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Aims To estimate the prevalence of LUTS and OAB in a large, ethnically diverse US study. Methods This cross‐sectional, population‐representative survey was conducted via the Internet in the US among 10,000 men and women aged 18–70 (2,000 African‐Americans [AA], 2,000 Hispanics, 6,000 whites). The LUTS tool assessed how often participants experienced LUTS during the past 4 weeks on a five‐point Likert scale. OAB was defined by the presence of urinary urgency ≥ “sometimes” or ≥ “often,” and/or the presence of urgency urinary incontinence (UUI). Descriptive statistics were used to evaluate group differences. Logistic regression analyses were conducted to examine the impact of racial/ethnic group on OAB. Results Response rate, 56.7%. Prevalent LUTS included terminal dribble and nocturia across gender, post‐micturition leaking (men), and stress incontinence (women). Prevalence of OAB ≥ “sometimes” and ≥ “often” were 17% and 8% in men and 30% and 20% in women—with significantly higher rates among AA men and women. A similar trend was found for UUI among men (AA, 10%; Hispanic and whites, 6%), while AA and white women had higher prevalence of UUI (19%) as compared to Hispanic women (16%). In logistic regression analyses, AA and Hispanic men and women were significantly more likely than whites to have OAB despite having lower prevalence of self‐reported comorbid conditions and risk factors. Conclusions LUTS and OAB are highly prevalent in both men and women and increase with advancing age. Further, racial/ethnic group is a robust predictor of OAB in men and women. Neurourol. Urodynam. 32: 230–237, 2013. © 2012 Wiley Periodicals, Inc.

SummaryWith the increasing prevalence of obesity, research has focused on the molecular mechanism(s) linking obesity and skeletal muscle insulin resistance. Metabolic alterations within muscle, such as changes in the cellular location of fatty acid transporter proteins, decreased mitochondrial enzyme activity, and defects in mitochondrial morphology, likely contribute to obesity and insulin resistance. These defects are thought to play a role in the reduced skeletal muscle fatty acid oxidation and increased intramuscular lipid (IMCL) accumulation that is apparent with obesity and other insulin-resistant states such as type 2 diabetes. Intramuscular triacylglycerol does not appear to be a ubiquitous marker of insulin resistance, although specific IMCL intermediates such as long-chain fatty acyl-CoAs, ceramide, and diacylglycerol may inhibit insulin signal transduction. In this review, we will briefly summarize the defects in skeletal muscle lipid metabolism associated with obesity, and discuss the proposed mechanisms by which these defects may contribute to insulin resistance. IUBMBIUBMB Life, 61(1): [47][48][49][50][51][52][53][54][55] 2009

Cultured myocytes from severely obese women express perturbations in FA metabolism and insulin signaling reminiscent of those observed in vivo. The obesity phenotype can be recapitulated in muscle cells from lean subjects via exposure to excess lipid, but not by overexpressing the FAT/CD36 FA transporter.

OBJECTIVETo determine whether the obesity-related decrement in fatty acid oxidation (FAO) in primary human skeletal muscle cells (HSkMC) is linked with lower mitochondrial content and whether this deficit could be corrected via overexpression of peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α).RESEARCH DESIGN AND METHODSFAO was studied in HSkMC from lean (BMI 22.4 ± 0.9 kg/m2; N = 12) and extremely obese (45.3 ± 1.4 kg/m2; N = 9) subjects. Recombinant adenovirus was used to increase HSkMC PGC-1α expression (3.5- and 8.0-fold), followed by assessment of mitochondrial content (mtDNA and cytochrome C oxidase IV [COXIV]), complete (14CO2 production from labeled oleate), and incomplete (acid soluble metabolites [ASM]) FAO, and glycerolipid synthesis.RESULTSObesity was associated with a 30% decrease (P < 0.05) in complete FAO, which was accompanied by higher relative rates of incomplete FAO ([14C]ASM production/14CO2), increased partitioning of fatty acid toward storage, and lower (P < 0.05) mtDNA (−27%), COXIV (−35%), and mitochondrial transcription factor (mtTFA) (−43%) protein levels. PGC-1α overexpression increased (P < 0.05) FAO, mtDNA, COXIV, mtTFA, and fatty acid incorporation into triacylglycerol in both lean and obese groups. Perturbations in FAO, triacylglycerol synthesis, mtDNA, COXIV, and mtTFA in obese compared with lean HSkMC persisted despite PGC-1α overexpression. When adjusted for mtDNA and COXIV content, FAO was equivalent between lean and obese groups.CONCLUSIONReduced mitochondrial content is related to impaired FAO in HSkMC derived from obese individuals. Increasing PGC-1α protein levels did not correct the obesity-related absolute reduction in FAO or mtDNA content, implicating mechanisms other than PGC-1α abundance.

Supplemental Digital Content is Available in the Text. The TRIAL-STIM randomised controlled trial found no evidence that a spinal cord stimulation screening trial strategy provides superior patient outcomes compared to a no trial screening approach.

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Given the apparent importance of triggers in attaining and maintaining asthma control, empirical research concerning optimal trigger management is needed. Results demonstrate that asthma triggers are similar across continents, suggesting a global checklist of triggers for use in research and clinical practice would be feasible.