Introduction There is no scientific evidence for the mechanism of male squirting, although the term is common in mass media. Here, we describe the first recording of male squirting using color Doppler ultrasonography. Case presentation We recruited a 25‐year‐old male volunteer who was able to have male squirting. A transrectal ultrasound probe was inserted into the rectum and male squirting was observed following normal ejaculation. With penis stimulation for a further 20 s after ejaculation, translucent misty fluids with a creatine level similar to that of urine came from the extraurethral orifice for about 60 s. Color Doppler ultrasonography recorded strong contraction of the prostate and pelvic striated muscles just before male squirting, and then the stream went from the urinary bladder through the prostatic urethra. Conclusion In male squirting, urine in the bladder gushes out from the external urethral orifice due to strong contraction of the prostate and pelvic striated muscles.

Introduction and Objectives Sexual dysfunction is one of the main factors that affects for quality of life (QOL) after prostatectomy. Previous research showed that sexual dysfunction after laparoscopic radical prostatectomy (LRP) was caused at 1 month, and refractory sexual dysfunction persisted for a long time. In recent years, robot-assisted laparoscopic radical prostatectomy (RALP) has been introduced at a large number of medical facilities. This time, we investigated change of sexual function after RALP using questionnaires related to sexual function. Materials and Methods Thirty-two patients were diagnosed localized prostate cancer and underwent RALP between January 2020 and June 2021 at our hospital. We investigated the change of sexual and voiding functions using International Index of Erectile Function (IIEF5), Expanded Prostate Cancer Index Composite (EPIC) at the time of diagnosis, 1, 3, 6, 12 month after RALP, and daily use numbers of urinary pad at 1, 3, 6, 12 month after RALP. Control was set at the time of diagnosis. This study was approved by the Ethics Committee of our facility (Approval No.3906-00). Results Patient age (median) was 67.5 (range 50-80) years old, body mass index (median) was 22.5 (range 17.4-28.7) kg/m2, and serum PSA (median) was 7.5 (range 4.0- 31.9) ng/ml at the time of diagnosis. Clinical stage T1c was accounted for 7 cases, T2a was 9 cases, T2b was 3 cases, T2c was 11 cases, and T3a was 2 cases. Fourteen patients (43.8%) underwent nerve-sparing RALP. IIEF5 and sexual function domain of EPIC showed deterioration at 1 month after RALP. However, sexual bother domain of EPIC showed not significant difference after RALP. The relevance between change of sexual function and nerve-sparing operation were not observed at our observation period. On the other hand, daily use numbers of urinary pad were significantly improved as time passed compared with that of at 1 month after RALP. The relevance between urinary continence and nerve-sparing operation were observed at 1 month after RALP. Conclusions Sexual dysfunction after RALP showed the same change as that after LRP. Besides, nerve-sparing operation might affect for urinary continence instead of sexual function. Disclosure Work supported by industry: no.

Introduction and Objectives Evidence-based treatment for chronic prostatitis (CP) has not been established so far. Innovative therapy for CP is needed to establish evidence-based therapy. Indoleamine 2,3-dioxygenase1 (IDO1) catalyzes the first and rate-limiting step of tryptophan catabolism through the kynurenine pathway. IDO1 expression in prostate is higher than that of other organs. IDO1 is induced in various tissues during inflammatory disease. Furthermore, protective effect of IDO1 inhibition for inflammation was indicated in some reports. We hypothesize that IDO1 plays a central role for immunological reaction in CP. We investigated the relevance between IDO1 inhibition and CP using autoimmune induced CP model mice. This study was approved by the safety committee for DNA experiments and the animal research committee of our facility (Approval No.18-07 and 20-89). Materials and Methods Ten to twelve weeks old, IDO1 knock out (IDO1 KO) mice were used through the research. Same conditional wild type (WT) mice were set as control. Prostate gland extracted from Wister rat were used as prostate antigen (Pag) for mice. PAg 100µg / 100µl were injected into mice subcutaneously. After creating autoimmune induced CP model mice, inflammatory change in the prostate was investigated using histological, biochemical and immunohistochemical analysis. Results Histological analysis showed suppressive effect of inflammatory cells infiltration and interstitial fibrosis were observed in IDO1 KO CP model mice compared with that of WT CP model mice. Proteomic analysis showed decreased effect of lymphocyte and monocyte related cytokines (CCL2, CCL3) and fibrosis related cytokine (TIMP-1) in IDO1 KO CP model mice compared with that of WT CP model mice. Same results were obtained from immunohistochemical analysis using immunofluorescent stain. Conclusions IDO1 is involved in chronic inflammation via cytokines/chemokines in the prostate. IDO1 inhibition contribute to suppressive effect of chronic inflammation and fibrosis in the prostate. Therefore, IDO1 inhibition might be a novel target therapy for chronic prostatitis. Disclosure Work supported by industry: no.

