{'fraction_non_alphanumeric': 0.016296296296296295, 'fraction_numerical': 0.0004938271604938272, 'mean_word_length': 5.962199312714777, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Coagulation abnormalities and cerebral infarction.

Thrombosis is central to the major pathophysiological mechanisms of ischaemic stroke-large vessel occlusive disease, embolism and small vessel occlusion. Whilst in the majority of cases the thrombotic process becomes activated secondarily to an underlying (cardio)vascular pathology, some cases of ischaemic strokes may result primarily from an abnormality of the haemostatic mechanisms which results in unchecked thrombus formation within the cerebral circulation. There is a requirement, in health, for the rapid and efficient sealing of breaches in the vascular endothelium, whilst at the same time uncontrolled vessel occlusion cannot be permitted. This has led to the evolution of an interactive system of cellular and fluid-phase components, activators and inhibitors designed to fulfil these requirements. The participants are blood platelets, components of the fluid phase of coagulation and their inhibitors, the fibrinolytic system and the vascular endothelium. Platelets are highly reactive, contractile and secretory anucleate cells which have the capacity to interact with components of the vascular subendothelium within seconds of their exposure. The response requires the availability of adhesive proteins and specific platelet membrane glycoprotein receptors. von Willebrand factor (vWF), a macromolecule synthesised by vascular endothelial cells and megakaryocytes, is the principal protein involved. Subsequently platelets may interact in a process of aggregation, to form an occlusive plug. In this process fibrinogen and other adhesive proteins act as intercellular bridges by interaction with platelet membrane glycoproteins. Inappropriate platelet activation is limited by the local secretion by vascular tissues of short-lived potent inhibitors of platelet adhesion and aggregation. The most important are prostaglandin I2 and nitric oxide, which exert their inhibitory action through the stimulation of cyclic nucleotide synthesis within platelets.