ABSTRACT
A felnottkori invaginatiók ritkák, klinikai megjelenésük eltér a gyerekkori formáktól. Klinikumuk igen változatos, gyakran atípusos, jellemzo, hogy egy klinikai sejtés nyomán gondolni kell az invaginatio lehetoségére. A kiegészíto vizsgálatok közül kiemelkedo szerep jut a computer tomográfiának (CT), ami magas érzékenységgel és fajlagossággal képes kimutatni a béltraktus invaginatióját. Gyógyításuk az esetek legnagyobb részében sebészi, sokszor csak a mutét során lehetséges felismerni a kiváltó okot. Esetismertetésünkben egy rendkívül ritka, felnottkori, passage-zavart okozó colo-colicus, a bal colonfelet érinto, a colon-flexura lienalis-descendens határra lokalizált invaginatio klinikai jellemzoit, diagnosztikáját és definitív megoldásaként a laparoscoposan asszisztált bal oldali haemicolectomia mutéti megoldását mutatjuk be. Munkánkban összefoglaljuk a felnottkori invaginatiókra vonatkozó kórélettani fogalmakat, diagnosztikai lehetoségeket, a leggyakoribb kiváltó tényezoket és terápiás lehetoségeket.
Subject(s)
Citrus , Intussusception , Adult , Humans , Colon , Colon, DescendingABSTRACT
This study is related to the accumulation of Cd(2+), its effects on oxidative stress biomarkers and its role in macromolecule damage in liver and kidney of common carp. We present evidence of an increased ratio of reduced to oxidized glutathione (GSH/GSSG) in both organs after 10 mg/L Cd(2+) exposure, with different underlying biological mechanisms and consequences. In the liver, the expressions and/or activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase increased to cope with the Cd(2+)-generated toxic effects during the first 48 h of treatment. In contrast, none of these selected antioxidant markers was significantly altered in the kidney, whereas the expression of glutathione synthetase was upregulated. These results suggest that the major defense mechanism provoked by Cd(2+) exposure involves the regeneration of GSH in the liver, while its de novo synthesis predominates in the kidney. High levels of accumulation of Cd(2+) and peroxynitrite anion (ONOO(-)) were detected in the kidney; the major consequences of ONOO(-) toxicity were enhanced lipid peroxidation and GSH depletion. The accumulation of ONOO(-) in the kidney suggests intensive production of NO and the development of nitrosative stress. In the liver the level of hydrogen peroxide was elevated.
Subject(s)
Antioxidants/metabolism , Cadmium/toxicity , Carps/metabolism , Kidney/metabolism , Liver/metabolism , Animals , Anions/metabolism , Cadmium/metabolism , Catalase/genetics , Catalase/metabolism , Fish Proteins/genetics , Fish Proteins/metabolism , Gene Expression Regulation, Enzymologic/drug effects , Glutathione/metabolism , Glutathione Disulfide/metabolism , Glutathione Peroxidase/genetics , Glutathione Peroxidase/metabolism , Glutathione Reductase/genetics , Glutathione Reductase/metabolism , Glutathione Synthase/genetics , Glutathione Synthase/metabolism , Hydrogen Peroxide/metabolism , Molecular Sequence Data , Peroxynitrous Acid/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Superoxide Dismutase/metabolism , Water Pollutants, Chemical/metabolism , Water Pollutants, Chemical/toxicity , Glutathione Peroxidase GPX1ABSTRACT
Heat shock proteins are chaperones that play a pivotal role in controling multiple regulatory pathways such as stress defense, hormone signaling, cell cycle control, cell proliferation and differentiation, and apoptosis. In this study, the expression patterns of four well-known heat shock genes (hsp70, hsc70-1, hsc70-2 and hsp90α) were characterized in the skin, spleen and blood cells of the common carp, under unstressed conditions and after Cd2+ treatment or hypothermia. The examined genes were expressed in a tissue-specific manner: hsc70-2 was expressed constitutively, and was at best only slightly inducible; hsp90α exhibited a high basic expression in all three tissues, whereas hsc70-1 did so only in the blood cells, the expression of hsp70 proved to be below the level of detection in unstressed fish. Cold shock induced the expression of hsp genes in the spleen (hsp90α) and blood cells (hsp70, hsc70-1 and hsp90α), while Cd2+ treatment has no effect on the expression pattern. The highest inducibilities were detected in the skin: for hsp70 an induction of at least 20-fold after cadmium exposure, for hsc70-1 of at least 30-fold and for hsp90α of 3-fold after hypothermia.