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Biomedical subjects

J E Carroll

Publications and source records attributed to J E Carroll.

At least 37 records · Page 2Linked to original sources
PubMed1990

Term infant asphyxia in Kuwait.

In the developing nation of Kuwait, we undertook a case-control study of 43 consecutively born, asphyxiated, term infants. The asphyxia incidence of 9.4/1000 was only slightly higher than that in more developed countries. Severe morbidity occurred in 1.1/1000, and mortality in 1.1/1000. We found significant associations between asphyxia and primiparity, maternal hypertension, consanguinity, increased length of labour, and instrumental deliveries. Maternal age, socio-economic class, maternal illnesses other than diabetes, and breech delivery did not seem to play a role. The fact that the chosen method of delivery failed for a number of the asphyxiated patients, necessitating emergency Caesarian section, suggests that obstetric factors may need closer analysis.

Apgar Score↗
PubMed1989

Acyl-CoA dehydrogenase enzymes during early postnatal development in the rat.

Fatty acid oxidation rates tend to increase with age in most developing tissues. In skeletal muscle, heart, and liver of developing rats, we measured activities of three acyl-CoA dehydrogenase enzymes, which constitute the first step in the mitochondrial beta-oxidation sequence. In skeletal muscle, activities of all three enzymes increased with age. In heart muscle, palmityl-CoA dehydrogenase increased, while the other two enzymes changed only minimally. In liver, palmityl-CoA dehydrogenase activity steadily increased with age. Decanoyl- and butyryl-CoA dehydrogenase also increased with age, but much more irregularly. We also examined the electrophoretic characteristics of these enzyme proteins in the three tissues. There were no changes in their electrophoretic patterns during development.

Acyl-CoA Dehydrogenase↗
PubMed1989

Deficiency of carnitine palmitoyltransferase I.

Defective activity of carnitine palmitoyltransferase I was demonstrated in fibroblasts derived from a patient with hypoketotic hypoglycemia. The level of activity observed was approximately 10% of the control mean. Oxidation of palmitate by intact fibroblasts was reduced to 5% of control values. The patient presented at age 14 months with seizures and was found to have marked hypoglycemia and no ketones in the urine. In response to fasting, she developed hypoglycemia, but the curves for acetoacetate and 3-hydroxybutyrate were flat. Administration of medium-chain triglycerides relieved the hypoglycemia and generated a brisk ketogenesis.

Acyltransferases↗
PubMed1988

Muscle imaging in neuromuscular disease using computerized real-time sonography.

The results of a study utilizing computerized real-time sonography (CRS) to image muscles in patients with neuromuscular disease are presented for 67 patients, 37 with neuromuscular disease and 4 with upper motor neuron disease, and 26 age-matched healthy controls between the ages of 2 days and 59 years. CRS is a safe, noninvasive, atraumatic method for evaluating a broad range of neuromuscular diseases. It is capable of differentiating myopathies or dystrophies from neurogenic atrophies and floppy infants with "central" hypotonia from those with neuromuscular diseases.

Humans↗
PubMed1988

Autonomic dysfunction and adrenocortical unresponsiveness to ACTH.

A child is reported with adrenocortical unresponsiveness to ACTH and autonomic dysfunction. The latter consisted of cold extremities, progressive loss of tear production, the development of achalasia of the esophagus, pupillary dysfunction, and an abnormal histamine skin test. These findings suggest progressive parasympathetic denervation as a cause for the adrenocortical abnormality.

17-Hydroxycorticosteroids↗
PubMed1988

Myopathies caused by disorders of lipid metabolism.

Myopathies due to abnormalities in fatty acid oxidation fall into several clinical categories. Rhabdomyolysis occurring with prolonged stress on the muscle is frequently found to be caused by carnitine palmityl transferase deficiency. The association of systemic metabolic derangements and muscle weakness is seen with defects in long-chain acyl-CoA dehydrogenase, medium-chain acyl-CoA dehydrogenase, or short-chain acyl-CoA dehydrogenase. The latter three are often associated with low muscle carnitine concentrations. In patients who present with only muscle weakness and triglyceride storage, muscle carnitine concentrations may be either normal or reduced.

Fatty Acids↗
PubMed1987

Effect of incompatibility stress on the fit of metal-ceramic crowns.

