Thin film GaAs photovoltaic solar energy cells

Fabrication process for thin film gallium arsenide photovoltaic solar energy cell

Materials and methods for large-area solar cells Final report, 17 Dec. 1964 - 16 Dec. 1965

Growth and evaluation of gallium arsenide-indium arsenide-aluminum foil structures in construction of thin film large area solar cells for satellite

Changes in Plasma Phospholipid Fatty Acid Patterns and their Impact on Plasma Triglyceride Levels Following Fish Oil Supplementation

The objective of the present study was to test for associations between changes in fatty acids (FAs) and changes in plasma triglyceride (TG) levels after an n-3 FA supplementation and to test whether SNPs from the FADS gene cluster were associated with plasma FA levels or with specific FA patterns. A total of 210 subjects completed a 2-wk run-in period followed by 6-wk supplementation with 5g/d of fish oil. FA profiles of plasma phospholipids (PPLs) were obtained and 19 SNPs from the FADS gene cluster were genotyped. Principal component analysis was conducted and scores were calculated. There was an increase in EPA, DPA and DHA levels in PPLs as well as a decrease in ALA and all n-6 FA levels after the supplementation. Factor analysis suggested 4 post-n-3 FA supplementation patterns. Changes in AA, ALA, DGLA, as well as changes in total n-3 and omega-6 FAs in absolute quantities of FAs were all associated with a change in TG levels whereas the correlation remained significant only for AA and DGLA when FAs were expressed as percentage of total FAs. Several SNPs from the FADS gene cluster were associated with post-supplementation FA levels. These results suggest that FAs alone or regrouped in factors could play a role in modulating plasma TG levels after fish oil supplementation. SNPs from the FADS gene cluster interact with both FAs and/or factors to modulate TG levels

Length Scales of Acceleration for Locally Isotropic Turbulence

Length scales are determined that govern the behavior at small separations of the correlations of fluid-particle acceleration, viscous force, and pressure gradient. The length scales and an associated universal constant are quantified on the basis of published data. The length scale governing pressure spectra at high wave numbers is discussed. Fluid-particle acceleration correlation is governed by two length scales; one arises from the pressure gradient, the other from the viscous force.Comment: 2 figures, 4 pages. Physical Review Letters, accepted August 200

Maternal reflective functioning and child internalising and externalising difficulties in the context of child sexual abuse / Le fonctionnement réflexif maternel et les symptômes intériorisés et extériorisés d’enfants victimes d’une agression sexuelle

Objectives were to examine 1) the relative contributions of childhood sexual abuse (CSA) and maternal reflective functioning (MRF) in explaining child internalising and externalising, and 2) whether MRF moderated the relationship between CSA and child difficulties. Participants were 154 mothers, including 64 mothers of children with histories of CSA. MRF was assessed with the Parent Development Interview-Revised and children’s psychosocial difficulties with the Child Behavior Checklist. MRF was the only significant predictor of child internalising and externalising difficulties in a model where CSA and MRF were considered simultaneously. MRF moderated the relationship between CSA and child internalising, suggesting that the parent’s capacity to mentalize and imagine the child’s psychological experience has a protective function in the context of CSA. / Cette étude avait pour objectifs d’évaluer les liens entre les agressions sexuelles en enfance (ASE), le fonctionnement réflexif maternel (FRM) et les difficultés psychosociales chez les enfants ainsi que le rôle modérateur du FRM dans la relation entre l’ASE et les difficultés chez les enfants. L’échantillon incluait 154 mères, dont 64 mères d’un enfant ayant vécu une ASE. Le Parent Development Interview-Revised et le Child Behavior Checklist ont permis de mesurer le FRM et les difficultés psychosociales respectivement. Une analyse acheminatoire montre que seul le FRM était significativement associé aux comportements intériorisés et extériorisés, et qu’il jouait un rôle modérateur dans la relation entre l’ASE et les difficultés intériorisées, suggérant un effet protecteur du FRM suite à une ASE

PPARα L162V underlies variation in serum triglycerides and subcutaneous fat volume in young males

