Australia's nursing workforce in perspective.
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Biomedical subjects
Publications and source records attributed to G F Williams.
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Methanol intoxication, a rare and potentially lethal form of poisoning, usually results from ingestion and occasionally inhalation of methanol. Initial symptoms of blurred vision, elongated anion gap and metabolic acidosis are typically delayed and may not at first be recognised as methanol-related complaints. Once diagnosed, treatment must be prompt and definitive. As well as general supportive care, ethanol infusion, dialysis and alkalinization from the mainstays of treatment. The cases described in this paper are compared to previous reports from other countries worldwide and contrast the variance in outcome often seen in methanol poisoning. The paper describes two tragic deaths and two lucky survivors, all of whom had consumed a cocktail of methanol and other alcoholic beverages at the same party. The ICU nurse's role in managing the methanol-intoxicated patient relies on that person's sound knowledge of the unusual biochemical reactions occurring in the body and the need to institute definitive and supportive measures to help both patient and family recover.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
One hundred twenty-one young adults 18 years of age or older who had been seen at this hospital with juvenile arthritis since 1955 were surveyed by a series of questionnaires to determine current social function and financial status. Chart reviews and patient questionnaires were used to determine modes of onset and the social circumstances of the family at the onset of the arthritis. The patients as a whole were functioning well: 45 were working full time, 25 were in school full time, 23 were in school and working, and 14 were married women at home. Females had a higher prevalence of persisting disability. Patients who had had a polyarticular onset had lower monthly salaries. No other disease or social variables at onset were statistically associated with any of the outcome variables measured. Fifty of the patients were compared to matched siblings and were found to have achieved comparable educations and salaries, and proportionate numbers of marriages and children.
Serum deoxycytidylate deaminase (EC 3.5.4.12, dCMP deaminase) activity was routinely estimated over 7 years in 2460 pregnancies. The results confirm that elevated dCMP deaminase activity (greater than 4.8 units) is associated with the development of pre-eclampsia but not with essential hypertension in pregnancy; a high rising level can precede eclampsia. Elevated enzyme activity was also found in women who developed jaundice in pregnancy and in some with apparently normal pregnancies. An unexpected finding was that these so called 'false positive' high levels were associated with all the unexplained intrauterine fetal deaths that occurred later in pregnancy. Although elevated dCMP deaminase levels may be associated with a normal outcome, persisting high levels indicate the need for careful monitoring of fetal well being and, in the presence of any other sign of placental insufficiency, delivery should be expedited.
A simple and reliable method for the estimation of cytidine deaminase (cytidine aminohydrolase; EC 3.5.4.5) activity in pregnancy serum is described. This enzyme does not require magnesium for activation and is also more stable than deoxycytidylate deaminase (dCMP deaminase, dCMP aminohydrolase; EC 3.5.4.12). There was excellent correlation between the two enzymes (r = 0.92). Both enzymes showed increased activity in abnormal pregnancy. Both enzymes activities were found to be similar in 1305 maternal serum samples and therefore due to the simplicity of cytidine deaminase estimation it is recommended for the screening of large numbers of antenatal sera for abnormal pregnancies.
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The value of measuring plasma urate and serum deoxycytidylate deaminase (dCMP deaminase) for the early diagnosis of pre-eclampsia has been investigated in 45 patients. A combination of increased blood pressure and increased plasma urate identified 19 patients with a high incidence of fetal and maternal morbidity ascribable to pre-eclampsia. Seventeen of the 19 patients also had an increased serum dCMP deaminase. Serial antenatal observations for a mean period of 104 days (36-179 days) on 33 of the patients demonstrated that plasma urate and serum dCMP deaminase increased together as early changes in the development of pre-eclampsia. In six patients, blood pressure, plasma urate and serum dCMP deaminase all increased but in only one was the rise in blood pressure the first change. Elevations of plasma urate and serum dCMP deaminase are therefore both early features of pre-eclampsia. Serial measurements can give warning of the disorder before the appearance of other clinical features. The change in dCMP deaminase is probably another reflection of early renal involvement in the pre-eclamptic process.
A method is described for determining the activity of deoxycytidylate deaminase in serum. The ammonia liberated from deoxycytidine monophosphate has been specifically determined by enzymatic amination of alpha-ketoglutarate using glutamate dehydrogenase. The concurrent oxidation of NADH2 at 340 nm was proportional to the ammonia liberated from deoxycytidine monophosphate. Using the technique described, a result would be available to the clinician in under 4.5 h. The "normal activity" for deoxycytidine deaminase in normal male, female and pregnancy sera has been determined.
Deoxycytidylate (DCMP) deaminase was assayed at various times during and after normal and abnormal pregnancies. The level in amniotic fluid was assessed at induction and at caesarean section, and cord blood levels were estimated after normal delivery and at caesarean section. A rise occurred during labour and after hysterectomy and caesarean section--returning to normal after 2-3, and 12 days respectively. Levels above 4.8 X 10-minus 4 ml-minus 1 were found in cases of preeclamptic toxaemia and early intrauterine death and in twin pregnancies over 36 weeks' gestation. It is suggested that because of its low incidence of false-negative and false-positive results this test is far superior to other enzyme tests in pregnancy, and a further trial is in progress to assess its role.
The antisera to the A and B isoenzymes found in placenta and fetal liver were raised in rabbits. No antigenic difference was found between the fetal liver and adult tissue isoenzymes. Antisera to the placental isoenzymes did not react with the isoenzymes of adult tissues. The antibody raised against the placental B and fetal B liver isoenzyme decreased the N-acetyl-beta-glucosaminidase activity in maternal serum at 38 weeks gestation to the value found in normal human serum. Immunological evidence has been presented that the isoenzyme of N-acetyl-beta-glucosaminidase found only in pregnancy serum was of placental origin.
An attempt has been made to show that the increase in enzyme activities in sera of pregnant women found with glucose-6-phosphate and adenosine 5'-monophosphate as substrates (described as glucose-6-phosphatase and 5'-nucleotidase) was due to the increase in alkaline phosphatase. The three enzyme activities has pH optima and heat stability characteristics of alkaline phosphatase. The response to the action of inhibitors and activators was typical for alkaline phosphatase. There was an identical increase in all three enzyme activities during pregnancy. As a control similar investigations were made with liver and placental tissue extracts.
Of 16 consecutive cases of previous sterilization treated by tubal surgery fifteen women tested had patent Fallopian tubes. Over 18 months since operation there were four full-term pregnancies and two abortions among 11 patients. At interview with the patient it is important to emphasize that reconstruction of the tubes is a major operation and carries an increased subsequent hazard of ectopic pregnancy.