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Biomedical subjects

E M Jones

Publications and source records attributed to E M Jones.

At least 73 records · Page 4Linked to original sources
PubMed1980

Mechanisms of increased brain glucose and glycogen after hydrocortisone: possible clinical significance.

We reported previously that chronic administration of hydrocortisone to normal developing mice increases the brain glucose content and cerebral energy reserve. The present report concerns possible mechanisms of this action. Increases in brain glucose (and glycogen) levels were not due to reduction of cerebral metabolic rate, and the effect of hydrocortisone in facilitating transport of hexose from blood to brain was not impressive. Chronic hydrocortisone treatment induced increases in the activities of brain glycerophosphate dehydrogenase and pyruvate carboxylase in vivo; there was no effect on eleven other enzymes of brain glucose and glycogen metabolism. In normal nursing mice, hydrocortisone produced consistent elevations in plasma beta-hydroxybutyrate (and glycerol) levels. Brain beta-hydroxybutyrate levels were also increased. Therefore, the brain glucose concentration may be elevated in these animals because of the availability of an increased supply of ketone bodies as alternative substrates for cerebral oxidative metabolism and biosynthesis. Ketonemia, elevated cerebral glucose and beta-hydroxybutyrate concentrations, and increased glycerophosphate dehydrogenase activity in brain suggest possible explanations for the beneficial action of adrenocorticotropic hormone and glucocorticoids in the treatment of infantile myoclonic epilepsy and other neurological disorders.

Animals↗
PubMed1978

Ocular penetration of topical chloramphenicol in humans.

Commercial ophthalmic chloramphenicol solutions and ointments were applied to human eyes, and the concentrations of chloramphenicol in aqueous humor and tear samples were analyzed using gas-liquid chromatography. Within several minutes after a single application of 0.5% chloramphenicol solution, the tear concentrations of the drug had fallen below 1 mg/liter, the minimal bacteriostatic concentration for many ocular pathogens. Repeated drops of 0.5% chloramphenicol solutions during several hours were required to produce an aqueous humor concentration of 1 mg/liter. A single application of 1% chloramphenicol ointment gave prolonged drug concentrations in the tears and aqueous humor, falling to 1 mg/liter in two to four hours. The repeated use of chloramphenicol solution or ointment was well tolerated by the patients. We conclude that the penetration of chloramphenicol in the anterior segment of the eye is best carried out by the repeated application of chloramphenicol ointment.

Administration, Topical↗
PubMed1975

Effects of alloxan diabetes, anti-insulin serum diabetes, and non-diabetic dehydration on brain carbohydrate and energy metabolism in young mice.

Alloxan-induced diabetes of 4 days duration produced metabolite changes in brain compatible with severe reduction in cerebral metabolism (phosphocreatine increased 70%), and reduced phosphofructokinase activity (fructose diphosphate levels fell 38%). There was a 56% reduction in brain lactate concentration, but pyruvate levels were unchanged. In 5 of 23 animals, brain glycogen levels increased; in the remainder blycogen levels decreased. Brain fructose concentration, 0.4 mmol/kg, was only 1/30 of the glucose concentration. The alloxan-treated animals were also severely dehydrated. Therefore, to determine the casual relation of insulin deficiency to these findings, the effects of chronic dehydration and acute insulin deficiency were investigated. Findings in the brains of severely dehydrated animals (water deprivation and mannitol injections for 4 days) were almost identical with those seen after alloxan treatment. The exceptions were that, in the dehydrated mice, reductions in lactate and pyruvate were proportional, and glycogen levels were consistently reduced. In acute diabetes (6 to 24 hours after repeated anti-insulin serum injections) P-creatine, fructose diphosphate, and lactate levels were normal. Pyruvate levels were normal at 6 hours, but increased 39% by 12 to 24 hours; glycogen was 36% higher at 6 hours and 63% at 12 to 24 hours. Insulin (and glucose) appeared to be specific in correcting the metabolic abnormalities found in the brains of animals with alloxan-induced diabetes. At 4 and one half hours after treatment with insulin and glucose, glucose 6-phosphate levels fell 25%, fructose diphosphate increased 28%, and lactate and the lactate to pyruvate ratio returned to normal; glycogen increased 50%. However, the treatment also had a dramatic clinical effect. Since animals gained 8 to 27% of body weight during therapy, at least some of the improvements in metabolite levels could be related to rehydration.

