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Biomedical subjects

D Dickson

Publications and source records attributed to D Dickson.

At least 109 records · Page 6Linked 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

Changes in ionized calcium concentrations and acid-base status during abdominal aortic vascular surgery.

Abdominal aortic surgery may produce significant haemodynamic instability (from a combination of factors: hypovolaemia, acid-base disturbances, vasoactive metabolite release from ischaemic tissues and hypocalcaemia). Calcium is often given after aortic unclamping to attenuate this instability. We studied 20 patients undergoing elective abdominal aortic surgery and observed a triphasic change in ionized calcium concentrations and acid-base status. Initially, during the cross-clamp period (when patients were cardiovascularly stable), ionized calcium concentrations decreased significantly (mean 1.06 (SD 0.08) to 0.91 (0.13) mmol litre-1; P < 0.01), while a significant metabolic acidosis developed (pH 7.38 (0.05) to 7.30 (0.05); P < 0.05). Second, release of the aortic cross-clamp resulted in further acidosis (pH 7.27 (0.05) (P < 0.05) mixed respiratory and metabolic) with a decrease in mean arterial pressure, with no change in ionized calcium concentrations. The third phase was associated with spontaneous restoration of acid-base status and ionized calcium concentrations to normal over 2 h. There was no correlation between units of blood given, volume of blood lost, fluid volume given or duration of aortic cross-clamping and degree of ionized hypocalcaemia. We conclude that ionized hypocalcaemia occurred during the cross-clamp period of aortic surgery, was unrelated to the volume of blood given and did not appear to be responsible for the changes in arterial pressure during surgery.

Acid-Base Equilibrium↗
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↗