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Institution

French Institute of Health and Medical Research

GovernmentParis, France
About: French Institute of Health and Medical Research is a government organization based out in Paris, France. It is known for research contribution in the topics: Population & Receptor. The organization has 109367 authors who have published 174236 publications receiving 8365503 citations.


Papers
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Journal ArticleDOI
TL;DR: In this paper, a comprehensive review of the relationship between sleep and depression is presented, focusing on the relationships between sleep disturbance and depression, and focusing on sleep-related hypotheses explaining the pathophysiology of depression.
Abstract: Background Of all the psychiatric disorders associated with insomnia, depression is the most common. It has been estimated that 90% of patients with depression complain about sleep quality. Since the first reports of short rapid eye movement (REM) latency in depressed patients and of the effect of sleep deprivation on depression in the 1970s, numerous sleep studies have provided extensive observations and theoretical hypotheses concerning the etiology and pathophysiology of depression. The aim of this review is to summarize knowledge regarding the relationships between sleep and depression. Data sources and selection MEDLINE and PsycINFO searches of the literature published in English or French between 1964 and 2005 that examined the relationships between sleep disturbance and depression were conducted. Search terms used were depression, depressive disorder, affective disorder, mood disorders, seasonal affective disorder, sleep, sleep disorders, insomnia, REM, polysomnography, sleep deprivation, electroencephalography, PET, SPECT, and fMRI. Data synthesis Two hundred five papers were identified and selected and then integrated into the following categories: sleep architecture, antidepressive therapies, age- and gender-associated differences, functional imaging results, and sleep-related hypotheses explaining the pathophysiology of depression. Conclusion Numerous studies provide findings indicating the remarkable relationship between sleep alterations and depression. Although the existing hypotheses are not likely to explain all aspects of the sleep alterations in depression, each may be worth being maintained for refinements of pathophysiologic models of depression as new data accumulate. Further research taking into account the heterogeneity of depressive disorder and linking the different areas of research is needed to develop more comprehensive theoretical models and new therapies for depression.

886 citations

Journal ArticleDOI
27 Mar 2008-Nature
TL;DR: Application of this method to liver and adipose gene expression data generated from a segregating mouse population results in the identification of a macrophage-enriched network supported as having a causal relationship with disease traits associated with metabolic syndrome.
Abstract: Identifying variations in DNA that increase susceptibility to disease is one of the primary aims of genetic studies using a forward genetics approach. However, identification of disease-susceptibility genes by means of such studies provides limited functional information on how genes lead to disease. In fact, in most cases there is an absence of functional information altogether, preventing a definitive identification of the susceptibility gene or genes. Here we develop an alternative to the classic forward genetics approach for dissecting complex disease traits where, instead of identifying susceptibility genes directly affected by variations in DNA, we identify gene networks that are perturbed by susceptibility loci and that in turn lead to disease. Application of this method to liver and adipose gene expression data generated from a segregating mouse population results in the identification of a macrophage-enriched network supported as having a causal relationship with disease traits associated with metabolic syndrome. Three genes in this network, lipoprotein lipase (Lpl), lactamase β (Lactb) and protein phosphatase 1-like (Ppm1l), are validated as previously unknown obesity genes, strengthening the association between this network and metabolic disease traits. Our analysis provides direct experimental support that complex traits such as obesity are emergent properties of molecular networks that are modulated by complex genetic loci and environmental factors. Complex human diseases result from the interplay of many genetic and environmental factors. To build up a picture of the factors contributing to one such disease, obesity, gene expression was evaluated as a quantitative trait in blood and adipose tissue samples from hundreds of Icelandic subjects aged 18 to 85. The results reveal a tendency to certain characteristic patterns of gene activation in the fatty tissues — though to a much lesser extent in the blood — of people with a higher body mass index. A transcriptional network constructed from the adipose tissue data has significant overlap with a network based on mouse adipose tissue data. Experimental support for the idea that complex diseases are emergent properties of molecular networks influenced by genes and environment comes from a study in mice. Mice were examined for disturbances in genetic expression networks that correlate with metabolic traits associated with obesity, diabetes and atherosclerosis. Three genes — Lpl, Lactb and Ppm1l — were identified as previously unknown obesity genes. This 'molecular network' approach raises the prospect that therapies might be directed at whole 'disease networks', rather than at one or two specific genes. Standard approaches to identify the genetic changes that lead to disease are reversed by examination of genetic networks for perturbations that are associated with disease states, and following up candidate genes from there. This begins with three genes in mice that lead to obesity when mutated, demonstrating that complex genetic–environmental traits can be dissected with this new approach.

886 citations

Journal ArticleDOI
01 Apr 1986-Nature
TL;DR: Evidence is presented that a change in the position of a visual target during a reaching movement can modify the trajectory even when vision of the hand is prevented, and the mechanisms that maintain the apparent stability of a target in space are dissociable from those that mediate the visuomotor outputdirected at that target.
Abstract: When we reach towards an object that suddenly appears in our peripheral visual field, not only does our arm extend towards the object, but our eyes, head and body also move in such a way that the image of the object falls on the fovea. Popular models of how reaching movements are programmed1,2 have argued that while the first part of the limb movement is ballistic, subsequent corrections to the trajectory are made on the basis of dynamic feedback about the relative positions of the hand and the target provided by central vision. These models have assumed that the adjustments are dependent on seeing the hand moving with respect to the target. Here we present evidence that a change in the position of a visual target during a reaching movement can modify the trajectory even when vision of the hand is prevented. Moreover, these dynamic corrections to the trajectory of the moving limb occur without the subject perceiving the change in target location. These findings demonstrate that (1) visual feedback about the relative position of the hand and target is not necessary for visually driven corrections in reaching to occur, and (2) the mechanisms that maintain the apparent stability of a target in space are dissociable from those that mediate the visuomotor outputdirected at that target.

886 citations

Journal ArticleDOI
TL;DR: A new light-measurement strategy taking account of the complex photoreceptive inputs to these non-visual responses is proposed for use by researchers, and simple suggestions for artificial/architectural lighting are provided for regulatory authorities, lighting manufacturers, designers, and engineers.

886 citations

Journal ArticleDOI
01 May 1987-Nature
TL;DR: New drugs selective for histamine H3-receptors can be used to establish that these receptors are involved in the feedback control of histamine synthesis and release, and to demonstrate their distribution in the brain and peripheral tissues.
Abstract: New drugs selective for histamine H3-receptors can be used to establish that these receptors are involved in the feedback control of histamine synthesis and release, and to demonstrate their distribution in the brain and peripheral tissues These drugs provide new tools for affecting physiological and possibly pathological conditions in which histamine is involved

882 citations


Authors

Showing all 109539 results

NameH-indexPapersCitations
Guido Kroemer2361404246571
Pierre Chambon211884161565
Peer Bork206697245427
Ronald M. Evans199708166722
Raymond J. Dolan196919138540
Matthew Meyerson194553243726
Charles A. Dinarello1901058139668
Julie E. Buring186950132967
Tadamitsu Kishimoto1811067130860
Didier Raoult1733267153016
Giuseppe Remuzzi1721226160440
Zena Werb168473122629
Nahum Sonenberg167647104053
Philippe Froguel166820118816
Gordon J. Freeman164579105193
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202368
2022306
20217,549
20207,367
20196,969
20186,607