Biomedical subjects
M A Baxter
Publications and source records attributed to M A Baxter.
Heel pad thickness is an insensitive index of biochemical remission in acromegaly.
The value of serial measurements of heel pad thickness as a clinical predictor of biochemical remission in acromegaly was assessed in 25 patients followed for up to 20 years after treatment by interstitial irradiation using yttrium-90 implantation. Growth hormone (GH) levels fell to 50% of baseline values within 12 months of therapy (P less than 0.001) and to 21% at 5 years, reaching normal levels after 10 years, constituting a biochemical cure maintained to the end of the study period. By contrast, heel pad thickness remained relatively stable, falling to 95% of baseline after 5 years (P less than 0.05) and to 87% after 20 years. There was no overall correlation between the measured parameters (r = 0.033, P greater than 0.05) suggesting that heel pad thickness is a poor predictor of biochemical remission in acromegaly.
Hypoglycaemia and atrial fibrillation.
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Inositol lipids and phosphates in the differentiation of blood cells.
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Prevalence of antibody indicating Lyme disease in farmers in Wigtownshire.
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Diabetic dietary prescriptions.
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The stimulation of superoxide anion production in guinea-pig peritoneal macrophages and neutrophils by phorbol myristate acetate, opsonized zymosan and IgG2-containing soluble immune complexes.
The kinetics of superoxide anion production in guinea-pig peritoneal macrophages and neutrophils were determined following in vitro stimulation with phorbol myristate acetate (PMA), opsonized zymosan (OZ) and soluble immune complexes of guinea-pig IgG2 (SIC). Superoxide production was recorded as chemiluminescence (CL) arising from the reductive cleavage of lucigenin. With PMA, both macrophages and neutrophils displayed a two-phase response consisting of a rapid initial burst of CL, which preceded ligand ingestion, followed by a plateau in the CL response which persisted for more than 30 min. By contrast, OZ induced a slow progressive increase in CL in both phagocytes which was consistent with the development of an oxidative burst concomitant with ingestion. The phagocytes differed in their responses to SIC, the macrophages displaying CL kinetics similar to those observed with PMA, whereas the neutrophils responded in the manner observed with OZ. The relationship between disparity in the patterns of macrophage and neutrophil CL responses to SIC and differences in their expression of Fc receptors for IgG2 (Coupland & Leslie, 1983) is discussed.
The effects of nitrogen mustard (HN2) on activities of the plasma membrane of PC6A mouse plasmacytoma cells.
Nitrogen mustard, HN2 (10(-5) M), inhibited the transport of the potassium congener 86rubidium into PC6A mouse plasmacytoma cells by 45% after a 4 hr incubation at 37 degree in vitro. HN2 (10(-3) M) had a rapid effect on the profile of 86rubidium transport into PC6A cells when added simultaneously with the 86rubidium whereas a monofunctional analogue of HN2((2-chloroethyl)dimethylamine) had no effect at 10(-3) M. The transport of the amino acid analogues alpha-aminoisobutyric acid and cycloleucine into PC6A cells was inhibited by 19% and 5% respectively after a 4 hr incubation with 10(-5) M HN2. The results suggest that the activity of plasma membrane Na+K+-ATPase may be affected by HN2. This enzyme may play a pivotal role in controlling cell growth and division. Crude cell membrane preparations from PC6A cells had variable Na+K+-ATPase activity which was possibly due to contamination with mitochondrial Mg2+-ATPase. Incubation of a crude cell membrane preparation in the presence of 40 nM dicyclohexylcarbodiimide gave constant Na+K+-ATPase activity which was inhibited by 44% on incubation with HN2 (10(-3) M) for 0.5 hr. The monofunctional analogue of HN2 inhibited this preparation by only 7% under the same conditions. It is suggested that inhibition of Na+K+-ATPase by HN2 may be an important facet of its cytotoxic activity.
