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Similar Publications

[Age-dependent possible role of contact-activated blood coagulation factor XII as a potential contributor to the “bradykinin storm” in COVID-19 patients].

Orv Hetil

December 2020

3 Általános Orvostudományi Kar, Kardiológiai Intézet, Kardiológiai Tanszék, Debreceni Egyetem, Debrecen.

Unlabelled: Összefoglaló. Bevezetés: Egy új, számítógép által segített betegminta-asszociációs analízis eredménye szerint a COVID-19 tüneteinek kialakításában kiemelt tényezőként jelenik meg a bradikinin. Eszerint a bradikinin lebontása lelassul az angiotenzinkonvertáló enzim aktivitásának csökkenése miatt, ami jelentősen megemelkedő bradikininszinthez vezet a tüdőben.

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Objective: Introduction: Abnormalities comorbidity - a frequent phenomenon in medical practice. This determines the relevance of research processes maintaining homeostasis with a combination of various diseases. The aim of this study was to examine and compare the character of vegetative, antioxidant, kallikrein-kinin system and parameters of endogenous intoxication disorders in the patients with isolated essential hypertension and with combination of hypertonic disease and chronic pancreatitis.

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The Search for Biomarkers in Hereditary Angioedema.

Front Med (Lausanne)

November 2017

Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.

The unpredictable nature of attacks of tissue swelling in hereditary angioedema requires the identification of reliable biomarkers to monitor disease activity as well as response to therapy. At present, one can assess a C4 level (by ELISA) to assist in diagnosis but neither C4 nor C1 inhibitor levels reflect clinical course or prognosis. We will here review a collection of plasma proteins involved in blood coagulation, fibrinolysis, and innate immunity (Figure 1).

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Unlabelled: Essentials Kallikrein amplifies contact activation and is a potential target for preventing thrombosis. We developed and characterized a kallikrein aptamer using convergent evolution and kinetic assays. Kall1-T4 prolongs intrinsic clotting time by inhibiting factor XIIa-mediated prekallikrein activation.

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Objective: To determine the Km, Vmax, and Ki of BOC-Leu-Ser-Thr-Arg-pNA (B3644) in the determination of kallikrein, and then to establish the procedure for plasma prekallikrein/kallikrein determination. Method Chromogenic substrate assays on a semi-auto spectrophotometer were employed.

Results: The apparent activities of seven substrates: B3644, S2238, S2251, ChromozymPCa, T6140, ChromozymPK, and T1637, for porcine kallikrein were 0.

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