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Institution

Paul Sabatier University

EducationToulouse, France
About: Paul Sabatier University is a education organization based out in Toulouse, France. It is known for research contribution in the topics: Population & Adipose tissue. The organization has 15431 authors who have published 23386 publications receiving 858364 citations.


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Journal ArticleDOI
TL;DR: A finite volume method based on the integration of the Laplace equation on both the cells of a primal almost arbitrary two-dimensional mesh and those of a dual mesh obtained by joining the centers of the cells, generally called "diamond-cells", of a third mesh is presented.
Abstract: We present a finite volume method based on the integration of the Laplace equation on both the cells of a primal almost arbitrary two-dimensional mesh and those of a dual mesh obtained by joining the centers of the cells of the primal mesh. The key ingredient is the definition of discrete gradient and divergence operators verifying a discrete Green formula. This method generalizes an existing finite volume method that requires "Voronoi-type" meshes. We show the equivalence of this finite volume method with a non-conforming finite element method with basis functions being P 1 on the cells, generally called "diamond-cells", of a third mesh. Under geometrical conditions on these diamond- cells, we prove a first-order convergence both in the H 1 norm and in the L 2 norm. Superconvergence results are obtained on certain types of homothetically refined grids. Finally, numerical experiments confirm these results and also show second-order convergence in the L 2 norm on general grids. They also indicate that this method performs particularly well for the approximation of the gradient of the solution, and may be used on degenerating triangular grids. An example of application on non- conforming locally refined grids is given.

231 citations

Journal ArticleDOI
TL;DR: Both animal and human epidemiological studies support the idea that air pollutants cause defects during gametogenesis leading to a drop in reproductive capacities in exposed populations.
Abstract: Air pollution is involved in many pathologies. These pollutants act through several mechanisms that can affect numerous physiological functions, including reproduction: as endocrine disruptors or reactive oxygen species inducers, and through the formation of DNA adducts and/or epigenetic modifications. We conducted a systematic review of the published literature on the impact of air pollution on reproductive function. Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included (1) ovary or follicle or oocyte or testis or testicular or sperm or spermatozoa or fertility or infertility and (2) air quality or O3 or NO2 or PM2.5 or diesel or SO2 or traffic or PM10 or air pollution or air pollutants. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the search terms and published in English. We have excluded articles whose results did not concern fertility or gamete function and those focused on cancer or allergy. We have also excluded genetic, auto-immune or iatrogenic causes of reduced reproduction function from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on fertility and the molecular pathways involved. Both animal and human epidemiological studies support the idea that air pollutants cause defects during gametogenesis leading to a drop in reproductive capacities in exposed populations. Air quality has an impact on overall health as well as on the reproductive function, so increased awareness of environmental protection issues is needed among the general public and the authorities.

231 citations

Journal ArticleDOI
TL;DR: In this paper, the authors investigated the electrochemical behavior of Ti3C2 MXene in 1M solution of 1-ethly-3-methylimidazolium bis- (trifluoromethylsulfonyl) -imide (EMITFSI) in acetonitrile and two other common organic electrolytes.

231 citations

Journal ArticleDOI
TL;DR: It is found that LARP1 associates with the mTOR complex 1 (mTORC1) and is required for global protein synthesis as well as cell growth and proliferation, and implicate Larp1 as an important regulator of cell Growth and proliferation.
Abstract: The mammalian target of rapamycin (mTOR) promotes cell growth and proliferation by promoting mRNA translation and increasing the protein synthetic capacity of the cell. Although mTOR globally promotes translation by regulating the mRNA 5′ cap-binding protein eIF4E (eukaryotic initiation factor 4E), it also preferentially regulates the translation of certain classes of mRNA via unclear mechanisms. To help fill this gap in knowledge, we performed a quantitative proteomic screen to identify proteins that associate with the mRNA 5′ cap in an mTOR-dependent manner. Using this approach, we identified many potential regulatory factors, including the putative RNA-binding protein LARP1 (La-related protein 1). Our results indicate that LARP1 associates with actively translating ribosomes via PABP and that LARP1 stimulates the translation of mRNAs containing a 5′ terminal oligopyrimidine (TOP) motif, encoding for components of the translational machinery. We found that LARP1 associates with the mTOR complex 1 (mTORC1) and is required for global protein synthesis as well as cell growth and proliferation. Together, these data reveal important molecular mechanisms involved in TOP mRNA translation and implicate LARP1 as an important regulator of cell growth and proliferation.

231 citations

Journal ArticleDOI
TL;DR: The differences in the lipolytic responses to epinephrine in adipocytes from different sites are linked to a variablealpha‐2 inhibiting effect (and alpha‐2 site number) rather than to a modified beta driven increase in lipolysis initiated by the physiological amine.
Abstract: Investigations have been carried out to explain the heterogeneity of response to catecholamines of human fat cells from various deposits. Adipocytes from two subcutaneous sites (abdominal and femoral) were studied concomitantly in women while omental fat cells were taken from another group of patients undergoing abdominal surgery. Alpha-2 and beta sites were identified in fat-cell membranes with [3H]yohimbine and [3H]dihydroalprenolol, respectively. Lipolytic responses were tested with isoproterenol (beta agonist), clonidine (alpha-2 agonist) and epinephrine. There are clear differences in the relative number of beta and alpha-2 sites according to the origin of the fat deposit; beta sites are less numerous than alpha-2 sites in subcutaneous fat cells of both regions (alpha-2:beta sites are in a ratio of 3 +/- 0.4:2 +/- 0.4). However, in membranes of omental fat cells, beta sites are at least as numerous as alpha-2 sites (ratio 0.9 +/- 0.2). Epinephrine always has a higher affinity for alpha-2 sites than for beta sites in the subcutaneous and omental deposits. In lipolysis studies, epinephrine, in the absence of adenosine in the incubation medium, initiated an anti-lipolytic effect in femoral fat cells and promoted inhibition of lipolysis at lower concentrations in abdominal subcutaneous fat cells, the effect being reversed at higher doses; epinephrine, however, was always lipolytic in omental adipocytes. There was no striking differences in the sensitivity to isoproterenol in the various deposits. Clonidine had a higher affinity for alpha-2 sites in femoral fat cells and was equipotent in the omental and abdominal ones. Thus, the differences in the lipolytic responses to epinephrine in adipocytes from different sites are linked to a variable alpha-2 inhibiting effect (and alpha-2 site number) rather than to a modified beta driven increase in lipolysis initiated by the physiological amine.

231 citations


Authors

Showing all 15486 results

NameH-indexPapersCitations
Yury Gogotsi171956144520
Tobin J. Marks1591621111604
L. Montier13840397094
Jean-Paul Kneib13880589287
Olivier Forni13754895819
J. Aumont13129995006
Julian I. Schroeder12031550323
Bruno Vellas118101170667
Christopher G. Goetz11665159510
Didier Dubois11374254741
Alain Dufresne11135845904
Henri Prade10891754583
Louis Bernatchez10656835682
Walter Wahli10536549372
Patrice D. Cani10037049523
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202332
202293
2021759
2020753
2019728
2018622