Clinical Background of Patients with Sperm in Their Urinary Sediment

<div><p>Introduction</p><p>The detection rate and associated factors of at least one sperm in urinary sediment is not well-known in real clinical practice.</p><p>Aims</p><p>The aim of the present study was to evaluate the clinical features associated with the presence of sperm in urinary sediment in a large number of samples.</p><p>Methods</p><p>We conducted a cross-sectional study at Tokyo Saiseikai Central Hospital. We identified 5,005 males who were aged ≥20 years in whom urinary sedimentation had been performed at least twice between May 2011 and June 2012. The sperm group included patients in whom at least one urinary sediment test performed under a microscope had detected at least one sperm. We evaluated the associations between the presence of at least one sperm in urinary sediment and clinical parameters such as various diseases and the use of particular oral medicines.</p><p>Main Outcomes</p><p>In total, 1.6% (339/20,937) of urinary sediment samples contained at least one sperm. The sperm group consisted of 282 subjects (5.6%), and the no-sperm group included 4,723 subjects (94.3%).</p><p>Results</p><p>Multivariate analysis demonstrated that younger age (<65) (odds ratio [OR]: 1.71, 95% confidence interval [CI]: 1.32–2.21), the total number of examinations (≥4) (OR: 1.46, 95%CI: 1.11–1.92), diabetes (OR: 1.72, 95%CI: 1.31–2.25), a history of pelvic surgery for colon cancer (OR: 4.89, 95%CI: 2.38–10.02), alpha-1 blocker use (OR: 1.55, 95%CI: 1.16–2.08), a history of trans-urethral resection of the prostate (OR: 2.77, 95%CI: 1.46–5.13), and selective serotonin reuptake inhibitor use (OR: 2.12, 95%CI: 1.07–4.19) were independent predictors of the presence of at least one sperm in urinary sediment.</p><p>Conclusion</p><p>There is considerable overlap between the factors associated with the presence of at least one sperm in urinary sediment and those that are strongly associated with ejaculatory disorders.</p></div

Possible Long-Term Efficacy of Sitagliptin, a Dipeptidyl Peptidase-4 Inhibitor, for Slowly Progressive Type 1 Diabetes (SPIDDM) in the Stage of Non-Insulin-Dependency: An Open-Label Randomized Controlled Pilot Trial (SPAN-S)

<p><strong>Article full text</strong></p> <p><br> The full text of this article can be found <a href="https://link.springer.com/article/10.1007/s13300-017-0299-7"><b>here</b>.</a><br> <br> <strong>Provide enhanced content for this article</strong><br> If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <u>[email protected]</u>.<br> <br> The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.<br> <br> Other enhanced features include, but are not limited to:<br> • Slide decks<br> • Videos and animations<br> • Audio abstracts<br> • Audio slides</p> <p> </p

data_sheet_1_Enhanced AKT Phosphorylation of Circulating B Cells in Patients With Activated PI3Kδ Syndrome.DOCX

<p>Activated PI3Kδ syndrome (APDS) is a primary immunodeficiency characterized by recurrent respiratory tract infections, lymphoproliferation, and defective IgG production. Heterozygous mutations in PIK3CD, PIK3R1, or PTEN, which are related to the hyperactive phosphoinositide 3-kinase (PI3K) signaling, were recently presented to cause APDS1 or APDS2 (APDSs), or APDS-like (APDS-L) disorder. In this study, we examined the AKT phosphorylation of peripheral blood lymphocytes and monocytes in patients with APDSs and APDS-L by using flow cytometry. CD19⁺ B cells of peripheral blood in APDS2 patients showed the enhanced phosphorylation of AKT at Ser473 (pAKT) without any specific stimulation. The enhanced pAKT in CD19⁺ B cells was normalized by the addition of a p110δ inhibitor. In contrast, CD3⁺ T cells and CD14⁺ monocytes did not show the enhanced pAKT in the absence of stimulation. These findings were similarly observed in patients with APDS1 and APDS-L. Among CD19⁺ B cells, enhanced pAKT was prominently detected in CD10⁺ immature B cells compared with CD10⁻ mature B cells. Enhanced pAKT was not observed in B cells of healthy controls, patients with common variable immunodeficiency, and hyper IgM syndrome due to CD40L deficiency. These results suggest that the enhanced pAKT in circulating B cells may be useful for the discrimination of APDS1, APDS2, and APDS-L from other antibody deficiencies.</p

Clinical and Genetic Characteristics of Non-Insulin-Requiring Glutamic Acid Decarboxylase (GAD) Autoantibody-Positive Diabetes: A Nationwide Survey in Japan

