Impactos da pós-graduação stricto sensu na formação de professores de português da educação básica do Distrito Federal

This study sought to investigate the impact of stricto sensu post-graduate growth in portuguese teachers training of basic education who work in DF’s public school, analyzing the growth of stricto sensu post-graduate in the last 10 years in Education and Languages’ areas together with the data of basic education teachers working in the DF’s public school system who obtained the titles of Masters and /or PhD in the same period, making it possible to observe the evolution of the continuing education of teachers at this level of education. It also pointed out aspects concerning the National System of Post-Graduate and the role of CAPES in the induction of teachers’ continuing education at this level of studies. Researches on continuing teacher educa-tion were analyzed. The findings confirm the progress in the involvement of basic education teachers active in DF’s public education with stricto sensu post-graduate and at the same time the importance of further efforts incentive for a more significant growth of incomes and entitlements.  Este trabalho procurou investigar o impacto do crescimento da Pós-graduação stricto sensu na formação de professores de português da Educação básica que atuam na rede pública de ensino do Distrito Federal (DF), avaliando o comparativo entre o crescimento da Pós-graduação stricto sensu, nas áreas de Educação e Letras, nos últimos 10 anos com a relação de professores da Educação Básica atuantes na rede pública de ensino do DF que ingressaram e obtiveram os títulos de mestrado e/ou doutorado no mesmo período, possibilitando observar a evolução da formação continuada dos professores nesse nível de ensino. Também foram apontados aspectos que dizem respeito ao Sistema Nacional de Pós-graduação e o papel da CAPES no incentivo da formação continuada de professores em nível de Pós-graduação stricto sensu. Pesquisas realizadas sobre a formação continuada de professores foram analisadas. As conclusões confirmam o avan-ço no envolvimento de professores da Educação Básica atuantes na rede pública de ensino do DF com a Pós-graduação stricto sensu e ao mesmo tempo a importância de esforços adicionais de incentivo para um crescimento mais expressivo de ingressos e titulações. &nbsp

Reduction of Diphenyl Diselenide and Analogs by Mammalian Thioredoxin Reductase Is Independent of Their Gluthathione Peroxidase-Like Activity: A Possible Novel Pathway for Their Antioxidant Activity

Since the successful use of the organoselenium drug ebselen in clinical trials for the treatment of neuropathological conditions associated with oxidative stress, there have been concerted efforts geared towards understanding the precise mechanism of action of ebselen and other organoselenium compounds, especially the diorganyl diselenides such as diphenyl diselenide, and its analogs. Although the mechanism of action of ebselen and other organoselenium compounds has been shown to be related to their ability to generally mimic native glutathione peroxidase (GPx), only ebselen however has been shown to serve as a substrate for the mammalian thioredoxin reductase (TrxR), demonstrating another component of its pharmacological mechanisms. In fact, there is a dearth of information on the ability of other organoselenium compounds, especially diphenyl diselenide and its analogs, to serve as substrates for the mammalian enzyme thioredoxin reductase. Interestingly, diphenyl diselenide shares several antioxidant and neuroprotective properties with ebselen. Hence in the present study, we tested the hypothesis that diphenyl diselenide and some of its analogs (4,4’-bistrifluoromethyldiphenyl diselenide, 4,4’-bismethoxy-diphenyl diselenide, 4.4’-biscarboxydiphenyl diselenide, 4,4’-bischlorodiphenyl diselenide, 2,4,6,2’,4’,6’-hexamethyldiphenyl diselenide) could also be substrates for rat hepatic TrxR. Here we show for the first time that diselenides are good substrates for mammalian TrxR, but not necessarily good mimetics of GPx, and vice versa. For instance, bis-methoxydiphenyl diselenide had no GPx activity, whereas it was a good substrate for reduction by TrxR. Our experimental observations indicate a possible dissociation between the two pathways for peroxide degradation (either via substrate for TrxR or as a mimic of GPx). Consequently, the antioxidant activity of diphenyl diselenide and analogs can be attributed to their capacity to be substrates for mammalian TrxR and we therefore conclude that subtle changes in the aryl moiety of diselenides can be used as tool for dissociation of GPx or TrxR pathways as mechanism triggering their antioxidant activities

Blockade of adenosine A2A receptors prevents staurosporine-induced apoptosis of rat hippocampal neurons

Since adenosine A2A receptor (A2ARs) blockade protects against noxious brain insults involving apoptosis, we directly tested if A2AR blockade prevents apoptosis induced by staurosporine (STS). Exposure of rat hippocampal neurons to STS (30 nM, 24 h) decreased neuronal viability while increasing the number apoptotic-like neurons and de-localizing mitochondria and cytochrome c immunoreactivities. This was prevented by the selective A2AR antagonists, SCH58261 and ZM241385 (50 nM). Shorter incubation periods (6 h) with STS caused no neuronal loss but decreased synaptophysin and MAP-2 immunoreactivities, which was prevented by SCH58261. Furthermore, STS (100 nM) decreased MTT reduction and increased caspase-3 activity in rat hippocampal nerve terminals, which was prevented by SCH58261. These results show that A2AR blockade inhibits STS-induced apoptotic-like neuronal cell death. This begins with an apoptotic-like synaptotoxicity, which later evolved into an overt neurotoxicity, and A2ARs effectively control this initial synaptotoxicity, in agreement with their predominant synaptic localization in the hippocampus.http://www.sciencedirect.com/science/article/B6WNK-4NTRT29-1/1/e8601014d0729171e70d9df284a4044

Neuronal Adenosine A2A Receptors Are Critical Mediators of Neurodegeneration Triggered by Convulsions

Neurodegeneration is a process transversal to neuropsychiatric diseases and the understanding of its mechanisms should allow devising strategies to prevent this irreversible step in brain diseases. Neurodegeneration caused by seizures is a critical step in the aggravation of temporal lobe epilepsy, but its mechanisms remain undetermined. Convulsions trigger an elevation of extracellular adenosine and upregulate adenosine A2A receptors (A2AR), which have been associated with the control of neurodegenerative diseases. Using the rat and mouse kainate model of temporal lobe epilepsy, we now tested whether A2AR control convulsions-induced hippocampal neurodegeneration. The pharmacological or genetic blockade of A2AR did not affect kainate-induced convulsions but dampened the subsequent neurotoxicity. This neurotoxicity began with a rapid A2AR upregulation within glutamatergic synapses (within 2 h), through local translation of synaptic A2AR mRNA. This bolstered A2AR-mediated facilitation of glutamate release and of long-term potentiation (LTP) in CA1 synapses (4 h), triggered a subsequent synaptotoxicity, heralded by decreased synaptic plasticity and loss of synaptic markers coupled to calpain activation (12 h), that predated overt neuronal loss (24 h). All modifications were prevented by the deletion of A2AR selectively in forebrain neurons. This shows that synaptic A2AR critically control synaptic excitotoxicity, which underlies the development of convulsions-induced neurodegeneration