Health care reforms in Europe
XVII, 177 s. : tab. ; 30 cm
- Conspectus
- Veřejné zdraví a hygiena
- NML Fields
- veřejné zdravotnictví
- NML Publication type
- publikace WHO
- MeSH
- Behavior and Behavior Mechanisms psychology MeSH
- Adult MeSH
- Humans MeSH
- Political Systems MeSH
- Surveys and Questionnaires MeSH
- Social Change psychology MeSH
- Life Change Events psychology MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Publication type
- Interview MeSH
- Geographicals
- Czech Republic MeSH
Cílem studie bylo vyhodnotit, zda se liší jednotlivé typy postižení centrálního nervového systému (CNS) u nemocných se systémovým lupus erytematodes (SLE) s neuropsychiatrickými projevy (NPSLE). V práci jsme prospektivně zpracovali a porovnali klinické nálezy, testy aktivity nemoci a výsledky pomocných vyšetřovacích metod u 70 nemocných s diagnózou NPSLE. Nemocní s NPSLE vykazují v MR nálezech ložiskové hyperintenzity v T2 vážených obrazech v bílé hmotě, velikost ložisek převážně nepřesahuje 3 mm, ložiska jsou nejčastěji uložena frontoparietálně a odpovídají nejspíše vaskulopatii, resp. vaskulitidě mozkových arteriol s mikrotrombózou a gliózou. Nález v likvoru je nespecifický, prokazuje přesněji poruchu hematoencefalické bariéry než postkontrastní MR zobrazení, a to až u 50 % nemocných. Postkontrastní MR zobrazení je ovlivněno kortikoterapií, a proto se u nemocných porucha bariéry nemusí zobrazit. Nenalezli jsme žádné specifické změny v paraklinických vyšetřeních u různých projevů neuropsychiatrického lupusu. Nebyla nalezena ani jejich korelace s aktivitou nemoci.
The aim of the study was to evaluate significant differences among the various types of central nervous system (CNS) affection in patients with systemic lupus erythematosus (SLE) with neuropsychiatric manifestation (NPSLE). The clinical findings of 70 patients with diagnosis of SLE with neuropsychiatric symptomatology were prospectively recorded and compared with activity indices and findings of other auxiliary methods. NPSLE patients have the focal hyperintensities in the white matter on MR findings in the T2 weighted images. The lesions mainly reach the size up to 3 mm and they are localized predominantly in frontal and parietal regions of both hemispheres. These signal changes are supposed to be caused by the vasculopathy or vasculitis of cerebral arterioles with microthrombosis and gliosis. Cerebrospinal fluid (CSF) analysis is nonspecific; it shows the blood brain barrier (BBB) disruption more precisely than postcontrast MR scans, being present in up to 50% of patients. Postcontrast MRI scans are influenced by corticotherapy and therefore need not show signal changes. We did not find any specific changes in paraclinical investigations caused by various types of neuropsychiatric symptomatology. There was no correlation between them and the activity of the disease.
- MeSH
- Autoantibodies blood MeSH
- Biomedical Research MeSH
- Research Support as Topic MeSH
- Blood-Brain Barrier abnormalities drug effects MeSH
- Humans MeSH
- Magnetic Resonance Imaging utilization MeSH
- Neurocognitive Disorders diagnosis classification MeSH
- Prospective Studies MeSH
- Psychiatry MeSH
- Sex Factors MeSH
- Lupus Erythematosus, Systemic diagnosis complications MeSH
- Lupus Vasculitis, Central Nervous System epidemiology mortality MeSH
- Check Tag
- Humans MeSH
- MeSH
- Adult MeSH
- Adrenal Cortex Hormones adverse effects MeSH
- Intelligence MeSH
- Cognition Disorders MeSH
- Humans MeSH
- Central Nervous System Diseases diagnosis etiology MeSH
- Arthritis, Rheumatoid psychology MeSH
- Lupus Erythematosus, Systemic psychology MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
1st ed. x, 390 s.
