54,672 research outputs found
Historical experiences, collective memory and willingness to fight for one’s country: Comments on Paez et al. (2008)
No full textThis paper considers Paez et al.’s (2008) article ‘“Remembering” World War II and willingness to fight: Sociocultural factors in the social representation of historical warfare across 22 societies.’ Despite the importance of their focus on social representations of history and willingness to fight for one’s country, it is argued that Paez et al.’s paper features a number of methodological flaws. Specifically, the way in which key variables (historical experience, collective memory and willingness to fight for one’s country) are operationalized is especially problematic. The implications of these weaknesses for their conceptual conclusions are discussed briefly, as are the more general limitations of statistical analyses of survey data for addressing these issues
L'identité en psychologie sociale : processus cognitifs, facteurs situationnels et représentations sociales
No full textDeschamps (J.-C.), Morales (J. -F.), Paez (D.) et Worchel (S.). — L’identité sociale. La construction de l’individu dans les relations entre groupes, Presses universitaires de Grenoble, 1999
No full textAlliot Liliane. Deschamps (J.-C.), Morales (J. -F.), Paez (D.) et Worchel (S.). — L’identité sociale. La construction de l’individu dans les relations entre groupes, Presses universitaires de Grenoble, 1999. In: Bulletin de psychologie, tome 53 n°448, 2000. pp. 517-519
"Closing the R&D Gap, Evaluating the Sources of R&D Spending"
No full textBoth spending and tax policies have been implemented in the United States with the goal of stimulating private sector research and development (R&D). Karier questions whether current R&D policy, especially the research and experimentation tax credit, can contribute to closing the gap between nondefense expenditures on R&D in the United States and such expenditures in other countries, such as Japan and Germany. He also explores possible changes to our current R&D policy to make it more effective.
Letter from C. D. Dawson, Tusayan Copper Mining and Smelting, to Carl Hayden
No full textLetter from C. D. Dawson to Carl Hayden urging him to consider the rights of miners and farmers when drawing up the boundaries for the proposed park
The role of oxidative stress in the pathogenesis of type 2 diabetes mellitus micro- and macrovascular complications : avenues for a mechanistic-based therapeutic approach
No full textA growing body of evidence suggests that oxidative stress plays a key role in the pathogenesis of micro- and macrovascular diabetic complications. The increased oxidative stress in subjects with type 2 diabetes is a consequence of several abnormalities, including hyperglycemia, insulin resistance, hyperinsulinemia, and dyslipidemia, each of which contributes to mitochondrial superoxide overproduction in endothelial cells of large and small vessels as well as the myocardium. The unifying pathophysiological mechanism that underlies diabetic complications could be explained by increased production of reactive oxygen species (ROS) via: (1) the polyol pathway flux, (2) increased formation of advanced glycation end products (AGEs), (3) increased expression of the receptor for AGEs, (4) activation of protein kinase C isoforms, and (5) overactivity of the hexosamine pathway. Furthermore, the effects of oxidative stress in individuals with type 2 diabetes are compounded by the inactivation of two critical anti-atherosclerotic enzymes: endothelial nitric oxide synthase and prostacyclin synthase. Of interest, the results of clinical trials in patients with type 2 diabetes in whom intensive management of all the components of the metabolic syndrome (hyperglycemia, hypercholesterolemia, and essential hypertension) was attempted (with agents that exert a beneficial effect on serum glucose, serum lipid concentrations, and blood pressure, respectively) showed a decrease in adverse cardiovascular end points. The purpose of this review is (1) to examine the mechanisms that link oxidative stress to micro- and macrovascular complications in subjects with type 2 diabetes and (2) to consider the therapeutic opportunities that are presented by currently used therapeutic agents which possess antioxidant properties as well as new potential antioxidant substances
Measurement of the D+/- production asymmetry in 7 TeV pp collisions
