Tuberkulózní postižení střev je v rozvinutých zemích vzácné onemocnění, které postihuje zejména imigranty a imunokompromitované pacienty. Klinický obraz může imitovat nitrobřišní infekce, nádorová onemocnění či Crohnovu chorobu. Diferenciální diagnostika Crohnovy choroby a břišní tuberkulózy může být pro klinika a patologa svízelná, v obou případech se jedná o chronický granulomatózní zánět s podobnou symptomatologií. Prezentujeme případ 53letého pacienta s perforační peritonitidou při tuberkulóze střeva, u kterého byla původně mylně diagnostikována Crohnova choroba. Průběh choroby, rozsah a povaha nálezu byly v každé fázi léčby příčinou kritických komplikací. S touto zkušeností předáváme i doporučení: břišní tuberkulózu zvažovat v diferenciálně diagnostické rozvaze každého chronického střevního onemocnění. Klíčová slova: střevní tuberkulóza − Crohnova choroba − kritické komplikace, Intestinal tuberculosis is a rare disease in developed countries, affecting mainly immigrants and immunocompromised patients. Clinical presentation may mimic many other abdominal diseases such as intra-abdominal infections, tumors, and Crohn´s disease. Differential diagnosis of Crohn´s disease and intestinal tuberculosis poses a dilemma to clinicians and pathologists as both are chronic granulomatous disorders with similar clinical features. We report the case of a 53 year-old man presenting with perforated intestinal tuberculosis in which the initial diagnostic work-up suggested Crohn´s disease. The severity of the findings resulted in critical complications during the course of treatment. This case points out the need for awareness of intestinal tuberculosis in the differential diagnosis of chronic intestinal disease. Key words: intestine tuberculosis − Crohn´s disease − critical complications, and P. Bavor, P. Kocián, J. Hoch
Crohn's disease is a chronic immune-mediated intestinal inflammation targeted against a yet incompletely defined subset of commensal gut microbiota and occurs on the background of a genetic predisposition under the influence of environmental factors. Genome-wide association studies have identified about 70 genetic risk loci associated with Crohn's disease. The greatest risk for Crohn's disease represent polymorphisms affecting the CARD15 gene encoding nucleotide-binding oligomerization domain 2 (NOD2) which is an intracellular sensor for muramyl dipeptide, a peptidoglycan constituent of bacterial cell wall. The accumulated evidence suggests that gut microbiota represent an essential, perhaps a central factor in the induction and maintaining of Crohn's disease where dysregulation of normal co-evolved homeostatic relationships between intestinal microbiota and host mucosal immune system leads to intestinal inflammation. Taken together, these findings identify Crohn's disease as a syndrome of overlapping phenotypes that involves variable influences of genetic and environmental factors. A deeper understanding of different genetic abnormalities underlying Crohn's disease together with the identification of beneficial and harmful components of gut microbiota and their interactions are essential conditions for the categorization of Crohn's disease patients, which enable us to design more effective, preferably causative, individually tailored therapy. and L. Hrnčířová, J. Krejsek, I. Šplíchal, T. Hrnčíř
Crohnova nemoc se často projevuje čistě jako zánětlivé onemocnění, ale u mnoha pacientů se vyvine v komplikované onemocnění charakterizované tvorbou striktur nebo píštělí. Přesná etiopatogeneze tohoto závažného onemocnění není zcela jednoznačně objasněna, a to i přes veškeré úsilí výzkumu a přes poznání řady dílčích patogenetických mechanizmů. Mnoho studií naznačuje, že se zvýšeným rizikem rozvoje komplikované formy onemocnění souvisí zejména varianty v NOD2/CARD15 genu. Samotná přítomnost variant v NOD2 genu je pouze jen jedním z faktorů přispívajících k rozvoji tohoto onemocnění. U geneticky predisponovaných jedinců v kombinaci s působením faktorů prostředí dochází k porušení vrozené (např. porušená střevní bariéra, dysfunkce Panethových buněk) i adaptivní (např. nerovnováha efektorových a regulačních T lymfocytů a cytokinů, migrace a retence leukocytů) imunitní odpovědi vůči snížené pestrosti střevních komenzálů. Data dosud provedených metaanalýz neposkytují jednoznačné důkazy k podpoře top-down strategie terapie závislé pouze na jediné variantě v NOD2 genu, ale na druhé straně v případě vysoce rizikových pacientů se dvěma variantami v NOD2 genu data ukazují, že cílená a časná intenzivní terapie by mohla být prospěšná. Na tyto otázky by mohly odpovědět další prospektivní studie., Crohn’s disease is often purely inflammatory, but most patients develop complicated disease with strictures or fistulae. Specific etiopathogenesis of this severe disease is not definitely clear despite research efforts and learning of many pathogenetic mechanisms. Many studies have suggested that NOD2 mutations are associated with increased risk of complicated disease. Presence of NOD2 mutation itself is just one of factors contributing to development of this disease. Genetically predisposed individuals in combination with influence of environmental factors result in a disturbed innate (i.e., disturbed intestinal barrier, Paneth cell dysfunction) and adaptive (i.e., imbalance of effector and regulatory T cells and cytokines, migration and retention of leukocytes) immune response towards a diminished diversity of commensal microbiota. Data of meta-analysis made so far provide ambiguous evidence to support top-down therapy based solely on single NOD2 mutations, but suggest that targeted early-intensive therapy for high-risk patients with two NOD2 mutations might be beneficial, but more prospective trials could answer these questions., and Tomáš Kupka, Jarmila Šímová, Lubomír Martínek, Pavel Svoboda, Pavel Klvaňa, Martina Bojková, Magdalena Uvírová, Lenka Dovrtělová, Petr Dítě
