PubMed Health⌕ Search

Biomedical subjects

A Hodson

Publications and source records attributed to A Hodson.

14 recordsLinked to original sources
PubMed1984

CT demonstration of hyperdense cerebral vasculature due to bromide therapy.

An increase in the effective atomic number of blood is among the factors allowing or influencing the visualization of the major cerebral vessels on noncontrast CT. Bromine (atomic number, 50) attenuates 70 keV X-rays significantly and was responsible for a striking enhancement of the major cerebral vessels on the noncontrast CT in a child being treated for epilepsy. Although oral bromides are only occasionally used in the treatment of epilepsy, their use causes an increase in blood density and thus bromides need to be considered along with other etiologies (reviewed) that allow visualization of the major cerebral vessels on noncontrast CT.

Brain↗
PubMed1984

Effect of transfusion therapy on arteriographic abnormalities and on recurrence of stroke in sickle cell disease.

Stroke is a relatively frequent and severe complication of sickle cell disease. We performed cerebral arteriograms in 30 patients with sickle cell disease to evaluate the cause of acute neurologic deficits and to assess the effects of transfusion therapy given for a year or more after the acute episode. Twenty-three patients with motor and speech deficits had multiple abnormalities of major cerebral arteries. The internal carotid and anterior and middle cerebral arteries showed stenosis and/or occlusion at their common junction. Irregular luminal surfaces suggested that endothelial damage and intimal hyperplasia were the basis of stroke. Prolonged transfusion therapy nearly stopped progression of stenosis and markedly decreased the irregularity of the luminal surfaces; in 4 untransfused patients, the degree of stenosis doubled and the luminal abnormalities persisted. Prior to transfusion, 90% of patients had recurrence of stroke. With transfusion therapy, only 10% of patients had recurrence despite persistent arterial abnormalities. Clinical recurrences per patient-month decreased 75-fold. The patients tolerated prolonged transfusion therapy well, despite progressive iron accumulation. Seven patients with smooth abnormalities of a single artery, nonocclusive changes, or with normal arteriograms did not receive transfusions. Only one of this group had recurrence of symptoms.

Acute Disease↗
PubMed1981

The metabolic response to hyperglycaemic clamping in insulin-dependent diabetes.

The metabolic and hormonal effects of stable hyperglycaemia (10-12 mmol/l) have been examined in five insulin-dependent diabetics and compared with the results of 8 h (1200 to 2000 h) normoglycaemic (5-6 mmol/l) clamping. Glucose levels were maintained using a glucose controlled insulin infusion system. Mean blood lactate, pyruvate, total ketone bodies, glycerol and plasma non-esterified fatty acids were similar during the period of stable glycaemia at the two glucose levels. In contrast mean blood alanine was markedly elevated during hyperglycaemic clamping (0.384 +/- 0.008 vs 0.298 +/- 0.021 mmol/l) and 3-hydroxybutyrate was slightly decreased (0.068 +/- 0.007 vs 0.084 +/- 0.008 mmol/l). Plasma glucagon levels were raised during hyperglycaemic clamping and growth hormone slightly decreased. There was a close positive correlation between mean blood alanine and mean blood glucose (r = 0.79, p less than 0.01), and a negative correlation of alanine with the amount of insulin infused (r = -0.72, p less than 0.01). It is suggested that the raised alanine results from increased peripheral glucose utilisation. In general a short period of stable hyperglycaemia is not associated with a worsening of metabolic abnormalities in insulin-dependent diabetic subjects.

Adult↗
PubMed1980

A possible mechanism for the anti-ketogenic action of alanine in the rat.