No full textThe asymmetry in the production cross-section \sigma of D+/- mesons, A_P = (\sigma(D+) - \sigma(D-))/(\sigma(D+) + \sigma(D-)), is measured in bins of pseudorapidity \eta and transverse momentum p_T within the acceptance of the LHCb detector. The result is obtained with a sample of D+ -> K_S pi+ decays corresponding to an integrated luminosity of 1.0 fb^-1, collected in pp collisions at a centre of mass energy of 7 TeV at the Large Hadron Collider. When integrated over the kinematic range 2.0 K_S pi+ decay is negligible. No significant dependence on \eta or p_T is observed
D* (D)over-bar* molecule interpretation of Z(c)(4025)
No full textWe have used QCD sum rules to study the newly observed charged state Z(c)(4025) as a hidden-charm D*(D) over bar* molecular state with the quantum numbers I-G(J(P)) =1(+)(1(+)). Using a D*(D) over bar* molecular interpolating current, we have calculated the two-point correlation function and the spectral density up to dimension eight at leading order in alpha(s). The extracted mass is m(X) = (4.04 +/- 0.24) GeV. This result is compatible with the observed mass of Z(c)(4025) within the errors, which implies a possible molecule interpretation of this new resonance. We also predict the mass of the corresponding hidden-bottom B*(B) over bar* molecular state: m(Zb) = (9.98 +/- 0.21) GeV.Physics, Particles & FieldsSCI(E)[email protected]; [email protected]; [email protected]; [email protected]
Prompt charm production in pp collisions at √<span style="text-decoration:overline">s</span>=7 TeV
No full textCharm production at the LHC in pp collisions at s√=7 TeV is studied with the LHCb detector. The decays D0→K−π+, D+→K−π+π+, D⁎+→D0(K−π+)π+, D+s→ϕ(K−K+)π+, Λ+c→pK−π+, and their charge conjugates are analysed in a data set corresponding to an integrated luminosity of 15 nb−1. Differential cross-sections dσ/dpT are measured for prompt production of the five charmed hadron species in bins of transverse momentum and rapidity in the region 0<pT<8 GeV/c and 2.0<y<4.5. Theoretical predictions are compared to the measured differential cross-sections. The integrated cross-sections of the charm hadrons are computed in the above pT-y range, and their ratios are reported. A combination of the five integrated cross-section measurements gives
σ(cc¯)pT<8 GeV/c,2.0<y<4.5=1419±12(stat)±116(syst)±65(frag) μb,
where the uncertainties are statistical, systematic, and due to the fragmentation functions
Identification of a Pathogenic Mutation of the Lipase Maturation Factor 1 (LMF1) Gene Causing Recurrent Pancreatitis and Requiring Critical Care
No full textBackground: Familial chylomicronemia syndrome (FCS) is a rare autosomal recessive disorder characterized by extreme hypertriglyceridemia (>1000 mg/dL), recurrent pancreatitis, and lipoprotein lipase (LPL) deficiency. Mutations in the LMF1 gene, encoding a chaperone protein required for LPL maturation, can lead to combined lipase deficiency. This study reports a case of a 33-year-old Ecuadorian mestizo woman presenting with recurrent pancreatitis secondary to severe hypertriglyceridemia, in whom two LMF1 variants of uncertain significance (VUS) were identified. Methods: Whole-exome sequencing (WES) was performed on the patient and her asymptomatic son using next-generation sequencing (NGS). Data analysis included computational pathogenicity predictors (REVEL, PolyPhen, SIFT, MutationTaster, etc.). Two LMF1 variants-c.1142C>T (p.Pro381Leu) and c.897G>A (p.Gln299Gln)-were identified. Their pathogenic potential was assessed based on allele frequency (gnomAD), bioinformatics predictions, and ACMG criteria. Results: Both variants were classified as VUS, with c.897G>A predicted to affect splicing, potentially leading to loss of function. The c.1142C>T (p.Pro381Leu) variant, despite its low frequency, remains unclassified due to insufficient evidence. The patient's son carried one variant but was asymptomatic. The patient's phenotype suggested an intermediate form between monogenic and polygenic hypertriglyceridemia. Conclusions: This is a new Ecuadorian report of LMF1-related hypertriglyceridemia, highlighting the need for functional studies to confirm pathogenicity. Given the classification of both variants as VUS, further research is required to elucidate their clinical significance. This case underscores the necessity of a combined genetic and biochemical approach for diagnosing and managing severe hypertriglyceridemia
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