Cystic fibrosis and control nasal epithelial cells harvested by a brushing procedure.
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Cell Separation↗
Biomedical subjects
A G Davidson
Publications and source records attributed to A G Davidson.
Epstein-Barr virus shedding in breast milk.
One hundred healthy women already donating to the Children's Hospital Breast Milk bank consented to provide a sample of breast milk for this study. Using a DNA-DNA hybridization dot-blot assay Epstein-Barr virus (EBV) genome (Bam HIW region) was detected in cells shed into breast milk of 46 out of 100 women studied and in 60 out of 132 (46%) of samples donated overall. The prevalence of EBV shedding increased postnatally to a peak of 74% (26/35 positive samples) between 3 and 12 weeks postdelivery. Women delivering prematurely had an initially lower prevalence of shedding with only six out of 30 (20%) positive samples in the first week after delivery, compared to 16 out of 35 (46%) for women delivering at term. Of the 18 women donating more than one sample, 13 showed consistently positive (n = 8) or negative (n = 5) results, and the remaining five had intermittent shedding detected. Only seven out of 42 (17%) breast milk samples studied were EBV-IgG antibody positive, and none showed IgM or IgA-EBV antibodies. Further studies and prospective followup of infants are needed to confirm that breast milk is a significant source for early EBV infection of infants, as indicated by serologic studies.
Antibodies, Viral↗
Biochemical investigation of a child with molybdenum cofactor deficiency.
A girl aged eight months, who presented with developmental delay and dislocated optic lenses, was diagnosed as having combined sulfite oxidase and xanthine dehydrogenase deficiencies consistent with molybdenum cofactor deficiency. The diagnosis was confirmed by demonstrating the absence in urine of urothione, a molybdenum cofactor metabolite. Prenatal diagnosis excluded the disease in the mother's second pregnancy. A summary of an in vitro study of molybdenum cofactor synthesis in the patient is given.
Coenzymes↗
The high incidence of valproate hepatotoxicity in infants may relate to familial metabolic defects.
The incidence of fatal hepatic failure associated with valproic acid (VPA) therapy is highest in children under the age of three years, particularly in those with developmental delay. The pathogenesis of VPA hepatotoxicity is unclear but may relate to the accumulation of a toxic metabolite of VPA which impairs fatty-acid oxidation. We describe two unrelated infants with developmental delay who developed hepatic failure while receiving VPA. Siblings of both children subsequently developed hepatic steatosis and intractable seizures without being exposed to VPA. This suggests that the two children who developed liver failure when receiving VPA may have had a familial metabolic disorder. Familial metabolic disorders may account partly for the higher incidence of fatal hepatotoxicity described in infants receiving VPA.
Chemical and Drug Induced Liver Injury↗
Second-derivative spectrofluorometric determination of sulphoxide impurity in phenothiazine drug substances and formulation.
A direct second-derivative spectrofluorimetric procedure for determining sulphoxide impurity in phenothiazines and their formulations has been developed. The method, which has been applied to the analysis of chlorpromazine hydrochloride and prochlorperazine mesylate, as examples of typical phenothiazine substances, and to their formulations, is based on the measurement of the amplitude taken from the minimum at ca. 270 nm to the longer wavelength maximum in the second-derivative excitation spectrum of the sulphoxide in pH 8 buffer solution. The method is rapid, accurate and precise, and can be used to measure the concentration of sulphoxide in phenothiazines and their formulations at concentrations down to 0.1% m/m of that of the parent phenothiazine.
Drug Contamination↗
Cardiomyopathy associated with nonendemic selenium deficiency in a Caucasian adolescent.
We describe a girl aged 17 y who died after a cardiac arrest secondary to septic shock. At autopsy, the enlarged, soft, and flabby heart showed microscopic evidence of acute myocardial infarction, myocardial edema, myocardiocyte loss, replacement fibrosis in the interventricular septum, and right and left ventricular hypertrophic nucleomegaly. The pathological diagnosis was that of cardiomyopathy due to prolonged selenium deficiency. The patient had been on total parenteral nutrition for 17 mo, following extensive bowel resection for intractable pain, nausea, and vomiting caused by chronic idiopathic intestinal pseudoobstruction. Seven months before death, when severe biochemical selenium deficiency was diagnosed, supplemental selenium was added to the infusion, and plasma selenium concentrations increased. In long-standing selenium deficiency, sepsis may contribute the final insult to a damaged myocardium, triggering symptomatic cardiac failure and sudden death.
Adolescent↗
Communicability of Pseudomonas infections in patients with cystic fibrosis.
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Cross Infection↗
Difference spectrophotometric assay of nitrazepam in tablet formulations.
