Perfil epidemiológico das crianças vítimas de queimaduras em um hospital infantil da Serra Catarinense / Epidemiological profile of the burned children at a children's hospital of the Serra Catarinense / Perfil epidemiológico de niños víctimas de quemaduras en un hospital infantil de la sierra catarinense

Objetivos: Identificar o perfil epidemiológico dos pacientes acometidos por queimadura internados em um hospital infantil da Serra Catarinense. Método: Estudo descritivo, retrospectivo e transversal realizado por meio de análise prontuários de crianças (0 a 15 anos, 11 meses e 29 dias) internadas por queimadura em um hospital infantil da Serra Catarinense, no período de janeiro de 2013 a dezembro de 2018. Variáveis analisadas foram idade, sexo, tempo médio de internação, necessidade de internação em unidade de terapia intensiva (UTI), desfecho final, agente causal, região do corpo acometida e superfície corporal queimada (SCQ). Resultados: Foram analisados 78 prontuários, com média de idade de 4,2 anos, sendo maior a prevalência do sexo masculino (n=47; 60,3%). O tempo médio de internação foi 11 dias (62,8%), sendo que 4 pacientes (5%) necessitaram de internação em UTI e, destes, um foi a óbito. O principal agente causal foi líquido aquecido (n=61; 78%). Em relação às áreas acometidas 41% (n=32) apresentaram envolvimento da cabeça e a maior parte do casos computados apresentaram SCQ maior que 20% (n=18; 23,1%). Conclusão: A fase mais suscetível à queimadura é a pré-escolar, com predominância no sexo masculino, sendo que o acidente é por escaldadura e que acomete várias regiões do corpo, principalmente parte superior do mesmo. Assim, programas preventivos devem chamar a atenção dos pais e cuidadores quanto à avaliação dos riscos, de modo a antecipá-los, afastando ou tornando-os indisponíveis às crianças.

Objective: To identify the epidemiological profile of burn patients admitted to a children hospital of Serra Catarinense. Methods: A descriptive, retrospective, and cross-sectional study carried out through the analysis of medical records of children (0 to 15 years, 11 months and 29 days) hospitalized by burns in a children hospital of Serra Catarinense, from January 2013 to December 2018. Variables assessed were age, gender, average length of stay, need for admission to the intensive care unit (ICU), final outcome, causative agent, affected body region and burned body surface (SCQ). Results: 78 medical records were analyzed, with a mean age of 4.2 years, most of the sample was male (n=47; 60.3%). The average length of stay was 11 days (62.8%), with 4 patients (5%) requiring ICU admission and one patient dying. The main causative agent was heated fluid (n=61; 78%) and in relation to the affected areas, 41% (n=32) of the cases presented head involvement and most of the computed cases presented SQ greater than 20% (n=18; 23.1%). Conclusion: The results of the study indicate that the most susceptible phase to burn is the preschool, with predominance in males, and the accident is by scalding and affecting various regions of the body, especially the upper part of it. Thus, preventive programs should draw the attention of parents and caregivers to risk assessment in order to anticipate them, driving them away or unavailable to children.

Objetivo: identificar el perfil epidemiológico de pacientes con quemaduras ingresados en un hospital de niños de la sierra catarinense. Método: Estudio descriptivo, retrospectivo y transversal realizado a través del análisis de historias clínicas de niños (0 a 15 años, 11 meses y 29 días) hospitalizados por quemaduras en un hospital de niños de la sierra catarinense, de enero de 2013 a diciembre de 2018. Las variables evaluadas fueron la edad, el sexo, la duración promedio de la estadía, la necesidad de ingreso a la unidad de cuidados intensivos (UCI), el resultado final, el agente causal, la región corporal afectada y la superficie corporal quemada (SCQ). Resultados: Fueron analisadas 78 histórias clínicas de pacientes com edad de 4,2 años, con mayor prevalencia de varones (n=47; 60,3%). El tiempo promedio de estadía fue de 11 días (62,8%), con 4 pacientes (5%) que requirieron ingreso a la UCI y de estos, uno falleció. El principal agente causal fue los liquidos calientes (n=61; 78%). Con respecto a las áreas afectadas, el 41% (n=32) la cabeza y la mayoría de los casos presentaron un SCQ superior al 20% (n=18; 23,1%). Conclusión: Los resultados del estudio indican que la fase más susceptible a las quemaduras es la preescolar, con predominio en los hombres, y el agente causador los líquidos calientes, afectando varias regiones del cuerpo. Por lo tanto, los programas preventivos deben llamar la atención de los padres y cuidadores sobre la evaluación de riesgos para anticiparlos, alejándolos o no disponibles para los niños.

Neurotoxicity of cadmium on immature hippocampus and a neuroprotective role for p38 MAPK.

