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Anafilaksja idiopatyczna

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Łukaszyk M., Łukaszyk-Spryszak A., Szpak A., Bodzenta-Łukaszyk A.
Alergia Astma Immunologia - przegląd kliniczny
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2019
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vol. 24
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issue 3
126-130
EN
Idiopathic anaphylaxis is a severe, life-threatening systemic or generalized immediate hypersensitivity reaction with symptoms similar to resembling other forms of anaphylaxis. It concers approximately 30-60% of cases in adults and 20% of cases in children. In the pathogenesis of idiopathic anaphylaxis, alpha-gal syndrome, mastocytosis, diseases associated with mast cell activation, and hidden allergens and cofactors -physical exertion, alcohol, drugs can play a significant role. The clinical manifestations of idiopathic anaphylaxis and therapeutic management are identical to those of anaphylaxis with a known causative agent. The paper discusses epidemiology of anaphylaxis, pathomechanism, diagnostics and therapeutic management according to international guidelines.
PL
Anafilaksja idiopatyczna jest ciężką, zagrażającą życiu systemową lub uogólnioną natychmiastową reakcją nadwrażliwości o objawach podobnych/zbliżonych do innych postaci anafilaksji. Dotyczy ok. 30-60% przypadków u dorosłych i ok. 20% przypadków u dzieci. W patogenezie anafilaksji idiopatycznej istotną rolę mogą odgrywać zespół alfa-gal, mastocytoza, schorzenia przebiegające z aktywacją komórki tucznej oraz ukryte alergeny i kofaktory – wysiłek fizyczny, alkohol, leki. Objawy kliniczne anafilaksji idiopatycznej oraz postępowanie terapeutyczne są identyczne jak w anafilaksji o znanym czynniku sprawczym. W pracy omówiono epidemiologię anafilaksji, patomechanizm, diagnostykę oraz postępowanie terapeutyczne według wytycznych międzynarodowych
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Involvement of Na+/H+ exchanger in desmopressin-induced platelet procoagulant response.

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Tomasiak M. M., Stelmach H., Bodzenta-Łukaszyk A., Tomasiak M.
Acta Biochimica Polonica
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2004
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vol. 51
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issue 3
773-788
EN
Desmopressin (DDAVP) action on platelets is associated with the development of procoagulant response but the underlying mechanism of this phenomenon is not known. We investigated whether this effect of DDAVP might be due to activation of plasma membrane Na+/H+ exchanger. The DDAVP-induced platelet procoagulant response, measured as phospholipid-dependent thrombin generation, was dose dependent and significantly weaker than that produced by collagen or monensin (mimics Na+/H+ antiport). Both the DDAVP- and collagen-produced procoagulant responses were less pronounced in the presence of EIPA, an Na+/H+ exchanger inhibitor. Flow cytometry studies revealed that in vitro treatment of platelets with DDAVP or collagen was associated with the appearance of both degranulated (and fragmented) and swollen cells. The DDAVP-evoked rise in size and granularity heterogeneity was similar to that produced by collagen or monensin and was not observed in the presence of EIPA. Using flow cytometry and annexin V-FITC as a probe for phosphatidylserine (PS) we demonstrated increased and uniform binding of this marker to all subsets of DDAVP-treated platelet population. The DDAVP-evoked PS expression was dose dependent, strongly reduced by EIPA and weaker than that caused by monensin or collagen. As judged by optical swelling assay, DDAVP in a dose dependent manner produced a rise in platelet volume. The swelling was inhibited by EIPA and its kinetics was similar to that observed in the presence of monensin. Electronic cell-sizing measurements showed an increase in mean platelet volume and a decrease in platelet count and platelet crit upon treatment with DDAVP. DDAVP elicited a slow (much slower than collagen) alkalinization of platelet cytosol. Altogether the data indicate an involvement of Na+/H+ exchanger in the generation of procoagulant activity in DDAVP-treated platelets.
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