Alcohol intake exacerbates experimental autoimmune prostatitis through gut microbiota driving cholesterol biosynthesis-mediated Th17 differentiation.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is very common worldwide, and alcohol consumption is a notable contributing factor. Researches have shown that gut microbiota can be influenced by alcohol consumption and is an important mediator in regulating Th17 cell immunity. However, it is still unclear the exact mechanism by which alcohol exacerbates the CP/CPPS and the role of gut microbiota in this process.

Gut Microflora Modulates Th17/Treg Cell Differentiation in Experimental Autoimmune Prostatitis the Short-Chain Fatty Acid Propionate.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a very common urological disorder and has been gradually regarded as an immune-mediated disease. Multiple studies have indicated that the gut microflora plays a pivotal part in immune homeostasis and autoimmune disorder development. However, whether the gut microflora affects the CP/CPPS, and the underlying mechanism behind them remain unclear.

IL-17 exacerbates experimental autoimmune prostatitis via CXCL1/CXCL2-mediated neutrophil infiltration.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a poorly understood disease. Accumulating evidence suggests that autoimmune dysfunction is involved in the development of CP/CPPS. Interleukin-17 (IL-17) is associated with the occurrence and development of several chronic autoimmune inflammatory diseases.

Melatonin attenuates prostatic inflammation and pelvic pain via Sirt1-dependent inhibition of the NLRP3 inflammasome in an EAP mouse model.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common male genitourinary system disease. As a neuroendocrine hormone, melatonin possesses a variety of biological functions, among which its anti-inflammatory effects have recently drawn substantial attention. The purpose of the current research was to study the effect of melatonin on CP/CPPS and the underlying mechanisms using a mouse model of experimental autoimmune prostatitis (EAP).

Diffuse neurofibroma of the chest and abdominal wall invading the diaphragm leads to diaphragmatic eventration: case report.

Background: Neurofibromatosis type 1 (NF1) is an autosomal dominant condition with a high rate of new mutation and variable expression. Diffuse neurofibroma of the epidermis invading deeper organs is rare.We report a case of diffuse subcutaneous neurofibroma in the thoracoabdominal wall which had invaded the diaphragm and caused diaphragmatic eventration.

Effect of Eriocalyxin B on prostatic inflammation and pelvic pain in a mouse model of experimental autoimmune prostatitis.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common disease in males. Eriocalyxin B (EriB), a natural diterpenoid purified from Isodon eriocalyx var. laxiflora, was previously reported to have antitumor effects via multiple immune-related pathways.

CaMK4-dependent phosphorylation of Akt/mTOR underlies Th17 excessive activation in experimental autoimmune prostatitis.

Chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) is a complicated syndrome characterized by genitourinary pain in the absence of bacterial infection. Th17 cell-driven autoimmunity has been proposed as a cause of CP/CPPS. However, the factors that promote Th17-driven autoimmunity in experimental autoimmune prostatitis (EAP) and the molecular mechanisms are still largely unknown.

Abnormal gut microbiota composition is associated with experimental autoimmune prostatitis-induced depressive-like behaviors in mice.

Background: Depressive symptoms are found in approximately 78% of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) patients, but the pathological mechanisms remain unknown. Increasing evidence suggests that abnormal gut microbiota may play an important role in depression. Thus, we aimed to investigate whether gut microbiota contributes to CP/CPPS-associated depression by using a mouse model of experimental autoimmune prostatitis (EAP).

Microglial activation and neurobiological alterations in experimental autoimmune prostatitis-induced depressive-like behavior in mice.

Background: Patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) frequently show depressive symptoms clinically and increasing evidence indicates a correlation between CP/CPPS and depression. However, the underlying mechanisms of CP/CPPS-related depression remain poorly understood. Here, we sought to determine the role of hippocampal microglial activation and neurobiological changes in a mouse model of experimental autoimmune prostatitis (EAP)-induced depression and the treatment efficacy of Chinese herb extract baicalein.

Effect of alcohol on chronic pelvic pain and prostatic inflammation in a mouse model of experimental autoimmune prostatitis.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent disease of the urogenital system. Alcohol has been reported to be closely related to CP/CPPS. Thus, we intended to verify the role of alcohol in CP/CPPS and determine the underlying mechanism.

MicroRNA expression profile in chronic nonbacterial prostatitis revealed by next-generation small RNA sequencing.

MicroRNAs (miRNAs) are considered to be involved in the pathogenic initiation and progression of chronic nonbacterial prostatitis (CNP); however, the comprehensive expression profile of dysregulated miRNAs, relevant signaling pathways, and core machineries in CNP have not been fully elucidated. In the current research, CNP rat models were established through the intraprostatic injection of carrageenan into the prostate. Then, next-generation sequencing was performed to explore the miRNA expression profile in CNP.

[Related immunologic mechanisms of chronic prostatitis: Advances in studies].

