's training route (a series of training epochs) to capture the category distribution of S; upon which, a regulatory factor is further devised to approximate T * over inherent gap, so as to generate "good" samples to S. Furthermore, during the distillation process, a sample-balanced strategy comes up to tackle the overfitting and missing knowledge issues between the generated partial and critical samples by training G. The theoretical and empirical studies verify the advantages of GapSSG over the state-of-the-arts.

Autonomic Nervous System Dysfunction Is Related to Chronic Prostatitis/Chronic Pelvic Pain Syndrome.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common and non-lethal urological condition with painful symptoms. The complexity of CP/CPPS's pathogenesis and lack of efficient etiological diagnosis results in incomplete treatment and recurrent episodes, causing long-term mental and psychological suffering in patients. Recent findings indicate that the autonomic nervous system involves in CP/CPPS, including sensory, sympathetic, parasympathetic, and central nervous systems. Neuro-inflammation and sensitization of sensory nerves lead to persistent inflammation and pain. Sympathetic and parasympathetic alterations affect the cardiovascular and reproductive systems and the development of prostatitis. Central sensitization lowers pain thresholds and increases pelvic pain perception in chronic prostatitis. Therefore, this review summarized the detailed processes and mechanisms of the critical role of the autonomic nervous system in developing CP/CPPS. Furthermore, it describes the neurologically relevant substances and channels or receptors involved in this process, which provides new perspectives for new therapeutic approaches to CP/CPPS.

The role of miR-155 in urologic malignancies.

MicroRNAs (miRNAs) are a class of short non-coding RNAs that play a crucial role in regulating gene expression across multiple levels. They are involved in a wide range of physiological processes, including proliferation, differentiation, apoptosis, and cell cycle control. In recent years, miRNAs have emerged as pivotal regulatory molecules in the development and progression of tumors. Among these, miR-155 has garnered significant attention due to its high expression in various diseases, particularly urologic malignancies. Since an extensive corpus of studies having focused on the roles of miR-155 in various urologic malignancies, it is essential to summarize the current evidence on this topic through a comprehensive review. Altered miR-155 expression is related to various physiological and pathological processes, including immune response, inflammation, tumor development and treatment resistance. Notably, alterations in miR-155 expression have been observed in urologic malignancies as well. The up-regulation of miR-155 expression is commonly observed in urologic malignancies, contributing to their progression by targeting specific proteins and signaling pathways. This article provides a comprehensive review of the significant role played by miR-155 in the development of urologic malignancies. Furthermore, the potential of miR-155 as a biomarker and therapeutic target in urologic malignancies is also discussed.

Crosstalk between m6A modification and autophagy in cancer.

Autophagy is a cellular self-degradation process that plays a crucial role in maintaining metabolic functions in cells and organisms. Dysfunctional autophagy has been linked to various diseases, including cancer. In cancer, dysregulated autophagy is closely associated with the development of cancer and drug resistance, and it can have both oncogenic and oncostatic effects. Research evidence supports the connection between m6A modification and human diseases, particularly cancer. Abnormalities in m6A modification are involved in the initiation and progression of cancer by regulating the expression of oncogenes and oncostatic genes. There is an interaction between m6A modification and autophagy, both of which play significant roles in cancer. However, the molecular mechanisms underlying this relationship are still unclear. m6A modification can either directly inhibit autophagy or promote its initiation, but the complex relationship between m6A modification, autophagy, and cancer remains poorly understood. Therefore, this paper aims to review the dual role of m6A and autophagy in cancer, explore the impact of m6A modification on autophagy regulation, and discuss the crucial role of the m6A modification-autophagy axis in cancer progression and treatment resistance.

Predictive value of controlling nutritional status score for prostate cancer diagnosis.

Objective: This study aims to explore the predictive value of the Controlling Nutritional Status (CONUT) score for prostate cancer (PCa) diagnosis. Methods: The data of 114 patients who underwent prostate needle biopsies from June 2020 to December 2022 were retrospectively analyzed. The relationship between CONUT score and various clinical factors as well as PCa diagnosis was evaluated. Results: The pathological results classified patients into the PCa (n = 38) and non-PCa (n = 76) groups. Compared with the non-PCa group, the PCa group exhibited statistically significant differences in age, prostate-specific antigen (PSA), PSA density (PSAD), the proportion of PI-RADS ≥ 3 in mpMRI, and the CONUT score, prostate volume, lymphocyte count, and total cholesterol concentration (p < 0.05). ROC curve analyses indicated the diagnostic accuracy as follows: age (AUC = 0.709), prostate volume (AUC = 0.652), PSA (AUC = 0.689), PSAD (AUC = 0.76), PI-RADS ≥ 3 in mpMRI (AUC = 0.846), and CONUT score (AUC = 0.687). When CONUT score was combined with PSA and PSAD, AUC increased to 0.784. The AUC of CONUT score combined with PSA, PSAD, and mpMRI was 0.881, indicates a higher diagnostic value. Based on the optimal cut-off value of CONUT score, compared with the low CONUT score group, the high CONUT score group has a higher positive rate of PCa diagnosis (p < 0.05). Conclusion: CONUT score is an excellent auxiliary index for PCa diagnosis in addition to the commonly used PSA, PSAD, and mpMRI in clinical practice. Further prospective trials with a larger sample size are warranted to confirm the present study findings.