Reduction of mitochondrial pyruvate dehydrogenase phosphatase activity in lactating rat mammary gland following starvation or insulin deprivation.
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Starvation of lactating rats leads to alterations in the behaviour of pyruvate dehydrogenase kinase which persist in the semi-purified pyruvate dehydrogenase complex of the mammary gland but are partly reversible in vitro.
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Absent pyruvate inhibition of pyruvate dehydrogenase kinase in lactating rat mammary gland following various treatments. Removal of circulating insulin and prolactin and exposure to protein synthesis inhibitors.
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Specificity of lactating rat mammary-gland pyruvate dehydrogenase phosphate phosphatase for the phosphorylated residues of the alpha-subunit [proceedings].
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The mode of regulation of pyruvate dehydrogenase of lactating rat mammary gland. Effects of starvation and insulin.
1. The ;initial activity' of the pyruvate dehydrogenase enzyme complex in whole tissue or mitochondrial extracts of lactating rat mammary glands was greatly decreased by 24 or 48h starvation of the rats. Injection of insulin and glucose into starved rats 60min before removal of the glands abolished this difference in ;initial activities'. 2. The ;total activity' of the enzyme complex in such extracts was revealed by incubation in the presence of free Mg(2+) and Ca(2+) ions (more than 10 and 0.1mm respectively) and a crude preparation of pig heart pyruvate dehydrogenase phosphatase. Starvation did not alter this ;total activity'. It is assumed that the decline in ;initial activity' of the enzyme complex derived from the glands of starved animals was due to increased phosphorylation of its alpha-subunit by intrinsic pyruvate dehydrogenase kinase. 3. Starvation led to an increase in intrinsic pyruvate dehydrogenase kinase activity in both whole tissue and mitochondrial extracts. Injection of insulin into starved animals 30min before removal of the lactating mammary glands abolished the increase in pyruvate dehydrogenase kinase activity in whole-tissue extracts. 4. Pyruvate (1mm) prevented ATP-induced inactivation of the enzyme complex in mitochondrial extracts from glands of fed animals. In similar extracts from starved animals pyruvate was ineffective. 5. Starvation led to a decline in activity of pyruvate dehydrogenase phosphatase in mitochondrial extracts, but not in whole-tissue extracts. 6. These changes in activity of the intrinsic kinase and phosphatase of the pyruvate dehydrogenase complex of lactating rat mammary gland are not explicable by current theories of regulation of the complex.
Persistent effects of starvation on pyruvate dehydrogenase kinase and phosphatase of lactating rat mammary gland [proceedings].
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Effects of starvation, diabetes and 2-bromo-alpha-ergocryptine treatment on pyruvate dehydrogenase activity in lactating rat mammary gland.
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The role of magnesium in diabetes mellitus. A possible mechanism for the development of diabetic complications.
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Audit of the change from twice daily to basal-bolus insulin regimens in insulin-dependent diabetes.
Basal-bolus insulin regimens have become popular with patients, but clinicians' enthusiasm for their use has been tempered by a number of reports that suggest that these regimens do not improve overall glycemic control when compared with conventional, twice daily, regimens. Indeed, it has been suggested that basal-bolus regimens may be abused by certain patients leading to an increase in body weight and deterioration in glycemic control. This paper reports the results of a retrospective audit of 145 insulin-dependent diabetic patients changed from conventional insulin therapy to a basal-bolus insulin regimen. After 3 months on the basal-bolus regimen, a small but significant fall in total insulin (10%; p < 0.001) and intermediate-acting insulin (50%; p < 0.001) dose was recorded. During this time period serum fructosamine measurements also fell by 10% (p < 0.001) indicating a small but significant improvement in glycemic control. Body-mass index (BMI) and body weight data did not support the view that basal-bolus regimens lead to an increase in body weight. Analysis of the data by gender did not support the view that the basal-bolus insulin regimen is prone to abuse by female patients.