A Educação na Prisão não é uma Mera Atividade

Education and prison have always formed an incoherent pair: the first, finding its universal reasons in the particular context of the second, which, by its nature, offers only a contradictory frame for the free expression of the first one. How can prison, being anti-educative by itself, offer people an opportunity to explore useful knowledge from now until the day they are released? We will try to demonstrate that, amidst these contradictions, education is possible with the proviso that it is effectively an education for life, and not only instruction or reeducation.A educação e a prisão sempre formaram um par incoerente: a primeira encontrando sua justificação universal no contexto particular da segunda que, no entanto, por natureza, oferece apenas um quadro contraditório para a livre expressão da primeira. Como a prisão, que é antieducativa em si, pode oferecer às pessoas, uma possibilidade de contar com aprendizados úteis no seu momento presente e que lhe servirão até a sua saída? O artigo tentará mostrar que, em meio a essas contradições, uma educação é possível com a condição de que esta última seja efetivamente uma educação para toda a vida e não o ensino ou a reeducação

Spatio-temporal modeling of soil characteristics for soilscape reconstruction

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Virus Evolution Reveals an Exclusive Role for LEDGF/p75 in Chromosomal Tethering of HIV

Retroviruses by definition insert their viral genome into the host cell chromosome. Although the key player of retroviral integration is viral integrase, a role for cellular cofactors has been proposed. Lentiviral integrases use the cellular protein LEDGF/p75 to tether the preintegration complex to the chromosome, although the existence of alternative host proteins substituting for the function of LEDGF/p75 in integration has been proposed. Truncation mutants of LEDGF/p75 lacking the chromosome attachment site strongly inhibit HIV replication by competition for the interaction with integrase. In an attempt to select HIV strains that can overcome the inhibition, we now have used T-cell lines that stably express a C-terminal fragment of LEDGF/p75. Despite resistance development, the affinity of integrase for LEDGF/p75 is reduced and replication kinetics in human primary T cells is impaired. Detection of the integrase mutations A128T and E170G at key positions in the LEDGF/p75–integrase interface provides in vivo evidence for previously reported crystallographic data. Moreover, the complementary inhibition by LEDGF/p75 knockdown and mutagenesis at the integrase–LEDGF/p75 interface points to the incapability of HIV to circumvent LEDGF/p75 function during proviral integration. Altogether, the data provide a striking example of the power of viral molecular evolution. The results underline the importance of the LEDGF/p75 HIV-1 interplay as target for innovative antiviral therapy. Moreover, the role of LEDGF/p75 in targeting integration will stimulate research on strategies to direct gene therapy vectors into safe landing sites