The characteristics of sexual behavior in blind men in Ganzhou, China: A cross-sectional study.

Visual stimuli play key roles in influencing men sexual behavior. However, few studies have explored the sexual behavior of blind men. To provide more information about blind men for the study of andrology by surveying the characteristics of their current sexual behavior. A questionnaire-based cross-sectional study design was performed. The questionnaire contained questions regarding demographic characteristics of participants, access to sexual knowledge, perception of the sexual partners' beauty, and sexual arousal. Blind men were interviewed face-to-face by the trained investigator. Complete questionnaires were collected from 54 participants, with an average age of 40.57 ±â€…9.80 years old. Eye diseases were the most frequent cause of blindness. In terms of sexual orientation, all participants were heterosexual. Notably, 90.7% of the participants reported to have had a sexual experience. Among those who had engaged in sexual behavior, 93.6% experienced sexual pleasure and 69.4% had a normal erectile function. Overall, 16.7% of the participants received sex education. The participants obtained sexual knowledge mainly through sounds from mobile phones, peer-to-peer communication, sounds of television and radio. Voice was the most frequent perception of the sexual partners' beauty, followed by figure, skin, and body fragrance. In terms of stimuli of sexual arousal, tactile sensation and auditory sensation in that order were the most frequent stimuli of sexual arousal. Stimuli of sexual arousal in blind men are mainly mediated by sound and touch. Blind men understand their sexual partners' beauty through auditory, tactile, and olfactory sensations. Blind men in Ganzhou lack formal and systematic sex education.

Critical roles of lncRNA-mediated autophagy in urologic malignancies.

Urologic oncology is a significant public health concern on a global scale. Recent research indicates that long chain non-coding RNAs (lncRNAs) and autophagy play crucial roles in various cancers, including urologic malignancies. This article provides a summary of the latest research findings, suggesting that lncRNA-mediated autophagy could either suppress or promote tumors in prostate, kidney, and bladder cancers. The intricate network involving different lncRNAs, target genes, and mediated signaling pathways plays a crucial role in urological malignancies by modulating the autophagic process. Dysregulated expression of lncRNAs can disrupt autophagy, leading to tumorigenesis, progression, and enhanced resistance to therapy. Consequently, targeting particular lncRNAs that control autophagy could serve as a dependable diagnostic tool and a promising prognostic biomarker in urologic oncology, while also holding potential as an effective therapeutic approach.

Autophagy in erectile dysfunction: focusing on apoptosis and fibrosis.

In most types of erectile dysfunction, particularly in advanced stages, typical pathological features observed are reduced parenchymal cells coupled with increased tissue fibrosis. However, the current treatment methods have shown limited success in reversing these pathologic changes. Recent research has revealed that changes in autophagy levels, along with alterations in apoptosis and fibrosis-related proteins, are linked to the progression of erectile dysfunction, suggesting a significant association. Autophagy, known to significantly affect cell fate and tissue fibrosis, is currently being explored as a potential treatment modality for erectile dysfunction. However, these present studies are still in their nascent stage, and there are limited experimental data available. This review analyzes erectile dysfunction from a pathological perspective. It provides an in-depth overview of how autophagy is involved in the apoptotic processes of smooth muscle and endothelial cells and its role in the fibrotic processes occurring in the cavernosum. This study aimed to develop a theoretical framework for the potential effectiveness of autophagy in preventing and treating erectile dysfunction, thus encouraging further investigation among researchers in this area.

MicroRNA-21 in urologic cancers: from molecular mechanisms to clinical implications.

The three most common kinds of urologic malignancies are prostate, bladder, and kidney cancer, which typically cause substantial morbidity and mortality. Early detection and effective treatment are essential due to their high fatality rates. As a result, there is an urgent need for innovative research to improve the clinical management of patients with urologic cancers. A type of small noncoding RNAs of 22 nucleotides, microRNAs (miRNAs) are well-known for their important roles in a variety of developmental processes. Among these, microRNA-21 (miR-21) stands out as a commonly studied miRNA with implications in tumorigenesis and cancer development, particularly in urological tumors. Recent research has shed light on the dysregulation of miR-21 in urological tumors, offering insights into its potential as a prognostic, diagnostic, and therapeutic tool. This review delves into the pathogenesis of miR-21 in prostate, bladder, and renal cancers, its utility as a cancer biomarker, and the therapeutic possibilities of targeting miR-21.