The interactive effect of coping thickness and a positive thermal contraction mismatch between metal and porcelain on the fit of metal-ceramic crowns has not yet been experimentally determined. Previous studies have suggested that marginal distortion may be due to contraction differences, although finite element analyses indicate that these distortion effects should be negligible. The marginal gap between metal-ceramic crowns and prepared dies was determined under conditions designed to exaggerate distortion effects. These included the use of thin metal copings (0.1 and 0.2 mm), a chamfer preparation, an alloy with relatively poor creep resistance, and a large thermal contraction mismatch between the alloy and porcelain layers. Gap changes which resulted during porcelain firing cycles were relatively small, but larger marginal discrepancies developed in crowns prepared with a compatible porcelain during grinding and abrasive blasting procedures. This study conclusively demonstrates that incompatibility stress induced by a positive contraction mismatch is not a primary cause of marginal or generalized distortion of metal-ceramic crowns and suggests that external grinding and internal abrasive blasting of crowns are more likely causes of this effect.

Aluminum Oxide↗
PubMed1986

Fatty acyl-CoA dehydrogenase enzymes in human skeletal muscle.

An electrophoretic and enzyme-substrate staining technique for acyl-CoA dehydrogenase (ACD) enzymes was developed for use with small (less than 100 mg) tissue samples. Based on their electrophoretic mobility and substrate staining specificity, at least two and perhaps three chain-length specific enzymes for dehydrogenation of saturated fatty acids were found in human skeletal muscle. ACD enzymes staining with octanoyl-CoA or palmitoyl-CoA were identified by this technique in human skeletal muscle, heart, and liver, but the ACD enzyme staining with butyryl-CoA was difficult to detect and was definitely visualized only in skeletal muscle.

Acyl-CoA Dehydrogenases↗
PubMed1986

Carnitine reduces fasting ketogenesis in patients with disorders of propionate metabolism.

Patients with disorders of propionate metabolism have low plasma levels of free carnitine and excrete higher than normal quantities of esterified carnitine. The response to a 19 h fast was assessed as a physiological index of carnitine deficiency. In patients with propionic acidaemia and methylmalonic acidaemia a substantial ketogenesis developed in response to fasting. Supplementation with L-carnitine significantly reduced this ketogenic response.

Carnitine↗
PubMed1986

'Dystrophic' lipid myopathy in two sisters.

Two sisters with progressive myopathy demonstrated microscopic and biochemical evidence of lipid storage in skeletal muscle. Their muscle biopsy specimens resembled those seen in Duchenne's muscular dystrophy and some of the biochemical features were similar, including increased muscle concentration of long-chain acyl-coenzyme A (a fatty oxidation intermediate) and decreased oxidation of radioactively labeled fatty acids by muscle homogenates in vitro. Although the site of the defect was not localized, the data suggested impairment of intramitochondrial beta-oxidation of fatty acids. These two patients may be important in understanding the pathogenesis of muscular dystrophy.

Child↗
PubMed1986

MRI of normal and pathologic skeletal muscle.

Lower extremity skeletal muscle of 22 individuals (five normal volunteers and 17 patients with muscular or neuromuscular diseases) was studied with magnetic resonance imaging. Axial images generated with spin-echo pulse sequences using short repetition times (500-900 msec TR) and short echo times (30-60 msec TE) provided excellent contrast between fat (high signal intensity) and muscle (intermediate signal intensity). Seventeen patients with clinically verified muscle disorders were evaluated in a manner similar to the normal volunteers. Conditions studied include Duchenne muscular dystrophy (three patients), limb-girdle muscular dystrophy (five), facioscapulohumeral dystrophy (three), and spinal muscular atrophy, amyotrophic lateral sclerosis, hereditary sensorimotor neuropathy, cerebral palsy, poliomyelitis, and Kearn-Sayre mitochondrial muscle disease (one each). General patterns of muscle abnormality were common among the diseases and included decreased or increased muscle size and a spectrum of muscle replacement by fat. Variable patterns were observed within disease groups and for each patient. Much phosphorus-31 spectroscopy has been performed in a blind fashion with no proton map of normal/abnormal muscle distribution to guide the spectroscopist. This study emphasizes the worth of having a muscle proton map of patients with muscle dysfunction to assure that meaningful phosphorus spectroscopic information is obtained from a volume of tissue limited to an appropriate muscle.

