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Biomedical subjects

D Shapcott

Publications and source records attributed to D Shapcott.

At least 37 records · Page 2Linked to original sources
PubMed1980

Cerebral hypoxia from bicarbonate infusion in diabetic acidosis.

To study the delivery of oxygen to the cerebral tissue during metabolic acidosis and its therapy with bicarbonate (NaHCO3), oxygen partial pressure of the cisternal fluid was measured in 12 experiments of HCl-induced acidemia and eight experiments of diabetic ketoacidosis in 16 unanesthetized dogs. Full correction of acidosis with bicarbonate caused a significant (P less than 0.05) decrease in Pcsf 2: in the HCl acidotic dogs, Pcsfo2 decreased from 53.9 +/- 2.2 torr to 45.9 +/- 2.3 torr within one hour; in the ketoacidotic dogs, Pcsfo2 decreased for 48.5 +/- 5.4 torr to 26.7 +/- 6.6 torr within six hours. In the ketoacidotic dogs not treated with bicarbonate, there was no significant change in Pcsfo2. An inverse relationship (P less than 0.01) between the cisternal lactic acid level and the cisternal PO2 was also observed. It is concluded that NaHCO3 therapy in diabetic ketoacidosis decreases the cerebral O2 availability and that cerebral hypoxia contributes to the brain dysfunction encountered after the initiation of such therapy in acidemia.

Acidosis↗
PubMed1980

Glycosylated hemoglobins in Friedreich's ataxia.

In a study of glycosylated hemoglobins in Friedreich's Ataxia patients and in family members, the level was found to be higher in insulin dependent diabetics than in healthy non-diabetic control subjects (p < 0.01), but was similar to non-ataxic diabetic control subjects. Results for non-diabetic Friedreich's Ataxia patients and siblings were similar to those for non-diabetic control subjects while levels were slightly increased in the heterozygotes. It is concluded that in Friedreich's Ataxia patients and family members (apart from the insulin dependent diabetics), there was no hyperglycemia sufficient to be detected as an increase in glycosylated hemoglobins.

Diabetes Complications↗
PubMed1979

Single column high pressure liquid chromatographic determination of drugs in blood.

1. Analysis of anticonvulsants (phenobarbital, diphenylhydantoin and carbamazepine), theophylline and an antiarrhythmic agent (disopyramide) in blood using a simple high pressure liquid chromatography apparatus equipped with a reversed -- phase column is described. A simple extraction of plasma or serum with organic solvent is used to isolate the anticonvulsants and theophylline. Disopyramide is extracted with ether and is further purified by a back extraction into acid. 2. Hexanesulfonic acid -- methanol solutions are used for chromatography of the anticonvulsants and disopyramide while the mobile phase for theophylline is a NH4H2PO4 -- methanol mixture. Chromatographic analysis time for the drugs is approximately 15 minutes. The drugs are monitored by a UV detector at 254 nm except for theophylline which is measured at 280 nm. Quantitation is accomplished by comparison of peak heights with those of internal standards. Quantities of serum or plasma routinely used for analysis are: 200 ul for the anticonvulsants, 100 ul for theophylline and 0.5 ml for disopyramide. Detection limits are less than 1 ug/ml for these quantities.

Anticonvulsants↗
PubMed1979

Glucose tolerance and erythrocyte insulin receptors in Friedreich's ataxia.

Detailed in vivo and in vitro studies of glucose and insulin metabolism in Friedreich's ataxia patients and unaffected family members have further defined the extent of the abnormalities in carbohydrate metabolism. The high incidence of glucose intolerance and a hyperinsulinemic response to a glucose challenge in a high percentage of Friedreich's ataxia patients has been confirmed. An increased incidence of glucose intolerance among heterozygotes is suggested, while the siblings show a more normal distribution of diabetes and a nearly normal insulin response to the glucose tolerance test. Human growth hormone patterns are normal for all groups. Preliminary studies of insulin binding to erythrocytes suggest a difference in the binding characteristics among diabetic Friedreich's ataxia patients, while the binding in the non-diabetic Friedreich's ataxia group is similar to that of non-diabetic controls. Results from a small group of non-diabetic siblings suggest a normal insulin binding, while a tendency toward increased binding at low insulin concentrations among diabetic family members is noted.

Diabetes Complications↗
PubMed1979

Erythrocyte membrane lipids in Friedreich's ataxia.

In a study of the lipid composition of erythrocyte membranes in Friedreich's ataxia, the concentration of the major membrane components (phospholipids, cholesterol and protein) in ataxic patients, family members, and control subjects were found to be the same. The total fatty acid distribution was also normal. However, an altered distribution of phospholipid classes in erythrocytes was noted (an increase of PI + PS and a decrease of PE in Friedreich's ataxia patients).

Adult↗
PubMed1979

Food intake patterns of infants with high serum cholesterol level at six months.

In our longitudinal study on the influence of nutrition upon health during infancy we found in a cohort of 556 infants in good health, 6.4% of infants at six months with a total serum cholesterol level above 200 mg/100 ml. Because of the known importance of hypercholesterolemia for health we studied the role of the food intake patterns during the first six months in relation to the serum cholesterol. We analysed the 24 hours dietary recalls, the dietary habits and a set of biochemical determinations used for evaluation of nutritional status: 35 infants, 21 girls and 14 boys, were compared with a control group matched for sex and birth date. There were no differences in mean body weight and socio-demographic characteristics. Daily energy and protein intake was higher in the study group. Analysing milk consumption we found that the daily intake was always higher in the high cholesterol group. The solid foods were introduced earlier in the study group, i.e. for 46% of infants in the second week of life. The serum levels of vitamins A, C, and E, and of triglyceride were higher in the high cholesterol groups. At twelve months 33% of infants with the cholesterol level above 200 mg/100 ml we included in the studied group remain still with a high level. This tendency underlines the need of further research.