<div><p>Aims</p><p>Glutamic acid decarboxylase autoantibodies (GADAb) differentiate slowly progressive insulin-dependent (type 1) diabetes mellitus (SPIDDM) from phenotypic type 2 diabetes, but many GADAb-positive patients with diabetes do not progress to insulin-requiring diabetes. To characterize GADAb-positive patients with adult-onset diabetes who do not require insulin therapy for >5 years (NIR-SPIDDM), we conducted a nationwide cross-sectional survey in Japan.</p><p>Methods</p><p>We collected 82 GADAb-positive patients who did not require insulin therapy for >5 years (NIR-SPIDDM) and compared them with 63 patients with insulin-requiring SPIDDM (IR-SPIDDM). Clinical and biochemical characteristics, HLA-DRB1-DQB1 haplotypes, and predictive markers for progression to insulin therapy were investigated.</p><p>Results</p><p>Compared with the IR-SPIDDM group, the NIR-SPIDDM patients showed later diabetes onset, higher body mass index, longer duration before diagnosis, and less frequent hyperglycemic symptoms at onset. In addition, C-peptide, LDL-cholesterol, and TG were significantly higher in the NIR-SPIDDM compared to IR-SPIDDM patients. The NIR-SPIDDM group had lower frequency of susceptible HLA-DRB1*04:05-DQB1*04:01 and a higher frequency of resistant HLA-DRB1*15:01-DQB1*06:02 haplotype compared to IR-SPIDDM. A multivariable analysis showed that age at diabetes onset (OR = 0.82), duration before diagnosis of GADAb-positive diabetes (OR = 0.82), higher GADAb level (≥10.0 U/ml) (OR = 20.41), and fasting C-peptide at diagnosis (OR = 0.07) were independent predictive markers for progression to insulin-requiring diabetes. An ROC curve analysis showed that the optimal cut-off points for discriminating two groups was the GADAb level of 13.6 U/ml, age of diabetes onset of 47 years, duration before diagnosis of 5 years, and fasting C-peptide of 0.65 ng/ml.</p><p>Conclusions</p><p>Clinical, biochemical and genetic characteristics of patients with NIR-SPIDDM are different from those of IR-SPIDDM patients. Age of diabetes onset, duration before GADAb-positivity, GADAb level, and fasting C-peptide at diagnosis must be carefully considered in planning prevention trials for SPIDDM.</p></div

Correction: A Genome-Wide Association Study for Diabetic Retinopathy in a Japanese Population: Potential Association with a Long Intergenic Non-Coding RNA

<p>Correction: A Genome-Wide Association Study for Diabetic Retinopathy in a Japanese Population: Potential Association with a Long Intergenic Non-Coding RNA</p

Regional association plot of the region around the SNP rs9362054.

<p>The -log₁₀P values of the Fisher's exact test under the allele model in the GWAS of diabetic retinopathy in stage 1 were plotted against relative chromosomal locations (UCSC human genome 19).</p

Summary of the study strategy.

<p>Summary of the study strategy.</p

Associations of rs9362054 in <i>RP1-90L14.1</i> with diabetic retinopathy (DR), proliferative diabetic retinopathy (PDR) and diabetic nephropathy (DN) in each stage and combined stages 1, 2 and 3, using logistic regression under genotype, dominant and recessive models after adjusting for sex, duration of diabetes and HbA1c.

a<p>With additive genetic effect.</p><p>Associations of rs9362054 in <i>RP1-90L14.1</i> with diabetic retinopathy (DR), proliferative diabetic retinopathy (PDR) and diabetic nephropathy (DN) in each stage and combined stages 1, 2 and 3, using logistic regression under genotype, dominant and recessive models after adjusting for sex, duration of diabetes and HbA1c.</p

SNPs showing associations with diabetic retinopathy (DR) in combined stages 1 and 2 samples with <i>P</i><10⁻³ using the allele model.

<p>SNPs showing associations with diabetic retinopathy (DR) in combined stages 1 and 2 samples with <i>P</i><10⁻³ using the allele model.</p

Optimal cut-off values of GADAb level, age at diabetes onset, duration before diagnosis of GADAb-positive diabetes, and FCPR for a progression to insulin-requiring diabetes by ROC curve analysis.

<p>Optimal cut-off values of GADAb level, age at diabetes onset, duration before diagnosis of GADAb-positive diabetes, and FCPR for a progression to insulin-requiring diabetes by ROC curve analysis.</p