<p>Abstract</p> <p>Background</p> <p>Of the five sub-phenotypes defining metabolic syndrome, all are known to have strong genetic components (typically 50–80% of population variation). Studies defining genetic predispositions have typically focused on older populations with metabolic syndrome and/or type 2 diabetes. We hypothesized that the study of younger populations would mitigate many confounding variables, and allow us to better define genetic predisposition loci for metabolic syndrome.</p> <p>Methods</p> <p>We studied 610 young adult volunteers (average age 24 yrs) for metabolic syndrome markers, and volumetric MRI of upper arm muscle, bone, and fat pre- and post-unilateral resistance training.</p> <p>Results</p> <p>We found the PPARα L162V polymorphism to be a strong determinant of serum triglyceride levels in young White males, where carriers of the V allele showed 78% increase in triglycerides relative to L homozygotes (LL = 116 ± 11 mg/dL, LV = 208 ± 30 mg/dL; p = 0.004). Men with the V allele showed lower HDL (LL = 42 ± 1 mg/dL, LV = 34 ± 2 mg/dL; p = 0.001), but women did not. Subcutaneous fat volume was higher in males carrying the V allele, however, exercise training increased fat volume of the untrained arm in V carriers, while LL genotypes significantly decreased in fat volume (LL = -1,707 ± 21 mm³, LV = 17,617 ± 58 mm³; p = 0.002), indicating a systemic effect of the V allele on adiposity after unilateral training. Our study suggests that the primary effect of PPARα L162V is on serum triglycerides, with downstream effects on adiposity and response to training.</p> <p>Conclusion</p> <p>Our results on association of PPARα and triglycerides in males showed a much larger effect of the V allele than previously reported in older and less healthy populations. Specifically, we showed the V allele to increase triglycerides by 78% (p = 0.004), and this single polymorphism accounted for 3.8% of all variation in serum triglycerides in males (p = 0.0037).</p

Disturbance in uniformly 13C-labelled DHA metabolism in elderly human subjects carrying the apoE ε4 allele

Carrying the apoE ε4 allele (E4+) is the most important genetic risk for Alzheimer's disease. Unlike non-carriers (E4 − ), E4+ seem not to be protected against Alzheimer's disease when consuming fish. We hypothesised that this may be linked to a disturbance in n-3 DHA metabolism in E4+. The aim of the present study was to evaluate [13C]DHA metabolism over 28 d in E4+v. E4 − . A total of forty participants (twenty-six women and fourteen men) received a single oral dose of 40 mg [13C]DHA, and its metabolism was monitored in blood and breath over 28 d. Of the participants, six were E4+ and thirty-four were E4 − . In E4+, mean plasma [13C]DHA was 31 % lower than that in E4 − , and cumulative β-oxidation of [13C]DHA was higher than that in E4 − 1–28 d post-dose (P≤ 0·05). A genotype × time interaction was detected for cumulative β-oxidation of [13C]DHA (P≤ 0·01). The whole-body half-life of [13C]DHA was 77 % lower in E4+ compared with E4 − (P≤ 0·01). In E4+ and E4 − , the percentage dose of [13C]DHA recovered/h as 13CO2 correlated with [13C]DHA concentration in plasma, but the slope of linear regression was 117 % steeper in E4+ compared with E4 − (P≤ 0·05). These results indicate that DHA metabolism is disturbed in E4+, and may help explain why there is no association between DHA levels in plasma and cognition in E4+. However, whether E4+ disturbs the metabolism of 13C-labelled fatty acids other than DHA cannot be deduced from the present study

