National Repository of Grey Literature 36 records found  1 - 10nextend  jump to record: Search took 0.00 seconds. 
Changes in individual isoforms of nitric oxide synthase in experimental hypertension and metabolic syndrome: genetic and molecular-biological aspects
Hojná, Silvie ; Kuneš, Jaroslav (advisor) ; Pelouch, Václav (referee) ; Kittnar, Otomar (referee) ; Cífková, Renata (referee)
Changes in individual isoforms of nitric oxide synthase in experimental hypertension and metabolic syndrome: genetic and molecular-biological aspects Powered by TCPDF (
The role of iNOS and fertile cells in the mechanism of development of hypoxic lung hypertension
Baňasová, Alena ; Hampl, Václav (advisor) ; Štípek, Stanislav (referee) ; Pelouch, Václav (referee) ; Ošťádal, Bohuslav (referee)
The role of iNOS and fertile cells in the mechanism of development of hypoxic lung hypertension Powered by TCPDF (
Examining the significance of peptides regulating the intake of food and the nutritional state of children and adolescents
Bronský, Jiří ; Průša, Richard (advisor) ; Pelouch, Václav (referee) ; Hyánek, Josef (referee)
Introduction: Regulation of food intake and nutritional status is mediated by complex interactions of regulatory peptides of the central nervous system, gastrointestinal tract and adipose tissue. These systems are connected by feedback loops which inform the centre about amount of ingested food and energy reserves in the organism. Dysfunction of any of these regulatory areas may lead to changes in nutritional status of the organism. Methods: We used radioimmunoassay to measure plasma levels of orexin A, total ghrelin and serum levels of leptin and enzyme immunoassay to measure serum levels of adiponectin in healthy subjects and in children with obesity, anorexia nervosa, Crohn's disease and celiac disease and we evaluated the influence of nutritional therapy on these levels. Moreover, we evaluated relationship of these regulatory peptides to other biochemical and anthropometrical factors of nutritional status. We also measured plasma levels of total and unreduced amylin by enzyme immunoassay with immunofluorescence detection in adult patients with osteoporosis, type II diabetes mellitus and in the control group. Results: During reduction of body weight in obese children and adolescents, there were statistically significant changes of plasma orexin A levels and total ghrelin levels, but we haven't seen any...
Peripheral metabolism of glucocorticoids in hypertensive rats
Vagnerová, Karla ; Pelouch, Václav (advisor) ; Kment, Milan (referee) ; Hampl, Richard (referee)
Klíčovým článkem periferního metabolismu glukokortikoidů Je llβ- hydroxysteroiddehydrogenasa (lI RSD), která katalyzuje přeměnu glukokortikoidů na jejich méně účinné ll-oxo deriváty a naopak a může tak ovlivnit koncentraci těchto hormonů přímo v tkáni. Existují dva isoenzymy 11HSD. llHSD2 je -schopna pouze snížit hladinu glukokortikoidů a je exprimovaná nejen v mi neralokortikoidně cílových tkáních ale i např. v p l acentě. Naproti tomu llRSDl in vivo převážně zvyšuje lokální koncentraci glukokortikoidů a je exprimovaná v nejrů znějšíc h tkáních. Přítomnost těchto isoenzymů v tkáni má obrovský význam při zprostředkování jak mineralokortikoidního tak glukokortikoidního signálu. Je známo, že mineralokortikoidy (aldosteron) glukokortikoidy (kortisol, kortikosteron) mají přibližně stejnou afinitu k mineralokortikoidnímu receptoru (MR) in vitro a navíc plazmatická hladina glukokortikodů je přibližně 1000x vyšší nežli mineralokortikoidů. In vivo dochází ovšem k specifické vazb ě aldosteronu na MR. Tato selektivní vazba je umožněna díky llHSD2, která konvertuje glukokortikoidy na méně účinné ll-oxo deriváty. Nedostatečná funkce tohoto isoenzymu vede k nadměrné aktivaci MR glukokortikoidem a tím k rozvoji hypertenze. Poslední dobou se uvažuje o tom, že v srdci a mozku, kde jsou exprimované MR a v malé míře lIRSD2,...
Sites and Consequences of Mitochondreal ROS Production
Mráček, Tomáš ; Houštěk, Josef (advisor) ; Pelouch, Václav (referee) ; Kolarov, Jordan (referee)
The thesis consists of 8 articles (6 published and 2 submitted), which may be divided into two major lines. The first (articles 1-4) deals with mitochondrial glycerophosphate dehydrogenase. We have shown that this enzyme is capable of massive ROS production and in the presented works we studied in more detail this ROS production as well as some aspects of enzyme biogenesis, so as to better understand its physiological significance. The second line (articles 5-8) represents our studies on the potential involvement of ROS in pathogenesis of mitochondrial diseases. 1. Glycerophosphate-dependent hydrogen peroxide production by brown adipose tissue mitochondria and its activation by ferricyanide; Drahota Z., Chowdhury SKR., Floryk D., Mráček T., Wilhelm J., Rauchová H., Lenaz G., Houštěk J.; J Bioenerg Biomembr. 2002; 34(2):105-13. Indeed, this was first article to demonstrate ROS production by mammalian mGPDH. We studied oxidation of glycerophosphate by brown adipose tissue mitochondria, which are known to contain high amounts of mGPDH. We found significant GP-dependent AA- stimulated production of H2O2. To further verify our findings, we used three independent methods for H2O2 measurement - fluorescence detection with p-hydroxyphenylacetic acid, antimycine A - insensitive oxygen consumption, and luminometric...
Švíglerová, Jitka ; Pučelík, Pavel (advisor) ; Ošťádal, Bohuslav (referee) ; Pelouch, Václav (referee)
Contractile functions and sympathetic innervation of the albino rat diabetic heart Thesis Summary: The aim of this thesis was to describe: 1. The impact of untreated long-termed diabetes induced by streptozotocin on cardiac contractile functions and their sympathetic regulation in rat. 2. The effect of insulin on cardiac contraction in control and diabetic myocardium. In the diabetic group, the contraction force was significantly decreased compared to control group. The norepinephrine-releasing mechanisms were altered in chronically diabetic rats and may contribute to the decreased norepinephrine concentration in the diabetic heart. Insulin exerted a significant negative inotropic effect in rat myocardium, both control and diabetic. This effect was probably related to processes of SR Ca2+ release triggering, whereas SR Ca2+ loading is not involved. MUDr. Jitka Švíglerová Plzeň, 2006

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