Tradução, adaptação transcultural e validação de conteúdo da versão em português do Coping Behaviours Inventory (CBI) para a população brasileira

Estratégias de coping relacionam-se diretamente com o sucesso de abstinência do uso de álcool. No Brasil não há instrumentos que identifiquem estratégias específicas para usuários de álcool. O objetivo deste estudo foi realizar a tradução, adaptação transcultural e validação de conteúdo do Coping Behaviours Inventory (CBI). Os procedimentos seguiram de tradução e retradução, adaptação transcultural, avaliação de conteúdo e estudo piloto. A versão final em português foi aplicada por telefone a 40 usuários de álcool que buscaram auxílio em um serviço de teleatendimento, o VIVAVOZ. A versão retraduzida aproximou-se da original. Quanto à validação de conteúdo, a maioria dos itens é satisfatória e aceitável. Além disso, a concordância entre os juízes, referente à dimensão teórica, apresentou índice kappa médio igual a 0,666, sendo o nível de concordância considerado substancial. Os resultados são satisfatórios e aceitáveis, o que demonstra que a escala está adequada para investigar as estratégias de coping para usuários de álcool.</jats:p

Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging

Defects in the DNA repair mechanism nucleotide excision repair (NER) may lead to tumors in xeroderma pigmentosum (XP) or to premature aging with loss of subcutaneous fat in Cockayne syndrome (CS). Mutations of mitochondrial (mt)DNA play a role in aging, but a link between the NER-associated CS proteins and base excision repair (BER)-associated proteins in mitochondrial aging remains enigmatic. We show functional increase of CSA and CSB inside mt and complex formation with mtDNA, mt human 8-oxoguanine glycosylase (mtOGG)-1, and mt single-stranded DNA binding protein (mtSSBP)-1 upon oxidative stress. MtDNA mutations are highly increased in cells from CS patients and in subcutaneous fat of aged Csbm/m and Csa−/− mice. Thus, the NER-proteins CSA and CSB localize to mt and directly interact with BER-associated human mitochondrial 8-oxoguanine glycosylase-1 to protect from aging- and stress-induced mtDNA mutations and apoptosis-mediated loss of subcutaneous fat, a hallmark of aging found in animal models, human progeroid syndromes like CS and in normal human aging

Deceleration of Fusion–Fission Cycles Improves Mitochondrial Quality Control during Aging

Mitochondrial dynamics and mitophagy play a key role in ensuring mitochondrial quality control. Impairment thereof was proposed to be causative to neurodegenerative diseases, diabetes, and cancer. Accumulation of mitochondrial dysfunction was further linked to aging. Here we applied a probabilistic modeling approach integrating our current knowledge on mitochondrial biology allowing us to simulate mitochondrial function and quality control during aging in silico. We demonstrate that cycles of fusion and fission and mitophagy indeed are essential for ensuring a high average quality of mitochondria, even under conditions in which random molecular damage is present. Prompted by earlier observations that mitochondrial fission itself can cause a partial drop in mitochondrial membrane potential, we tested the consequences of mitochondrial dynamics being harmful on its own. Next to directly impairing mitochondrial function, pre-existing molecular damage may be propagated and enhanced across the mitochondrial population by content mixing. In this situation, such an infection-like phenomenon impairs mitochondrial quality control progressively. However, when imposing an age-dependent deceleration of cycles of fusion and fission, we observe a delay in the loss of average quality of mitochondria. This provides a rational why fusion and fission rates are reduced during aging and why loss of a mitochondrial fission factor can extend life span in fungi. We propose the ‘mitochondrial infectious damage adaptation’ (MIDA) model according to which a deceleration of fusion–fission cycles reflects a systemic adaptation increasing life span

Efeitos da Difenilhidantoína sobre a reatividade vascular no sapo (Bufo Arenarum)

Efeitos da Diefenilhidantoína sobre a reatividade vascular no sapo (Bufo Arenarum

Efeitos da Difenilhidantoína sobre a reatividade vascular no sapo (Bufo Arenarum)

Efeitos da Diefenilhidantoína sobre a reatividade vascular no sapo (Bufo Arenarum