... of systems upon which life depends: an ecological perspective Climate change: overview ol recent scientific ... ... Weather and climate: changing human exposures -- Introduction -- The climate system and greenhouse gases ... ... Weather, climate and climate variability Climate change -- Climate variability and change over the twentieth ... ... Climate change and infectious diseases 103 -- Introduction 103 iv -- CLIMATE CHANGE AND HUMAN HEALTH ... ... How much disease could climate change cause? ...
xi, 322 s. : il. ; 26 cm
- MeSH
- Risk Assessment MeSH
- Disasters history economics classification prevention & control statistics & numerical data MeSH
- Climate MeSH
- Disease Transmission, Infectious MeSH
- Greenhouse Effect MeSH
- Ultraviolet Rays adverse effects MeSH
- Health Status MeSH
- Conspectus
- Veřejné zdraví a hygiena
- NML Fields
- environmentální vědy
- veřejné zdravotnictví
- NML Publication type
- publikace WHO
Systémový lupus erythematosus (SLE) patrí k orgánovo-nešpecifickým autoimunitným chorobám. Podobne ako iné autoimunitné choroby aj SLEje geneticky determinovaný, pričomide o polygénovú dedičnosť. Pomerne dávno je známe, že na genetickej predispozícii sa zúčastňujú gény hlavného histokompatibilného komplexu (HLA) a gény pre zložky komplementového systému C2, C4, C1q a MBP. Novšie k nim pribudli gény regulujúce apotózu (Fas, FasL), gén pre Fc-receptor IgG (FcγRIIA) a gén pre faktor nekrotizujúci nádory. Výrazným spôsobom na vývoji SLE sa podpisujú hormóny, najmä estrogény. Príčinný vzťah medzi estrogénmi a imunitným systémomje daný tým, že estrogény stimulujú lymfocyty do syntézy cytokínov (IL-4, IL-6, IL-10), ktoré podporujú B-lymfocyty v produkcii protilátok a potláčajú bunkovú imunitu. SLE je typická choroba, pri ktorej za vývoj klinických príznakov zodpovedajúpriamoalebo nepriamo,prostredníctvomimunokomplexov, protilátky. Ďalej sa zisťuje, že lymfocyty B sa nachádzajú v aktivovanom stave, počty CD4+-lymfocytov sú znížené, kým dvojito-negatívne bunky (CD4-CD8-) sú naopak zvýšené. Pozorujú sa poruchy aj v cytokínovej sieti, najmä zvýšené hladiny IFN-α, IL-4, IL-6, receptora pre IL-2 a adhezívnej molekuly ICAM-1.
Systemic lupus erythematosus (SLE) belongs to organ non-specific autoimmunedisorders. Similarly to other autoimmune diseases, SLE is also genetically determined. Among many genes involved in the predisposition to SLE those of the major histocompatibility complex (HLA) and the complement system (C2, C4, C1q, and MBP) have already been known for many years. Recently new genes were added to this list – the FcγRIIA gene (the receptor for Fc-fragment of IgG), the Fas and FasL genes involved in the regulation of apoptosis, and the TNF (tumour necrosis factor) gene. Hormones, especially oestrogens, substantially contribute to the pathogenesis of the disease as they stimulate lymphocytes to produce cytokines (IL-4, IL-6, IL-10) supporting antibody production by B-lymphocytes; moreover they suppress cellular immunity. SLE is a prototypic disease in which antibodies are responsible directly or indirectly, via immunocomplexes, for clinical symptoms. B cells are activated, thenumberofCD4+-lymphocytes is decreasedcompared todouble negativeT-lymphocytes (CD4-CD8-), the number of which is increased. Changes in the cytokine network are also observed, esp. increased levels of IFN-α, IL-4, IL-6, IL-2 receptor, and adhesive molecule ICAM-1 have been reported.
- MeSH
- Autoantibodies adverse effects MeSH
- B-Lymphocytes immunology pathology MeSH
- Cytokines blood MeSH
- HLA Antigens immunology adverse effects MeSH
- Hormones adverse effects MeSH
- Lupus Erythematosus, Systemic genetics immunology MeSH
- T-Lymphocytes immunology pathology MeSH
- Publication type
- Review MeSH