PPARα: energy combustion, hypolipidemia, inflammation and cancer

The peroxisome proliferator-activated receptor α (PPARα, or NR1C1) is a nuclear hormone receptor activated by a structurally diverse array of synthetic chemicals known as peroxisome proliferators. Endogenous activation of PPARα in liver has also been observed in certain gene knockout mouse models of lipid metabolism, implying the existence of enzymes that either generate (synthesize) or degrade endogenous PPARα agonists. For example, substrates involved in fatty acid oxidation can function as PPARα ligands. PPARα serves as a xenobiotic and lipid sensor to regulate energy combustion, hepatic steatosis, lipoprotein synthesis, inflammation and liver cancer. Mainly, PPARα modulates the activities of all three fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal ω-oxidation, and thus plays a key role in energy expenditure. Sustained activation of PPARα by either exogenous or endogenous agonists leads to the development of hepatocellular carcinoma resulting from sustained oxidative and possibly endoplasmic reticulum stress and liver cell proliferation. PPARα requires transcription coactivator PPAR-binding protein (PBP)/mediator subunit 1(MED1) for its transcriptional activity

The PPARGC1A Gly482Ser polymorphism is associated with left ventricular diastolic dysfunction in men

<p>Abstract</p> <p>Background</p> <p>The Gly482Ser polymorphism in peroxisome proliferator-activated receptor gamma coactivator-1 alpha (<it>PPARGC1A</it>) has been demonstrated to be associated with diabetes, obesity and hypertension, all of which are important risk factors for left ventricular diastolic dysfunction.</p> <p>Methods</p> <p>The <it>PPARGC1A </it>Gly482Ser polymorphism was genotyped in a community-based cohort of 499 men and 533 women, who also underwent an echocardiographic examination to determine their left ventricular diastolic function. The association between the polymorphism and the presence of diastolic dysfunction was evaluated using logistic regression models.</p> <p>Results</p> <p>The Ser allele of the <it>PPARGC1A </it>Gly482Ser polymorphism was significantly associated with a lower risk of diastolic dysfunction in men, but not in women. In a model adjusting for potential confounders (age, body mass index, leisure time physical activity, hypertension and diabetes) the results were still significant and substantial (odds ratio 0.13, 95% confidence interval 0.03–0.54, p for trend = 0.004). The results were consistent in a series of models, and they imply a multiplicative, protective effect of the Ser allele, with lower risk of diastolic dysfunction for each copy of the allele.</p> <p>Conclusion</p> <p>The Ser allele of the <it>PPARGC1A </it>Gly482Ser polymorphism was associated with decreased risk of diastolic left ventricular dysfunction in men, but not in women, in our large community-based sample. It was associated with a substantially decreased risk, even after adjustment for potential confounders. The clinical importance of the findings has to be established in further studies.</p

The Transcriptome of Human Epicardial, Mediastinal and Subcutaneous Adipose Tissues in Men with Coronary Artery Disease

The biological functions of epicardial adipose tissue (EAT) remain largely unknown. However, the proximity of EAT to the coronary arteries suggests a role in the pathogenesis of coronary artery disease (CAD). The objectives of this study were to identify genes differentially regulated among three adipose tissues, namely EAT, mediastinal (MAT) and subcutaneous (SAT) and to study their possible relationships with the development of cardiovascular diseases.Samples were collected from subjects undergoing coronary artery bypass grafting surgeries. Gene expression was evaluated in the three adipose depots of six men using the Illumina® HumanWG-6 v3.0 expression BeadChips. Twenty-three and 73 genes were differentially up-regulated in EAT compared to MAT and SAT, respectively. Ninety-four genes were down-regulated in EAT compared to SAT. However, none were significantly down-regulated in EAT compared to MAT. More specifically, the expression of the adenosine A1 receptor (ADORA1), involved in myocardial ischemia, was significantly up-regulated in EAT. Levels of the prostaglandin D2 synthase (PTGDS) gene, recently associated with the progression of atherosclerosis, were significantly different in the three pairwise comparisons (EAT>MAT>SAT). The results of ADORA1 and PTGDS were confirmed by quantitative real-time PCR in 25 independent subjects.Overall, the transcriptional profiles of EAT and MAT were similar compared to the SAT. Despite this similarity, two genes involved in cardiovascular diseases, ADORA1 and PTGDS, were differentially up-regulated in EAT. These results provide insights about the biology of EAT and its potential implication in CAD