Abstract In this study, the liquid-liquid equilibrium (LLE) data of systems containing ethyl linoleate/oleate/palmitate/laurate, ethanol and glycerol at temperatures ranging from 323.15 to 353.15 K were used to evaluate the performance of the NRTL, UNIFAC, Cubic-Plus-Association Equation of State (CPA EoS), and artificial neural network (ANN) models. The systems evaluated correspond to the most important components formed at the end of the ethanolysis reaction of soybean, palm and coconut oils. The temperature range selected is very important for heterogeneous catalysts, especially for high-pressure systems. The accuracy of the models was evaluated by average global deviation. UNIFAC, UNIFAC-LLE and CPA EoS models showed lower accuracy with deviations of 10.1, 8.01 and 5.95%, respectively. In spite of this predictive limitation, these models show high extrapolation capability for the description of LLE behavior when few experimental data are available in the literature. The ANN model shows the best agreement between experimental and predicted data with an average deviation of 1.12%. In this regard, ANN is offered in this work as an alternative to equations of state and activity coefficient models to be used in a more reliable and less cumbersome way for process simulators of biodiesel production and separation equipment design.

RESUMONovos estudos sugerem que os ácidos graxos poliinsaturados, como o ômega-3, podem reduzir os sintomas da esquizofrenia. O presente estudo avaliou o efeito preventivo do ômega-3 sobre os níveis de interleucinas (IL) e o fator neurotrófico derivado do cérebro (BDNF) em cérebros de ratos jovens submetidos a um modelo de esquizofrenia. O tratamento foi feito por 21 dias, iniciando no 30º dia de vida dos animais. Depois de 14 dias de tratamento com ômega-3 ou veículo, um tratamento concomitante com salina ou ketamina (25 mg/kg) foi iniciado e mantido até o último dia do experimento. No cortex pré-frontal dos ratos, os níveis de BDNF diminuíram em 1 h e 24 h depois da última administração de ketamina enquanto que o grupo administrado com ketamina e ômega-3 mostrou uma diminuição nos níveis de BDNF somente após as 24 h. Em contraste, ambas as intervenções induziram respostas similares quanto aos níveis de IL-1β e IL6. Esses achados sugerem que a similaridade nos níveis de IL-1β e IL6 em nossos grupos de experimento é devida ao mecanismo de ação da ketamina sobre o sistema imune. Mais estudos são necessários para explicar essa patologia. Em conclusão, de acordo com estudos prévios e considerando o atual estudo, nós sugerimos que o ômega-3 tem um papel profilático no desenvolvimento de sintomas associados à esquizofrenia.

ABSTRACTNew studies suggest that polyunsaturated fatty acids, such as omega-3, may reduce the symptoms of schizophrenia. The present study evaluated the preventive effect of omega-3 on interleukines (IL) and neurotrophin brain-derived neurotrophic factor (BDNF) levels in the brains of young rats subjected to a model of schizophrenia. Treatment was performed over 21 days, starting on the 30th day of rat's life. After 14 days of treatment with omega-3 or vehicle, a concomitant treatment with saline or ketamine (25 mg/kg) was started and maintained until the last day of the experiment. BDNF levels in the rat's prefrontal cortex were decreased at 1 h and 24 h after the last administration of ketamine, whereas the group administered with ketamine and omega-3 showed a decrease in BDNF levels only after 24 h. In contrast, both interventions induced similar responses in levels of IL-1β and IL6. These findings suggest that the similarity of IL-1β and IL6 levels in our experimental groups is due to the mechanism of action of ketamine on the immune system. More studies have to be carried out to explain this pathology. In conclusion, according to previous studies and considering the current study, we could suggest a prophylactic role of omega-3 against the outcome of symptoms associated with schizophrenia.

Concentrações elevadas de frutose são a principal carac-terística bioquímica da frutosemia, um grupo de doenças hereditárias na via metabólica deste carboidrato. Os principais achados clínicos observados nos pacientes afetados pela frutosemia incluem anormalidades neurológicas com retardo do desenvolvimento, cuja fisiopatologia ainda não está definida. No presente trabalho investigou-se os efeitos in vitro e in vivo da frutose sobre a atividade da enzima acetilcolinesterase (AChE) em diferentes estruturas cerebrais de ratos em desenvolvimento. Para os experimentos in vitro, a frutose foi adicionada em concentrações crescentes ao meio de incubação. Observou-se que a frutose inibiu a atividade da AChE em córtex cerebral de ratos de 30 de vida, mesmo em baixas concentrações (0,1 mM). Para os experimentos in vivo, os ratos sofreram eutanásia 1 hora após uma administração única de frutose (5 µmol/g; subcutânea). O grupo controle recebeu o mesmo volume de solução salina. A atividade da AChE encontrou-se aumentada em córtex cerebral de ratos com 30 e 60 dias de vida que receberam administração de frutose. Finalmente, não se observou diferença significativa entre os grupos controle e frutose em cérebro de animais de 15 e 90 dias de vida. Os resultados do presente trabalho sugerem que um desequilíbrio na homeostase colinérgica pode estar envolvido na fisiopatologia do dano cerebral observado em pacientes jovens afetados pela frutosemia.

Increased fructose concentrations are the biochemical hallmark of fructosemia, a group of inherited disorders on the metabolic pathway of this sugar. The main clinical findings observed in patients affected by fructosemia include neurological abnormalities with developmental delay, whose pathophysiology is still undefined. In the present work we investigated the in vitro and in vivo effects of fructose on acetylcholinesterase (AchE) activity in brain structures of developing rats. For the in vitro experiments, fructose was added at increasing concentrations to the incubation medium. It was observed that fructose provoked an inhibition of acetylcholinesterase activity in cerebral cortex of 30-day-old-rats, even at low concentrations (0.1 mM). For the in vivo experiments, rats were killed 1 h after a single fructose administration (5 µmol/g). Control group received the same volume of saline solution. We found that AchE activity was increased in cerebral cortex of 30- and 60-day-old rats receiving fructose administration. Finally, we observed that AchE activity was unaffected by acute fructose administration in cerebral cortex, striatum or hippocampus of 15- and 90-day-old rats. The present data suggest that a disruption in cholinergic homeostasis may be involved in the pathophysiology of brain damage observed in young patients affected by fructosemia.