Publications by authors named "E A Proper"

Article Synopsis
  • The study aimed to create a prioritized list of research themes and essential data points related to mental health issues in children and adolescents presenting to emergency departments (ED).
  • A Delphi survey involving various stakeholders, including clinicians and patients, was conducted to gather and prioritize these research themes and data points.
  • The final results highlighted 71 key items, focusing on safety in the ED, the effectiveness of mental health spaces, follow-up care, and important data like risk factors and behavioral disturbances.
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Objective This study aimed to describe and compare the proportion of patients classified as an emergency department (ED) mental health presentation under different definitions, including the Australian Institute of Health and Welfare (AIHW) definition. Methods This retrospective cohort study enrolled all patients that presented to the EDs of a multi-centre Victorian health service between 1 January 2020 and 30 June 2023. Varying definitions of a mental health presentation were applied to each ED attendance, applying the current AIHW definition (using selected diagnosis codes), broader diagnosis-based coding, the presenting complaint recorded at triage and whether the patient was seen by or referred to the emergency psychiatric service (EPS).

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Rationale: Altered expression of glutamate transporter EAAT2 protein has been reported in the hippocampus of patients with temporal lobe epilepsy (TLE). Two alternative EAAT2 mRNA splice forms, one resulting from a partial retention of intron 7 (I7R), the other from a deletion of exon 9 (E9S), were previously implicated in the loss of EAAT2 protein in patients with amyotrophic lateral sclerosis.

Methods: By RT-PCR we studied the occurrence of I7R and E9S in neocortical and hippocampal specimens from TLE patients and non-neurological controls.

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Molecular misreading of the ubiquitin-B (UBB) gene results in a dinucleotide deletion in UBB mRNA. The resulting mutant protein, UBB+1, accumulates in the neuropathological hallmarks of Alzheimer disease. In vitro, UBB+1 inhibits proteasomal proteolysis, although it is also an ubiquitin fusion degradation substrate for the proteasome.

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Glial fibrillary acidic protein (GFAP) is considered to be a highly specific marker for glia. Here, we report on the expression of GFAP in neurons in the human hippocampus. Intriguingly, this neuronal GFAP is coded by out-of-frame splice variants and its expression is associated with Alzheimer pathology.

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