In this work, we evaluated the effect of adaptation to heat on the fall of blood pressure (BP) induced by heat shock (HS) and the interrelation between nitric oxide (NO) and heat shock protein, HSP70. Experiments were carried out on Wistar rats. It was shown that HS resulted in a generalized and transient increase in NO production (the electron paramagnetic resonance method) and a fall of BP from 113± 3 to 88± 1 mm Hg (?<0.05). Adaptation to heat itself did not affect BP, but completely prevented the NO overproduction and hypotension induced by HS. The adaptation simultaneously increased the brain NO-synthase content and induced HSP70 synthesis (the Western blot analysis) in various organs. Both the antihypotensive effects of adaptation and HSP70 accumulation were completely prevented by L-NNA, an inhibitor of NO synthesis, or quercetin, an inhibitor of HSP70 synthesis. The data suggest that adaptation to heat stimulates NO synthesis and NO activates synthesis of HSP70. HSP70, which hampers NO overproduction, thus restricts the BP fall induced by heat shock., I. Yu. Malyshev, L.A. Bayda, A.I. Trifonov, N.P. Larionov, L.D. Kubrina, V.D. Mikoyan, A.F. Vanin, E.B. Manukhina., and Obsahuje bibliografii
The aim of this study was to determine the effect of chronic crowding on the cardiovascular system of Wistar-Kyoto (WKY) rats. Rats were randomly divided into the control (480 cm2 per rat) or crowded (200 cm2 per rat) group for eight weeks. Body weight, blood pressure (BP), heart rate and plasma nitrate/nitrite levels of the crowded rats were not different from controls at the end of the experiment. Plasma corticosterone exhibited an increasing trend (5.7±1.8 vs. 12.6±3.7 ng/ml, p=0.08) while blood glucose was significantly reduced in the crowded rats in comparison with the controls. Nitric oxide (NO) synthase activity and nitrate/nitrite levels of the crowded rats were significantly elevated in the aorta by ∼80 % and ∼20 %, respectively, but unchanged in the left ventricle. Moreover, acetylcholine-induced relaxation was significantly increased in the crowded rats in both the femoral artery (61±5 % vs. 76±5 %, p<0.001) and mesenteric artery (51±6 % vs. 72±7 %, p<0.001). In conclusion, results suggest that chronic crowding may increase vasorelaxation and vascular NO production in normotensive rats. This may be considered as an adapting mechanism preventing the development of the stress-related elevation of BP. Additionally, results also suggest caution in the housing of rats because an inappropriate crowding may affect results of the experiment significantly., I. Bernátová, A. Púzserová, J. Navarová, Z. Csizmadiová, M. Zeman., and Obsahuje bibliografii a bibliografické odkazy
Converted from MARCXML to MODS version 3.5 using MARC21slim2MODS3-5.xsl (Revision 1.106 2014/12/19)(EE patch 2015/05/15), obrázky z venkovského života od Henryka Sienkiewicze ; z polštiny přeložil Cyril S. Moudrý, Rok vyd. a název originálu z bibliografického katalogu 19. stol., Přívazek k: Historické arabesky / Z. Winter, and Converted from MODS 3.5 to DC version 1.8 (EE patch 2015/06/25)
Thessaly lies on the Aegean (micro-)plate, undergoing internal crustal deformation due to the plate relative motion against the adjacent Anatolian and Nubian plates. As a result, the whole Thessalian Basin was supposed to be under an extensional tectonic regime of N-S direction. However, the recent earthquake sequence of March 2021 which occurred close to the northwestern margin of the basin revealed NE-SW direction of extension. Based on 7-year GPS measurements recorded by stations installed within and around the basin we assessed four deformational parameters for Thessaly aiming at the understanding of the deformation processes that control the region. These parameters are i) the Maximum Horizontal Extension (MAHE), ii) the Total Velocity (TV), iii) the Maximum Shear Strain (MSS), and iv) the Area Strain (AS). The results show that during the monitoring period, Thessaly moved toward the S-SW with a simultaneous clockwise rotation and underwent dispersed deformation mostly associated with dilatation. Focusing on the epicentral area of the 2021 sequence, strain during the 7-year period was rather low in all three strain parameters, implying a mature stage of elastic strain accumulation before the fault rupture., Ilias Lazos, Sotirios Sboras, Konstantinos Chousianitis, Stylianos Bitharis, Evaggelos Mouzakiotis, Vassilios Karastathis, Christos Pikridas, Aristeidis Fotiou and Dimitris Galanakis., and Obsahuje bibliografii