Pierre-and-Marie-Curie University

About: Pierre-and-Marie-Curie University is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Raman spectroscopy. The organization has 34448 authors who have published 56139 publications receiving 2392398 citations.

Global sea-air CO2 flux based on climatological surface ocean pCO2, and seasonal biological and temperature effects

Abstract: Based on about 940,000 measurements of surface-water pCO2 obtained since the International Geophysical Year of 1956–59, the climatological, monthly distribution of pCO2 in the global surface waters representing mean non-El Nino conditions has been obtained with a spatial resolution of 4°×5° for a reference year 1995. The monthly and annual net sea–air CO2 flux has been computed using the NCEP/NCAR 41-year mean monthly wind speeds. An annual net uptake flux of CO2 by the global oceans has been estimated to be 2.2 (+22% or ?19%) Pg C yr?1 using the (wind speed)2 dependence of the CO2 gas transfer velocity of Wanninkhof (J. Geophys. Res. 97 (1992) 7373). The errors associated with the wind-speed variation have been estimated using one standard deviation (about±2 m s?1) from the mean monthly wind speed observed over each 4°×5° pixel area of the global oceans. The new global uptake flux obtained with the Wanninkhof (wind speed)2 dependence is compared with those obtained previously using a smaller number of measurements, about 250,000 and 550,000, respectively, and are found to be consistent within±0.2 Pg C yr?1. This estimate for the global ocean uptake flux is consistent with the values of 2.0±0.6 Pg C yr?1 estimated on the basis of the observed changes in the atmospheric CO2 and oxygen concentrations during the 1990s (Nature 381 (1996) 218; Science 287 (2000) 2467). However, if the (wind speed)3 dependence of Wanninkhof and McGillis (Res. Lett. 26 (1999) 1889) is used instead, the annual ocean uptake as well as the sensitivity to wind-speed variability is increased by about 70%. A zone between 40° and 60° latitudes in both the northern and southern hemispheres is found to be a major sink for atmospheric CO2. In these areas, poleward-flowing warm waters meet and mix with the cold subpolar waters rich in nutrients. The pCO2 in the surface water is decreased by the cooling effect on warm waters and by the biological drawdown of pCO2 in subpolar waters. High wind speeds over these low pCO2 waters increase the CO2 uptake rate by the ocean waters. The pCO2 in surface waters of the global oceans varies seasonally over a wide range of about 60% above and below the current atmospheric pCO2 level of about 360 ?atm. A global map showing the seasonal amplitude of surface-water pCO2 is presented. The effect of biological utilization of CO2 is differentiated from that of seasonal temperature changes using seasonal temperature data. The seasonal amplitude of surface-water pCO2 in high-latitude waters located poleward of about 40° latitude and in the equatorial zone is dominated by the biology effect, whereas that in the temperate gyre regions is dominated by the temperature effect. These effects are about 6 months out of phase. Accordingly, along the boundaries between these two regimes, they tend to cancel each other, forming a zone of small pCO2 amplitude. In the oligotrophic waters of the northern and southern temperate gyres, the biology effect is about 35 ?atm on average. This is consistent with the biological export flux estimated by Laws et al. (Glob. Biogeochem. Cycles 14 (2000) 1231). Small areas such as the northwestern Arabian Sea and the eastern equatorial Pacific, where seasonal upwelling occurs, exhibit intense seasonal changes in pCO2 due to the biological drawdown of CO2.

A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer's disease

Abstract: There is increasing evidence that subjective cognitive decline (SCD) in individuals with unimpaired performance on cognitive tests may represent the first symptomatic manifestation of Alzheimer's disease (AD). The research on SCD in early AD, however, is limited by the absence of common standards. The working group of the Subjective Cognitive Decline Initiative (SCD-I) addressed this deficiency by reaching consensus on terminology and on a conceptual framework for research on SCD in AD. In this publication, research criteria for SCD in pre-mild cognitive impairment (MCI) are presented. In addition, a list of core features proposed for reporting in SCD studies is provided, which will enable comparability of research across different settings. Finally, a set of features is presented, which in accordance with current knowledge, increases the likelihood of the presence of preclinical AD in individuals with SCD. This list is referred to as SCD plus.

Genetic Determinants of Response to Clopidogrel and Cardiovascular Events

Abstract: Background Pharmacogenetic determinants of the response of patients to clopidogrel contribute to variability in the biologic antiplatelet activity of the drug. The effect of these determinants on clinical outcomes after an acute myocardial infarction is unknown. Methods We consecutively enrolled 2208 patients presenting with an acute myocardial infarction in a nationwide French registry and receiving clopidogrel therapy. We then assessed the relation of allelic variants of genes modulating clopidogrel absorption (ABCB1), metabolic activation (CYP3A5 and CYP2C19), and biologic activity (P2RY12 and ITGB3) to the risk of death from any cause, nonfatal stroke, or myocardial infarction during 1 year of follow-up. Results Death occurred in 225 patients, and nonfatal myocardial infarction or stroke in 94 patients, during the follow-up period. None of the selected single-nucleotide polymorphisms (SNPs) in CYP3A5, P2RY12, or ITGB3 were associated with a risk of an adverse outcome. Patients with two variant alleles of ABCB1 (TT at nucleotide 3435) had a higher rate of cardiovascular events at 1 year than those with the ABCB1 wild-type genotype (CC at nucleotide 3435) (15.5% vs. 10.7%; adjusted hazard ratio, 1.72; 95% confidence interval [CI], 1.20 to 2.47). Patients carrying any two CYP2C19 loss-offunction alleles (*2, *3, *4, or *5), had a higher event rate than patients with none (21.5% vs. 13.3%; adjusted hazard ratio, 1.98; 95% CI, 1.10 to 3.58). Among the 1535 patients who underwent percutaneous coronary intervention during hospitalization, the rate of cardiovascular events among patients with two CYP2C19 loss-of-function alleles was 3.58 times the rate among those with none (95% CI, 1.71 to 7.51). Conclusions Among patients with an acute myocardial infarction who were receiving clo pid ogrel, those carrying CYP2C19 loss-of-function alleles had a higher rate of subsequent cardiovascular events than those who were not. This effect was particularly marked among the patients undergoing percutaneous coronary intervention. (ClinicalTrials. gov number, NCT00673036.)

Genome evolution in yeasts

Abstract: Identifying the mechanisms of eukaryotic genome evolution by comparative genomics is often complicated by the multiplicity of events that have taken place throughout the history of individual lineages, leaving only distorted and superimposed traces in the genome of each living organism. The hemiascomycete yeasts, with their compact genomes, similar lifestyle and distinct sexual and physiological properties, provide a unique opportunity to explore such mechanisms. We present here the complete, assembled genome sequences of four yeast species, selected to represent a broad evolutionary range within a single eukaryotic phylum, that after analysis proved to be molecularly as diverse as the entire phylum of chordates. A total of approximately 24,200 novel genes were identified, the translation products of which were classified together with Saccharomyces cerevisiae proteins into about 4,700 families, forming the basis for interspecific comparisons. Analysis of chromosome maps and genome redundancies reveal that the different yeast lineages have evolved through a marked interplay between several distinct molecular mechanisms, including tandem gene repeat formation, segmental duplication, a massive genome duplication and extensive gene loss.