1. The anti-ketogenic effect of alanine has been studied in normal starved and diabetic rats by infusing l-alanine for 90min in the presence of somatostatin (10mug/kg body wt. per h) to suppress endogenous insulin and glucagon secretion. 2. Infusion of alanine at 3mmol/kg body wt. per h caused a 70+/-11% decrease in [3-hydroxybutyrate] and a 58+/-9% decrease in [acetoacetate] in 48h-starved rats. [Glucose] and [lactate] increased, but [non-esterified fatty acid], [glycerol] and [3-hydroxybutyrate]/[acetoacetate] were unchanged. 3. Infusion of alanine at 1mmol/kg body wt. per h caused similar decreases in [ketone body] (3-hydroxybutyrate plus acetoacetate) in 24h-starved normal and diabetic rats, but no change in other blood metabolites. 4. Alanine [3mmol/kg body wt. per h] caused a 72+/-9% decrease in the rate of production of ketone bodies and a 57+/-8% decrease in disappearance rate as assessed by [3-(14)C]acetoacetate infusion. Metabolic clearance was unchanged, indicating that the primary effect of alanine was inhibition of hepatic ketogenesis. 5. Aspartate infusion at 6mmol/kg body wt. per h had similar effects on blood ketone-body concentrations in 48h-starved rats. 6. Alanine (3mmol/kg body wt. per h) caused marked increases in hepatic glutamate, aspartate, malate, lactate and citrate, phosphoenolpyruvate, 2-phosphoglycerate and glucose concentrations and highly significant decreases in [3-hydroxybutyrate] and [acetoacetate]. Calculated [oxaloacetate] was increased 75%. 7. Similar changes in hepatic [malate], [aspartate] and [ketone bodies] were found after infusion of 6mmol of aspartate/kg body wt. per h. 8. It is suggested that the anti-ketogenic effect of alanine is secondary to an increase in hepatic oxaloacetate and hence citrate formation with decreased availability of acetyl-CoA for ketogenesis. The reciprocal negative-feedback cycle of alanine and ketone bodies forms an important non-hormonal regulatory system.

Alanine↗
PubMed1979

Freeze-fracture studies of erythrocyte plasma membrane in human neuromuscular diseases.

Freeze-fracture studies were conducted in erythrocyte plasma membrane from 8 patients with Duchenne muscular dystrophy (DMD), 8 age-matched controls, 3 adult controls, 10 patients with myotonic muscular dystrophy, and 26 other neuromuscular disease controls. There was marked depletion of intramembranous particles in Duchenne dystrophy, whereas intramembranous particle density counts in other neuromuscular diseases were within normal limits. Therefore, the internal molecular architecture of the erythrocyte membrane is abnormal in Duchenne dystrophy, supporting the concept that a membrane defect involving multiple tissues is present in this disorder.

Erythrocyte Membrane↗
PubMed1978

Alteration in erythrocyte membrane structure in Duchenne muscular dystrophy.

Freeze-fracture studies of erythrocytes from patients with Duchenne muscular dystrophy revealed depletion of particles on both fracture faces of the plasma membrane. This study indicates that the structure of the erythrocyte plasma membrane is abnormal in Duchenne dystrophy and supports the concept that a generalized membrane abnormality is present in this disease.

Adolescent↗
PubMed1977

Erythrocyte cation-activated adenosine triphosphatases in Duchenne muscular dystrophy.

The cation-stimulated adenosine triphosphatase (ATPase) activities of erythrocyte ghosts and erythrocyte ghost plasma membrane fragments of patients with Duchenne muscular dystrophy (DMD) were compared with activities in age-matched normal male controls. DMD Mg++-stimulated ATPase activity was within the normal range. The specific activity of DMD erythrocyte ghost Na+,K+-stimulated, Mg++-dependent ATPase was also normal, and was inhibited by 10(-4) M ouabain to an extent comparable with controls. Ca++-stimulated, Mg++-dependent ATPase activity of DMD erythrocyte ghost plasma membrane fragments, assayed at 0.5 mM free Ca++, was 21% above that in age-matched male controls (n = 22, 2-tailed paired t-test, P less than 0.01). Kinetic studies indicated that the DMD erythrocyte Ca++-stimulated, Mg++-dependent ATPase has greater affinity for MgATP than the enzyme in control erythrocytes.

Adenosine Triphosphatases↗
PubMedDate not supplied

A case for long-term treatment with anticonvulsants.

Seizures occurring in the neonatal period are one of the most significant discriminating factors in predicting childhood neurologic mortality and morbidity (epilepsy, cerebral palsy and mental retardation). Data derived from retrospective and prospective studies indicate that different variables, such as cause and severity of seizure activity, birth weight, neurologic examination and electroencephalogram, help predict which of these children will be severely affected. Most physicians treat such children with an anticonvulsant (phenobarbital) for the first year of life on the supposition that this therapy will minimize mortality and long-term morbidity. There are no controlled studies to indicate whether anticonvulsant therapy affects the outcome in children with neonatal seizures. It may now be possible to select those who are at significantly higher risk for neurologic morbidity, and these infants may benefit from anticonvulsant prophylaxis with phenobarbital.

Anticonvulsants↗