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D Dickson

Publications and source records attributed to D Dickson.

At least 37 records · Page 2Linked to original sources
PubMed1998

A survey of communication skills training in UK schools of medicine: present practices and prospective proposals.

It is now widely accepted that effective interpersonal communication is at the heart of quality health care delivery but that current standards in medicine must be improved (Numann 1988; Cowan et al. 1992). One approach acknowledged by the General Medical Council (1991) devotes more attention during training to the theme of communication, and quite significant modifications of the undergraduate medical curriculum are presently taking place. This article documents the results of a postal survey of the 26 UK Schools of Medicine, designed to illuminate current practices and future plans in respect of communication skills training (CST). As such, it takes advantage of the present period of ongoing curricular innovation and change to extend and update earlier reviews (Whitehouse 1991; Frederikson & Bull 1992). A total of 19 responses was received. Following preliminary analysis, the four schools who had already implemented their new curriculum were selected for further in-depth investigation by means of telephone interviews. In addition to reporting frequencies and percentages for responses to questions, cross-tabulations were carried out to explore relationships between certain of the findings. Apart from some consistency in CST teaching methods adopted, the overall picture to emerge is one of considerable variability in such areas as course content, timing, duration and assessment. Foremost among the difficulties encountered in implementing CST appeared to be lack of adequate physical resources and suitably trained staff. Future plans were often sketchy and inchoate. Results are discussed and tentative recommendations for the further development of CST in the medical curriculum proffered.

Clinical Competence↗
PubMed1998

Receptors for advanced glycosylation endproducts in human brain: role in brain homeostasis.

BACKGROUND: Advanced glycation end products (AGEs) are the reactive derivatives of nonenzymatic glucose-macromolecule condensation products. Aging human tissues accumulate AGEs in an age-dependent manner and contribute to age-related functional changes in vital organs. We have shown previously that AGE scavenger receptors are present on monocyte/macrophages, lymphocytes, and other cells. However, it remains unclear whether the human brain can efficiently eliminate AGE-modified proteins and whether excessive AGEs can contribute to inflammatory changes leading to brain injury in aging. MATERIALS AND METHODS: To explore the expression and characteristics of AGE-binding proteins on CNS glia components and their putative function, such as degradation of AGE-modified proteins, primary human astrocytes and human monocytes (as a microglial cell surrogate) and murine microglia (N9) cells and cell membrane extracts were used. Immunohistochemistry was used to examine the distribution of AGE-binding proteins in the human hippocampus; RT-PCR techniques were used to examine the biologic effects of AGEs and a model AGE compound, FFI, on AGE-binding protein modulation and cytokine responses of human astrocytes and monocytes. RESULTS: Our results showed that AGE-binding proteins AGE-R1, -R2, and -R3 are present in glial cells. Western blot analyses and radiolabeled ligand binding studies show that AGE-R1 and -R3 from human astrocytes bind AGE-modified proteins; binding could be blocked by anti-AGE-R1 and anti-AGE-R3 antibodies, respectively. Immunohistochemistry showed that AGE-R1 and -R2 are expressed mainly in neurons; only some glial cells express these AGE-binding proteins. In contrast, AGE-R3 was found only on those astrocytes whose positively stained foot processes extend and surround the sheath of microcapillaries. RT-PCR results showed that mRNAs of the three AGE-binding proteins are expressed constitutively in human astrocytes and monocytes, and receptor transcripts are not regulated by exogenous AGEs, the model AGE compound FFI, or phorbol ester. At the concentrations used, GM-CSF appears to be the only cytokine whose transcript and protein levels are regulated in human astrocytes by exogenous AGEs. CONCLUSIONS: The selective presence of AGE-binding proteins in pyramidal neurons and glial cells and their roles in degrading AGE-modified protein in glial cells suggest that the human brain has a mechanism(s) to clear AGE-modified proteins. Without this capacity, accumulation of AGEs extracellularly could stimulate glial cells to produce the major inflammatory cytokine GM-CSF, which has been shown to be capable of up-regulating AGE-R3. It remains to be determined whether AGE-binding proteins could be aberrant or down-regulated under certain pathological conditions, resulting in an insidious inflammatory state of the CNS in some aging humans.

Aging↗
PubMed1997

Pathological diagnostic criteria for dementia associated with cortical Lewy bodies: review and proposal for a descriptive approach.

In recent years dementia histologically characterised by the presence of cortical Lewy bodies has been increasingly recognised. There is now need for a scheme for an internationally acceptable scheme for pathological diagnosis and classification so that clinical, pathological and molecular features of disease can be correlated. Recent observations made by different groups in large patient series have used slightly different pathological criteria resulting in at least seven different diagnostic terms. In some patients the only cortical pathology is the presence of Lewy bodies, while in the majority of patients there are coexisting pathological changes which either overlap with those seen in Alzheimer's disease (AD). Cortical Lewy bodies can also be present in patients who do not have any obvious cognitive abnormality. A problem with equating studies from different groups is that different criteria have been used to define AD, so that establishing the relevance of cortical Lewy bodies themselves to cognitive decline and separating this from the contribution which may be related to the AD pathology is problematic. The lesions which appear to be of most relevance to potential cognitive decline in DLB are cortical Lewy bodies, Lewy-related neurites, senile plaques, neurofibrillary tangles, neuronal and synaptic loss, spongiform change, and cortical cholinergic deficits. It is possible to operationally classify patients with cognitive decline and cortical Lewy bodies into three main groups, Cortical Lewy body disease, Cortical Lewy body disease with plaques, and Cortical Lewy body disease with plaques and tangles. There are frequent cases which overlap these groups making operational classification difficult in practice. A descriptive classification, in which the severity of different pathological changes is rated, is easy to use in practice. As new molecular risk factors for AD or DLB are revealed they will need to be related to morphological and clinical features. A descriptive diagnostic assessment for DLB will facilitate such studies and makes no judgements as to what these relationships will be.

Aged↗