Age Factors↗
PubMed1978

Simple and rapid system for screening and identification of reducing sugars in urine.

As part of our screening programme for metabolic disorders we needed a rapid, simple, inexpensive means to detect reducing sugars in urine, with a simple but precise test for their identification. Our system comprises a bismuth reduction test for reducing sugars, with unidimensional thin layer chromatography on silica gel and color development with diphenylamine--aniline for definitive identification.

Carbohydrates↗
PubMed1978

Taurine in cerebrospinal fluid in Friedreich's ataxia.

In a previous study we reported low values of taurine and aspartic acid in the CSF of patients with Friedreich's ataxia, when the results were compared to the literature. Further studies have revealed that unforetold difficulties with the advertised methodology of sequential multi-sample amino acid analysis were responsible for low values in the determination of these two amino acids in the small volumes necessary for CSF. A corrected method is presented. With the latter method the differences disappear for CSF taurine and aspartic acid, but they remain valid for the previously reported blood and urine values in Friedreich's ataxia. GABA levels are also normal in Friedreich's ataxia CSF.

Adolescent↗
PubMed1978

Purine metabolism in Friedreich's ataxia.

In a detailed investigation of nucleotide synthesis, interconversion and degradation, no difference was found between subjects with Friedreich's Ataxia and normal controls. It appears improbable that this disorder is related to a primary defect in purine metabolism.

Adolescent↗
PubMed1978

Oxygen transport in patients with Friedreich's ataxia.

The hypothesis is that an abnormal oxygen-hemoglobin dissociation curve is a primary or a secondary defect in patients with Friedreich's ataxia was investigated in 12 subjects with this disease. Hemoglobin and P50 were measured and compared with age and sex matched controls. The mean hemoglobin concentration was 14.2 g% and the P50 was 26.25 torr for the patients and 13.8 g% and 26.27 torr in the controls. These results indicate that the oxygen transport system is normal in this disease and likely exclude an abnormal oxygen dissociation curve as a primary or a secondary factor in the pathophysiology of the cardiomyopathy and the neuromyopathy found in this disease.

Friedreich Ataxia↗
PubMed1977

The measurement of volatile chromium in biological materials.

Chromium is an essential trace element in mammals since dietary chromium deficiency results in glucose intolerance due to decreased sensitivity to insulin. In humans, both adults and children with glucose intolerance have been improved by treatment with chromium. Furthermore, chromium deficiency has been implicated as a causative factor in hypercholesterolemia and atherosclerosis. However, little is known of the metabolism of chromium in humans, primarily because of analytical difficulties. The biologically active form of chromium is the "glucose tolerance factor" (GTF) which is a co-ordination complex of trivalent chromium with nicotinic acid and certain amino acids. At physiological pH, ionic chromium as a simple inorganic salt is insoluble in water, but trivalent chromium forms stable complexes with ascorbic acid, amino acids and other substances present in blood and tissue. Chromium is present in serum, bound to protein and also as dialysable or ultrafiltrable chromium (free chromium). The free chromium includes G.T.F. and other coordination complexes and represents the metabolically active form of the element; the ratio free/protein bound chromium in serum varies within the individual according to the diet and the metabolic state.

Animals↗
PubMed1976

Clinical laboratory findings in Friedreich's ataxia.

All clinical laboratory tests carried out in 4 groups of patients with the diagnosis of typical or atypical Friedreich's ataxia have been found to be within the normal range. In this prospective study of 50 patients, a number of findings previously reported to be abnormal in the literature, have not been confirmed.

Alanine Transaminase↗
PubMed1976

Glucose and insulin metabolism in Friedreich's ataxia.

Our prospective survey of 50 ataxic patients confirms the previous finding of frequent clinical or chemical diabetes in Friedreich's ataxia. Eighteen percent of our typical cases have clinical diabetes and 40% at least an abnormal glucose tolerance curve. However, this finding does not appear to be specific to that form of ataxia. Furthermore, we have shown that most patients with ataxia have normal or low fasting insulin levels, but a hyperinsulinic response to a glucose load.

Blood Glucose↗
PubMed1976

Amino acid metabolism in Friedreich's ataxia.

A study of amino acids determined by sequential Multi-sample Amino Acid Automatic Analyzer in plasma, urine and cerebrospinal fluid (CSF) in patients with Friedreich's ataxia and control subjects has revealed a number of mathematically significant variations from normal. Of practical physiological importance are the following: a high urinary excretion of alanine with slightly elevated plasma levels; a low plasma and CSF concentration of aspartic acid in the presence of normal urinary values and finally a low CSF concentration of taurine accompanied by normal plasma levels, but elevated urinary output and renal clearance rates. We postulate that the modifications in alanine and aspartic acid are less specific and probably secondary, but there could be a genetic defect in the membrane transport of taurine and the other beta-amino acids in Friedreich's ataxia.

Alanine↗
PubMed1976

Pyruvate metabolism in Friedreich's ataxia.

Friedreich's ataxia patients show evidence of an abnormally elevated and prolonged response of pyruvate and lactate to a glucose load, with normal fasting levels. However, ther is a bimodal distribution of this response with high and low pyruvate responders. This trait appears to be determined genetically, However, although in vivo tests suggest low oxidation of pyruvate, we were unable to confirm any in vitro impairment of each of the components of the pyruvate dehydrogenase (PDH) complex. We conclude that the defect is in the metabolic regulation of PDH, probably at the E3 (lipoamide dehydrogenase) step.

Alanine Transaminase↗