Název: Prolaktin a systémový lupus erythematodes
Překlad názvu: Prolactin And Systemic lupus erythematosus
Autoři: Moszkorzová, Ludmila ; Dostál, Ctibor (vedoucí práce) ; Pokorný, Jaroslav (oponent) ; Hrnčíř, Zbyněk (oponent)
Typ dokumentu: Disertační práce
Rok: 2007
Jazyk: cze
Abstrakt: Prolactin (PRL) is a polypeptide hormone of 23 kDa molecular weight made up of 199 amino acids, and produced by lactotropes, acidophilic cells of the anterior lobe of the pituitary. PRL is also synthetized in some other parts of the brain and in certain peripheral blood elements. Whether this extra-pituitary PRL, also known as PRL-like hormone, interferes with serum PRL radioimmunoassay (RIA) and whether it also has a feedback effect on PRL secretion in the pituitary, has yet to be elucidated. There is, however, proof of its apocrine and paracrine function of cellular growth factor, a function enhancing mitogenesis and lymphocyte differentiation at the site of inflammation and thereby their own production of yet other mediators and immunomodulators - including interleukines (IL) and growth factors. PRL also directly interferes with the synthesis of some acute-phase proteins in the liver (stimulating, e.g., alpha-2-macroglobulin synthesis). As a result of these discoveries, PRL was classed among immunomodulators, and the hypothesis was advanced of its part in the pathogenesis of autoimmune diseases. The aim of the thesis was to verify the presence of hyperprolactinemia (hyper- PRL) in SLE patients compare to patients with other auto-immune diseases and to healthy controls and to find its association...

Instituce: Fakulty UK (VŠKP) (web)
Informace o dostupnosti dokumentu: Dostupné v digitálním repozitáři UK.
Původní záznam: http://hdl.handle.net/20.500.11956/11351

Trvalý odkaz NUŠL: http://www.nusl.cz/ntk/nusl-286987


Záznam je zařazen do těchto sbírek:
Školství > Veřejné vysoké školy > Univerzita Karlova > Fakulty UK (VŠKP)
Vysokoškolské kvalifikační práce > Disertační práce
 Záznam vytvořen dne 2017-04-25, naposledy upraven 2022-03-04.


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