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L Whelan

Publications and source records attributed to L Whelan.

7 recordsLinked to original sources

Serving on an enquiry panel: one nurse's experience.

Liz Whelan is Clinical Nurse Manager at Gloucestershire Royal Hospital and recently served on the panel of inquiry into the death of a patient in A&E at Whipp's Cross Hospital, London (Mr Thomas Rogers, Review of Care at Whipps Cross Hospital Accident and Emergency Department, Report of the Panel of Inquiry, October 2001). The following is a transcript of the talk (supported by slides) she gave as a concurrent session at the RCN A&E Association's Conference in November 2001.

Advisory Committees↗

Effect of posture on body temperature of young men in cold air.

We studied eight young adult men to see whether a supine posture caused a fall in body core temperature in the cold, as it does in thermoneutral conditions. In air at 31 degrees C (thermoneutral), a supine posture for 3 h reduced mean aural, gastric, oesophageal and rectal temperatures by 0.2-0.4 degree C, compared to upright and increased femoral artery blood flow from 278 (SEM 42)ml.min-1 whilst upright to 437 (SEM 42) ml.min-1 whilst supine. In cold air (8 degrees C) the supine posture failed to reduce these temperatures [corrected] significantly, or to increase femoral blood flow: it reduced heart rate, and increased arterial systolic and pulse pressures adjusted to carotid sinus level, less than in thermoneutral conditions. However, the behaviour of core temperature at the four sites was significantly nonuniform between the two postures in the cold, mainly because the supine posture tended to reduce rectal temperature. It may have done so by reducing heat production in the muscles of the pelvis, since it reduced overall metabolic rate from 105 (SEM 8) to 87 (SEM 4) W.m-2 in the cold. In other respects the results indicated that posture ceased to have an important effect on body core temperatures during cold stress.

Adult↗

Antithyroglobulin monoclonal and autoantibodies cross-react with an orbital connective tissue membrane antigen: a possible mechanism for the association of ophthalmopathy with autoimmune thyroid disorders.

The possibility that Graves' ophthalmopathy and autoimmune thyroid disorders may be associated because of autoimmune reactions against antigens shared between human orbital and thyroid tissues was investigated using anti-thyroglobulin (Tg) monoclonal and autoantibodies. Eleven of 16 mouse monoclonal antibodies (MCAB) tested reacted, in an enzyme-linked immunosorbent assay (ELISA), with an antigen in human orbital connective tissue membranes (OCTmem), but not with the OCT soluble fraction, or with membrane or soluble fractions of human eye muscle, lacrimal gland or skin connective tissue. The anti-OCTmem activity was absorbed by OCTmem and Tg, but not by liver membranes or bovine serum albumin (BSA). In preliminary studies four out of 113 human MCAB against thyroid or orbital tissue antigens showed reactivity restricted to Tg and OCTmem. Sera from approximately 50% of patients with autoimmune thyroid disorders, with or without ophthalmopathy, also reacted with OCTmem. The autoantibody activity correlated closely with serum titres of antithyroglobulin but not with the presence, duration, or severity of the eye disease. The OCTmem reactivity was absorbed by Tg, thyroid membranes, and OCTmem but not liver membranes, membranes prepared from other orbital tissues, or BSA. The OCTmem-Tg shared antigen site appeared not to be native thyroglobulin since, (i) MCAB and serum autoantibodies did not react with the cytosol fraction of OCT, and (ii) because the membrane antigen was not solubilizable. Because not all patients with ophthalmopathy have detectable anti-Tg antibodies and, conversely, because not all patients with detectable anti-Tg antibodies develop ophthalmopathy it is unlikely that autoimmunity against a OCTmem-Tg shared antigen is the primary mechanism of Graves' ophthalmopathy, although this possibility has not been excluded. On the other hand the reaction of anti-Tg autoantibodies with OCT membranes may be a model for other autoimmune reactions against other thyroid-orbital tissue-shared antigens. While the pathogenesis of Graves' ophthalmopathy is likely to be multifactorial, humoral and cellular reactions against primary orbital antigens, thyroid-orbitol tissue shared antigens, or both, are likely to play important roles.

Adult↗