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Biomedical subjects

J Iliffe

Publications and source records attributed to J Iliffe.

At least 37 records · Page 2Linked to original sources
PubMed1996

Nurse practitioners legitimised!

The formal nurse practitioner debate began in NSW at the 1990 NSW Nurses' Association Annual Conference, when a question was put to the then NSW Minister for Health, Peter Collins, on the Government's position on independent nursing practice. A subsequent letter from Mr Collins invited submissions on the issue and a joint submission was prepared by the Association and the NSW College of Nursing. A NSW Department of Health Taskforce, under the direction of the Nursing Branch and the Chief Nursing Officer, Judith Meppem, was established.

Humans↗
PubMed1996

Nurse practitioner report. The recommendations.

The Final Report of the Steering Committee for Stage 3 of the Nurse Practitioner Project was released by the NSW Minister for Health on April 24, 1996. The release of the Final Report and its 48 recommendations represents the completion of a process which has been both a difficult and an exhausting one for the State Steering Committee. The major recommendation of the Report is the recognition of nurse practitioners as 'legitimate providers of health services in NSW'.

Humans↗
PubMed1996

The Association says no to Mandatory Continuing Education.

Mandatory Continuing Education (MCE) for nurses is a compulsory requirement for nurses to participate in continuing education in order to continue practising as a nurse. Should MCE be introduced, the most likely method of enforcing that requirement would be for it to be linked to a nurses' authority to practice, that is, it would be necessary to demonstrate the required MCE before annual registration would be renewed and a current practising certificate issued.

Education, Nursing, Continuing↗
PubMed1973

The effect of glucose, insulin and noradrenaline on lipolysis, and on the concentrations of adenosine 3':5'-cyclic monophosphate and adenosine 5'-triphosphate in adipose tissue.

Glycerol release and tissue concentrations of ATP and cyclic AMP were followed during the incubation of adipose tissue with or without glucose, insulin and noradrenaline. Glucose plus insulin or, to a lesser extent, glucose alone increased the accumulation of glycerol during incubations both with and without noradrenaline by slowing the decline in the rate of glycerol release with time. Insulin alone decreased the accumulation by accelerating the fall in glycerol release. In the absence of noradrenaline, ATP and cyclic AMP concentrations were not significantly affected by insulin or glucose. With noradrenaline or noradrenaline plus insulin the ATP concentration gradually fell. With noradrenaline plus glucose the ATP concentration fell rapidly and then stabilized, or, if insulin was also present, returned to the control value. In the presence of noradrenaline, the concentration of cyclic AMP rose during the first 20min and then fell. Insulin lowered the peak concentration of cyclic AMP, but glucose had no effect either on the peak value or the fall in the concentration of the nucleotide. The increase and fall in the concentration of cyclic AMP with noradrenaline or noradrenaline plus insulin bore similarities to the increase and decline in the lipolytic rate in incubations without glucose. It is proposed that glucose stimulates ATP production by furnishing glycerol 1-phosphate and thus removing free fatty acids, but that it can influence lipolysis by a mechanism which is distinct from any which is mediated by free fatty acids, possibly by inhibiting the inactivation of the lipase.

Adenosine Triphosphate↗
PubMed1970

The sensitivity of acetyl-coenzyme A carboxylase to citrate stimulation in a homogenate of rat liver containing subcellular particles.

1. Although citrate is known to activate purified preparations of acetyl-CoA carboxylase, it had no stimulatory effect on the incorporation of [(14)C]acetate into long-chain fatty acids in a whole homogenate of rat liver (S(0.7)) under conditions in which the activity of acetyl-CoA carboxylase was rate-limiting for fatty acid synthesis. 2. The rate of incorporation of acetyl carbon into fatty acids was estimated in S(0.7) preparations incubated with [(14)C]acetate, by measuring the specific radioactivity of the acetyl carbon of acetyl-CoA and the incorporation of (14)C into fatty acids. These estimates were compared with estimates of acetyl-CoA carboxylase activity in the S(0.7) preparation obtained by direct assay in conditions in which the enzyme was in the fully activated state. 3. In the absence of citrate, incorporation of acetyl carbon into fatty acids was about 75% of the value expected if the acetyl-CoA carboxylase in the S(0.7) preparation were in the fully activated state. 4. Incorporation of acetyl carbon into fatty acids in the S(0.7) preparation was stimulated by citrate, but the effect was many times less than the stimulation of [(14)C]acetate incorporation by citrate in particle-free preparations. 5. When the mitochondria and microsomes were removed from the S(0.7) preparation, [(14)C]acetate incorporation into fatty acids fell to a negligible value and the preparation became highly sensitive to stimulation by citrate. 6. It is suggested that in the presence of mitochondria and microsomes, and in the intact liver cell, the degree of activation of acetyl-CoA carboxylase is such that citrate activation may not be of physiological significance.

Acetates↗