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Conversely, these adverse events caused by AngII and MS were obviously reversed by ML3404 and SP600125. The present study indicated that PRDX6 overexpression inactivated p38 MAPK and JNK pathway through decrease AngII-induced inflammation, oxidative stress and endothelial dysfunction leading to attenuation of endothelial cell damage.I recently reported induction of chromatid-type aberrations in human peripheral blood lymphocytes after a single 15 min exposure to universal mobile telecommunications system (UMTS) mobile telephony (MT) electromagnetic field (EMF) from a mobile phone. Eganelisib in vitro Lymphocytes from six healthy subjects were stimulated for mitosis, and exposed during the G2/M phase at 1 cm distance from the handset during an active phone call in "talk" mode. The same type of cells from the same subjects treated with a high caffeine dose (~ 290 times above the permissible single dose for an adult human) exhibited the same type of aberrations in a little smaller but comparable degree. The combination of this caffeine dose and the 15 min MT EMF exposure increased dramatically the number of aberrations in all subjects. The combined effect increased almost linearly with increasing duration of exposure to the MT EMF. Thus, MT EMF exposure ~ 136 times below the official limit (ICNIRP 2020) exerts a genotoxic action even greater than that of a caffeine dose ~ 290 times above the corresponding limit. Therefore, with a reasonable approximation, the limit for MT EMFs should be lowered by at least ~ 4 × 104 times (136 × 290) for short-term exposures, and ~ 4 × 106 times for long-term exposures.Myoblast damage by oxidative stress has been proposed as one of the main causes of skeletal muscle loss due to induction of muscle damage. Platycodin D, a triterpenoid saponin found in the root of Platycodon grandiflorum (Jacq.) A. DC., has been known to possess strong antioxidant activity. However, whether platycodin D can defend myoblasts against oxidative injury remains to be elucidated. Therefore, this study was conducted to investigate the potential protective effects of platycodin D against oxidative stress in mouse myoblast C2C12 cells. The results demonstrated that platycodin D inhibited hydrogen peroxide (H2O2)-induced cytotoxicity and DNA damage by blocking abnormal reactive oxygen species (ROS) generation. Furthermore, platycodin D protected cells from the induction of mitochondria-mediated apoptosis by oxidative stress. In addition, platycodin D markedly promoted the activation of nuclear factor-erythroid-2-related factor 2 (Nrf2), which was associated with the enhanced expression of heme oxygenase-1 (HO-1) in the presence of H2O2. However, inhibiting the expression of HO-1 by Nrf2 siRNA significantly attenuated the protective effect of platycodin D, indicating that platycodin D activates the Nrf2/HO-1 signaling pathway to protect against oxidative stress. Based on current data, platycodin D may be useful as a potential therapeutic agent against various oxidative stress-related muscle disorders.Previously detected βsp and γ1sp dielectric relaxations on the spectrin-based membrane skeleton (MS) of human red blood cells (RBCs) have been shown sensitive to the attachment of MS to the lipid-protein membrane. Such relaxations were now detected on the MS of mammal (rat, horse, bovine, sheep and goat) and "unstrained" chicken RBCs. To become "unstrained" chicken RBCs were subjected consecutively to cold (4°C, >20 h) and either colchicine (15 mM) or vinblastine (30 μM) (4°C, 1 h) that led to irreversible disassembly of their marginal band and an additional portion of their cytoskeleton. With the exception of bovine RBCs, the critical frequency (fc) of either relaxation increased, although at different rates, with the decrease in the volume of RBC species. The strong increase in fc of γ1sp relaxation from 2.5 MHz ("unstrained" chicken RBCs) to 13 MHz (goat RBCs) could indicate denser state of MS in smaller RBC species. The low values of fc of γ1sp relaxation in "unstrained" chicken RBCs (2.5 MHz) and bovine RBCs (4.5 instead of 9 MHz) could be related to their extraordinary thermal stability at the temperature of spectrin denaturation.Összefoglaló. Az áramütés súlyos esetben hirtelen halállal vagy több szervrendszer kiterjedt károsodásával járhat. A magasfeszültségű áramütés (>1000 V) általában súlyosabb égési sérülésekkel és magasabb kórházi mortalitással jár, mint az alacsonyfeszültségű, de a sérülések súlyosságát a feszültségen kívül a test ellenállása, az áramexpozíció ideje, az áram fajtája, erőssége és útja is befolyásolja. A kritikus állapotú vagy súlyos égési sérüléseket szenvedett betegek sürgősségi ellátása komplex és multidiszciplináris szemléletet igényel. A súlyos szövődményekkel járó áramütéses balesetek ugyanakkor a fejlett országokban ritkák az áramütés következtében sürgősségi osztályon jelentkező betegek döntő többsége panaszmentesen vagy minor panaszokkal kerül felvételre. A ritmuszavarok az áramütéses balesetek messze leggyakoribb cardialis szövődményei, és rendszerint közvetlenül az áramütés után jelentkeznek. Az elektromos áram kamrafibrillációt vagy asystoliát is kiválthat, mely a baleset helyszínén ellátás nélkül hay ill patients with severe burns and/or other injuries require a multidisciplinary intensive treatment. However, such complications are rare in the developed countries most patients present in the emergency department with no or minor symptoms and do not require hospital admission. Arrhythmias are the most frequent cardiac complications after EA. Electrical current may cause ventricular fibrillation or asystolia which can lead to death on the scene. In patients presenting in the emergency department, clinically relevant arrhythmias are rare and can be diagnosed by a 12-lead ECG, therefore a systematic monitoring may not be indicated. Aim of our work is to review the most frequent complications after an electrical accident with special focus on cardiac complications and arrhythmias. The other aim of the manuscript is to summarize the most important aspects of emergency treatment and indication for ECG monitoring after electrical accident. Orv Hetil. 2020; 161(47) 1979-1988.

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