A difference spectrophotometric procedure is described for the assay of nitrazepam in tablet formulations. The method is based on the measurement of absorbance at 282 nm of a solution of the tablet extract in 0.1 M hydrochloric acid (pH 1) relative to that of an equimolar solution in 0.1 M sodium hydroxide (pH 13). The method is precise and selective for nitrazepam in the presence of the tablet excipients and 2-amino-5-nitrobenzophenone, the principal hydrolysis product of nitrazepam. The absence of a constant isosbestic point in the difference spectrum of nitrazepam during hydrolysis in alkaline solution indicates the presence of a previously unrecognized intermediate hydrolysis product.
Hydrogen-Ion Concentration↗
Determination of low levels of phenothiazine sulphoxides in phenothiazine drug substances and formulations by thin-layer chromatography-second-derivative spectrofluorimetry.
A thin-layer chromatographic-second derivative spectrofluorimetric procedure has been developed for low levels of sulphoxide (down to 0.01%, w/w) in phenothiazine drug substances and formulations. The method has been applied to prochlorperazine maleate, chlorpromazine hydrochloride and promethazine hydrochloride. It has also been applied to pharmaceutical formulations of promethazine hydrochloride and comparison of the results with those obtained by a published difference spectrophotometric procedure for promethazine sulphoxide showed that there was good agreement. The method is simple, rapid, accurate and precise and seems to have general application to the determination of low levels of sulphoxide in phenothiazine drug substances or formulations.
Chromatography, Thin Layer↗
Coeliac disease: an analysis of aetiological possibilities and re-evaluation of the enzymopathic hypothesis.
Although it is well established that components of wheat gluten and structurally-related cereal proteins produce intestinal damage in Coeliac disease (CD), the primary defect which confers upon the host susceptibility to these dietary substances remains a mystery. To date, three main hypotheses have been framed to explain this susceptibility, but none has yet been proven. Diagrammatic representation of these aetiologic hypotheses facilitates their analysis and illustrates the potential importance of a relatively ignored possibility, i.e., that there may be a defect in the intraluminal phase of the in vivo processing of dietary gluten. We suggest that future work should be directed towards investigating the potential role of abnormalities of this phase in the aetiology of CD.
Celiac Disease↗
The simultaneous assay of triprolidine, pseudoephedrine and dextromethorphan in combined preparations by derivative-difference spectrophotometry.
Difference spectrophotometric procedures are described for the assay of triprolidine hydrochloride, dextromethorphan hydrobromide and pseudoephedrine hydrochloride in Actifed preparations. Triprolidine is assayed by the measurement of the difference absorbance at 301 nm between equimolar solutions of the sample extract in 0.1 M sulphuric acid and 0.1 M sodium hydroxide in ethanol (20% v/v). Dextromethorphan and pseudoephedrine are assayed by measurement of the amplitudes in the second and fourth derivative spectra of the difference absorption spectrum of the sample solutions. The measured values are proportional to the concentrations of the drugs. The accuracy, precision and selectivity of the procedures are discussed. Applications of the assay are described for Actifed Compound Linctus, Actifed Syrup and Actifed Tablets.
Journal Article↗
Difference spectrophotometric assay of 5-hydroxymethylfurfuraldehyde in hydrolysed pharmaceutical syrups-II. Isoniazid reagent.
A rapid difference spectrophotometric assay of 5-hydroxymethylfurfuraldehyde (5-HMF) in certain degraded syrups is described. The method involves the measurement of the difference absorbance at 340 nm of the isonicotinoyl hydrazone of 5-HMF, formed at room temperature in an acidic solution of isoniazid, relative to an equimolar solution of 5-HMF, which has been reduced by sodium borohydride, and isoniazid reagent. The procedure is accurate, precise and selective for 5-HMF in the syrups examined. The limits of detection and determination are 0.91 mug ml(-1) and 12.4 mug ml(-1), respectively. The method has been applied to codeine linctus, paracetamol elixir (paediatric) opiate squill linctus, ipecacuanha and squill linctus, Phensedyl Linctus and invert syrup.
Journal Article↗
Coeliac disease: a critical review of aetiology and pathogenesis.
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Celiac Disease↗
Difference spectrophotometric assay of 5-hydroxymethylfurfuraldehyde in hydrolysed pharmaceutical syrups--I. Sodium borohydride reagent.