Adult↗
PubMed1986

Effects of pH on adrenal angiotensin receptors and responses.

Ambient hydrogen ion concentration modulates the effects of angiotensin II (AII) on adrenal aldosterone secretion, but the mechanism of this modulation is unknown. We examined the influence of pH on AII receptors and responses in bovine adrenal glomerulosa cells. Lowering pH from 7.4 to 6.8 increased AII binding 20.5% and increased maximal All-stimulated aldosterone secretion 43%. By contrast, at pH 8.0, All binding and stimulation of aldosteronogenesis fell by 56.6% and 39%, respectively. Effects on All binding intermediate to these changes were observed at pH 7.1 and 7.7. Similar effects of altered pH were observed on All binding to a crude membrane fraction of bovine glomerulosa cells. Analysis indicated that pH primarily affected receptor number rather than affinity. In studies of proposed postreceptor mediators of All actions, pH had no effect on All stimulation of phosphatidylinositol turnover or All inhibition of calcium influx. The results show that pH affects All interaction with its receptors. The larger magnitude of the change in aldosterone compared with receptor binding suggests that a postreceptor step is also altered by pH; however, this postreceptor step is not reflected in calcium influx or phospholipid turnover.

Adrenal Glands↗
PubMed1985

A single therapeutic dose of valproate affects liver carbohydrate, fat, adenylate, amino acid, coenzyme A, and carnitine metabolism in infant mice: possible clinical significance.

We have previously reported that chronic valproate administration reduced ketonemia in suckling mice and fasting epileptic children. The present study demonstrates that even a single dose of valproate in the therapeutic range for man caused a prolonged reduction of plasma beta-hydroxybutyrate levels in normal infant mice; the plasma glucose concentration was also significantly lowered. In the livers of these animals, there were extraordinary decreases in levels of free coenzyme A, acetyl CoA and free carnitine. Concomitantly concentrations of acid-soluble fatty acid (short-chain, non-acetyl) coenzyme A esters and of acid-insoluble (long-chain) fatty acid carnitine esters increased. There was evidence for inhibition of the metabolic flux through the Krebs citric acid cycle at those enzyme reactions which require coenzyme A. While valproate doubled liver alanine levels, concentrations of liver aspartate, glutamate and glutamine were reduced. All of the valproate-induced metabolite changes can be explained by the decrease of coenzyme A due to the accumulation of acid-soluble (non-acetyl) coenzyme A esters (presumably valproyl CoA and further metabolites). Decreased coenzyme A would limit the activities of one or more enzymes in the pathway of fatty acid oxidation and the Krebs citric acid cycle. Secondary decreases in acetyl CoA would limit both ketogenesis and gluconeogenesis. Decreased levels of selected hepatic amino acids could reflect their use as alternative fuels. The effect of clinical doses of valproate in infant mice may relate to the valproate-associated syndrome of hepatic failure and Reye-like encephalopathy in some infants and children and suggest a simple screen for those who may be at particular risk.

3-Hydroxybutyric Acid↗
PubMed1984

Androgen modulation of adrenal angiotensin receptors.

Several polar androgens increased the binding of angiotensin and its stimulation of aldosteronogenesis in bovine adrenal glomerulosa cells. The effect was seen only if the steroids were applied to the cells and then washed away. This phenomenon and the technique for demonstrating it may have implications for studies of receptor modulation and for clinical states in which responsiveness to angiotensin is increased.

Adrenal Cortex↗
PubMed1984

Brominated vegetable oil myopathy: inhibition at multiple sites.

Skeletal muscle lipid storage was induced by feeding rats brominated vegetable oil (BVO). The defect was examined by measuring radioactive substrate oxidation, intermediates of fatty acid oxidation, and activities of oxidative enzymes. One- and U-[14C] palmitate and 1-[14C] pyruvate oxidation were reduced in muscle after four doses of BVO. Inhibition of U-[14C] palmitate oxidation occurred after two doses. Short chain acylcoenzyme A(CoA) derivatives accumulated in the muscle. Several enzymes of beta-oxidation were significantly reduced, with the greatest reduction in 3-ketoacyl-CoA thiolase. The inhibition probably affected multiple sites of CoA and CoA-derivative metabolism.

Animals↗