Institution
Collège de France
Education•Paris, France•
About: Collège de France is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Receptor. The organization has 6541 authors who have published 11983 publications receiving 648742 citations. The organization is also known as: College de France.
Topics: Population, Receptor, Dopamine, Dopaminergic, Neural crest
Papers published on a yearly basis
Papers
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TL;DR: In this article, the authors discuss the problem of the relation between reason and history in the context of the workshop, and propose the notion of workshop as a way of understanding and knowing a practice.
Abstract: I would like first to analyze what, borrowing an expression of Austin, I will call the "scholastic point of view," the point of view of the skhole, that is, the academic vision. What does the fact of thinking within a scholastic space, an academic space, imply? What does our thinking owe to the fact that it is produced within an academic space? Isn't our deepest unconscious related to the fact that we think in such an academic space? This would be the first question. From there, I will try to give some indications on the particular problem (it was present throughout the discussion, particularly around the notion of mimesis but also, obviously, this morning, in the presentation of Jacques Bouveresse [1989]) that the understanding of practice poses and which makes for such a difficult task for the human sciences. Does the very ambition of understanding practice make any sense? And what is involved in understanding and knowing a practice with an approach that is intrinsically theoretical? Then, if time allows, I would like to raise the issue that has been up in the air since the birth of the social sciences: the problem of the relations between reason and history. Isn't sociology, which apparently undermines the foundations of reason and thereby its own foundations, capable of producing instruments for forging a rational discourse and even of offering techniques for waging a politics of reason, a Realpolitik of reason? The scope of the problematic I adumbrate here is disproportionate to the time at my disposal. This is why I welcome the idea of "workshop," which fits perfectly what I want to do and can do today.
232 citations
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TL;DR: The data suggest a modest contribution of the CYP11B2 gene to essential hypertension in hypertensive patients and normotensive individuals.
Abstract: —Anomalies in either of the tightly linked genes encoding the enzymes CYP11B1 (11β-hydroxylase) or CYP11B2 (aldosterone synthase) can lead to important changes in arterial pressure and are responsible for several monogenically inherited forms of hypertension. Mutations in these genes or their regulatory regions could thus contribute to genetic variation in susceptibility to essential hypertension. To test this hypothesis, we performed 2 complementary studies of the CYP11B1 / CYP11B2 locus in essential hypertension. After characterizing a DNA contig containing the CYP11B1 gene and mapping the gene in the Centre d’Etudes du Polymorphisme Humain reference panel of families, we performed a linkage study with 292 hypertensive sibling pairs and a highly informative microsatellite marker near CYP11B1 . We also analyzed the association of 2 frequent biallelic polymorphisms of the CYP11B2 gene, 1 in the promoter at position −344 (−344C/T) and the other, a common gene conversion in intron 2, with hypertension in 380 hypertensive patients and 293 normotensive individuals. Statistical analyses did not show significant linkage of the CYP11B1 microsatellite marker to hypertension. No positive association with hypertension was found with the gene conversion in intron 2, but a positive association with hypertension was found with the −344T allele. The hypertensive and normotensive samples differed significantly in both genotype ( P =0.023) and allele frequencies ( P =0.010). Our data suggest a modest contribution of the CYP11B2 gene to essential hypertension.
231 citations
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TL;DR: It is concluded that the presence of FN is required for cell migration during gastrulation, and that the formation of a neural plate is not prevented when late gastrula stage embryos are treated with antibodies to FN.
Abstract: Gastrulation and formation of the neural plate are major steps in early vertebrate embryogenesis. Although morphogenetic movements leading to the formation of the primary germ layers have been extensively described1–3, the mechanisms governing migration of mesodermal cells and their interactions with ectoderm remain ill-defined. A large body of evidence indicates that fibronectin (FN), a high molecular weight cell-surface-associated glycoprotein, promotes cell adhesion and cell migration throughout embryogenesis4–6. FN has been detected at an early blastula stage in Pleurodeles waltlii7. We now show that FN is a component of a dense fibrillar matrix underlying the blastocoel roof; in contrast, the exterior surface of the embryo is devoid of FN. Microsurgical inversion of part of the blastocoel roof does not prevent mesodermal cell migration except at the site of inversion where no FN matrix is available. Perturbation experiments using antibodies to FN demonstrate that the invagination of presumptive mesodermal cells does not occur when the monovalent antibodies are injected before or at the onset of gastrulation; on the other hand, the formation of a neural plate is not prevented when late gastrula stage embryos are treated with antibodies to FN. We conclude that the presence of FN is required for cell migration during gastrulation.
231 citations
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TL;DR: In this article, a high precision measurement at 15m from a 2800 MWth reactor in which 300 000 events of electron antineutrino interactions with proton have been detected using an integral method was reported.
231 citations
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TL;DR: The results suggest that the high-affinity system for the transport of choline is present in cholinergic synaptosomes and plays an important role in sustaining and perhaps regulating the synthesis of the transmitter.
Abstract: Hemicholinium (HC-3), a neuromuscular blocking agent which inhibits the synthesis and the release of acetylcholine (ACh) was investigated for its effects both on [14C]ACh synthesis from [2-14C]pyruvate or [6-14C]glucose and on [3H]choline uptake in purified rat striatal synaptosomes. The synthesis of the transmitter was reduced to 15% of control by 1 µM HC-3 in the presence of eserine (170 µM). The drug produced half-maximal inhibition at 0.06 µM; this effect was totally reversed by 30 µM choline. Choline concentrations as low as 10 µM stimulated significantly the synthesis of [14C]ACh in a diluted suspension of synaptosomes. The existence of a high-affinity uptake system for choline, recently observed by Yamamura and Snyder, was confirmed in our preparation: its Km was found to be 3.5 µM. Eserine (170 µM) produced only 10% inhibition of the uptake process in the presence of 1 µM choline. HC-3 was found to be a purely competitive inhibitor of the choline high-affinity uptake (Ki = 25 nM). A very good correlation was found between the inhibitory effects of HC-3 on [14C]ACh synthesis and on [3H]choline high-affinity uptake. The results suggest that the high-affinity system for the transport of choline is present in cholinergic synaptosomes and plays an important role in sustaining and perhaps regulating the synthesis of the transmitter.
230 citations
Authors
Showing all 6597 results
Name | H-index | Papers | Citations |
---|---|---|---|
Pierre Chambon | 211 | 884 | 161565 |
Irving L. Weissman | 201 | 1141 | 172504 |
David R. Williams | 178 | 2034 | 138789 |
Kari Alitalo | 174 | 817 | 114231 |
Pierre Bourdieu | 153 | 592 | 194586 |
Stanislas Dehaene | 149 | 456 | 86539 |
Howard L. Weiner | 144 | 1047 | 91424 |
Alain Fischer | 143 | 770 | 81680 |
Yves Agid | 141 | 669 | 74441 |
Michel Foucault | 140 | 499 | 191296 |
Jean-Pierre Changeux | 138 | 672 | 76462 |
Jean-Marie Tarascon | 136 | 853 | 137673 |
K. Ganga | 132 | 272 | 99004 |
Jacques Delabrouille | 131 | 354 | 94923 |
G. Patanchon | 128 | 241 | 87233 |