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Biomedical subjects

L Thomas

Publications and source records attributed to L Thomas.

At least 469 records · Page 26Linked to original sources
PubMed1983

Granular cell tumor of the bronchus: a previously unreported cause of hypercalcemia.

Hypercalcemia was found in a patient with an endobronchial granular cell tumor. To the best of our knowledge, the association of hypercalcemia and granular cell tumor has not been previously reported in the literature. Resection of the tumor resulted in the return of the serum calcium levels to normal. Investigation of the metabolic status of the patient suggested that the tumor was not producing parathormone.

Adult↗
PubMed1983

Sensory distinction between H-2b and H-2bm1 mutant mice.

Genetic polymorphism in the H-2:Qa:Tla region of chromosome 17 is associated with constitutive variation of bodily odor phenotypes which permit individual olfactory recognition among mice. To determine whether known genes in the H-2:Qa:Tla complex are concerned in the constitution of odor phenotypes, mice were tested for their ability to sense a difference between the B6/By (H-2b) and congeneic B6.C-H-2bm1 strains, which differ genetically by mutation of the H-2K gene. As in previous studies of the sensory discrimination of H-2:Qa:Tla phenotypes, mice were trained by reward in a Y maze to distinguish the odors of urine samples, and the successful distinctions of B6/By from B6.C-H-2bm1 were confirmed by transfer of training, without reward, to coded samples of urine from genetically equivalent urine donor mice which the trained mice had not previously encountered. Cosegregation of odor phenotype with H-2b and H-2bm1 was demonstrated by transfer of training to typed H-2b and H-2bm1 homozygous segregants of F2 generations of appropriate crosses. Although it is not excluded that the differences in odor phenotype which distinguish H-2b and H-2bm1 mice are directly related to the structure of the H-2b and H-2bm1 products, it is equally possible that H-2-related odor phenotypes arise from effects of H-2 genetic variation on metabolic pathways either directly, or indirectly through developmental polymorphism.

Animals↗
PubMed1983

Energy cost of walking in normal children and teenagers.

Oxygen consumption during free level walking was determined in 114 children and teenaged subjects between the ages of 6 and 19 years and compared with a group of 47 normal adults. Subjects were divided into two age groups: children (6-12 years) and adolescents (13-19 years). The mean rate of oxygen uptake for children was significantly greater, 15.3 ml/kg/min, than the value for teenaged subjects, 12.9 ml/kg/min. The oxygen cost to walk a unit distance (meter) was higher in children than adolescent subjects. The mean values averaged .22 ml/kg/min and .18 ml/kg/min respectively. The data on heart rate paralleled the findings on oxygen consumption. The mean heart rate for children, 114 beats per minute (bpm), was significantly higher than the mean values for adolescent subjects, 97 bpm.

Adolescent↗
PubMed1983

Energy cost of walking and of wheelchair propulsion by children with myelodysplasia: comparison with normal children.

The oxygen consumption of 15 myelodysplastic children during walking and propelling a wheelchair was studied. In comparison to normal children, they walked more slower and consumed more oxygen per meter, but had a similar rate of oxygen consumption. A swing-through gait pattern was 33 per cent more energy-efficient than a four-point gait pattern for these children. Wheelchair propulsion produced velocities and energy efficiencies similar to normal children walking. Oxygen consumption and velocity measurements were found to be significantly related to the clinical factors of level of lesion and strength of hip and knee extension. Regression lines and equations are presented to permit prediction of energy cost and efficiency from heart-rate data of myelodysplastic children.

Child↗
PubMed1983

Examination of the role of the pituitary-adrenocortical axis, counterregulatory hormones, and insulin clearance in variable nocturnal insulin requirements in insulin-dependent diabetes.

In insulin-dependent diabetics, insulin requirements increase significantly after 0600 h, resulting in prebreakfast hyperglycemia with either conventional insulin therapy or constant insulin infusions with insulin infusion devices. In order to clarify the role of the pituitary-adrenocortical axis and further examine the mechanisms of the phenomenon of nocturnal variability in insulin requirements, we studied five IDDs using a closed-loop insulin infusion device (Biostator, GCIIS). The subjects were given saline (SAL) or dexamethasone (DEX) i.v. from 1800 to 0900 h on successive nights. From 2400-0300 to 0600-0900 h, mean insulin infusion rates required to maintain blood glucose values between 109 and 120 mg/dl increased by 0.21 +/- 0.05 mU/kg/min during the SAL infusion, and 0.16 +/- 0.04 mU/kg/min during the DEX infusion, when plasma cortisols were suppressed to less than or equal to 2 micrograms/dl. Mean free insulin concentrations did not increase and remained constant throughout both study nights in spite of the significantly higher 0600-0900-h insulin infusion rates. Growth hormone, glucagon, epinephrine, and norepinephrine concentrations showed normal nocturnal and early morning patterns during both study nights. We conclude that the nocturnal variability in insulin requirements persists despite suppression of the pituitary-adrenocortical axis, and that increased free insulin clearance or degradation may contribute to the "dawn phenomenon" of rising prebreakfast glucose despite constant insulin infusion.

Adult↗
PubMed1982

Two DNA glycosylases in Escherichia coli which release primarily 3-methyladenine.

Two enzymes have been partially purified from Escherichia coli and designated 3-methyladenine DNA glycosylases I and II. The glycosylase I is that described by Riazuddin & Lindahl [Riazuddin, S., & Lindahl, T. (1978) Biochemistry 17, 2110-2118]. The apparent molecular weight of glycosylase I is 20 000, and that of II is 27 000. Glycosylase I releases 3-methyladenine (3-MeA) while II releases 3-MeA, 3-methylguanine (3-MeG), 7-methylguanine (7-MeG), and 7-methyladenine (7-MeA). The rate of release of 3-MeA by glycosylase II is 30 times that of 7-MeG. Glycosylase I is missing in mutants tag 1 and tag 2 [Karran, P., Lindahl, T., Ofsteng, I., Evenson, G. B., & Seeberg, E. (1980) J. Mol. Biol. 140, 101-127]. In crude extracts, the 3-MeA activity of II is approximately 10% of the total 3-MeA activity. A 50% inactivation at 48 degrees C required 5 min for I and 65 min for II. The apparent Km for 3-MeA residues for glycosylase I was 1.4 x 10(-8) M. The enzyme was inhibited noncompetitively by 3-MeA with an average apparent Ki of 1.6 mM. The apparent Km for 3-MeA, for glycosylase II, was 9.2 x 10(-9)M, and it was not inhibited by 3-MeA. The 3-MeA and 7-MeG activities of the glycosylase II preparation could not be separated by isoelectric focusing, by chromatography on DEAE, Sephadex G-100, phosphocellulose, DNA-cellulose, or carboxymethylcellulose, or by heating at 50 degrees C. The apparent Km for 7-MeG was 1.1 x 10(-8)M. Glycosylase II released N1-(carboxyethyl)adenine and N7-(carboxymethyl)guanine from DNA treated with beta-[3H]propiolactone but did not release the aflatoxin B-1 adduct at N-7 of guanine.

Adenine↗