Biomedical subjects
Publications and source records attributed to J T Wilson.
The rate of reassociation of denatured DNA was determined for two selected diploid species, Gossypium thurberi (D genome) and G. arboreum (A genome), and one allotetraploid species, G. hirsutum (AD genome). The relative genome size and DNA content of the chromosomes of the diploids were A greater than D. Renaturation curves indicated that the differences in genome sizes were due primarily to the repetitive DNA content.
Resistance to the organophosphorus acaricides diazinon, dimethoate and formothion in the Biarra (B), Mackay (M) and Ridgelands (R) strains respectively of the cattle tick B. microplus has been shown previously to be controlled in each strain by a single incompletely dominant autosomal genetic factor. A very similar mode of inheritance of fenthion resistance in strain B has now been demonstrated with no departure in degree of dominance of resistance from the mean value of +0-57 common to these strains exposed to these chemicals. No F1 larval progeny from the following crossings were appreciably more resistant than their parents to these chemicals: R x B--bromophos ethyl and fenthion; B x M--carbaryl, chlorfenvinphos, chlorpyrifos, diazinon, dimethoate, ethion, fenthion and formothion; M x R--chlorfenvinphos, diazinon, dimethoate, ethion, formothion. The field importance of this absence of overdominance is discussed. There were no susceptible double recessive F2 larval progeny of B x M crossings of F2 or F3 larval progeny of R x M crossings when tested against dimethoate to which the three parental types were similarly resistant; 1/16 of the larval progeny would be expected to be completely susceptible if the resistance genes were unlinked. F1 adult progeny of B x M and R x M crossings exhibited the incompletely recessive mutant-type decreased brain acetylcholinesterase (AChE) activity common to strains B, M and R, thus satisfying the test for allelism. No ticks with normal levels of brain AChE were detected in F2 adult progeny of B x M or R x M crossings. This evidence was strongly suggestive of a series of closely linked genes or alleles controlling dimethoate resistance and a series of alleles controlling decreased brain AChE activity in strains B, M and R.
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Wide variations in drug dose recommendations for children of the same or different ages reflect the inadequacy of data on pharmacokinetics and pharmacodynamics in children. Selected aspects of available literature on pharmacokinetics of drugs used in older infants and children has been reviewed with special attention to calculation of an age-appropriate dose. During the neonatal period and early infancy the elimination of many drugs that are excreted in the urine in unchanged form is restricted by the immaturity of glomerular filtration and renal tubular secretion. On the other hand, in late infancy and/or in childhood, a similar or greater rate of elimination from plasma than in adults has been observed for many drugs, notably digoxin, phenobarbitone, phenytoin, carbamazepine, ethosuximide, diazoxide, clindamycin and propoxyphene. Consistent with this, it has been shown that some drugs exhibit a lower plasma level/dose ratio in infancy and early childhood as compared with the adult. This is true for phenobarbitone, phenytoin and ethosuximide. Some age groups of children remain uninvestigated with regard to pharmacokinetics, even for the drugs reviewed. Therefore, pediatric therapy remains empirically based for many drugs.
Infant twins sustained severe circumoral and pharyngeal burns from a concentrated solution of benzalkonium (Zephiran) chloride prescribed for treatment of candidiasis. This report emphasizes the unnecessary hazard accompanying use of a potentially toxic drug-especially when prepared in error by the pharmacist-when a safer drug (nystatin) is available for treatment of oral candidiasis. Risks from use of a prescription drug for other than the intended patient are also highlighted by this episode of poisoning.
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Time course studies of rho-nitroanisole O-demethylation revealed formaldehyde production in excess of rho-nitrophenol (PNP) and 4-nitrocatechol (NTC) formation by rat liver microsomes. This indicated that these products (PNP, NTC) were metabolised further. The hydroxylation reaction PNP yields NTC showed substrate and product inhibition and a requirement for reduced nicotinamide adenine dinucleotide phosphate and O2 and was localized in liver microsomes. It was strongly activated by ascorbic acid, cysteine, adenosine triphosphate or hydroxylamine in vitro and enhanced by phenobarbital treatment in vivo. Mercapturic derivatives were metabolized to the corresponding hydroxy compounds with the same speed as their parent compounds. Both PNP and NTC were metabolized to the corresponding glucuronide and sulfate conjugates. On the other hand, the PNP or NTC glucuronides and sulfates were metabolized with liver microsomes to PNP and NTC.
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