Knockout of phosphatidylethanolamine binding protein4 (PEBP4) promotes chronic non-bacterial prostatitis by mediating the activation of NF-κB signaling.

BACKGROUND: The etiology of chronic prostatitis remains unclear; consequently, this disease is associated with recurrence and ineffective clinical therapy. Therefore, there is an urgent need to investigate the underlying pathogenesis of chronic prostatitis in order to develop more efficacious treatments. OBJECTIVE: The previous study found that knocking out of PEBP4 leads to chronic prostatitis in the male mice. This research aimed to identify the role of PEBP4 in prostatitis, determine the molecular pathogenic mechanisms associated with chronic prostatitis, and provide guidelines for the development of new treatment strategies for chronic prostatitis. MATERIALS AND METHODS: A PEBP4 exon knockout strain (PEBP4-/-) was established in C57BL/6 mice via the Cre-loxP system. Hematoxylin-eosin (H&E) staining was used to investigate histological changes. RNA-sequencing was used to investigate the gene expression signature of the prostate and the levels of inflammatory cytokines were determined by real-time polymerase chain reaction (RT-PCR). The expression of PEBP4 protein in prostate tissue was determined by immunohistochemistry in specimens from patients with BPH and BPH combined with chronic prostatitis. Finally, we used a CRISPR-Cas9 plasmid to knockout PEBP4 in RWPE-1 cells; western blotting was subsequently used to measure the level of activation in the NF-κB signaling pathway after activating with TNF-α. RESULTS: Hemorrhage and inflammatory cell infiltration were incidentally observed in the seminal vesicles and prostate glands of PEBP4-/- mice after being fed with a normal diet for 1 year. In addition, we found significantly lower (p < 0.001) expression levels of PEBP4 protein in prostate tissues from patients with benign prostate hyperplasia (BPH) and chronic and non-bacterial prostatitis (CNP) when compared to those with BPH only. The reduced expression of PEBP4 led to a higher risk of prostatitis recurrence in patients after 2 years of follow-up. Increased levels of NF-κB and IκB phosphorylation were observed in PEBP4-knockout RWPE-1 cells and prostate glands from PEBP4-/- mice. CONCLUSION: The knockout of PEBP4 in experimental mice led to chronic prostatitis and the reduced expression of PEBP4 in patients with higher risk of chronic and non-bacterial prostatitis suggested that PEBP4 might act as a protective factor against chronic prostatitis. The knockout of PEBP4 in RWPE-1 cells led to the increased activation of NF-κB and IκB, thus indicating that inhibition of PEBP4 faciliated the NF-κB signaling cascade. Our findings provide a new etiology and therapeutic target for chronic prostatitis.

Insights into vitamin A in bladder cancer, lack of attention to gut microbiota?

Vitamin A has long been associated with bladder cancer, and many exogenous vitamin A supplements, vitamin A derivatives, and synthetic drugs have been investigated over the years. However, the effectiveness of these strategies in clinical practice has not met expectations, and they have not been widely adopted. Recent medical research on intestinal flora has revealed that bladder cancer patients exhibit reduced serum vitamin A levels and an imbalance of gut microbiota. In light of the close relationship between gut microbiota and vitamin A, one can speculate that a complex regulatory mechanism exists between the two in the development and occurrence of bladder cancer. As such, further exploration of their interaction in bladder cancer may help guide the use of vitamin A for preventive purposes. During the course of this review, attention is paid to the influence of intestinal microbiota on the vitamin A metabolism and the RA signaling pathway, as well as the mutual promotion relationships between them in the prevention of bladder cancer, In addition, it emphasizes the importance of intestinal microbiota for bladder cancer prevention and treatment.

Preclinical models and evaluation criteria of prostatitis.

Prostatitis is a common urological condition that affects almost half of all men at some point in their life. The prostate gland has a dense nerve supply that contributes to the production of fluid to nourish sperm and the mechanism to switch between urination and ejaculation. Prostatitis can cause frequent urination, pelvic pain, and even infertility. Long-term prostatitis increases the risk of prostate cancer and benign prostate hyperplasia. Chronic non-bacterial prostatitis presents a complex pathogenesis, which has challenged medical research. Experimental studies of prostatitis require appropriate preclinical models. This review aimed to summarize and compare preclinical models of prostatitis based on their methods, success rate, evaluation, and range of application. The objective of this study is to provide a comprehensive understanding of prostatitis and advance basic research.