Institution
Paris Descartes University
Government•Paris, France•
About: Paris Descartes University is a government organization based out in Paris, France. It is known for research contribution in the topics: Population & Immune system. The organization has 20987 authors who have published 37456 publications receiving 1206222 citations. The organization is also known as: Université Paris V-Descartes & Université de Paris V.
Topics: Population, Immune system, Cancer, Transplantation, Pregnancy
Papers published on a yearly basis
Papers
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TL;DR: The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidance of pathogenic cell loss.
Abstract: Cells may die from accidental cell death (ACD) or regulated cell death (RCD). ACD is a biologically uncontrolled process, whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms. A growing number of novel non-apoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies. Here, we critically review the current state of the art regarding non-apoptotic types of RCD, including necroptosis, pyroptosis, ferroptosis, entotic cell death, netotic cell death, parthanatos, lysosome-dependent cell death, autophagy-dependent cell death, alkaliptosis and oxeiptosis. The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidance of pathogenic cell loss.
1,071 citations
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TL;DR: A new classification of CC into six molecular subtypes that arise through distinct biological pathways that improves the current disease stratification based on clinicopathological variables and common DNA markers is described.
Abstract: Background
Colon cancer (CC) pathological staging fails to accurately predict recurrence, and to date, no gene expression signature has proven reliable for prognosis stratification in clinical practice, perhaps because CC is a heterogeneous disease. The aim of this study was to establish a comprehensive molecular classification of CC based on mRNA expression profile analyses.
1,065 citations
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New York University1, Lunenfeld-Tanenbaum Research Institute2, Northwood University3, Ghent University Hospital4, Johns Hopkins University School of Medicine5, Brigham and Women's Hospital6, Paris Descartes University7, Cornell University8, University of Fribourg9, University of Cincinnati Academic Health Center10, Yale University11
TL;DR: The PI-RADS Steering Committee, using a consensus-based process, has recommended several modifications to PI- RADS v2, maintaining the framework of assigning scores to individual sequences and using these scores to derive an overall assessment category.
1,053 citations
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TL;DR: The clearance systems of the brain as they relate to proteins implicated in AD pathology are described, with the main focus on Aβ.
Abstract: Accumulation of toxic protein aggregates-amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles-is the pathological hallmark of Alzheimer disease (AD). Aβ accumulation has been hypothesized to result from an imbalance between Aβ production and clearance; indeed, Aβ clearance seems to be impaired in both early and late forms of AD. To develop efficient strategies to slow down or halt AD, it is critical to understand how Aβ is cleared from the brain. Extracellular Aβ deposits can be removed from the brain by various clearance systems, most importantly, transport across the blood-brain barrier. Findings from the past few years suggest that astroglial-mediated interstitial fluid (ISF) bulk flow, known as the glymphatic system, might contribute to a larger portion of extracellular Aβ (eAβ) clearance than previously thought. The meningeal lymphatic vessels, discovered in 2015, might provide another clearance route. Because these clearance systems act together to drive eAβ from the brain, any alteration to their function could contribute to AD. An understanding of Aβ clearance might provide strategies to reduce excess Aβ deposits and delay, or even prevent, disease onset. In this Review, we describe the clearance systems of the brain as they relate to proteins implicated in AD pathology, with the main focus on Aβ.
1,047 citations
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TL;DR: This article will review the mechanisms of activation of alternative, classical, and lectin pathways, the formation of C3 and C5 convertases, the action of anaphylatoxins, and the membrane-attack-complex, and discuss the importance of structure–function relationships.
Abstract: Complement is a complex innate immune surveillance system, playing a key role in defense against pathogens and in host homeostasis. The complement system is initiated by conformational changes in recognition molecular complexes upon sensing danger signals. The subsequent cascade of enzymatic reactions is tightly regulated to assure that complement is activated only at specific locations requiring defense against pathogens, thus avoiding host tissue damage. Here we discuss the recent advances describing the molecular and structural basis of activation and regulation of the complement pathways and their implication on physiology and pathology. This article will review the mechanisms of activation of alternative, classical and lectin pathways, the formation of C3 and C5 convertases, the action of anaphylatoxins and the membrane attack complex. We will also discuss the importance of structure-function relationships using the example of atypical hemolytic uremic syndrome. Lastly we will discuss the development and benefits of therapies using complement inhibitors.
1,042 citations
Authors
Showing all 21023 results
Name | H-index | Papers | Citations |
---|---|---|---|
Guido Kroemer | 236 | 1404 | 246571 |
Cyrus Cooper | 204 | 1869 | 206782 |
Jean-Laurent Casanova | 144 | 842 | 76173 |
Alain Fischer | 143 | 770 | 81680 |
Maxime Dougados | 134 | 1054 | 69979 |
Carlos López-Otín | 126 | 494 | 83933 |
Giuseppe Viale | 123 | 740 | 72799 |
Thierry Poynard | 119 | 668 | 64548 |
Lorenzo Galluzzi | 118 | 477 | 71436 |
Shahrokh F. Shariat | 118 | 1637 | 58900 |
Richard E. Tremblay | 116 | 685 | 45844 |
Olivier Hermine | 111 | 1026 | 43779 |
Yehezkel Ben-Ari | 110 | 459 | 44293 |
Loïc Guillevin | 108 | 800 | 51085 |
Gérard Socié | 107 | 920 | 44186 |