Distribution of SUA and psychiatric outcomes across genotypes of <i>SLC2A9 rs6855911</i> in men and women.

<p>GAD = generalized anxiety disorder; and SUA = serum uric acid.</p><p>The results are expressed as numbers and percentages except for SUA which is expressed as mean and standard deviation.</p><p>Sex-by-genotype interaction were significant for its effect on lifetime and current any anxiety disorders and social phobia (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0076336#pone-0076336-t004" target="_blank">Table 4</a>).</p

Crude and adjusted logistic regression analysis of SUA (per 100 µmol/L) and psychiatric disorders in overall sample.

<p>MDD = major depressive disorder; GAD = generalized anxiety disorder; and SUA = serum uric acid.</p><p>If P value for the quadratic term (SUA²) is significant, ORs derived from models with quadratic term are presented.</p><p>Adjusted for age, sex, socio-economic status, alcohol consumption, smoking, diabetes, hypertension, GFR (calculated according to Modification in Diet in Renal Disease equation) and drugs that influence uric acid and additionally for anxiety (in the association between SUA and depression) and depression (in the association between SUA and anxiety).</p><p>P_interaction = P value for multiplicative interaction parameter between SUA and sex; Interaction for models with a quadratic term was assessed using a likelihood ratio test (LRT) comparing a model which included SUA*sex and SUA²* sex and a model without; and §indicates P value of the LRT.</p>*<p>Logistic regression not possible due to zero prevalence; NA = not available.</p

Distribution of psychiatric disorders across sex-specific quintiles of SUA.

<p>MDD =  major depressive disorder; GAD = generalized anxiety disorder; and SUA =  serum uric acid.</p>*<p>P-value <0.05 for quadratic trend tested by a crude logistic model which included a quadratic term (SUA squared) for continuous value of SUA.</p

Age-adjusted prevalence and mean values of selected cardiovascular risk factors by level of education and age group among men (N = 2960).

<p>BP: blood pressure; CI: confidence interval; HDL: high-density lipoprotein; LDL: low-density lipoprotein. Prevalence and mean values are adjusted for age and place of birth (Switzerland or outside Switzerland).</p>a<p><i>p</i> for linear trend across socioeconomic categories.</p>b<p>Difference in prevalence/mean between the highest and the lowest educational category.</p>c<p><i>p</i> for interaction between educational level and age group.</p>d<p>Analyses restricted to current smokers (N = 515 in the 35–54 years group and N = 293 in the 55–75 years group). 32 smokers with missing information on pack-years were not included.</p>e<p>Overweight: BMI ≥25 kg/m² and <30 kg/m²; obesity: BMI ≥30 kg/m²; abdominal obesity: waist circumference ≥102/88cm in men/women; hypertension: BP≥140/90 mmHg or taking BP treatment; low HDL-cholesterol: <1.0/1.2 mmol/l in men/women; high LDL-cholesterol: ≥3.4 mmol/l; high triglycerides: ≥1.7 mmol/l; diabetes:fasting glucose ≥7.0 mmol/l or taking diabetes treatment.</p

Crude and adjusted logistic regression analysis of <i>SLC2A9 rs6855911</i> and psychiatric disorders according to sex.

<p>GAD = generalized anxiety disorder.</p><p>ORs represent the effect of <i>SLC2A9 rs6855911</i> used as a continuous score of 0, 1 and 2 corresponding to GG, AG and AA genotype respectively with AA being the genotype associated with elevated levels of serum uric acid.</p><p>Adjusted for age, sex, socio-economic status, alcohol consumption, smoking, diabetes, hypertension, GFR (calculated according to Modification in Diet in Renal Disease equation) and drugs that influence uric acid and additionally for anxiety (in the association between SUA and depression) and depression (in the association between SUA and anxiety).</p><p>P_interaction = P value for sex-by-genotype interaction for its effect on psychiatric disorders.</p

Socio-demographic characteristics by gender and age group.

<p>SD: standard deviation.</p

Use of oscillometric devices in atrial fibrillation: a comparison of three devices and invasive blood pressure measurement