Introduction & Objectives Testicular ischemia represented by torsion needs emergency surgery to reperfuse testicular blood flow. However, spermatic dysfunction is often led despite appropriate treatment. Pathology of spermatic dysfunction following testicular ischemia-reperfusion injury (IRI) is still unclear. In previous research, Inflammation and excessive oxidative stress were thought to be involved in tissue dysfunction following IRI. We hypothesized that inflammation and excessive oxidative stress plays key role in spermatic dysfunction following testicular IRI. We investigated relevance between Inflammation / excessive oxidative stress and spermatic dysfunction using testicular IRI model mice. Materials & Methods Ten to fifteen weeks old, C57BL/6 male were used through the study. Unilateral (left side) testicular vessels were clamped and de-clamped 1 hour later. Testicular blood flow was resumed. Sham operation mice were set as control. Bilateral testes were removed at 0(during ischemia), 1, 3, 5 weeks after modeling testicular IRI mice. Inflammation and oxidative stress changes in bilateral testis were investigated using histological, biochemical and immunohistochemical analysis. Spermatic changes extracted from the epididymal cauda were investigated using computer aided sperm analysis (CASA). Results Histological analysis using HE and Masson-Trichrome (MT) stain showed invasion of inflammatory cells and destruction of tissue structure from week 1. Inflammatory analysis using comprehensive protein assay and immunofluorescent stain showed increased expression of cytokines (IL-2, IL-3, IL-17A, IL-23), chemokines (CCL2, CCL5, CXCL1, CX3CL1), testes were showed from week1. Oxidative stress and cell death analysis using representative candidates (8-OHdG, ROS) showed increased expression of representative candidates from week0. Spermatic analysis showed that obvious decreased spermatic concentration and motility were showed from week 1. In contralateral testes, slow decreased spermatic concentration and motility was showed from week 1. Conclusions Spermatic dysfunction following testicular-ischemia reperfusion injury was induced in inflammatory and excessive oxidative stress changes. Inflammatory and excessive oxidative stress changes might be a novel regulatory factor for spermatic dysfunction following testicular ischemia-reperfusion injury. Disclosure Work supported by industry: no.

Introduction and Objective Even though antimicrobial therapy is received, some patients with epididymitis remaining inflammatory changes and led to refractory condition. Innovative therapy focused on the inflammatory changes is needed for epididymitis. Indoleamine 2,3-dioxygenase 1 (IDO1) catalyzes the first and rate-limiting step of tryptophan catabolism. IDO1 plays a key role in immune response and shows high expression in male genitalia. Furthermore, protective effect of IDO1 inhibition for various inflammatory disease was indicated in some reports. We hypothesize that IDO1 plays a central role for immunological reaction in epididymal inflammation. We investigated the relevance between IDO1 inhibition and epididymal inflammation. This study was approved by the safety committee for DNA experiments and the animal research committee of our facility (Approval No.14-35, 18-52). Materials and Methods Ten to twelve weeks old, C57BL/6 IDO1 knock out (IDO1 KO) mice were used through the research. Same conditional wild type (WT) mice were set as control. Lipopolysaccharide (LPS) 5μg/g(weight) was injected into epididymis from the vas deferens side. Epididymis was removed at a to 7 days after epididymitis modeling. Inflammatory changes in epididymis were investigated using histological, biochemical and immunohistochemical analysis. Series of these analysis were duplicated at least. Results Histological analysis using HE staining showed decreased effect of inflammation in IDO1 KO mice compared with WT mice. Proteomic analysis showed decreased effect of both inflammatory promoting cytokines (IL-1α, IL-6) and chemokines (CCL3, CXCL1) in IDO KO mice. On the other hand, increased effect of inflammatory inhibiting cytokines (IL-4, IL-10) were showed in IDO KO mice. Same results were obtained from immunohistochemical analysis using immunofluorescent staining. Conclusions IDO1 is involved in epididymal inflammation via cytokine and chemokine. IDO1 inhibition contribute to tissue protection for epididymitis. Therefore, IDO1 inhibition might be an innovative therapy for epididymitis. Disclosure Work supported by industry: no.