Platelets and Aspirin-Induced Asthma. Pathogenesis and - download pdf or read online

By Helen Evsyukova

ISBN-10: 0128000333

ISBN-13: 9780128000335

ISBN-10: 0128001038

ISBN-13: 9780128001035

Platelets and Aspirin-Induced bronchial asthma is the 1st booklet to be released that displays study performed on aspirin-induced bronchial asthma pathogenesis. it really is tested via positions of neuroimmunoendocrine interactions in organism. The Melatonin hormone performs a key function, being the regulator and coordinator of complex and interrelated organic strategies. This new inspiration of aspirin-induced bronchial asthma pathogenesis indicates new tools for therapy of this sickness via correcting the melatonin content material within the patient's organism. Investigations into the mechanisms of aspirin-induced bronchial asthma as a pathology of melatonin generating cells of platelets is helping to figure out high-risk teams and strengthen preventive measures and enough therapy.

  • The first booklet to check the position of platelets, melatonin and diffuse neuroimmunoendocrine approach within the pathogenesis of aspirin-induced asthma
  • Proposes a brand new thought of aspirin-induced bronchial asthma pathogenesis that implies new diagnostic and remedy equipment for the disease

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Additional resources for Platelets and Aspirin-Induced Asthma. Pathogenesis and Melatonin

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However, if it has an effect on processes related to mobilization of calcium ions from intracellular stores in healthy subjects, due to which the first phase of ADP-induced platelet aggregation becomes shorter, then in AIA patients, as MT production increases, the platelet aggregation is reinforced because of its higher rate, which is caused by the inductor binding to receptors on the platelet membrane. In ATA patients, an equally-high MT production was observed at daytime and nighttime, without any correlation between its level and platelet functional activity.

Thus, MT enhances the decline of body temperature at night and acts as a natural inductor of physiological sleep [5,76,192]. m. helps synchronize the impaired “sleep-wake” cycle by suppressing the reaction that results in them falling asleep during the daytime [492]. Seasonal fluctuations of the MT production underlie the seasonal alterations in humans, and pineal deficiency is manifested in disadaptive disorders underlying the seasonal recurrence of chronic diseases. This is confirmed by the absence of seasonal cycling of the MT production in patients with malignancies, as well as by more frequent depressions and alcoholism in people with impaired seasonal rhythms of MT secretion due to relocating from middle latitudes to the far north [21,46,584].

This effect of MT has been demonstrated in respect of both the constitutive and inducible isoforms of NOS. In the first instance, MT changes the binding of cNOS to calmodulin [446,447], and in the second instance it inhibits the enzyme expression, suppressing its transcription in part by suppressing the activated transcription factor NF-κB [55,195]. Studies of MT’s effect on NO production by endothelial cells under the impact of bradykinin, carbachol, and histamine have proved its inhibiting action mediated by MT association with G-protein-coupled receptors and suppression of Ca21 mobilization from intracellular stores [529].

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Platelets and Aspirin-Induced Asthma. Pathogenesis and Melatonin by Helen Evsyukova

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