Biomedical subjects

T Stephan

Publications and source records attributed to T Stephan.

At least 19 recordsLinked to original sources

PubMed1992

Direct measurement of spin-lattice relaxation times of phosphorus metabolites in human myocardium.

T1 values of phosphorus metabolites visible in human cardiac 31P-MR spectra were determined in 12 volunteers at 1.5 T. Consecutive spectra were acquired with varying pulse repetition time (TR) from 1.6 to 24 s; volume selection was achieved with ISIS. T1's of creatine phosphate (CP), [gamma-P], [alpha-P], and [beta-P]ATP, 2-3 diphosphoglycerate, and phosphodiesters were 6.1 +/- 0.5, 5.4 +/- 0.5, 5.5 +/- 0.5, 5.8 +/- 1.0, 7.6 +/- 1.0, and 5.0 +/- 1.0 s, respectively. CP/ATP ratios showed little change with varying TR; linear regression of CP/ATP vs TR was of borderline significance (r = 0.28, P = 0.06). T1's for CP and ATP were also determined in standard solution (20 mM CP, 10 mM ATP) yielding T1CP of 8.7 +/- 0.2 and T1[gamma-P]-ATP of 9.9 +/- 0.7 s. Thus, T1's for CP and ATP were similar at 1.5 T in both human heart and standard solution. In human cardiac 31P-MR spectra, CP/ATP ratios may need little correction for partial saturation.

2,3-Diphosphoglycerate↗

PubMed1977

Endocrine abnormalities and myopathy in Bloom's syndrome.

Abnormal endocrine indices and myopathy have been variably present in two brothers with Bloom's syndrome (congenital teleangiectatic erythema, hypersensitivity to light, and growth retardation). These consisted of: (1) growth retardation with height and weight below the third centiles; in the younger one at age 14, hypoglycaemia failed to elicit a rise in growth hormone but did so in the older one at age 17; (2) serum TSH was raised in the older one in whom serum FSH and LH were also above the normal range; and (3) myopathy characterised by pronounced dilatation of the sarcoplasmic reticulum was present in the younger one; distinct reduction of muscle strength was shown in his older brother with ultrastructural alteration of skeletal muscle of unknown significance.

Abnormalities, Multiple↗

PubMed1977

Transient insulin increase in reactive hypoglycemia in obese and non-obese subjects.

(1). Insulin levels at the moment of glucose-induced reactive hypoglycemia have been compared with zero-hour insulin levels in 108 subjects in whom the blood glucose had decreased to 50 mg percent or less (50 to 31 mg) at the third, fourth, or fifth hour in the course of an oral glucose tolerance test (1.75 g/kg of body weight). (2). Of the 47 obese subjects, insulin levels at the time of the reactive hypoglycemia were inappropriately high, ie exceeded the fasting insulin level by 20 uU/ml or more in 38 percent and by 40 microunits/ml or higher in 26 percent of the tests. (3). In 61 non-obese subjects, employing the same criteria, inappropriately high insulinemia at the time of reactive hypoglycemia was recorded with about the same frequency. (4). In each instance of reactive hypoglycemia of 50 mg percent or less with concomitant insulin levels above the starting value to the degree stipulated, the so-termed inappropriate hyperinsulinemia was transient. In other words, judging by levels preceding and/or following the reactive hypoglycemia, insulin titers were decreasing and hence, the inappropriately high insulin level at the moment of hypoglycemia represented a lag phenomenon. (5). The above data suggest that insulin levels elevated above the starting value may play a role in reactive hypoglycemia. In subjects with insulin levels at the time of reactive hypoglycemia equal to or below the starting value, the low blood glucose level cannot be attributed to insulin. In such instances, delay or lag in hepatic glucose output and/or counter-regulatory responses probably play the dominant or sole role in the reactive hypoglycemia.

Blood Glucose↗

PubMed1977

Unresponsiveness to exogenous TSH in obesity.

(1). Assessment of thyroidal and other indices in 275 instances of obesity with body weight excesses up to 200 percent or more of the ideal revealed absent thyroidal I131 uptake responses to TSH in about one out of five patients. Moreover, basal thyroidal I131 uptake of 10 percent or less, prolongation of ankle reflex time, or high levels of serum cholesterol were present in a minority. Also, occasional instances of unduly elevated serum TSH titers were found. Some of the indices deviated from normal more often with the greater excesses of body weight or with increased age. (2). These findings are consonant with a hypothesis that routine thyroidal or related indices are sporadically abnormal in massive obesity almost always without overt hypothyroidism or myxedema, that total unresponsiveness to exogenous TSH is surprisingly frequent, and that such unresponsiveness represents an unexplained endocrine anomaly in association with gross overweight. (3). Our data suggest that some obese persons are not able to respond to exogenous TSH, nor, presumably, to increases of endogenous TSH. This could result in an economy of caloric expenditure and play a contributory role in the genesis or the perpetuation of the obesity.

Achilles Tendon↗

PubMed1976

Thyroid hormone-like effects without thyrotoxicosis during one year's therapy with NA-DT3 for hypercholesterolemia.

A thyroid hormone analogue, sodium dextro-triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na-DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.

Adult↗

PubMed1975

Clinical and ultrastructural observations in a kindred with normo-hyperkalaemic periodic paralysis.

Electron microscopic studies of muscle biopsies from clinically unaffected sibs in a family with normo-hyperkalaemic periodic paralysis with variable myotonia have revealed dilatation of the sarcoplasmic reticulum similar to that observed in affected members. This supports the view that such dilatation is not only a significant and likely primary ultrastructural change but that it may precede clinical manifestations and represent an anatomical marker of the genetic trait. Identical dilatation of the sarcoplasmic reticulum was found in the clinically unaffected father of the affected and unaffected grandchildren of the propositus. This raises the possibility that this non-consanguineous member contributed to the genetic trait or its manifestations in the grandchildren of the index patient since similar dilatation of the sarcoplasmic reticulum was not observed in the muscles of healthy control subjects.

Adolescent↗

PubMed1975

Obesity.

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Adult↗

PubMed1975

Hypoglycemia.

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Alcohol Drinking↗

PubMed1975

Electron microscopical study of a family with myotonia congenita.

Biopsy specimens of skeletal muscle from a family that had three female siblings with clinical features of recessive-type myotonia congenita were examined by light and electron microscopy. Fibers examined by the former technique appeared normal. Although some variation in size and shape of mitochondria and sarcomere fragmentation were focally observed by electron microscopy in affected members, they were also encounted in those without clinical manifestations. Importantly, no changes in sarcolemma, sarcoplasmic reticulum, or transverse tubular system were encountered. Capillary basement membrane thickness was within normal limits. The evidence strongly suggests that myotonia congenita represents an entity distinct from myotonia dystrophica and that its pathogenesis may be related to a biochemical rather than ultrastructal aberration.

Adolescent↗

PubMed1974