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1
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Mechanizmy molekularne przekazywania sygnału aktywacji przez wybrane receptory błonowe płytek krwi

100%
Golański J., Watała C., Jacek Golański - Akademia Medyczna w Łodzi I. K., Cezary Watała - Akademia Medyczna w Łodzi K. D. L.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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2001
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vol. 15
EN
This review paper concerns molecular mechanisms of signal transduction by various receptor systems and the role of various agonists in the activation of blood platelets. Authors present the physiological pathways leading to platelet activation and release reaction, as well as those responsible for the natural feedback inhibition of platelet activation. The significance of the conformational changes in platelet receptor glycoproteins, the reorganisation of platelet cytoskeleton, the mobilisation of calcium, processes of phosphorylation/déphosphorylation, and lipid bilayer fluidity in the modulation of the triggering of platelet signal transduction is discussed.
2
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Regulation of cell function by isoforms of C-reactive protein: A comparative analysis

100%
Boncler M., Watała C.
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issue 1
17-31
EN
Despite the emerging evidence suggesting a proatherogenic role of C-reactive protein (CRP) in atherosclerosis, the contribution of CRP in pathogenesis of atherosclerosis and atherothrombosis has not been unequivocally defined. The role of CRP in pathophysiology/pathology seems to largely depend on its structure. Two CRP isoforms, the native pentameric and the modified monomeric one, differ substantially in their physiological functions, which is thought to origin from the considerable structural heterogeneity of the CRP molecule. The present review provides an overview of the experimental evidence with relevance to the clinical role(s) of various CRP isoforms. The biological role of the protein, its structure and distribution are discussed with particular emphasis on the diverse properties of the pentameric and monomeric forms of CRP. Some methodological aspects, related to experimental models and techniques of CRP preparation, are also critically reviewed.
3
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Modulacja aktywacji płytek krwi - antagoniści receptora tromboksanu i modulatory receptorów eikozanoidowych

100%
Więcławska B., Watała C., Łodzi A. M. w.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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1999
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vol. 14
4
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In vitro effect of insulin on the osmotic fragility of human diabetic erythrocytes

81%
Bryszewska M., Watała C., Leyko W., Uniwersytet Łódzki I. B. i. B.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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1986
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vol. 4
5
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Decreased erythrocyte ghost membrane fluidity as a result of lipid composition changes in plasma of adult Insulin-dependent diabetics

81%
Watała C., Bryszewska M., Leyko W., University of Łódź I. o. B. a. B.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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1986
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vol. 5
6
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Przegląd krajowych gatunków rodziny Cicindelidae (Coleoptera)

81%
Burakowski B., Jadwiszczak A., Watała C., Nauk B. B. I. Z. P. A., Nauk A. J. I. Z. P. A., Cezary Watała - Akademia Medyczna w Łodzi K. D. L.
Acta Universitatis Lodziensis. Folia Zoologica
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1994
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vol. 2
EN
Ten species of tiger-beetles (Coleoptera, Cicindelidae) occuring in Central Europe are described and figured. Keys to the adults and known larvae, with brief notes on their distribution and bionomics, are provided.
7
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Znaczenie uwarunkowań genetycznych w dysfunkcjach układu hemostazy w cukrzycy - potencjalne czynniki ryzyka powikłań naczyniowych

81%
Watała C., Boncler M., Różalski M., Łodzi A. M. w.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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1999
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vol. 14
EN
The unambiguous determination of etiopathogenetic factors underlying the increased risk of vascular disease in diabetic patients remains to be established. Evidence accumulated hitherto points that such an increased risk might be a constellation of metabolic disorders and genetic background. Thus, the impairments in coagulation and fibrinolysis, which are believed to partly result from metabolic disorders encountered in diabetes, and genetic factors might be compounding in predisposing a diabetic individual to develop the late diabetic sequelae sooner. The role of the latter seems superior with respect to some dysfunctions in haemostasis. Hence, the monitoring of the frequency and distribution of genetic polymorphisms of selected haemostatic proteins might be promising in an attempt to define the reasons of altered haemostatic imbalance in patients with diabetes mellitus. Based on such a knowledge one could discriminate the groups of patients with high risk for the development of vascular disease, in whom pharmacological strategy to attenuate haemostatic impairments would be desirable.
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