Vladimír Riljak, Katerina Jandová, Milos Langmeier
{"title":"[Kainic acid and neurobiology].","authors":"Vladimír Riljak, Katerina Jandová, Milos Langmeier","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Kainic acid, the analog of excitatory amino acid L-glutamate, interacts with specific receptors in the central nervous system. During last 25 years it has become a tool for studying many human brain disorders, for example human temporal lobe epilepsy, Huntington's chorea etc. Systemic administration of kainic acid results in neuronal death in experimental animals. The mechanism, by which kainic acid produces neuronal damage is still unclear, as well as physiological function of kainate receptors remain to be elucidate. This review attempts to survey the major achievements reached in the studies, which were publicized throw the last three decades.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"55 3","pages":"115-22"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Development of the mammalian circadian system].","authors":"Kristýna Laurinová, Alena Sumová","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Many behavioral, physiological and molecular processes exhibit diurnal rhythms. Endogenous rhythms with period close to 24 hours are called circadian rhythms. Light entrains circadian rhythms to a 24 period of solar day. Circadian system consists of pacemaker, which is in mammals located in the suprachiasmatic nuclei of hypothalamus (SCN), its input and output pathways and peripheral clocks in numerous tissues. The generation of circadian rhytmicity is based on interactive transcription-translational feedback loops in SCN. These feedback loops consist of so called clock genes and their protein products which positively or negatively regulate their own transcription. Studies in rodent embros and neonates demonstrate that individual components of circadian system matures gradually during prenatal and postnatal period Mechanism of light entrainment of the circadian system develops postnatally. During early postnatal period, the developing circadian system is synchronized mainly by maternal cues.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"55 4","pages":"148-54"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Streptozotocin-induced model of type 1 diabetes mellitus].","authors":"Jitka Svíglerová, Jitka Kuncová, Zbynĕk Tonar","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Diabetes mellitus is the important health problem in the developed countries. Type 1 diabetes mellitus and its complications can be studied either on genetic models or it can be induced postnatally. One of the most frequently used postnatal models is the experimental diabetes induced by streptozotocin (STZ). This article presents an overview of STZ use in small and bigger experimental animals and their sensitivity to the diabetogenic effect of this drug. Some new aspects of the long-term STZ diabetes in albino rats (12 months) are provided.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"55 3","pages":"96-102"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26874932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Protection of hypothermic rat liver against gentle manipulation injury].","authors":"A Kebis, LutterováM, M Kukan, D Kuba","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hypothermic preservation can increase hepatocyte sensitivity to various insults. Here we studied the hypothesis that hepatocytes are injured by manipulation with cold-preserved liver. Livers from Wistar rats were divided into two groups. In the 1st group (n = 6) the livers were placed after harvesting into a polyethylene (PE) bag. After the preservation period they were placed into the perfusion chamber--developed in our laboratory. Connection of livers from PE bag to the perfusion chamber required a contact manipulation with the liver. This contact manipulation was eliminated in the second group of livers (n = 6) by using the perfusion chamber for preservation. Lavage and perfusion were done in both groups under the same conditions. We found in the lavage solution of livers of the 1st group 2-times more LDH and 3.7-times higher release of TNF-alpha compared to the 2nd group. Further, bile flow of livers from the 1st group during reperfusion was significantly lower compared to the 2nd group (0.179 +/- 0,12 vs 0.398 +/- 0.15 ml/min/g liver). Manipulation with hypothermic liver leads to hepatocyte injury. Our new model of chamber can protect hypothermic liver against manipulation injury and can allow to perform physiological and pharmacological experiments on liver ex vivo.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 4","pages":"136-41"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24951706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Fibroblast growth factor-2].","authors":"J Faitová","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Fibroblast growth factor-2 is a member of a large family of proteins that bind heparin and heparan sulfate and modulate the function of a wide range of cell types. FGF-2 occurs in several isoforms resulting from alternative initiations of traslation: an 18 kDa cytoplasmic isoform and four larger molecular weight nuclear isoforms (22, 22.5, 24 and 34 kDa). It acts mainly through a paracrine/autocrine mechanism involving high affinity transmembrane receptors and heparan sulfate proteoglycan low affinity receptors. It is expressed mostly in tissues of mesoderm and neuroectoderm origin, and plays an important role in mesoderm induction, stimulates the growth and development of the new blood vessels (angiogenesis), normal wound healing and tissue development. FGF-2 positively regulates hematopoiesis by acting on various cellular targets: stromal cells, early and committed hematopoietic progenitors and possibly some mature blood cells. FGF-2 is a potent hematopoietic growth factor that is likely to play an important role in physiological and pathological hematopoiesis.