The developing brain is very sensitive to damage by toxic agents, many of which only manifest in adulthood. Cadmium [Cd(II)] is an environmental pollutant which is widely used in industry and is a constituent of tobacco smoke. Exposure to Cd(II) has been linked to detrimental effects on mammalian cells including neural cells. We have investigated the action of Cd(II) on immature hippocampus by assessing cell viability and modulation of AKT/PKB and mitogen-activated protein kinase (MAPK) family members including extracellular signal-regulated kinase (ERK)-1/2, p38 MAPK and c-Jun N-terminal kinases (JNK). Hippocampal slices from immature rats (postnatal day 14; PN14) were incubated with Cd(II) (5-200 microM) for 3h and the effects on protein phosphorylation were analyzed by western blotting. Phosphorylation of p38(MAPK) was enhanced by Cd(II) at all doses tested. Cd(II) also stimulated the phosphorylation of ERK1/2 in a concentration-dependent manner. However, the phosphorylation of JNK and AKT was not altered by the metal. Moreover, Cd(II) reduced cell viability, as measured by MTT reduction. Inhibition of p38 MAPK by SB203580 aggravated the acute Cd(II)-induced impairment of cell viability, whereas inhibition of MEK by PD98059 did not alter the effects of Cd(II). The present data suggest that in immature hippocampal cells p38 MAPK may be a part of signaling pathway that counteracts acute Cd(II) neurotoxicity. In conclusion, our results showed that Cd(II) impairs cell viability and disturbs MAPKs pathways in an important developmental stage for synaptic organization.

Diphenyl diselenide confers neuroprotection against hydrogen peroxide toxicity in hippocampal slices.

The present study aimed at investigating the potential in vitro protective effect of the organochalcogenide diphenyl diselenide - (PhSe)2 - against hydrogen peroxide (H2O2)-induced toxicity in rat hippocampal slices. Hippocampal slices were treated for 1 h with H2O2 (2 mM) in the presence or absence of (PhSe)2 (0.1-10 microM). H2O2 treatment significantly decreased cell viability (measured by MTT test) and the co-incubation with (PhSe)(2) (10 microM) significantly blunted such phenomenon. The non permeable thiol compounds dithiothreitol (DTT) (100 microM) or reduced glutathione (GSH) (100 microM), which did not display protective effects against H2O2-induced loss of cell viability per se, significantly improved the protective effects elicited by (PhSe)2. Conversely, the permeable form of GSH (GSH monoethyl ester) was unable to alter the neuroprotection mediated by (PhSe)2. The treatment of rat hippocampal slices with H2O2 also increased the lipid peroxidation and decreased the intracellular GSH levels. Moreover, (PhSe)2 (from 0.1 microM) significantly decreased H2O2-induced lipid peroxidation. Interestingly, H2O2 decreased GSH levels and this phenomenon was partially prevented by (PhSe)2. The potential effects of H2O2 on MAPKs phosphorylation (ERK1/2, p38 MAPK and JNK1/2) were also evaluated. Even though H2O2 (2 mM) did not alter p38 MAPK and JNK1/2 phosphorylation in hippocampal slices, it stimulated ERK1/2 phosphorylation and the co-incubation with (PhSe)2 (10 microM) blocked this effect. Taken together, the present results indicate that (PhSe)2 exerts protective effects against H2O2-induced oxidative damage in hippocampal slices and avoided the increase in ERK1/2 phosphorylation promoted by H2O2. The neuroprotective effect of compound seems to be related to its thiol-peroxidase-like activity and appears to occur at the extracellular milieu because a permeable form of GSH was unable to improve the protective effect of the compound as did the impermeable GSH.

The activation of ERK1/2 and p38 mitogen-activated protein kinases is dynamically regulated in the developing rat visual system.

Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases that play an instrumental role in signal transduction from the cell surface to the nucleus. These enzymes are major intracellular mediators of developmental events and recently have been shown to control also synaptic plasticity processes [Sweatt, J.D., 2004. Mitogen-activated protein kinases in synaptic plasticity and memory. Curr. Opin. Neurobiol. 14, 311-317; Thomas, G.M., Huganir, R.L., 2004. MAPK cascade signalling and synaptic plasticity. Nat. Rev. Neurosci. 5, 173-183]. Mammalian members of this family are extracellular signal-regulated kinases 1/2 (ERK 1/2), c-Jun amino-terminal kinases or stress-activated protein kinases (JNK/SAPKs) and p38 kinases (p38(MAPK)). At the level of the visual system, it has been demonstrated that the ERK pathway regulates developmental plastic processes at both retino-thalamic and thalamo-cortical level and that p38(MAPK) controls a peculiar form of long-term depression in the visual cortex [Di Cristo, G., Berardi, N., Cancedda, L., Pizzorusso, T., Putignano, E., Ratto, G.M., Maffei, L., 2001. Requirement of ERK activation for visual cortical plasticity. Science 292, 2337-2340; Naska, S., Cenni, M.C., Menna, E., Maffei, L., 2004. ERK signaling is required for eye-specific retino-geniculate segregation. Development 131, 3559-3570; Xiong, W., Kojic, L.Z., Zhang, L., Prasad, S.S., Douglas, R., Wang, Y., Cynader, M.S., 2006. Anisomycin activates p38 MAP kinase to induce LTD in mouse primary visual cortex. Brain Res. 1085, 68-76]. Here, as a first approach to gain more insight on the role of two MAPKs - ERK1/2 and p38(MAPK) - in visual system maturation, we characterized by western blot the regulation of their phosphorylation/activation in rat retina, superior colliculus and visual cortex, during postnatal development from birth to adult age. Our main results show that: (i) in the retina p38(MAPK) activation peaks at P4, and then, from P15 to P45, both ERK1/2 and p38(MAPK) phosphorylation increases; (ii) in the superior colliculus phosphorylation of both MAPKs increases between P4 and P15; (iii) in the visual cortex ERK1/2 phosphorylation increases from P15 to P45, while phosphorylation of p38(MAPK) increases starting from P4. The present data demonstrate a distinct regulation of the activation of ERK1/2 and p38(MAPK) in the three visual areas analyzed which occurs in temporal correlation with critical events for visual system maturation. These results suggest an important role for ERK1/2 and p38(MAPK) in the postnatal development of the rat visual system.

