Sleep in Infants with Congenital Heart Disease

OBJECTIVES: To investigate hypoxia and sleep disordered breathing in infants with congenital heart disease. METHODS: Prospective study. In-hospital full polysomnography was performed on 14 infants with congenital heart disease, age 7 ±1 months, and in 7 normal infants, age 10 ±2 months. Congenital heart disease infants were classified as acyanotic (n=7) or cyanotic (n=7). RESULTS: Nutritional status, assessed by the Gomez classification and expressed as % weight for age, was 70 ±7, 59 ±11 and 94 ±16 in the acyanotic, cyanotic congenital heart disease and control infants, respectively (p<0.001). The respiratory disturbance index (AHI, events per hour) was [median (25-75%)]: 2.5 (1.0-3.4), 2.4 (1.5-3.1) and 0.7 (0.7-0.9) in acyanotic, cyanotic CHD infants and controls, respectively (p=0.013). Almost all congenital heart disease infants (11 out of 14) and only one control infant had an AHI >1 event/hour. The minimum oxygen saturation was 79% (74-82), 73% (57-74) and 90% (90-91) in the acyanotic, cyanotic congenital heart disease infants and controls, respectively (p <0.001). The arousal index (events/hour) was similar among the three groups at 8.4 ±2.4, 10.3 ±8.7 and 6.5 ±3, respectively (p=0.451). CONCLUSIONS: Infants with congenital heart disease frequently present with sleep-disordered breathing associated with oxygen desaturations but not arousals. Therefore, sleep may represent a significant burden to infants with congenital heart disease

Quantiication of coumarins in wine spirit aged by different technologies using Chestnut wood

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RECORRÊNCIA DE ALAGAMENTOS NA CIDADE DE TEÓFILO OTONI, MINAS GERAIS: UM ESTUDO INICIAL NO BAIRRO NOVO HORIZONTE

A desarmonia entre ocupação, uso do solo e planejamentos estrutural e ambiental geralmente levam a ocorrência de sérios problemas à população. Nesse sentido, este estudo busca relatar o histórico do local, pesquisar motivos dos casos ocorridos e apresentar providências iniciais. Os alagamentos decorrem da habitação descontrolada, falta de fiscalização por parte das autoridades e inexistência de ações para diminuir os riscos e prevenir desastres futuros

Insulin therapy modulates mitochondrial dynamics and biogenesis, autophagy and tau protein phosphorylation in the brain of type 1 diabetic rats

AbstractThe main purpose of this study was to examine whether streptozotocin (STZ)-induced type 1 diabetes (T1D) and insulin (INS) treatment affect mitochondrial function, fission/fusion and biogenesis, autophagy and tau protein phosphorylation in cerebral cortex from diabetic rats treated or not with INS. No significant alterations were observed in mitochondrial function as well as pyruvate levels, despite the significant increase in glucose levels observed in INS-treated diabetic rats. A significant increase in DRP1 protein phosphorylated at Ser616 residue was observed in the brain cortex of STZ rats. Also an increase in NRF2 protein levels and in the number of copies of mtDNA were observed in STZ diabetic rats, these alterations being normalized by INS. A slight decrease in LC3-II levels was observed in INS-treated rats when compared to STZ diabetic animals. An increase in tau protein phosphorylation at Ser396 residue was observed in STZ diabetic rats while INS treatment partially reversed that effect. Accordingly, a modest reduction in the activation of GSK3β and a significant increase in the activity of phosphatase 2A were found in INS-treated rats when compared to STZ diabetic animals. No significant alterations were observed in caspases 9 and 3 activity and synaptophysin and PSD95 levels. Altogether our results show that mitochondrial alterations induced by T1D seem to involve compensation mechanisms since no significant changes in mitochondrial function and synaptic integrity were observed in diabetic animals. In addition, INS treatment is able to normalize the alterations induced by T1D supporting the importance of INS signaling in the brain

A new perspective on vescalagin, castalagin, and their degadation pathways in wine spirits ageing

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Nanoparticles In Treatment Of Thermal Injured Rats: Is It Safe?

