Fuentes Información 1 1

Urbano García Rodolfo Daniel.

Grupo: 2218

FUENTES DE INFORMACIÓN. Parte I.
CLASIFICACIÓN. ESTRUCTURA DE LAS CITAS BIBLIOGRÁFICAS
DESARROLLO DEL EJERCICIO
a) Lectura de comprensión de textos en inglés
Como primer ejercicio de esta sesión, el alumno deberá intentar la traducción técnica y de
comprensión de los siguientes cuatro textos (problemas), que tienen grados de dificultad
creciente:
i)Platelet adhesion and aggregation is a central feature of arterial thrombosis.
The inhibitory effect of conventional antiplatelet drugs, such as aspirin and
adenosine diphosphate (ADP)-analogues (clopidogrel or ticlopidine), depends
on either inhibiting prostaglandin synthesis or blocking signal transduction
pathways induced by the activated receptors. However, there are additional
agonist pathwaysnot affected by these agents, leading to an activated state of
GP IIb/IIIa receptors. GP IIb/IIIa antagonists are effective because fibrinogen
binding to activated GP IIb/IIIa complex is the final common event in platelet
aggregation and platelet aggregation induced by all agonists. (Mandava P,
Thiagarajan P, Kent TA. Glycoprotein IIb/IIIa antagonists in acute ischaemic
stroke. Drugs 2008;68(8):1019-1028). CALIFICACIÓN:______7______

ii)

Abciximab is a recombinant Fab fragment of a monoclonal anti-IIb/IIIa antibody
with high molecular weight, tirofiban is a small non peptide compound and
eptifibatide is a small peptide. Both tirofiban and eptifibatide are specific for GP
IIb/IIIa receptors. Abciximab has cross reactivity with vitronectin receptors
found on endotelial cells and b3integrins found on leukocytes.
Thus, it has added features including an anti-inflammatory y role and reducing
the formation of platelet-leukocyte aggregates. Abciximab is also thought to
have some affinity for GP Ib receptors, thus affecting the interaction between
GP Ib receptors and von Willebrand factor, reducing thrombin generation.
(Mandava P, Thiagarajan P, Kent TA. Glycoprotein IIb/IIIaantagonists in acute

ischaemic

stroke.

Drugs

2008;

68(8):

1019-1028).

CALIFICACIÓN:_____6____

iii)

Stroke is clinically defined as the abrupt development of a focal neurologic
deficit

whose origin can be traced to either the occlusion of a

cerebral vessel, which deprives neurons of needed oxygen and high energy
metabolites, or the spontaneous rupture of an intracranial artery, which causes
braininjury by direct cell trauma, mass effect, elevated intracranial pressure,
and/or the release of deleterious biochemical substances. The majority of all
strokes is ischemic in nature and caused by vessel thrombosis, which occurs
when clot formation is superimposed on insidious and slowly progressive
narrowing or alterations in the luminal lining of the vessel. Atherosclerotic
disease is the mostcommon cause of thrombotic stroke. Atherosclerosis
primarily affects the larger intracranial and extracranial arteries and causes
hyperplasia and fibrous disposition in the subintimal area with plaque formation.
Plaques cause narrowing and platelet adhesion, which lead to vessel
thrombosis. Cerebral ischemia occurs when blood flow decreases as a result of
arterial narrowing (Rodriguez R y cols.Bilateral sequential common carotid
artery sectioning in mice as a new model for testing neuroprotective drugs. J
Stroke Cerebrov Dis 2000; 9:45-53). CALIFICACIÓN:_____6_____

iv)

A target for acute intervention in ischaemic stroke is the penumbra, a zone of
incomplete cerebral ischaemia, where neurones are functionally inactive but
still viable. The development of the penumbra is a time-limitedcondition where
cells will die in the ensuing hours to days, owing to a cascade of biochemical
events, the so-called 'ischaemic cascade'. Compounds that interfere with these
biochemical steps have been demonstrated to be neuroprotective in preclinical
models of stroke. A fraction of these have entered clinical development and
some of those that survived early safety trials have been studied in...