PubMed Health⌕ Search

Biomedical subjects

J F Mitchell

Publications and source records attributed to J F Mitchell.

At least 55 records · Page 3Linked to original sources
PubMed1976

Pharmacist involvement as a member of a renal transplant team.

A renal transplant service is described in which the pharmacist attends daily rounds, monitors drug dosage and conducts a medication instruction program aimed at improving patient compliance. A renal transplant handbook was developed to provide the patient with pharmacy, nursing and dietary instructions. Prior to patient discharge, the pharmacist provides a final medication consultation. As an active member of a renal transplant team, the pharmacist serves as a valuable source of drug information to medical personnel and patients.

Diet↗
PubMed1974

The output per stimulus of acetylcholine from cerebral cortical slices in the presence or absence of cholinesterase inhibition.

1 The release of endogenous acetylcholine (ACh) from cerebral cortical slices stimulated at 0.25, 1, 4, 16 and 64 Hz was measured in the presence either of physostigmine or of physostigmine and atropine.2 Atropine potentiated the evoked release of endogenous ACh especially at low frequencies resulting in an output per stimulus which sharply declined with increasing frequency of stimulation, while in the absence of atropine the output of ACh per stimulus was low and fairly constant.3 The evoked release of [(3)H]-ACh per stimulus following the incubation of the slices with [(3)H]-choline, as estimated by means of rate constants of the evoked release of total radioactivity, showed a frequency dependence similar to endogenous ACh when the two were tested under identical conditions.4 In the absence of an anticholinesterase the evoked release of [(3)H]-ACh per stimulus was dependent on frequency of stimulation in a similar way to that in the presence of physostigmine and atropine.5 Results suggest that under physiological conditions, i.e. in the absence of an anti-cholinesterase, the release of ACh per stimulus decreases with increasing frequency of stimulation and that this decrease is due to a lag in the mobilization of stored ACh rather than in the synthesis of new ACh.

Acetylcholine↗
PubMed1971

The release of gamma-aminobutyric acid during inhibition in the cat visual cortex.

1. The release of gamma-aminobutyric acid (GABA) from the surface of the posterior lateral gyrus of the cerebral cortex was measured by a sensitive enzymic fluorimetric assay procedure. Experiments were performed with anaesthetized cats during resting conditions and during cortical inhibition produced by electrical stimulation of the brain surface or of the lateral geniculate nucleus (l.g.n.).2. The average resting release of endogenous GABA was 0.20 n-mole/ 7 min.cm(2) cortex; this was increased during stimulation of both the cortical surface (2.9 times resting release during monopolar stimulation and 7.4 times resting release during bipolar stimulation) and the l.g.n. (5.7 times resting release).3. Removal of calcium ions from the collection fluid did not affect the resting release of endogenous GABA but prevented the increase in GABA release normally evoked by stimulation of the cortical surface.4. The stimulus parameters used to increase the release of GABA also inhibited the glutamate-induced firing of single cells in the visual cortex and this inhibition was abolished in the absence of calcium ions.5. In three experiments the total amino acid content of cortical samples was examined using an amino acid analyser. With the exception of GABA, there were no significant differences between the rates of release of any other detected amino acids during periods with and without electrical stimulation of the cortex.6. It is suggested that since the release of GABA observed during inhibitory stimulation of the cortex is calcium-dependent and specific, it may originate from inhibitory nerve terminals in the cortex. The present findings support the view that GABA is a central inhibitory neurotransmitter.

Action Potentials↗