A rapid difference spectrophotometric procedure is described for the assay of 5-hydroxymethylfurfuraldehyde (5-HMF) in hydrolysed pharmaceutical syrups. The assay involves measurement of the difference absorbance at 283 nm (DeltaA(283)) of a solution of 5-HMF at pH 8 relative to that of an equimolar solution in which the absorption of the 5-HMF has been destroyed by reduction of the carbonyl group by sodium borohydride. The DeltaA(283) is proportional to the concentration of 5-HMF and is unaffected by the presence of sucrose (the sugar component of syrup) or of dextrose or laevulose (the principal sugars of invert syrup). The accuracy, precision and selectivity of the method are discussed. The limits of detection and determination are 0.78 microg ml(-1) and 9.6 microg ml(-1) respectively. The assay has been applied successfully to samples of syrup containing hydroxybenzoate (paraben) preservatives, invert syrup, simple linctus, ephedrine elixir and raspberry syrup.
Journal Article↗
The difference spectrophotometric assay of 5-hydroxymethylfurfuraldehyde in parenteral formulations of dextrose.
A selective difference spectrophotometric assay for 5-hydroxymethylfurfuraldehyde (5-HMF) in injectable solutions of dextrose is described, which eliminates the interference that occurs in simple direct spectrophotometric procedures from other ultraviolet absorbing substances in the solution. The assay is based on the measurement of the absorbance of 5-HMF in an aliquot of the injection relative to that of an equimolar solution in which the 5-HMF has been reduced by sodium borohydride. The difference absorbance, which is due to the loss of absorption after reduction of 5-HMF, is proportional to the concentration of 5-HMF and is free from interference from the ingredients of the formulations and from other UV-absorbing decomposition products of dextrose.
Drug Stability↗
Guanosine triphosphate cyclohydrolase I deficiency: early diagnosis by routine urine pteridine screening.
A deficiency of hepatic guanosine triphosphate cyclohydrolase I is reported in a 4-month-old infant in whom positive results on a Guthrie phenylketonuria test in the neonatal period were found. Because of the significantly elevated serum phenylalanine levels a diagnosis of classical phenylketonuria was made, and dietary therapy was started. Urinary pteridine screening for cofactor variants, however, revealed extremely low levels of both neopterin and biopterin. This suggested the possibility of guanosine triphosphate cyclohydrolase I deficiency and led to additional confirmatory assays. Repeat urine, serum, and CSF pteridine profiles, combined with tetrahydrobiopterin-loading studies and the assay of guanosine triphosphate cyclohydrolase I activity in a liver biopsy, confirmed the defect. It is significant to note that the diagnosis was made before the onset of major clinical symptoms. This case illustrates the need for routine cofactor variant screening of all infants in whom hyperphenylalaninemia is diagnosed in the neonatal period.
Aminohydrolases↗
Biochemical and histologic pathology in an infant with cross-reacting material (negative) pyruvate carboxylase deficiency.
An infant with the acute neonatal form of pyruvate carboxylase deficiency (cross-reacting material negative) presented with severe intractable lactic acidosis within 4 h after birth. He also had hyperammonemia, hypercitrullinemia, and hyperlysinemia. Plasma glutamine was not elevated. He had a rapidly deteriorating clinical course with severe liver dysfunction, repeated septicemia and seizures; he was comatose and was on a ventilator throughout; death occurred at 8 wk of age. Skin fibroblast study confirmed the enzyme deficiency. Detailed biochemical parameters and histopathology of the brain and liver are presented. The evidence from this infant suggests that disturbances of intracellular oxaloacetate levels as a result of the primary enzyme defect might also contribute to deficiency in ATP generation which may explain the various other biochemical changes and liver pathology.
Acidosis↗
Difference spectrophotometric assay of 1,2-diphenolic drugs in pharmaceutical formulations -III. The simultaneous assay of levodopa and benserazide.
A simultaneous assay of levodopa and benserazide in combined formulations is described that utilizes the different spectral properties of the drugs in the presence of germanium dioxide. Difference absorbances are measured at 238 and 292.5 nm between pH 6 solutions of the drugs complexed with germanium dioxide relative to equimolar solutions of the uncomplexed drugs. The concentrations are calculated using two simultaneous equations derived from the difference absorptivities of the individual drugs at 238 and 292.5 nm. The choice of wavelengths for maximum accuracy and precision is discussed. Good recoveries of the drugs in standard mixtures were obtained and satisfactory precision was demonstrated by the relative standard deviations of 0.46% and 1.07% for levodopa and benserazide, respectively, obtained in the replicate analyses of a sample of Madopar capsules. The accuracy of the procedure and the absence of interference from excipients were confirmed by the good agreement in the results for the assay of several batches of Madopar capsules and one of Madopar tablets with those obtained by the manufacturer by an HPLC procedure.
Journal Article↗