Matsuda Y.,Sapporo Medical University |
Hisasue S.-I.,Sapporo Medical University |
Hisasue S.-I.,Juntendo University |
Kumamoto Y.,Sapporo Medical University |
And 4 more authors.
Journal of Sexual Medicine | Year: 2014
Introduction: The Erection Hardness Score (EHS) and the Sexual Health Inventory for men (SHIM) are patient-reported outcome scoring systems for erectile function. It is unclear which is more reliable for predicting the objective erectile function. Aim: The aim of this study was to evaluate whether the EHS could predict objective erectile function by measuring the maximal penile circumferential change (MPCC) with an erectometer. Methods: The study included 98 patients who visited our clinic from 2005 to 2010. The erectile function was evaluated using the SHIM, EHS, and MPCC. The MPCC was measured with the largest circumferential change of three consecutive occurrences of nocturnal penile tumescence (NPT) determined using the erectometer. Main Outcome Measures: We defined erectile dysfunction (ED) as MPCC<20mm and carried out multivariate analysis using logistic regression analysis to clarify the predictors for ED, with the variables including age, the SHIM score, and the EHS. We compared the tendency for MPCC≥20mm when EHS was 3 or more with that when EHS was 2 or less. Results: The median age of the patients was 59.5 years (range 18-83). In logistic regression analysis, the EHS was the only predictor for ED with MPCC<20mm. The mean EHS in the MPCC<20mm group was 1.64±0.20 (mean±SEM) and that in the MPCC≥20mm group was 2.46±0.13 (P=0.0018). There was a correlation between the EHS and the MPCC (correlation coefficient=0.33). In comparison with the group having an EHS of 2 or less, that with an EHS of 3 or more tended to have MPCC≥20mm (P=0.013). Conclusions: The EHS was correlated with the MPCC. The EHS represents the objective erectile function shown by the measurement of NPT. © 2014 International Society for Sexual Medicine.
Hackett G.,The Good |
Krychman M.,Southern California Center for Sexual Health and Survivorship Medicine |
Baldwin D.,University of Southampton |
Bennett N.,Lahey Hospital |
And 3 more authors.
Journal of Sexual Medicine | Year: 2016
Erectile dysfunction (ED) has been well recognized as a marker of increased cardiovascular risk for more than 15 years, especially in younger men. Early detection of ED represents an opportunity to intervene to decrease the risk of future cardiovascular events and limit the progression of ED severity. Evidence suggests there is a window of opportunity of 3 to 5 years from the onset of ED to subsequent cardiovascular events. This opportunity is usually missed if the onus is placed on the patient to seek care for his sexual problems. Unfortunately, these clear messages have not been incorporated into routine cardiovascular care. The reasons for these disparities within specialties are discussed in this article, in addition to management algorithms. Lifestyle modification is usually recommended as the first-line treatment to correct ED and lessen cardiovascular risk, but evidence suggests that this might be effective only in men without established cardiovascular comorbidities. In men with type 2 diabetes mellitus and established cardiovascular disease, lifestyle modification alone is unlikely to be effective. Cardiovascular medications are often associated with sexual dysfunction but changes in medication are more likely to be beneficial in men with milder recent-onset ED. A balanced view must be taken related to medication adverse events, taking into account optimal management of established cardiovascular disease. Testosterone deficiency has been associated with different metabolic disorders, especially metabolic syndrome and type 2 diabetes mellitus. Testosterone deficiency syndrome has been associated with an independent burden on sexual function globally and increased cardiovascular and all-cause mortality. Testosterone replacement therapy has been shown to improve multiple aspects of sexual function and, in some studies, has been associated with a decrease in mortality, especially in men with type 2 diabetes mellitus. Recent studies have suggested that phosphodiesterase type 5 inhibitors, the first-line medications to treat ED, could decrease cardiovascular and all-cause mortality, through multiple mechanisms, predominantly related to improved endothelial function. © 2016 International Society for Sexual Medicine.
Yasui T.,Nagoya City University |
Okada A.,Nagoya City University |
Urabe Y.,Tokyo Medical University |
Usami M.,Nagoya City University |
And 10 more authors.
