Institution
Université de Sherbrooke
Education•Sherbrooke, Quebec, Canada•
About: Université de Sherbrooke is a education organization based out in Sherbrooke, Quebec, Canada. It is known for research contribution in the topics: Population & Receptor. The organization has 14922 authors who have published 28783 publications receiving 792511 citations. The organization is also known as: Universite de Sherbrooke & Sherbrooke University.
Topics: Population, Receptor, Health care, Angiotensin II, Poison control
Papers published on a yearly basis
Papers
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TL;DR: A combined density functional theory (DFT)/time-dependent DFT study was conducted in order to understand the origin of the transitions in the absorption and emission spectra and to predict accurately emission energies for these complexes.
Abstract: The synthesis of a family of 4′-functionalized 5,5′-diaryl-2,2′-bipyridines (bpy*; 6a−6g) is reported. These ligands were reacted with the dimer [(ppy)2IrCl]2 (ppyH = 2-phenylpyridine) and afforded, after subsequent counterion exchange, a new series of luminescent cationic heteroleptic iridium(III) complexes, [(ppy)2Ir(bpy*)]PF6 (8a−8g). These complexes were characterized by electrochemical and spectroscopic methods. The crystal structures of two of these complexes (8a and 8g) are reported. All of the complexes except for 8c and 8f exhibit intense and long-lived emission in both 2-MeTHF and ACN at 77 K and room temperature. The origin of this emission has been assigned by computational modeling to be an admixture of ligand-to-ligand charge-transfer [3LLCT; π(ppy) → π*(bpy*)] and metal-to-ligand charge-transfer [3MLCT; dπ(Ir) → π*(bpy*)] excited states that are primarily composed of the former. The luminescent properties for 8a−8c are dependent upon the functionalization at the 4′ position of the aryl subs...
147 citations
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TL;DR: It is observed that TGF-β1 increased susceptibility of the human alveolar epithelial cell line A549 to H2O2-mediated cytotoxicity, and decreased the activities of the antioxidant enzymes glutathione reductase and catalase by 31%, and markedly decreased GSH content in A549 cells.
Abstract: Glutathione (GSH) is an essential antioxidant tripeptide that protects mammalian cells against oxidants and xenobiotics. Patients with fibrotic lung disorders have very low levels of GSH in their alveolar epithelial lining fluid (ELF), whereas transforming growth factor (TGF)-beta is overexpressed in their alveolar epithelial cells. We observed that TGF-beta1 increased susceptibility of the human alveolar epithelial cell line A549 to H2O2-mediated cytotoxicity (P < 0.05), decreased the activities of the antioxidant enzymes glutathione reductase and catalase by 31%, and markedly decreased GSH content in A549 cells (P < 0.01). GSH depletion was associated with an equivalent decrease in the activity of the rate-limiting enzyme in GSH synthesis, gamma-glutamylcysteine synthetase (gamma-GCS) (P < 0.01). Western blot analysis confirmed that the loss of gamma-GCS activity was associated with a marked decrease in gamma-GCS heavy subunit (gamma-GCShs) protein. TGF-beta1 suppressed the steady-state level of messenger RNA (mRNA) for the gamma-GCShs gene, with a maximal effect at 24 h. The half-life of gamma-GCShs mRNA was not affected by TGF-beta1, but transcription of the gene was downregulated as determined with nuclear run-on assays. Our findings indicate for the first time that TGF-beta1 is a potent inhibitor of GSH synthesis in human lung epithelial cells, and that the inhibition is mediated, at least in part, by a transcriptional effect on the gene encoding gamma-GCShs. Regulation of gamma-GCShs gene expression by TGF-beta1 is likely to play an important role in lower respiratory tract GSH homeostasis, and may represent a novel target for therapeutic efforts in lung fibrosis.
147 citations
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TL;DR: Evidence of roles for mammalian Rad9 in telomere stability and HR repair as a mechanism for promoting cell survival after ionizing radiation (IR) exposure is provided.
