Wednesday, July 8, 2009

Hairstyles How To Do Plats

Haemostasis and Thrombosis Platelet-and Coagulation

These are my plans haemostasis, thrombosis, platelets and the coagulation system, prepared for the examination of Professor lectures on General Pathology. Dobrina.






To download, click here: DOWNLOAD
clarification on the role of cAMP in the activation of ADP and platelet
ADP released from platelets has the same two receptors on platelets, the P2Y1 and P2Y12.
Activation of P2Y1 receptor involves the activation of PLC, production of inositol phosphate and the release of Ca + +, which mediates the morphological changes of the plate.
P2Y12 receptor activation activates the AC instead, which is stimulated to produce cAMP, which promotes the exposure of GP IIb / IIIa, the mediator of the combination. On this act the thienopyridine P2Y12 receptor (ticlopidine, clopidogrel). In the diagrams is stressed that cAMP blocks the platelet functions, it is actually a simplification in order to emphasize the primary role in the activation of Ca + +, because the field does not enter the activation time, but in the aggregate, when the plates have already been activated. It remains the role of PGI2 in the control of platelet activation, inhibiting it (in the key to its own action is mediated by cAMP). Furthermore, the PGI2 also has vasodilatory action, and action away from the vasospasm induced by platelet here because the coxib (selective inhibitor of COX-2) were related to vascular events, because it blocks the COX-2 endothelial cell, thereby nullifying the production of PGI2 and maintaining one of TxA2 by COX-1 and platelet endothelial.



NEW MODEL OF AGGREGATION PIASTRINICA

Vi segnalo anche un articolo molto importante, uscito a giugno su Nature Medicine:
A shear gradient–dependent platelet aggregation


mechanism drives thrombus formation
(W Nesbitt et al.)

In poche parole, รจ stato scoperto che tra il momento dell'adesione e quello dell'aggregazione piastrinica, mediata dall'integrina GPIIb/IIIa e dai fattori solubili rilasciati dai granuli, avviene una prima aggregazione (Reversible) regardless whether the same plate. This initial aggregation is induced by changes in shear stress, shear stress, which occur in the case of vascular alteration (eg a blood clot): essentially, it adheres to platelets (via GPIb / IX), and then is pulled away from the shear, but it remains immobilized by a filament of membrane, the decrease in the downstream shear induces the remodeling of this filament, which becomes more resistant. Finally, the aggregation becomes less reversible with the action of the integrin and, secondly, of soluble factors.
you place the translation of the abstract:

"
Platelet aggregation at sites of vascular injury is essential for homeostasis and arterial thrombosis. It has long been thought that platelet aggregation and thrombus growth were started by soluble factors generated at sites of vascular injury. Using intravital imaging techniques, high-resolution hydrodynamic analysis, we show that platelet aggregation is primarily driven by changes in the parameters of blood flow (rheology), with the soluble factors that maintain the secondary role of stabilizing the aggregates formed . We found that, in response to vascular damage, thrombus develops initially through the stabilization of aggregates of discoid platelets. Analysis of the dynamics of blood flow revealed that the disc-shaped platelets adhere preferentially in areas of low shear stress, on the downstream face of the thrombus, with the stabilization of the aggregates that depends on the dynamic restructuring of the membrane layers
(the English term "Tethers" would indicate precisely the formation of a "lead", with which the plate and away from the clot, is then approached by shortening it)
. These tests allow the understanding of the prothrombotic effects of changes in the parameters of blood flow, and suggest a fundamental reinterpretation mechanisms that drive the growth of platelet aggregation and thrombus. "
from the article page, you can also find videos of the experiments are very useful for understanding. I found a nice page that lists the conditions predisposing to thromboembolic events, a page dedicated to the arterial thrombophilia:
conditions predisposing them to thromboembolism
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