Het afweersysteem van planten, een fascinerend compromis

Plantenecologi

Evolutionary Dynamics of Seed Size and Seedling Competitive Ability

We present a model for the evolutionary dynamics of seed size when seedlings from large seeds are better competitors than seedling from small seeds and there is a trade-off between seed size and seed number. We first consider two limiting cases where seed size either has no effect on the competitive ability of seedlings, or where seedlings from larger seeds always win from seedlings from smaller seeds if together from the same germination site. In the first case there is a single evolutionary optimal seed size excluding all other, whereas in the second case there is an evolutionary stable seed polymorphism with a continuous variation of seed sizes where plants with small (but numerous seeds) survive by exploiting sites that by chance remain unoccupied by plants with larger (but less numerous) seeds. We investigate how these two cases connect to one another via intermediate levels of competitive asymmetry. We find that strong competitive asymmetry and high resource levels favor coexistence of plants with different seed sizes when seed and seedling survival is moderately low but large seeds have a substantial competitive advantage over small seeds. Assuming mutation-limited evolution and assuming that single mutations have only a small phenotypic effect, an initially monomorphic population with a single seed size will reach the final evolutionarily stable polymorphic state through a series of discrete evolutionary branching events. At each branching event, a given lineage already present in the population divides into two daughter lines, each with its own seed size. If precompetitive seed and seedling survival is high for small and large seeds alike, evolutionary branching may be followed by extinction of one or more lineages (including mass-extinction), and thus not necessarily gives rise to evolutionarily stable seed polymorphism. Various results presented here are model-independent and point the way to a more general evolutionarily bifurcation theory describing how the number and stability properties of evolutionary equilibria can change as a consequence of changes in model parameters

De aantalsfluctuaties van de St. Jacobsvlinder, wat zit daar achter?

De aantalsfluctuaties van de St. Jacobsvlinder, wat zit daar achter? Zebrarupsen, de opvallende geel-zwart gekleurde larven van de fel rood-zwarte St. Jacobsvlinder, zijn in de duinen in juni en juli soms zo algemeen, dat ze hele velden Jacobskruiskruid kaalvreten en alleen maar de kale stengels laten staan. Maar in een ander jaar vind je op datzelfde veld geen enkele rups en moet je moeite doen om een paar kleine rozetten van die plant te vinden. In weer een ander jaar staat het Jacobskruiskruid weer uitbundig geel te bloeien, maar moet je op de knieen om weer een paar rupsen te vinden. Ook de tellingen aan de St. Jacobsvlinder laten reusachtige schommelingen in de tijd zien. We leggen vlindertellingen onder een vergrootglas. Plant science

Targeting platelet receptor function in thrombus formation: The risk of bleeding

In this review, we presume that the process of thrombus formation, as assessed in whole blood flow studies and in experimental (murine) thrombosis studies, reflects the platelet responses in human haemostasis and thrombosis. Following this concept, we give an up-to-date overview of the main platelet receptors and signalling pathways that contribute to thrombus formation and are used as targets in (pre)clinical intervention studies to prevent cardiovascular disease. Discussed are receptors for thrombin, thromboxane, ADP, ATP, prostaglandins, von Willebrand factor, collagen, CLEC-2 ligand, fibrinogen and laminin. Sketched are the consequences of receptor deficiency or blockage for haemostasis and thrombosis in mouse and man. Recording of bleeding due to (congenital) platelet dysfunction or (acquired) antiplatelet treatment occurs according to different protocols, while common laboratory methods are used to determine platelet function

Managed Entry Agreements and Orphan Drugs: A European Comparative Study (2006-2012)

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Rate-limiting roles of the tenase complex of factors VIII and IX in platelet procoagulant activity and formation of platelet-fibrin thrombi under flow

The importance of factor Xa generation in thrombus formation has not been studied extensively so far. Here, we used mice deficient in either factor VIII or factor IX to determine the role of platelet-stimulated tenase activity in the formation of platelet-fibrin thrombi on collagen. With tissue factor present, deficiency in factor VIII or IX markedly suppressed thrombus growth, fibrin formation and platelet procoagulant activity (phosphatidylserine exposure). In either case, residual fibrin formation was eliminated in the absence of tissue factor. Effects of factor deficiencies were antagonized by supplementation of the missing coagulation factor. In wild-type thrombi generated under flow, phosphatidylserine-exposing platelets bound (activated) factor IX and factor X, whereas factor VIII preferentially co-localized at sites of von Willebrand factor binding. Furthermore, proteolytic activity of the generated activated factor X and thrombin was confined to the sites of phosphatidylserine exposure. With blood from a hemophilia A or B patient, the formation of platelet-fibrin thrombi was greatly delayed and reduced, even in the presence of high concentrations of tissue factor. A direct activated factor X inhibitor, rivaroxaban, added to human blood, suppressed both thrombin and fibrin formation. Together, these data point to a potent enforcement loop in thrombus formation due to factor X activation, subsequent thrombin and fibrin generation, causing activated factor X-mediated stimulation of platelet phosphatidylserine exposure. This implies that the factor VIII/factor IX-dependent stimulation of platelet procoagulant activity is a limiting factor for fibrin formation under flow conditions, even at high tissue factor concentrations

Stabilizing role of platelet P2Y(12) receptors in shear-dependent thrombus formation on ruptured plaques

Background: In most models of experimental thrombosis, healthy blood vessels are damaged. This results in the formation of a platelet thrombus that is stabilized by ADP signaling via P2Y(12) receptors. However, such models do not predict involvement of P2Y(12) in the clinically relevant situation of thrombosis upon rupture of atherosclerotic plaques. We investigated the role of P2Y(12) in thrombus formation on (collagen-containing) atherosclerotic plaques in vitro and in vivo, by using a novel mouse model of atherothrombosis. Methodology: Plaques in the carotid arteries from Apoe(-/-) mice were acutely ruptured by ultrasound treatment, and the thrombotic process was monitored via intravital fluorescence microscopy. Thrombus formation in vitro was assessed in mouse and human blood perfused over collagen or plaque material under variable conditions of shear rate and coagulation. Effects of two reversible P2Y(12) blockers, ticagrelor (AZD6140) and cangrelor (AR-C69931MX), were investigated. Principal Findings: Acute plaque rupture by ultrasound treatment provoked rapid formation of non-occlusive thrombi, which were smaller in size and unstable in the presence of P2Y(12) blockers. In vitro, when mouse or human blood was perfused over collagen or atherosclerotic plaque material, blockage or deficiency of P2Y(12) reduced the thrombi and increased embolization events. These P2Y(12) effects were present at shear rates >500 s(-1), and they persisted in the presence of coagulation. P2Y(12)-dependent thrombus stabilization was accompanied by increased fibrin(ogen) binding. Conclusions/Significance: Platelet P2Y(12) receptors play a crucial role in the stabilization of thrombi formed on atherosclerotic plaques. This P2Y(12) function is restricted to high shear flow conditions, and is preserved in the presence of coagulation