Cadmium stimulates MAPKs and Hsp27 phosphorylation in bovine adrenal chromaffin cells.

Cadmium (Cd(2+)) is a common environmental pollutant, which is widely used in industry and is a constituent of tobacco smoke. Exposure to this heavy metal has been linked to a wide range of detrimental effects on mammalian cells. In this study, the action of Cd(2+) on protein phosphorylation in bovine adrenal chromaffin cells (BACCs) was examined. Cells were incubated with (32)Pi in the presence of Cd(2+) (1-50 microM) and proteins were separated by one- or two-dimensional electrophoresis. An increase in the phosphorylation of BACCs proteins, without changing cell viability, was observed in response to Cd(2+) (5-50 microM). Particularly at three spots, with molecular weight of 25kDa and isoeletric point range 4.0-4.5, which were identified as phosphorylated isoforms of the heat shock protein of 27kDa (Hsp27). Phosphorylation of the p38(MAPK), a member of mitogen-activated protein kinase (MAPK) family, was stimulated by Cd(2+) over the same concentration range and it was the major upstream protein kinase involved in the phosphorylation of all three spots of Hsp27. Cd(2+) also stimulated the phosphorylation of other MAPK family member, the extracellular signal-regulated kinase (ERK)-1/2. Therefore, primary adrenal chromaffin cells are a target for Cd(2+) and both the ERK1/2 and the p38(MAPK) are activated. Additionally, Hsp27 is highly phosphorylated in response to the metal exposure, due to p38(MAPK) activation. These biochemical effects of Cd(2+) might disrupt the normal secretory function of these cells.

Modulation of ERK1/2 and p38(MAPK) by lead in the cerebellum of Brazilian catfish Rhamdia quelen.

Lead (Pb2+) is a neurotoxic trace metal, widespread in aquatic environment that can change physiologic, biochemical and behavioral parameters in diverse fish species. Chemical exposure may drive modulation of mitogen-activated protein kinases (MAPKs) that are a family of highly conserved enzymes which comprise ubiquitous groups of signaling proteins playing critical regulatory roles in cell physiology. Extracellular signal-regulated kinases (ERK1/2) and p38(MAPK) control complex programs such as gene expression, embryogenesis, cell differentiation, cell proliferation, cell death and synaptic plasticity. Little information is available about MAPKs in aquatic organisms and their modulation by trace metals. The aim of this work was to determine the modulation of ERK1/2 and p38(MAPK) phosphorylation by Pb2+ in vivo and in vitro, in cerebellar slices of the catfish, Rhamdia quelen. In the in vitro model, slices were incubated for 3 h with lead acetate (1-10 microM). In the in vivo studies, the animals were exposed for 2 days to lead acetate (1 mg L(-1)). ERK1/2 and p38(MAPK) (total and phosphorylated forms) were immunodetected in cerebellar slices by Western blotting. Pb2+ added in vitro at 5 and 10 microM increased significantly the phosphorylation of both MAPKs. The in vivo exposed animals also showed a significant increase of ERK1/2 and p38(MAPK) phosphorylation without changes in the total content of the enzymes. In conclusion, the present work indicates that it is possible to evaluate the ERK1/2 and p38(MAPK) activation in the central nervous system (CNS) of a freshwater fish largely distributed in South America. Moreover, Pb2+, an important environmental pollutant may activate in vitro and in vivo ERK1/2 and p38(MAPK) enzymes. These findings are important considering the functional and ecologic implications associated to Pb2+ exposure of a freshwater fish species, such as R. quelen, and the roles of ERK1/2 and p38(MAPK) in the control of brain development, neuroplasticity and cell death.