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Start Over Format svazek Subject psychiatrie Date Unknown

2. Mechanismus vášní v "économie animale": k otázce vášní duše v osvícenské medicíně

Creator:
Tinková, Daniela
Format:
print, bez média, and svazek
Type:
model:article and TEXT
Subject:
láska, melancholie, osvícenství, fyziologie, psychiatrie, love, melancholy, enlightenment, physiology, psychiatry, vášně duše, passions of soul, 8, and 94(437)
Language:
Czech and English
Description:
The aim of this study is to show how the emotions - in particular the so-called "passions of the soul" - were understood and interpreted in the medical thinking of the late Enlightenment. We focus chiefly on three innovations in 18th century medicine: the "discovery" of the neuro-cerebral system (the ’birth’ of neurology); the search for the "seat" of illnesses in particular organs (the "birth" of pathological anatomy); and the gradual separation of the body and the soul as objects of medical enquiry (the "birth of psychiatry). We consider whether, and to what extent, these innovations contributed to the breakdown of the "old" diagnostic paradigms of the "passions of the soul", or whether in fact they helped to maintain them. We also discuss to what extent the consideration of these passions fostered a new approach to the relationship between the body and the soul in Enlightenment medicine. Some of the phenomena studied are illustrated by specific examples of (erotic) love and melancholy. and Obsahuje bibliografické odkazy
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

3. Neurobiological aspects of depressive disorder and antidepressant treatment: role of glia

Creator:
Marek Páv, Hana Kovářů, Anežka Fišerová, Eva Havrdová, and Věra Lisá
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, psychiatrie, biochemie, deprese, nálada, antidepresiva, stres (psychologie), gliomy, imunitní systém, signální transdukce, psychiatry, biochemistry, depression, mood (psychology), antidepressants, stress (psychology), gliomas, immune system, signal transduction, hippocampus, neurogenesis, astrocyte, natural killer cells, guanine-binding proteins, G proteins, 14, and 612
Language:
English
Description:
Depression is a complex disorder related to chronic inflammatory processes, chronic stress changes and a hippocampal response. There is a increasing knowledge about the role of glial cells in nutrient supply to neurons, maintenance of synaptic contacts and tissue homeostasis within the CNS. Glial cells, viewed in the past as passive elements with a limited influence on neuronal function, are becoming recognized as active partners of neurons and are starting to be discussed as a possible therapeutic target. Their role in the pathogenesis of depressive disorders is also being reconsidered. Attention is devoted to studies of the different types of antidepressants and their effects on transmembrane signaling, including levels of α subunits of G proteins in C6 glioma cells in vitro as a model of postsynaptic changes in vivo. These models indicate similarities in antidepressant effects on G proteins of brain cells and effector cells of natural immunity, natural killers and granulocytes. Thus, an antidepressant response can exhibit certain common characteristics in functionally different systems which also participate in disease pathogenesis. There are, however, differences in the astrocyte G-protein responses to antidepressant treatment, indicating that antidepressants differ in their effect on glial signalization. Today mainstream approach to neurobiological basis of depressive disorders and other mood illnesses is linked to abnormalities in transmembrane signal transduction via G-protein coupled receptors. Intracellular signalization cascade modulation results in the activation of transcription factors with subsequent increased production of a wide array of products including growth factors and to changes in cellular activity and reactivity., M. Páv, H. Kovářů, A. Fišerová, E. Havrdová, V. Lisá., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public