<p><b>Background:</b> The use of automated (oscillometric) blood pressure (BP) devices is not validated in atrial fibrillation (AF) patients.</p> <p><b>Objectives:</b> To assess the reliability of three oscillometric BP devices, and the agreement with invasive arterial blood pressure(IBP) in AF patients.</p> <p><b>Methods:</b> 48 AF patients with randomized sequences of 10 consecutive BP measurements with two pairs of devices: (1) OmronR7™(wrist) and OmronHEM907™(arm); (2) OmronR7™ and Microlife WatchBPhome(arm). Reliability and agreement of each device were assessed by the intra-class correlation coefficient (ICC) for the continuous BP measurements and Bland & Altman methodology, respectively. In 10 additional AF patients, 10 consecutive measurements with IBP and OmronHEM907™, and IBP and Microlife WatchBPhome were performed.</p> <p><b>Results:</b> The OmronR7™ was not able to obtain any BP Readings. Arm devices presented better ICC for systolicBP(SBP) than for diastolicBP(DBP) (Omron HEM907™:0.94 [0.90; 0.97] vs. 0.77 [0.67; 0.89]; Microlife WatchBPhome:0.92 [0.88; 0.96] vs.0.79 [0.69; 0.89]).The correlation coefficient between Microlife WatchBPhome and IBP computed using the average of repeated measurements from two to ten measurements improved up to the third and remained stable afterwards.</p> <p>The agreement between IBP and SBP, and IBP and DBP, was moderate as illustrated by a wide limit of agreement [−24; 26](SBP) and [−15;17](DBP) for Microlife WatchBPHome, respectively and [−30; 13](SBP) and [−7; 15](DBP) for OmronHEM907.</p> <p><b>Conclusions:</b> BP measurement using the two arm oscillometric devices achieved a high reliability for SBP. The agreement between IBP and arm devices was low but using the average of three consecutive measurements improved the results substantially.</p

Diabetic RIP-REST transgenic mice are hyperglycemic and show poor insulin secretion.

<p><i>A</i>. Blood glucose levels were assessed at different ages in male and female diabetic RIP-REST transgenic (dark diamonds; n = 7) and wild type mice (open diamonds; n = 5). Diabetic RIP-REST mice feature hyperglycemia from weaning onward. Results are mean ± SD. ***<i>P</i><0.001 versus values of wild type mice. <i>B</i>. Diabetic RIP-REST mice (black circles, n = 3) and wild type littermates (open squares, n = 4) were subjected to <i>in situ</i> pancreatic perfusion at 1.5 ml/min rate. After a 30-min equilibration period at basal 1.4 mmol/l glucose, the pancreas was perfused sequentially at different glucose concentrations, first at 1.4 mmol/l for 20 min, next at 8.0 mmol/l for 20 min, then at 16.0 mmol/l for 20 min, followed by a 30-min stimulation at 8.0 mmol/l plus 1 nmol/l GLP-1, and finally at 1.4 mmol/l for 15 min. Results are mean ± SD.</p

CDK5R2 protects beta cells against cytokines and palmitate.

<p><i>A</i>. Left panel, immunoblotting of total proteins from INS-1E cells, 72 h after transfection with a negative siRNA (siNeg) or siRNAs against <i>Cdk5r2</i> (siCdk5r2#1 and siCdk5r2#2). Right panel, quantification of the corresponding Cdk5r2 protein levels. Results are mean ± SEM of three independent experiments. **<i>P</i><0.01 versus values of siNeg-transduced INS-1E cells. <i>B</i>. Quantification of apoptotic nuclei in non-transfected INS-1E cells (NT) and INS-1E cells transfected with a negative siRNA (siNeg) or with siRNAs against <i>Cdk5r2</i> (siCdk5r2#1 and siCdk5r2#2), treated 24 h with a mix of cytokines (black bars) or not (white bars). Results are mean ± SEM of six independent experiments. **<i>P</i><0.01 versus controls. <i>C</i>. Immunoblotting of total proteins from INS-1E cells transfected with a negative siRNA (siNeg) or siRNAs against <i>Cdk5r2</i> (siCdk5r2#1 and siCdk5r2#2), treated 24 h with a mix of cytokines (Cyt) or not (Ctrl). The cleavage of caspase-9 and −3, induced by cytokines, is higher in siCdk5r2- than in siNeg-treated cells. <i>D</i>. Quantification of apoptotic nuclei in non-transfected INS-1E cells (NT) and INS-1E cells transfected with a negative siRNA (siNeg) or siRNAs against <i>Cdk5r2</i> (siCdk5r2#1 and siCdk5r2#2), exposed 15 h to control medium (white bars) or palmitate (black bars). Results are mean ± SEM of six independent experiments. **<i>P</i><0.01 versus controls.</p

Beta cell loss in diabetic RIP-REST mice occurs through apoptosis.

<p><i>A</i>. Nuclear PCNA (green) and insulin (red) staining show same level of proliferating beta cells (arrows) in both wild type (WT, left panel) and diabetic RIP-REST mice (right panel) at P2. Blue staining is the DAPI labeling of nuclei. Scale bar, 50 μm. <i>B</i>. Representative images of nuclear TUNEL (green) and insulin (red) staining showing apoptotic nuclei of beta cells in sections of P2 diabetic RIP-REST mice. No apoptotic beta cells were detected in wild type animals (not shown). Blue staining is the DAPI labeling of nuclei. Scale bar, 25 μm. C. Quantification of apoptotic nuclei in non-infected INS-1E cells (NI) and INS-1E cells transfected with a control (Ad-GFP) or REST-expressing adenovirus (Ad-REST) at different multiplicity of infection (MOI) as indicated, and treated 24 h with a mix of cytokines (black bars) or not (white bars). Results are mean ± SD of six independent experiments. *<i>P</i><0.05 versus respective controls in treated or untreated conditions. # <i>P</i><0.05 versus MOI 2 of Ad-REST infection.</p