2 results
Mortality and recruitment in a lowland tropical rain forest of French Guiana: effects of soil type and species guild
- C. Madelaine, R. Pélissier, G. Vincent, J.-F. Molino, D. Sabatier, M.-F. Prévost, C. de Namur
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- Journal:
- Journal of Tropical Ecology / Volume 23 / Issue 3 / May 2007
- Published online by Cambridge University Press:
- 24 April 2007, pp. 277-287
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- Article
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A variety of processes have been identified as playing a key role in maintenance of hyper-rich tropical forest, among which ecological sorting caused by niche partitioning challenges stochastic dispersal processes. However, demographic responses to spatio-temporal resource variation that could result in biased species distributions are still little studied. In this paper we investigate from two censuses, c. 15 y apart, of a 12-ha permanent forest sample in French Guiana, how tree recruitment and mortality rates vary among hydrological soil types known to affect species habitat preferences and among ecological guilds related to species light requirement. The results indicate that both recruitment and mortality vary significantly with respect to these factors. While the mean instantaneous mortality and recruitment rates are estimated to 0.98 and 0.81%, respectively, pioneer species, canopy trees and hydromorphic bottomland soils depart significantly from these values. In particular, the pioneers, regenerating either from the soil seed bank or from post-opening seed rain, show faster dynamics than other species. These two guilds harbour probabilities of mortality elevated by a factor of 1.9 and 3.2, respectively, and probabilities of recruitment elevated by a factor of 4.9 and 3.1, respectively. Conversely, canopy trees show slower dynamics, with probabilities of mortality and recruitment lowered by a mean factor of about 0.5 with respect to other species. We also observe that trees growing in hydromorphic bottomlands prove to have significantly higher mortality and recruitment probabilities, by a factor of about 2 with respect to those growing in terra firme.
8 - Platelet receptors for thrombin
- from PART I - PHYSIOLOGY
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- By Lawrence F. Brass, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA, Marina Molino, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy, Peter J. O'Brien, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA, Mark Kahn, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Clive P. Page, Valentin Fuster, Jos Vermylen, Universiteitsbibliotheek-K.U., Leuven
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- Book:
- Platelets in Thrombotic and Non-Thrombotic Disorders
- Published online:
- 10 May 2010
- Print publication:
- 30 May 2002, pp 113-126
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- Chapter
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Summary
Introduction
Thrombin is one of the most potent agonists that platelets will encounter in vivo, but unlike most of the others it is a protease. For years after thrombin was shown to be a platelet activator as well as an effector in the clotting cascade, the precise mechanism by which it activates platelets remained obscure. Binding studies demonstrated high affinity interactions with several sites on the platelet surface, including glycoprotein (GP) Ibα, but efforts to establish that any of these constituted a receptor in the signalling sense were not entirely successful. Substrates on the platelet surface for proteolytic cleavage by thrombin were also identified, including GP V, but cleavage of these sites did not appear to be required for platelet activation by thrombin. Before discussing the receptors that have been identified, it is worth considering what some of the criteria might be for establishing a protein as a true signalling receptor for thrombin. Such criteria would include (i) demonstrating its presence on the platelet surface, (ii) showing that it was a substrate for thrombin or closely associated with a substrate for thrombin, (iii) demonstrating an association of the candidate receptor with mediators or effectors for intracellular signalling cascades, (iv) showing that expression of the candidate receptor could render a cell that was otherwise unresponsive to thrombin capable of responding, and (v) showing that blocking, dismantling or otherwise removing the candidate receptor would reduce platelet responses to thrombin.