The Impact of Breast Care Nurses: An Evaluation of the McGrath Foundation's Breast Care Nurse Initiative.

Objective: Over the four years to 30 June, 2017 the McGrath Foundation's Second Federal Government Breast Care Nurse (BCN) Initiative funded 57 McGrath BCNs (MBCNs) to deliver better continuity of care and provide specialized support to those diagnosed with and undergoing treatment for breast cancer. This article summarizes the findings generated through a mixed-method evaluation of the program's appropriateness, effectiveness, and efficiency.

Methods: The evaluation comprised surveys and semi-structured interviews with patients, multidisciplinary clinicians and MBCNs.

Projecting the radiation oncology workforce in Australia.

Research on radiation oncologists has indicated that there is a shortage in supply of specialist workers in this field internationally, and also within Australia. However, there are no current estimates as to what the future Australian radiotherapy workforce will look like. This paper aims to review the current status and capacity of the three main disciplines that make up the radiation oncology workforce in Australia and project the workforce supply and demand for 2014 and 2019.

Sialin, an anion transporter defective in sialic acid storage diseases, shows highly variable expression in adult mouse brain, and is developmentally regulated.

Sialin is a lysosomal membrane protein encoded by the SLC17A5 gene, which is mutated in patients with sialic acid storage diseases (SASD). To further understand the role of sialin in normal CNS development and in the progressive neuronal atrophy and dysmyelination seen in SASD, we investigated its normal cellular distribution in adult and developing mice. Overall, sialin showed granular immunoreactivity, consistent with a vesicular protein.

Gene knockout of amyloid precursor protein and amyloid precursor-like protein-2 increases cellular copper levels in primary mouse cortical neurons and embryonic fibroblasts.

Alzheimer's disease is characterised by the accumulation of amyloid-beta peptide, which is cleaved from the copper-binding amyloid-beta precursor protein. Recent in vivo and in vitro studies have illustrated the importance of copper in Alzheimer's disease neuropathogenesis and suggested a role for amyloid-beta precursor protein and amyloid-beta in copper homeostasis. Amyloid-beta precursor protein is a member of a multigene family, including amyloid precursor-like proteins-1 and -2.

Alpha7-nicotinic acetylcholine receptors mediate an Abeta(1-42)-induced increase in the level of acetylcholinesterase in primary cortical neurones.

The beta-amyloid protein (Abeta) is the major protein component of amyloid plaques found in the Alzheimer brain. Although there is a loss of acetylcholinesterase (AChE) from both cholinergic and non-cholinergic neurones in the brain of Alzheimer patients, the level of AChE is increased around amyloid plaques. Previous studies using P19 cells in culture and transgenic mice which overexpress human Abeta have suggested that this increase may be due to a direct action of Abeta on AChE expression in cells adjacent to amyloid plaques.

Glycosylation of acetylcholinesterase and butyrylcholinesterase changes as a function of the duration of Alzheimer's disease.

The identification of biochemical markers of Alzheimer's disease (AD) may help in the diagnosis of the disease. Previous studies have shown that Abeta(1-42) is decreased, and tau and phospho-tau are increased in AD cerebrospinal fluid (CSF). Our own studies have identified glycosylated isoforms of acetylcholinesterase (Glyc-AChE) and butyrylcholinesterase (Glyc-BuChE) that are increased in AD CSF.

Acetylcholinesterase is increased in mouse neuronal and astrocyte cultures after treatment with beta-amyloid peptides.

The cellular origin of the acetylcholinesterase (AChE) associated with amyloid plaques in the Alzheimer's disease (AD) brain is unknown. In this study we report that amyloid beta-peptides (Abeta) increased AChE levels in both neuronal and astrocytic primary cultures, supporting the possibility that both neurons and glia may make a direct contribution to the pool of AChE seen around amyloid deposits in the AD brain.

Cholinergic regulation of synaptic plasticity as a therapeutic target in Alzheimer's disease.

There is increasing evidence for disturbances in nicotinic acetylcholine receptor (nAChR) function in Alzheimer's disease (AD). nAChRs are involved in the regulation of many processes, including synaptic plasticity and memory. Levels of nAChRs are altered in the Alzheimer brain and there is evidence that the amyloid betaprotein (Abeta) can directly bind to nAChRs.

Altered glycosylation of acetylcholinesterase in APP (SW) Tg2576 transgenic mice occurs prior to amyloid plaque deposition.

Previous studies have shown that a minor glycoform of acetylcholinesterase (AChE) is increased in Alzheimer's disease brain and cerebrospinal fluid. This glycoform can be distinguished from other AChE species by its lack of binding to concanavalin A (Con A). In this study, the temporal relationship between AChE glycosylation and Abeta deposition was examined in Tg2576 mice.

Wheat germ agglutinin-binding glycoproteins are decreased in Alzheimer's disease cerebrospinal fluid.

A number of biomarkers (e.g. Abeta, tau) has been identified in Alzheimer's disease CSF.