On the fatigue response of a bonded repaired aerospace composite using thermography

Lock-in thermography was employed to investigate the repair efficiency of a bonded repaired aerospace composite subjected to step-wise cycling mechanical loading. The studied component (substrate) was artificially damaged with a 5 mm circular notch and subsequently repaired with a tapered bonded patch. Critical and sub-critical damage of the repaired component was monitored via thermography during 5 Hz tension–tension fatigue. The examination of the acquired thermographs enabled the identification of the patch debonding propagation as well as the quantification of the stress magnification at the patch ends and the locus of the circular notch. It was found that fatigue mechanical loading yields both thermoelastic and hysterestic phenomena with the latter being more prominent prior to the failure of the studied repaired component

FADS2 Function Loss at the Cancer Hotspot 11q13 Locus Diverts Lipid Signaling Precursor Synthesis to Unusual Eicosanoid Fatty Acids

Background: Genes coding for the fatty acid desaturases (FADS1, 2, 3) localized at the cancer genomic hotspot 11q13 locus are required for the biosynthesis of 20 carbon polyunsaturated fatty acids (PUFA) that are direct eicosanoid precursors. In several cancer cell lines, FADS2 encoded D6 and D8 desaturation is not functional. Methodology/Principal Findings: Analyzing MCF7 cell fatty acids with detailed structural mass spectrometry, we show that in the absence of FADS2 activity, the FADS1 product D5-desaturase operates to produce 5,11,14–20:3 and 5,11,14,17–20:4. These PUFA are missing the 8–9 double bond of the eicosanoid signaling precursors arachidonic acid (5,8,11,14–20:4) and eicosapentaenoic acid (5,8,11,14,17–20:5). Heterologous expression of FADS2 restores D6 and D8-desaturase activity and normal eicosanoid precursor synthesis. Conclusions/Significance: The loss of FADS2-encoded activities in cancer cells shuts down normal PUFA biosynthesis, deleting the endogenous supply of eicosanoid and downstream docosanoid precursors, and replacing them with unusual butylene-interrupted fatty acids. If recapitulated in vivo, the normal eicosanoid and docosanoid cell signaling milieu would be depleted and altered due to reduction and substitution of normal substrates with unusual substrates, with unpredictable consequences for cellular communication

Metabolically Healthy Obesity and High Carotid Intima-Media Thickness in Children and Adolescents: International Childhood Vascular Structure Evaluation Consortium

OBJECTIVE It has been argued that metabolically healthy obesity (MHO) does not increase cardiovascular disease (CVD) risk. This study examines the association of MHO with carotid intima-media thickness (cIMT), a proxy of CVD risk, in children and adolescents. RESEARCH DESIGN AND METHODS Data were available for 3,497 children and adolescents aged 6–17 years from five population-based cross-sectional studies in Brazil, China, Greece, Italy, and Spain. Weight status categories (normal, overweight, and obese) were defined using BMI cutoffs from the International Obesity Task Force. Metabolic status (defined as "healthy" [no risk factors] or "unhealthy" [one or more risk factors]) was based on four CVD risk factors: elevated blood pressure, elevated triglyceride levels, reduced HDL cholesterol, and elevated fasting glucose. High cIMT was defined as cIMT ≥90th percentile for sex, age, and study population. Logistic regression model was used to examine the association of weight and metabolic status with high cIMT, with adjustment for sex, age, race/ethnicity, and study center. RESULTS In comparison with metabolically healthy normal weight, odds ratios (ORs) for high cIMT were 2.29 (95% CI 1.58–3.32) for metabolically healthy overweight and 3.91 (2.46–6.21) for MHO. ORs for high cIMT were 1.44 (1.03–2.02) for unhealthy normal weight, 3.49 (2.51–4.85) for unhealthy overweight, and 6.96 (5.05–9.61) for unhealthy obesity. CONCLUSIONS Among children and adolescents, cIMT was higher for both MHO and metabolically healthy overweight compared with metabolically healthy normal weight. Our findings reinforce the need for weight control in children and adolescents irrespective of their metabolic status

Efficacy of anthropometric measures for identifying cardiovascular disease risk in adolescents: review and meta-analysis.

INTRODUCTION: To compare the ability of Body Mass Index (BMI), waist circumference (WC) and waist to height ratio (WHtR) to estimate cardiovascular disease (CVD) risk levels in adolescents. EVIDENCE ACQUISITION: A systematic review and meta-analysis was performed after a database search for relevant literature (Cochrane, Centre for Review and Dissemination, PubMed, British Nursing Index, CINAHL, BIOSIS citation index, ChildData, metaRegister). EVIDENCE SYNTHESIS: The study included 117 records representing 96 studies with 994,595 participants were included in the systematic review, 14 of which (13 studies, N.=14,610) were eligible for the meta-analysis. The results of the meta-analysis showed that BMI was a strong indicator of systolic blood pressure, diastolic blood pressure, triglycerides, high-density lipoprotein cholesterol and insulin; but not total cholesterol, low-density lipoprotein or glucose. Few studies were eligible for inclusion in the meta-analysis considering WC or WHtR (N.≤2). The narrative synthesis found measures of central adiposity to be consistently valid indicators of the same risk factors as BMI. CONCLUSIONS: BMI was an indicator of CVD risk. WC and WHtR were efficacious for indicating the same risk factors BMI performed strongly for, though there was insufficient evidence to judge the relative strength of each measure possibly due to heterogeneity in the methods for measuring and classifying WC