Advances in experimental medicine and biology ; vol. 174
649 s. : il.
Background: Despite the fact that the genetic basis of schizophrenia has been intensively studied for more than two decades, our contemporary knowledge in this field is rather fractional, and a substantial part of it is still missing. The aim of this review article is to sum up the data coming from genome‑wide association genetic studies in schizophrenia, and indicate prospective directions of further scientific endeavour. Methods: We searched the National Human Genome Research Institute’s Catalog of genome‑wide association studies for schizophrenia to identify all papers related to this topic. In consequence, we looked up the possible relevancy of these findings for etiology and pathogenesis of schizophrenia using the computer gene and PubMed databases. Results: Eighteen genome‑wide association studies in schizophrenia have been published till now, referring to fifty‑seven genes supposedly involved into schizophrenia’s etiopathogenesis. Most of these genes are related to neurodevelopment, neuroendocrinology, and immunology. Conclusions: It is reasonable to predict that complex studies of sufficiently large samples, involving detection of copy number variants and assessment of endophenotypes, will produce definitive discoveries of genetic risk factors for schizophrenia in the future.
... Trojan 301 -- The functional state of CNS in young rats after repeated exposure to aerogenic hypoxia ... ... Tomášová 405 -- 15Development of the behavior functions and memory -- Feeding, food reward, and learning ... ... Brodsky 523 -- Developmental electrophysiology -- Ordinary and partial coherence functions in the EEG ... ... Zezuláková 539 -- Functional maturation of visual cortex during prenatal and early postnatal ontogenesis ... ... Nikitina 579 -- Development of infant attention and evoked potentials -- B. Z. Karmel, M. ...
609 s. : il.
Functional gastrointestinal disorders are among the most common diseases. The treatment of these conditions must be comprehensive. The foundation of therapy includes lifestyle modifications, appropriate dietary adjustments, physiotherapy, and pharmacotherapy. Herbal medicines can also play a significant role in self-treatment.
- MeSH
- Antacids pharmacology therapeutic use MeSH
- Dyspepsia * drug therapy MeSH
- Phytotherapy * methods MeSH
- Gastrointestinal Diseases drug therapy MeSH
- Carum MeSH
- Plants, Medicinal MeSH
- Humans MeSH
- Mentha MeSH
- Opuntia MeSH
- Plant Extracts pharmacology therapeutic use MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
362 s. : il. ; 24 cm
- MeSH
- Electrophysiology MeSH
- Evoked Potentials MeSH
- Cognition physiology MeSH
- Brain physiology MeSH
- Publication type
- Congress MeSH
- Conspectus
- Lékařské vědy. Lékařství
- NML Fields
- neurovědy
- fyziologie
Amiodaron je považován za antiarytmikum s nejširším spektrem účinku. Elektrofyziologické funkce myokardu ovlivňuje na základě většiny dosud známých mechanismů. Kromě intenzivní blokády K+ kanálů je antogonistou Na+ a Ca + kanálů a β1-receptorů. Jeho systémový vliv má antiadrenergni povahu. Dochází k poklesu automacie v SA uzlu i v ektopických centrech, zpomaluje se vedení vzruchu v myokardu. Prodlužuje se efektivní i funkční refrakterní období síní i komor, zvyšuje se elektrická homogenita myokardu i práh pro vznik fibrilace komor. Nevýhodou je, že většina těchto účinků nastupuje s individuálně variabilní dlouhou dobou latence. V cévním a koronárním řečišti amiodaron vyvolává vazodilataci, klesá periferní cévní rezistence a stoupá perfuze tkání včetně myokardu. Hlavním důvodem pro omezení širšího klinického použití amiodaronu zůstávají nežádoucí účinky Pri nekontrolované terapii jsou časté a pestré. Nejzávažnější je plicní fibróza a hepatopatie. Nejčastější naopak korneální mikrodepozita, fotosenzibilita kůže a alergické reakce. Známé jsou poruchy funkce štítné žlázy (tyreotoxikóza nebo hypotyreóza) a priznaky plynoucí z poškození CNS a gastrointestinálního traktu.
Amiodarone is considered an antiarrhythmic drug with the broadest spectrum of action. It influences electrophysiological myocardial functions on the basis of the majorioty of hitherto known mechanisms. Apart from intensive block of the K+ channels, it is an antagonist of Na+ and Ca2+ channels and betai-receptors. Its systemic effect is antiadrenergic. A decline of the automatism in the SA node and ectopic centres occures, the conduction of impulses in the heart muscle slows down. The effective and functional atrial and ventricular refractory period is prolonged, the electric homogeneity of the heart muscle and threshold for the development of : ventricular fibrillation increases. The disadvantage is that the majority of these elBfects starts, after an individually variable latent period. In the vascular and coronary circulation amiodarone causes vasodilatation, the peripheral vascular resistance declines and the perfusion of tissues incl. the myocardium increases. The main reason for a limited wider clinical use of amiodarone are its undesirable effects. In uncontrolled therapy they are frequent and varied. The most serious ones include fibrosis and hepatopathy. The most frequent undesirable effects are corneal microdeposits, photosensitization ot the skin and allergic reactions. Impaired thyroid function (thyrotoxicosis, hypothyroidism) were encountered as well as symptoms caused by damage of the CNS and gastrointestinal tract.