The aim of this study was to assess whether thermal trauma induced oxidative stress altered the balance between oxidant and antioxidant systems in the blood of burn wound rats in the absence and presence of silver nanoparticles and S-nitrosoglutathione, GSNO. Free silver nanoparticles, free GSNO and silver nanoparticles + GSNO had no cytotoxic effects. Under anesthesia, the shaved dorsum of the rats was exposed to 90°C (burn group) water bath. Studied compounds were administered topically immediately and at 28 days after the burn injury, four times a day. Silver nanoparticles and silver nanoparticles + GSNO were no toxic in vitro and in vivo. There were no significant differences in the levels of urea, creatinine, aminotransferases and hematological parameters, in control-burn groups (free silver nanoparticles) and treated-burn groups (free GSNO or silver nanoparticles + GSNO). There were no differences in lipid peroxidation and in the levels of protein carbonyls and glutathione, used as oxidative stress markers. A little inflammatory cell response, papillary dermis vascularization, fibroblasts differentiated into contractile myofibroblasts and the presence of a large amount of extracellular matrix were evidenced in treated groups following skin injury. These results indicate that silver nanoparticles and GSNO may provide an effective action on wound healing.3041Tian, J., Wong, K.K.Y., Ho, C.M., Lok, C.N., Yu, W.Y., Che, C.M., Chiu, J.F., Tam, P.K.H., (2007) J. Chem. Med. Chem., 2, p. 129Teli, M.K., Mutalik, S., Rajanikant, G.K., (2010) Cur. Pharm. Design., 16, p. 1882Schaller, M., Laude, J., Bodewaldt, H., Hamm, G., Korting, H.C., (2004) Skin Pharmacol. Physiol., 17, p. 31Seabra, A.B., Da Silva, R., De Souza, G.F.P., De Oliveira, M.G., (2008) Artif. Organs, 32, p. 262Seabra, A.B., Pankotai, E., Fehér, M., Somlai, A., Kiss, L., Bíró, L., Szabó, C., Lacza, Z., (2007) Br. J. Dermatol., 156, p. 814Seabra, A.B., Martins, D., Simes, M.M.S.G., Da Silva, R., Brocchi, M., De Oliveira, M.G., (2010) Artif. Organs, 34, p. 204Durán, N., Marcato, P.D., Alves, O.L., De Souza, G.I.H., Esposito, E., (2005) J. Nanobiotechnol., 3, p. 1Durán, N., Marcato, P.D., De Souza, G.I.H., Alves, O.L., Esposito, E., (2007) J. Biomed. Nanotechnol., 3, p. 203Amadeu, T.P., Seabra, A.B., De Oliveira, M.G., Costa, A.M.A., (2007) J. Eur. Acad. Dermatol. Venereol., 21, p. 629Amadeu, T.P., Seabra, A.B., De Oliveira, M.G., Costa, A.M.A., (2008) J. Surg Res., 149, p. 84Correa, D.H.A., Melo, P.S., De Carvalho, C.A.A., De Azevedo, M.B.M., Durán, N., Haun, M., (2005) Eur. J. Pharmacol., 510, p. 17De Conti, R., Oliveira, D.A., Fernandes, A.M.A.P., Melo, P.S., Rodriguez, J.A., Haun, M., Castro, S.L., Durán, N., (1998) Vitro Mol. Toxicol, 11, p. 153Borefreund, E., Puerner, J.A., (1984) J. Tissue Cult. Methods, 9, p. 7Denizot, F., Lang, R., (1986) J. Immunol. Methods, 89, p. 271Michailidis, Y., Jamurta, A.Z., Nikolaidis, M.G., Fatouros, I.G., Koutedakis, Y., Papassotiriou, I., (2007) Med. Sci. Sport Exerc., 39, p. 1107Davis, T.A., Amare, M., Naik, S., Kovalchuk, A.L., Tadaki, D., (2007) Wound Repair Regen., 15, p. 57