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 3","pages":"92-101"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25118521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Development of the views on the function of the pineal gland].","authors":"A Strunecká","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Physiology has been collecting the knowledge about the functional significance of the pineal gland during the last 30 years. The recent scientific knowledge about the physiological functions of this gland is compared with the historical development of the views about the role of the pineal gland in the human body.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 1","pages":"23-8"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25118534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Tumor necrosis factor alfa (TNFalpha) and insulin resistance].","authors":"S Gwozdziewiczová, R Lichnovská, J Hrebícek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Obesity and diabetes mellitus type 2 belong among the most frequent illnesses and are categorized among the dominant risk factors for cardiovascular disease in all developed countries. There is a causal relation between insulin resistance and the origin of these risk factors of the cardiovascular morbidity and mortality. Numerous studies have attemted to identify the mechanisms linking obesity with insulin resistance and type 2 diabetes. Numbers of factors have been suggested as having a role in pathogenesis of obesity-related insulin resistance. One of these factors is tumor necrosis factor alfa (TNFalpha).</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 4","pages":"167-75"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24951710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Renin-angiotensin system: molecular biology].","authors":"J Zidzik, J Salagovic, B Fleischer, I Kalina","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Renin-angiotensin system (RAS) have been extensively studied in last few decades. RAS regulates blood pressure, water and electrolytes balance. The disorders in function of RAS may play a potential role in development of some complex diseases like: hypertension, myocardial infarction, stroke, nephropathies and renal failure, chronic obstruction pulmonary disease and many more. RAS may take part in formation and progression of these diseases. In this work we focus on molecular biology of RAS and polymorphisms of RAS genes.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 4","pages":"142-51"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24952954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[History and the present of metabotropic GABAB receptor].","authors":"M Franĕk","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>GABAB receptor is the main inhibitory metabotropic receptor in mammalian central nervous system. This receptor is a member of the Family 3 G-protein coupled receptors (GPCR). It is related to the metabotropic glutamate receptors, the calcium-sensing receptor and some vomeronasal receptors. The receptor is a heterodimer consisting of two subunits designated BR1 and BR2. Presynaptically. GABAB suppresses transmitter release via inhibition of Ca2+ channels, postsynaptically it increases K+ conductance resulting in hyperpolarization. The receptor is coupled to Gi/Go proteins and its activation can inhibit adenylyl cyclase activity. GABAs is widely distributed in CNS and peripheral tissues and plays an important role in many physiological and pathological processes. Recently, a novel GPCR with close relation to GABAB was cloned. It was termed GABABL, its role in GABAB activation has not been discovered yet.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 3","pages":"117-24"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25118523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[PPARs: the role in glucose and lipid homeostasis, insulin resistance and atherosclerosis].","authors":"J Hrebícek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This review deals with general mechanisms of peroxisome proliferator-activated receptors (PPARs) functions, describes the mode of action of various PPAR subtypes in different tissues and their participation in transcription of genes governing lipid and glucose homeostasis. The hypothetic role of free fatty acids in mediating metabolic effects of PPARs, their role in insulin resistance and genetic studies highlighting the ligand-independent activation and post-translational modification of PPARgamma are disscussed in details. A possible role for PPARs in atherosclerosis, especially in connection with macrophage function in this process, is also explained.</p>","PeriodicalId":75688,"journal":{"name":"Ceskoslovenska fysiologie","volume":"53 1","pages":"4-16"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25118532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}