Institution
University of Bordeaux
Education•Bordeaux, France•
About: University of Bordeaux is a education organization based out in Bordeaux, France. It is known for research contribution in the topics: Population & Laser. The organization has 28811 authors who have published 55536 publications receiving 1619635 citations. The organization is also known as: UB.
Topics: Population, Laser, Raman spectroscopy, Polymerization, Crystal structure
Papers published on a yearly basis
Papers
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TL;DR: A change of strategy in the modulation of autophagy might hold promise for future disease-modifying therapies for patients with neurodegenerative disorders.
Abstract: Cells rely on surveillance systems such as autophagy to handle protein alterations and organelle damage. Dysfunctional autophagy, an evolutionarily conserved cellular mechanism for degradation of intracellular components in lysosomes, frequently leads to neurodegeneration. The neuroprotective effect of autophagy stems from its ability to eliminate pathogenic forms of proteins such as α-synuclein or tau. However, the same pathogenic proteins often affect different types and steps of the autophagic process. Furthermore, genetic studies have shown that some proteins related to neurodegeneration, such as huntingtin, participate in autophagy as one of their physiological functions. This complex interplay between autophagy and neurodegeneration suggests that targeting autophagy as a whole might have limited applicability in neurodegenerative diseases, and that future efforts should focus instead on targeting specific types and steps of the autophagic process. This change of strategy in the modulation of autophagy might hold promise for future disease-modifying therapies for patients with neurodegenerative disorders.
230 citations
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TL;DR: These observations of lithium are believed to be the first by electron microscopy, and that they show promise for direct visualization of the ordering of lithium and vacancies in transition metal oxides.
Abstract: LiCoO2 is the most common lithium storage material for lithium rechargeable batteries, used widely to power portable electronic devices such as laptop computers. Lithium arrangements in the CoO2 framework have a profound effect on the structural stability and electrochemical properties of LixCoO2 (0 < x < 1), however, probing lithium ions has been difficult using traditional X-ray and neutron diffraction techniques. Here we have succeeded in simultaneously resolving columns of cobalt, oxygen, and lithium atoms in layered LiCoO2 battery material using experimental focal series of LiCoO2 images obtained at sub-Angstrom resolution in a mid-voltage transmission electron microscope. Lithium atoms are the smallest and lightest metal atoms, and scatter electrons only very weakly. We believe our observations of lithium to be the first by electron microscopy, and that they show promise to direct visualization of the ordering of lithium and vacancy in LixCoO2.
230 citations
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TL;DR: It is concluded that assessment of the C3d-binding capacity of DSA at the time of AMR diagnosis allows for identification of patients at risk for allograft loss.
Abstract: Antibody-mediated rejection (AMR) is a major cause of kidney graft loss, yet assessment of individual risk at diagnosis is impeded by the lack of a reliable prognosis assay. Here, we tested whether the capacity of anti-HLA antibodies to bind complement components allows accurate risk stratification at the time of AMR diagnosis. Among 938 kidney transplant recipients for whom a graft biopsy was performed between 2004 and 2012 at the Lyon University Hospitals, 69 fulfilled the diagnosis criteria for AMR and were enrolled. Sera banked at the time of the biopsy were screened for the presence of donor-specific anti-HLA antibodies (DSAs) and their ability to bind C1q and C3d using flow bead assays. In contrast with C4d graft deposition, the presence of C3d-binding DSA was associated with a higher risk of graft loss ( P P =0.06). The prognostic value of a C3d-binding assay was further confirmed in an independent cohort of 39 patients with AMR ( P =0.04). Patients with C3d-binding antibodies had worse eGFR and higher DSA mean fluorescence intensity. In a multivariate analysis, only eGFR 2 (hazard ratio [HR], 3.56; 95% confidence interval [CI], 1.46 to 8.70; P =0.005) and the presence of circulating C3d-binding DSA (HR, 2.80; 95% CI, 1.12 to 6.95; P =0.03) were independent predictors for allograft loss at AMR diagnosis. We conclude that assessment of the C3d-binding capacity of DSA at the time of AMR diagnosis allows for identification of patients at risk for allograft loss.
229 citations
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TL;DR: The R package lcmm as mentioned in this paper provides a series of functions to estimate statistical models based on linear mixed model theory, including the estimation of mixed models and latent class mixed models for Gaussian longitudinal outcomes.
