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T Page

Publications and source records attributed to T Page.

70 records · Page 4Linked to original sources
PubMed1984

Human GMP synthetase.

The specific activity of GMP synthetase was measured in several human tissues and found to be highest in cultured skin fibroblasts, followed by bone marrow, leukocytes, erythrocytes, placenta, and liver. The enzyme from fibroblasts was purified approximately 50-fold by ammonium sulfate fractionation and gel filtration. The Km values were determined to be 4.9 microM for XMP, 270 microM for ATP, and 340 microM for glutamine. Ammonium sulfate could replace glutamine as the amino donor but was much less efficient. The enzyme was specific for ATP as the energy source. Unlike the calf thymus enzyme, the human enzyme has no requirement for a reduced sulfhydryl compound. Human GMP synthetase is inhibited by ATP, dATP, azaserine, and hydroxylamine.

Carbon-Nitrogen Ligases↗
PubMed1984

Plasma immunoreactive gastric inhibitory polypeptide in obese hyperglycaemic (ob/ob) mice.

Gastric inhibitory polypeptide (GIP), a recognized component of the enteroinsular axis, is raised in the plasma and intestine of obese hyperglycaemic (ob/ob) mice. To evaluate the control of plasma GIP and its role in the hyperinsulinaemia of the ob/ob syndrome, GIP and insulin were determined at different ages in fed mice, and at 10-12 weeks of age after fasting/refeeding and administration of GIP, different nutrients and insulin to mice fasted for 18 h. Plasma GIP and insulin were raised in adult (10- and 20-week-old) compared with younger (3- and 5-week-old) mice, although GIP was not increased in the presence of hyperinsulinaemia at 3 weeks of age. Fasting suppressed and refeeding promptly restored plasma GIP and insulin concentrations. Administration of GIP to mimic postprandial concentrations evoked a marked but transient insulin response which was protracted in the presence of rising hyperglycaemia. Orally administered fat, glucose and amino acids raised GIP concentrations with fat having a particularly strong effect. Glucose and amino acids also evoked prominent increases of insulin, but fat produced only a small rise in insulin in the absence of increasing glucose concentrations. Consistent with glucose-potentiation, a mixture of all three nutrients greatly augmented the insulin response without further increase of plasma GIP. Glucose-induced increase in endogenous insulin and doses of exogenous insulin up to 100 units/kg did not suppress basal, fat-stimulated or glucose-stimulated GIP release. The results indicate that raised GIP concentrations make an important contribution to the hyperinsulinaemia and related metabolic abnormalities of the ob/ob syndrome.

Amino Acids↗
PubMed1983

[Lesch-Nyhan disease studied in intact fibroblasts].

A 5 year old spanish boy was studied in whom the clinical phenotype was that of classic Lesch-Nyhan syndrome. Activity of hypoxanthine guanine phosphoribosyl transferase (HGPRT) was studied in an intact fibroblast system in which the pattern of incorporation of isotope of 14C-labeled hypoxanthine into its purine products was assessed. This method has been effective in distinguishing among HGPRT variants even when activity in erythrocyte lysates is zero. In this patient the activity was 0,4 percent of normal, consistent with Lesch-Nyhan disease.

Adenine Phosphoribosyltransferase↗
PubMed1982

An improved procedure for detection of hypoxanthine--guanine phosphoribosyl transferase heterozygotes.

The absence of activity of the enzyme hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8) is known to be the cause of the Lesch-Nyhan syndrome. Previous methods for detection of heterozygous carriers of this genetic defect either are quite time consuming, require specialized equipment, or lack the necessary sensitivity. We present here a method in which thin-layer chromatography and autoradiography are used to assay the activity of this enzyme in individual hair roots collected from the scalp of the possible carrier. This method is fast and sensitive, and requires no specialized equipment.

Adenine Phosphoribosyltransferase↗
PubMed1981

Hypoxanthine-guanine phosphoribosyltransferase variants: correlation of clinical phenotype with enzyme activity.

A deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase(HGPRT) is associated with a varying clinical picture which may include hyperuricaemia, neurological abnormalities and bizarre self-mutilating behaviour. Due to technical problems with the usual in vitro enzyme assays, it has not been possible to establish a correlation between the degree of the enzyme deficiency and the severity of the clinical manifestations. In this study, the HGPRT activity of 12 patients with various clinical features was measured by quantitative analysis of the incorporation of radioactive precursors into purine compounds in intact fibroblasts. The results demonstrate that a correlation between the severity of the clinical symptoms and the degree of the enzyme deficiency as measured in intact fibroblasts does in fact exist.

Animals↗
PubMed1976

Drinking water and cancer mortality in Louisiana.

Multivariant regression analysis indicates a statistically significant relation between cancer mortality rates in Louisiana and drinking water obtained from the Missippi River. This is true for total cancer, cancer of the urinary organs, and cancer of the gastrointestinal tract.

Breast Neoplasms↗
PubMedDate not supplied

Clinical correlations in partial hypoxanthine guanine phosphoribosyltransferase deficiency.

Erythrocyte assays for hypoxanthine guanine phosphoribosyltransferase (HGPRT) activity performed on two male half-siblings with hyperuricemia, produced results consistent with classic Lesch-Nyhan syndrome. Due to the absence of neurologic abnormalities, cognitive deficits, or self-mutilation, HGPRT activity was measured by intact fibroblast assay which revealed partial enzyme deficiency. The presence of an unstable mutant enzyme may have led to the discrepancy between the erythrocyte and fibroblast studies. This discrepancy emphasizes the difficulty in assaying this enzyme solely utilizing red blood cell studies to determine a patient's course. In order to provide an accurate prognosis and relevant genetic counseling, measurement of this enzyme utilizing intact fibroblasts is critical after establishing a diagnosis of HGPRT deficiency in a hyperuricemic male lacking typical clinical manifestations of Lesch-Nyhan syndrome, but having enzyme activity of erythrocytes consistent with the diagnosis.

Child, Preschool↗
PubMedDate not supplied

A novel polymorphism in the 5' flanking region of the glucose transporter (GLUT1) gene is strongly associated with diabetic nephropathy in patients with Type 1 diabetes mellitus.

Glucose transporter 1 (GLUT1) activity has been implicated in renal hypertrophy and extracellular matrix formation in mesangial cells. Recent studies have suggested that polymorphisms in the GLUT1 gene are associated with susceptibility to diabetic nephropathy (DN) in patients with diabetes mellitus. In this study, a novel polymorphism (A-2841T) in the 5' flanking region of GLUT1 was examined in 288 patients with Type 1 diabetes mellitus (T1DM) and 101 normal controls. The polymorphisms were amplified and the fragment digested with the enzyme HpyCH4V. There was a highly significant increase in the frequency of the TT-2841 genotype in patients with nephropathy (n=131) compared with those with either no microvascular complications after a 20-year duration of diabetes (uncomplicated; n=72; 54.5% vs. 2.7%, chi=79.4, P<.000001). There was no difference between the uncomplicated group and those who only had retinopathy (n=50; 2.7% vs. 4.0%, respectively). The frequency in recently diagnosed patients was 17.1% and only 2.0% in normal controls. In contrast, the AA genotype was found in 13.6% of the nephropaths, 76.3% of uncomplicated, 48.0% of retinopaths, and 65% of normal controls. These results confirm previous reports of an association between the GLUT1 gene and susceptibility to DN but not retinopathy. The localisation of this polymorphism suggests that it may be involved in the expression of the gene.

5' Untranslated Regions↗
PubMedDate not supplied

Safe use of electroconvulsive therapy in pregnancy.

A 22-year-old woman who was 32 weeks pregnant was given a course of electroconvulsive therapy (ECT) as a life-saving measure to treat a severe psychotic illness. The ECT was highly effective and careful monitoring of both the mother and the fetus demonstrated that this was a safe procedure.

Adult↗