Journal of Human Genetics | Year: 2013
A previous genome-wide association study (GWAS) reported three novel nephrolithiasis-susceptibility loci at 5q35.3, 7p14.3 and 13q14.1. Here, we investigated the association of these loci with nephrolithiasis by using an independent Japanese sample set. We performed case-control association analysis using 601 patients with nephrolithiasis and 201 control subjects. We selected seven single-nucleotide polymorphisms (SNPs): rs12654812 and rs11746443 from 5q35.3 (RGS14-SLC34A1-PFN3-F12); rs12669187 and rs1000597 from 7p14.3 (INMT-FAM188B-AQP1); and rs7981733, rs1170155, and rs4142110 from 13q14.1 (DGKH (diacylglycerol kinase)), which were previously reported to be significantly associated with nephrolithiasis. rs12654812, rs12669187 and rs7981733 were significantly associated with nephrolithiasis after Bonferroni's correction (P=3.12 × 10 -3, odds ratio (OR)=1.43; P=6.40 × 10 -3, OR=1.57; and P=5.00 × 10 -3, OR=1.41, respectively). Meta-analysis of current and previous GWAS results indicated a significant association with nephrolithiasis (P=7.65 × 10 -15, 7.86 × 10 -14 and 1.06 × 10 -9, respectively). We observed a cumulative effect with these three SNPs; individuals with three or more risk alleles had a 5.9-fold higher risk for nephrolithiasis development than those with only one risk allele. Our findings elucidated the significance of genetic variation at these three loci in nephrolithiasis in the Japanese population. © 2013 The Japan Society of Human Genetics All rights reserved.
Kojima Y.,Sapporo Medical University |
Takasawa A.,Sapporo Medical University |
Murata M.,Sapporo Medical University |
Akagashi K.,Sanjukai Hospital |
And 6 more authors.
Pathology International | Year: 2013
The lipid cell variant of urothelial carcinoma is a rare variant of urinary bladder cancer, comprised of lipoblast-like cells. In this report, we describe a case of the lipid cell variant of aggressive urothelial carcinoma. A 78-year-old man was admitted to the hospital because of gross hematuria. On cystoscopy, an ulcerative lesion, non-papillary architecture, was observed in the lateral wall of the bladder. Transurethral resection was performed. Histopathological findings of the bladder tumor indicated neoplastic cells forming irregular solid nests and sheets. Lipoblast-like neoplastic cells that had eccentric nuclei and cytoplasmic vacuoles were observed, not only in the resected specimen, but also in urine samples. On mucin histochemistry, the tumor cell cytoplasm contained no neutral or acidic mucus. The lipoblast-like cells were positive for cytokeratins (AE1/AE3, CK7) and adipophilin, known as a protein associated with neutral lipid synthesis. In general, it is difficult to prove the existence of intracytoplasmic lipid in formalin-fixed paraffin-embedded materials. This is the first report in which the presence of lipid in vacuoles of the lipid cell variant has been verified by immunohistochemistry. © 2013 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd.
Hashimoto K.,Sapporo Medical University |
Kyoda Y.,Sapporo Medical University |
Tanaka T.,Sapporo Medical University |
Maeda T.,Sapporo Medical University |
And 6 more authors.
Laboratory Investigation | Year: 2015
Neuroendocrine (NE) cells in prostate cancer have been shown to be associated with the progression of prostate cancer. However, little is known about the molecular basis of this association. We have previously demonstrated that NE cells promote metastasis of a human prostate cancer cell line (LNCaP) with overexpression of the gelsolin gene. The purpose of this study was to investigate the interactions between NE cells and LNCaP cells and the involvement of gelsolin in contributing to the invasive potential of LNCaP cells. In addition, we examined whether neurotensin induced gelsolin-mediated invasion. We used the NE cell line NE-CS that was established from the prostate of the LPB-Tag 12T-10 transgenic mouse. Small interfering RNA (siRNA) targeting gelsolin or not targeting it was transfected into LNCaP cells. Cell invasion was assessed by Matrigel invasion assay. The supernatant of NE-CS cells and neurotensin induced the transformation of LNCaP cells. Neurotensin was observed in the supernatant of NE-CS cells but not in LNCaP cells. The siRNA targeting of gelsolin resulted in inhibition of invasion of LNCaP cells in the culture medium with neurotensin added, and in the supernatant of NE-CS cells with epidermal growth factor. The invasive potential of LNCaP cells enhanced by neurotensin or the supernatant of NE-CS cells through neurotensin receptor 1 (NTSR1) was blocked by a phospholipase Cγ inhibitor and an intracellular calcium chelator, with concomitant gelsolin suppression. This study indicates that NE cells and neurotensin induce gelsolin-mediated invasion of LNCaP cells through NTSR1 activation. © 2015 USCAP, Inc.