Animals↗
PubMed1975

Failure of adrenaline to induce hyperglycaemia after fructose injection in young mice.

In control animals a 2-fold increase in liver phosphorylase activity 10min after adrenaline treatment was associated with a 55% increase in plasma glucose (P less than 0.001); at 20 min plasma glucose was 247% of the control value (P less than 0.001). Liver phosphorylase activity was decreased by 74%, 20 min after fructose injection (P less than 0.001), and, although phosphorylase activity increased 5-fold within 5 min of adrenaline injection, no increases in plasma glucose concentration over that found in fructose-injected animals which did not receive adrenaline occurred at either 5, 10 or 20 min. The data confirm inactivation of liver phosphorylase after fructose injection and suggest inhibition of the adrenaline-activated enzyme by the decrease in Pi and elevation of fructose 1-phosphate concentrations produced by the injection of fructose. These findings may be causally related to the hypoglycaemia and the lack of response to glucagon seen in patients with hereditary fructose intolerance after fructose ingestion.

Animals↗
PubMed1972

Epidemiological aspects of the 1969 yellow fever epidemic in Nigeria.

The Virus Research Laboratory of the University of Ibadan, Nigeria, was notified on 23 October 1969 that cases of suspected yellow fever had occurred in the Jos area. The diagnosis was confirmed by virus isolation and the existence of a widespread outbreak on the Jos Plateau and adjacent areas was established. This was the first recognized epidemic of yellow fever in Nigeria since 1953. Between September and the end of December 1969, an estimated total of 252 patients with yellow fever were hospitalized. The case-fatality ratio for hospitalized patients was approximately 40%. The diagnosis of yellow fever was confirmed by virus isolation, serology, or pathology in 55 patients. It is estimated that up to 100 000 cases of yellow fever may have occurred during the epidemic.

Adolescent↗
PubMed1972

Clinical features of yellow fever cases at Vom Christian Hospital during the 1969 epidemic on the Jos Plateau, Nigeria.

Between 27 September and 27 December 1969, 103 patients diagnosed as having yellow fever were admitted to Vom Christian Hospital, near Jos, Nigeria. Headache and vomiting were the commonest presenting complaints, and 95% of the patients showed scleral icterus or bile pigments in the urine. Haemorrhage, signs of renal failure, and CNS involvement (agitation, seizures) were associated with a grave prognosis. The overall case-fatality ratio was 45.6%. The average duration of illness for fatal cases was 6.4 days and for non-fatal cases 17.8 days. Six illustrative case histories are presented.

Adolescent↗
PubMed1970

Reduced brain glucose with normal plasma glucose in salicylate poisoning.

After the intraperitoneal injection into young mice of 700-800 mg/kg of salicylate, brain glucose fell to one-third or less of control values despite normal plasma glucose levels; brain lactate was nearly doubled and there were small decreases in phosphocreatine (18%) and in glycogen (17%). ATP, pyruvate, alpha-ketoglutarate, and glutamate were unchanged. In liver, glycogen was reduced 79% and lactate was five times higher than in control animals; glucose, glucose-6-phosphate, and ATP were unchanged. Since salicylate uncouples oxidative phosphorylation, it is postulated that high energy phosphate in the brain is maintained near normal levels by a compensatory increase in cerebral glycolysis. Apparently the brain glucose level falls because the rate of utilization exceeds the rate at which glucose can be supplied from the blood. Concurrent administration of glucose with salicylate elevated brain glucose concentration and was associated with striking improvement in the condition and the increased survival of the animals. These findings stress the fact that in salicylate poisoning the supply of glucose to the brain may be inadequate even when blood glucose levels are normal.

Adenosine Triphosphate↗