Publications by authors named "A E Trezise"

Objectives: Depression is a significant mental health issue for older adults. Rumination is a key risk factor for depressive symptoms, and self-compassion is a protective factor. The aim of the current study was to test the processes by which self-compassion might act as a protective factor among older adults by investigating a mediation model, and whether the model is conditional on gender.

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Objectives: Depression is a significant mental health issue among older Australian adults. Research has indicated that insomnia is a key risk factor for the development of depressive symptoms in older adults, and that dispositional hope may be protective against the development of depressive symptoms in this population. This study examined whether dispositional hope and its dimensions, agency and pathways, moderated the relationship between insomnia symptoms and depressive symptoms among older Australian adults.

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Mammals express the sialic acids N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc) on cell surfaces, where they act as receptors for pathogens, including influenza A virus (IAV). Neu5Gc is synthesized from Neu5Ac by the enzyme cytidine monophosphate-N-acetylneuraminic acid hydroxylase (CMAH). In humans, this enzyme is inactive and only Neu5Ac is produced.

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Post-transcriptional regulation of gene expression through 5' untranslated region (5'UTR)-encoded cis-acting elements is an important mechanism for the control of protein expression levels. Through controlling specific aspects of translation initiation, expression can be tightly regulated while remaining responsive to cellular requirements. With respect to cystic fibrosis (CF), the overexpression of cystic fibrosis transmembrane conductance regulator (CFTR) protein trafficking mutants, such as delta-F508, is of great biological and clinical interest.

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The MYB oncogene is widely expressed in acute leukemias and is important for the continued proliferation of leukemia cells, suggesting that MYB may be a therapeutic target in these diseases. However, realization of this potential requires a significant therapeutic window for MYB inhibition, given its essential role in normal hematopoiesis, and an approach for developing an effective therapeutic. We previously showed that the interaction of c-Myb with the coactivator CBP/p300 is essential for its transforming activity.

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