Chronic prostatitis is a common male disease with a high incidence rate and a serious impact on the patients' quality of life. The pathogenesis of chronic prostatitis remains unclear though it is considered to be possibly related to infection, inflammation, and abnormal pelvic nerve muscle activity. Recently, a growing number of studies have reported immune imbalance and changes of inflammatory cytokines in patients with chronic prostatitis as well as a close correlation of abnormal immune response with the occurrence of diseases, pelvic pain symptoms, mental symptoms, hyperalgesia, and so on.

[Expressions of E-cadherin and N-cadherin in prostate cancer and their implications].

Objective: To investigate the differences in the expressions of E-cadherin and N-cadherin between high-risk prostate cancer and low- and medium-risk prostate cancer, and analyze their correlation with the age, serum PSA level, and Gleason score of the patients.

Methods: We retrospectively analyzed the clinical data of 42 cases of prostate cancer, which were divided into a low- and medium-risk group (group A, n = 15) and a high-risk group (group B, n = 27). We measured the expressions of E-cadherin and N-cadherin by immunohistochemical staining, compared their differences between the two groups, and analyzed their correlation with the age, serum PSA level, and Gleason score of the patients.

Increased chromogranin A and neuron-specific enolase in rats with chronic nonbacterial prostatitis induced by 17-beta estradiol combined with castration.

Although chronic nonbacterial prostatitis (CNBP) is a common diagnosis in middle-aged men, the etiology of this disease remains poorly understood. Neuroendocrine cells play an important role in the neuroendocrine regulation of the prostate, and chromogranin A (CgA) and neuron-specific enolase (NSE) are regarded as classic markers of neuroendocrine cells. This study aimed to determine CgA and NSE levels in a CNBP rat model to evaluate the role of neuroendocrine cells in the pathogenesis of CNBP.

mTOR regulate EMT through RhoA and Rac1 pathway in prostate cancer.

Recently, an increasing number of studies have suggested that mTOR plays a critical role in the regulation of tumor cell motility, invasion and cancer metastasis. However, little is known about the signaling mechanisms in regulating epithelial-mesenchymal transition (EMT) of prostate cancer. In this study, we found that the expression levels of Raptor and Rictor in prostate cancer tissues were elevated, which may suggest that Raptor and Rictor signaling pathways are associated with prostate cancer progression and metastasis.

Risk factors for hypospadias in China.

This case-controlled study was designed to evaluate the association between various baseline parental factors and the risk of hypospadias in China. Patients were selected from tertiary referral hospitals in Anhui, a province in mid-eastern China. A questionnaire was given to the parents of each patient.

[Mammalian target of rapamycin regulates androgen receptor and Akt phosphorylation in prostate cancer 22RV1 cells].

Objective: To investigate the roles of the mammalian target of rapamycin-1 and -2 (mTORC1 and TORC2) in the proliferation and apoptosis of prostate cancer 22RV1 cells.

Methods: After silencing mTORC1 and TORC2, we examined the proliferation and apoptosis of prostate cancer 22RV1 cells by methylthiazol tetrazolium (MTT) assay and flow cytometry, respectively, and detected the expressions of the androgen receptor (AR) and Akt phosphorylation in the prostate cancer 22RV1 cells by Western blot after transfecting Raptor-siRNA and Rictor-siRNA to the 22RV1 cells.

Results: MTT showed that the prostate cancer 22RV1 cells had no significant change in the growth rate after mTORC1 silence (P > 0.

[Clinical features on chromophobe renal cell carcinoma].

Objectives: To explore the clinical, pathological features and prognosis of patients with chromophobe renal cell carcinoma.

Methods: From January 1998 to January 2008, clinical data of 29 patients with chromophobe renal cell carcinoma including clinical manifestations, imaging examinations, treatment models, pTNM stages and follow-up results, were summarized to investigate its features and prognosis.

Results: All cases had no obvious clinical and preoperative imaging presentation.

Rapamycin regulates Akt and ERK phosphorylation through mTORC1 and mTORC2 signaling pathways.

Numerous studies have shown that mammalian target of rapamycin (mTOR) inhibitor activates Akt signaling pathway via a negative feedback loop while inhibiting mTORC1 signaling. In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin-mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors. Moreover, we analyzed the effect of mTORC1 and mTORC2 on regulating cell cycle progression.

[The mTOR inhibitor enhances chemosensitivity of androgen-independent prostate cancer cell line].

Objective: To investigate the effect of the mammalian target of rapamycin (mTOR) inhibitor CCI-779 on the chemosensitivity of androgen-independent prostate cancer cell line PC-3.

Methods: Prostate cancer cells PC-3 were cultured and treated with CCI-779, Paclitaxel and combination of the two. Then the inhibitory effects of the three medications on the growth of the PC-3 cells were determined by MTT, and the their cell cycle and apoptosis were detected by flow cytometry.

[Effects of rapamycin on prostate cancer PC-3 cells].

Background And Objective: The mammalian target of rapamycin (mTOR) signaling network regulates cell growth, proliferation, survival and apoptosis. This study was to investigate the effect and the underlying mechanism of rapamycin on prostate cancer PC-3 cells.

Methods: PC-3 cells were treated with 1 nmol/L rapamycin.