Abstract: The R package lcmm provides a series of functions to estimate statistical models based on linear mixed model theory. It includes the estimation of mixed models and latent class mixed models for Gaussian longitudinal outcomes (hlme), curvilinear and ordinal univariate longitudinal outcomes (lcmm) and curvilinear multivariate outcomes (multlcmm), as well as joint latent class mixed models (Jointlcmm) for a (Gaussian or curvilinear) longitudinal outcome and a time-to-event that can be possibly left-truncated right-censored and defined in a competing setting. Maximum likelihood esimators are obtained using a modified Marquardt algorithm with strict convergence criteria based on the parameters and likelihood stability, and on the negativity of the second derivatives. The package also provides various post-fit functions including goodness-of-fit analyses, classification, plots, predicted trajectories, individual dynamic prediction of the event and predictive accuracy assessment. This paper constitutes a companion paper to the package by introducing each family of models, the estimation technique, some implementation details and giving examples through a dataset on cognitive aging.
229 citations
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University of Helsinki1, Aalto University2, Harvard University3, Broad Institute4, Queen's University Belfast5, University College Dublin6, University of Miami7, University of Oulu8, University of Toronto9, University of Dundee10, Eastern Michigan University11, University of Michigan12, National Institute for Health and Welfare13, Karolinska Institutet14, Aintree University Hospitals NHS Foundation Trust15, Swansea University16, University of Copenhagen17, Aarhus University18, Novo Nordisk19, University of Paris20, University of Liège21, University of Bordeaux22, Vita-Salute San Raffaele University23, Umeå University24, University of Bucharest25, University of Medicine and Pharmacy of Craiova26, Carol Davila University of Medicine and Pharmacy27, National Institutes of Health28, University of Poitiers29, French Institute of Health and Medical Research30, The Heart Research Institute31, Belfast Health and Social Care Trust32
TL;DR: A meta-analysis of genome-wide association studies of T1D DN revealed association of two SNPs with ESRD in the AFF3 gene and an intergenic SNP on chromosome 15q26 between the genes RGMA and MCTP2, which represent new signals in the pathogenesis of DN.
Abstract: Diabetic kidney disease, or diabetic nephropathy (DN), is a major complication of diabetes and the leading cause of end-stage renal disease (ESRD) that requires dialysis treatment or kidney transplantation. In addition to the decrease in the quality of life, DN accounts for a large proportion of the excess mortality associated with type 1 diabetes (T1D). Whereas the degree of glycemia plays a pivotal role in DN, a subset of individuals with poorly controlled T1D do not develop DN. Furthermore, strong familial aggregation supports genetic susceptibility to DN. However, the genes and the molecular mechanisms behind the disease remain poorly understood, and current therapeutic strategies rarely result in reversal of DN. In the GEnetics of Nephropathy: an International Effort (GENIE) consortium, we have undertaken a meta-analysis of genomewide association studies (GWAS) of T1D DN comprising similar to 2.4 million single nucleotide polymorphisms (SNPs) imputed in 6,691 individuals. After additional genotyping of 41 top ranked SNPs representing 24 independent signals in 5,873 individuals, combined meta-analysis revealed association of two SNPs with ESRD: rs7583877 in the AFF3 gene (P = 1.2 x 10(-8)) and an intergenic SNP on chromosome 15q26 between the genes RGMA and MCTP2, rs12437854 (P = 2.0 x 10(-9)). Functional data suggest that AFF3 influences renal tubule fibrosis via the transforming growth factor-beta (TGF-beta 1) pathway. The strongest association with DN as a primary phenotype was seen for an intronic SNP in the ERBB4 gene (rs7588550, P = 2.1 x 10(-7)), a gene with type 2 diabetes DN differential expression and in the same intron as a variant with cis-eQTL expression of ERBB4. All these detected associations represent new signals in the pathogenesis of DN.
229 citations
Authors
Showing all 28995 results
Name | H-index | Papers | Citations |
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Nicholas G. Martin | 192 | 1770 | 161952 |
George F. Koob | 171 | 935 | 112521 |
Daniel J. Jacob | 162 | 656 | 76530 |
Arthur W. Toga | 159 | 1184 | 109343 |
James M. Tour | 143 | 859 | 91364 |
Floyd E. Bloom | 139 | 616 | 72641 |
Herbert Y. Meltzer | 137 | 1148 | 81371 |
Jean-Marie Tarascon | 136 | 853 | 137673 |
Stanley Nattel | 132 | 778 | 65700 |
Michel Haïssaguerre | 117 | 757 | 62284 |
Liquan Chen | 111 | 689 | 44229 |
Marion Leboyer | 110 | 773 | 50767 |
Jean-François Dartigues | 106 | 631 | 46682 |
Alexa S. Beiser | 106 | 366 | 47457 |
Robert Dantzer | 105 | 497 | 46554 |