Abstract: The protein products of several rad checkpoint genes of Schizosaccharomyces pombe (rad1+, rad3+, rad9+, rad17+, rad26+, and hus1+) play crucial roles in sensing changes in DNA structure, and several function in the maintenance of telomeres. When the mammalian homologue of S. pombe Rad9 was inactivated, increases in chromosome end-to-end associations and frequency of telomere loss were observed. This telomere instability correlated with enhanced S- and G2-phase-specific cell killing, delayed kinetics of γ-H2AX focus appearance and disappearance, and reduced chromosomal repair after ionizing radiation (IR) exposure, suggesting that Rad9 plays a role in cell cycle phase-specific DNA damage repair. Furthermore, mammalian Rad9 interacted with Rad51, and inactivation of mammalian Rad9 also resulted in decreased homologous recombinational (HR) repair, which occurs predominantly in the S and G2 phases of the cell cycle. Together, these findings provide evidence of roles for mammalian Rad9 in telomere stability and HR repair as a mechanism for promoting cell survival after IR exposure.
147 citations
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Royal Devon and Exeter Hospital1, University of Queensland2, Queen Mary University of London3, University of Exeter4, Northwestern University5, University of Oxford6, Wellcome Trust Centre for Human Genetics7, Statens Serum Institut8, Norwegian Institute of Public Health9, University of Bristol10, Erasmus University Rotterdam11, Children's Hospital of Philadelphia12, University of Copenhagen13, Copenhagen University Hospital14, University of Oulu15, St Thomas' Hospital16, Boston University17, QIMR Berghofer Medical Research Institute18, VU University Amsterdam19, VU University Medical Center20, Centre Hospitalier Universitaire de Sherbrooke21, University of Southampton22, Pompeu Fabra University23, University of Western Australia24, Newcastle University25, Cincinnati Children's Hospital Medical Center26, March of Dimes27, UCL Institute of Child Health28, Université de Sherbrooke29, University of Pennsylvania30, University of Helsinki31, University of Bergen32, University of Potsdam33, Jinan University34, University Hospital Southampton NHS Foundation Trust35, University of Ferrara36, University of Iowa37, Haukeland University Hospital38, University of Southern Denmark39, Charité40, Health Protection Agency41, Sahlgrenska University Hospital42, University of Crete43, Stanford University44, National Institute for Health Research45, Harvard University46, University of South Australia47
TL;DR: The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth.
Abstract: Genome-wide association studies (GWAS) of birth weight have focused on fetal genetics, while relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86,577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5x10-8. In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.
147 citations
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TL;DR: In this article, the contextuality of two-level states with real density matrices is shown to be necessary for quantum computation. But it is not shown that rebits can be used as well as qubits.
Abstract: Quantum computation commonly relies on qubits, but rebits---states with real density matrices---can be used as well. Researchers show how the contextuality of two-level states is necessary for quantum computation.
147 citations
Authors
Showing all 15051 results
Name | H-index | Papers | Citations |
---|---|---|---|
Masashi Yanagisawa | 130 | 524 | 83631 |
Joseph V. Bonventre | 126 | 596 | 61009 |
Jeffrey L. Benovic | 99 | 264 | 30041 |
Alessio Fasano | 96 | 478 | 34580 |
Graham Pawelec | 89 | 572 | 27373 |
Simon C. Robson | 88 | 552 | 29808 |
Paul B. Corkum | 88 | 576 | 37200 |
Mario Leclerc | 88 | 374 | 35961 |
Stephen M. Collins | 86 | 320 | 25646 |
Ed Harlow | 86 | 190 | 61008 |
William D. Fraser | 85 | 827 | 30155 |
Jean Cadet | 83 | 372 | 24000 |
Vincent Giguère | 82 | 227 | 27481 |
Robert Gurny | 81 | 396 | 28391 |
Jean-Michel Gaillard | 81 | 410 | 26780 |