Biomedical subjects
Publications and source records attributed to M K Baker.
Pregnant female mice of various congenic strains were injected on days 11 through 14 of gestation with phenytoin, and the fetuses were examined for the occurrence of cleft palate. The pattern of susceptibility indicates that two genes in the H-2 complex and another gene linked to H-3 are involved in the determination of this trait.
Three cases of pancreatic pseudocysts involving the kidney are presented in which clinical findings or diagnostic imaging favored intrinsic renal disease. Correct diagnosis was established in all cases by sonographically guided cyst aspiration with amylase determinations on the cyst fluid. In addition, laboratory studies ruled out infection, a well known complication of pancreatic pseudocysts. The findings were instrumental in guiding clinical management and insuring correctly timed and properly guided surgical intervention. It is concluded that any patient with a fluid collection in the kidney region may have a pancreatic pseudocyst even without a clear-cut history of pancreatitis or trauma. Fine-needle aspiration is safe and efficacious, and laboratory analysis of cyst fluid should always include amylase determination, in addition to bacteriologic and cytologic evaluation, even if serum amylase is normal.
Inbred and congenic strains of mice have been studied for susceptibility to phenytoin-induced cleft lip with or without cleft palate (CLP) and isolated cleft palate (CP). The role of genes linked to the H-2 complex on chromosome 17 has been confirmed. Congenic strains with the A background have identical levels of spontaneous CLP, whereas those strains having the A background with the H-2a haplotype have significantly higher rates of induced CLP than their congenic partners with the H-2b or H-2s haplotype. No such significant difference in the degree of CLP produced by phenytoin is demonstrable in strains with the B background. Rates of isolated CP produced by phenytoin are significantly higher in strains with H-2a than in their congenic partner strains with either H-2b or H-2s, whether the background is A or B.
In an in vitro model cortisol and phenytoin inhibit the precisely timed process of palatal development, the lysosomally mediated cell death of the medial edge palatal epithelium. This inhibition of programmed cell death of the palatal midline epithelium by each drug is virtually completely blocked by the antiglucocorticoid, cortexolone, whose blocking action results from competitive binding of the glucocorticoid receptor site. The inhibition produced by each of these drugs is prevented by the protein synthesis blocker, cycloheximide. Thus, blockade of programmed cell death by each of these drugs involves the glucocorticoid receptor site and requires protein synthesis.
Evidence for the binding of 5,5-diphenylhydantoin and glucocorticoids to a common receptor is presented for pulmonary and hepatic cytosols and thymocytes of A/J female mice. The 5,5-diphenylhydantoin-protein complex is absorbed by DNA cellulose, and is incorporated into nuclei, 5,5-Diphenylhydantoin, like glucocorticoids, inhibits the production of prostaglandins in thymocytes. Thus a common receptor is probably responsible for the inhibitory and teratogenic effects of these drugs.
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The binding of dexamethasone to its receptor in hepatic cytosol preparations from pregnant mice of four congenic and recombinant strains, C57BL/10, B10.A, B10.A(2R) and B10.A(5R), which have almost identical genetic backgrounds other than the H-2 complex, on day 12 of gestation was analyzed by plotting the binding of ligand against cytosol concentration. The plots of C57BL/10 and B10.A(5R) mice were straight lines, but those of the strains B10.A and B10.A(2R) were upward concave curves. The curvature probably did not result from denaturation of the receptor, as indicated by the time course of the dexamethasone binding and by the fact that at a lower concentration of the ligand, at which the receptor would be less stable, there was less curvature than at a higher concentration of the ligand. The curvature can be explained by the presence of endogenous modifier(s) using an analogy from enzymology. Mathematical analysis, partial removal of the modifier(s) by gel filtration, and mixing of the cytosols from the two types of strains indicated the presence of an unsaturated amount of a modifier(s) in the cytosol of the B10.A and B10.A(2R) strains, and the presence of a saturated amount of the cytosol of the C57BL/10 and B10.A(5R) strains. Thus, the H-2 complex contains a gene(s) which regulates the level of a modifier(s) in hepatic cytosol which affects the binding of glucocorticoid to its hepatic cytosolic receptor.
The binding of 3H-dexamethasone to cytosolic receptors in fetal jaws and in cytosols and nuclei of primary cell cultures of fetal palates was studied in various congenic strains of mice. The amount of specific binding was greater in palatal tissues from B10.A and B10.A(2R) mice than in B10 or B10.A(5R) preparations. These differences were not observed in the liver. Since the strains with higher levels of glucocorticoid receptor are known to be more susceptible to cortisone-induced cleft palate than the strains with low receptor levels, it is suggested that quantitative variation in receptor levels may be involved in determining H-2-linked differences in cleft-palate susceptibility. Whether or not this is the case, it appears that an H-2-linked gene affects the quantity of a cytosolic glucocorticoid-binding protein which translocates to the nucleus.
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A method whereby resistance data can be analysed by means of frequency distributions is described. This method established that Rhipicephalus appendiculatus and R. evertsi evertsi show either little or only developing resistance to the pesticides chlorfenvinphos and dioxathion. Boophilus spp., however, show more instances and higher levels of resistance to these 2 pesticides.
The genetic, clinical and clinical pathological findings of a neurological syndrome in Abyssinian kittens are described. The findings are compared with similar cases in the literature and a tentative diagnosis of a lysosomal storage disease is proposed.
The histopathological and ultrastructural findings in the central nervous system and lymphoid tissue of Abyssinian kittens suffering from a disease which was clinically characterised by neurological disturbances, are described. The lesions were vacuolisation of neurones and macrophages with light microscopy and lamellated membranous cytoplasmic bodies, initially in lysosomes with electron microscopy. Irregularly shaped membrane-bound bodies with an amorphous substance were eventually formed in the cytoplasm of affected cells. It is considered that this is a lysosomal storage disease.
Two new synthetic steroid analogues, (I) 16beta-bromo-3beta,17alpha-dihydroxy-5alpha-pregnane-11,20-dione and (II) 17beta-ureido-1,4-androstadien-3-one have been shown to give kinetic patterns consistent with active-site-directed irreversible inhibition of adult rat testicular microsomal steroid 17alpha-hydroxylase and C17-20 lyase in vitro. Administration of both analogues to adult male rats for 24 h produced potent inhibition of these testicular enzymes in vivo. Given to pregnant rats during the critical period of male organogenesis they produced hypospadias: a characteristic of the syndrome in man in which these enzymes are defective genetically. Given to male rat pups during the first 9 days of life, inhibitor II produced significantly smaller prostates and seminal vesicles in adulthood, indicating the usefulness of this inhibitor in studies on the role of testosterone in neonatal programming of target organ size in adulthood. Thus, two new enzyme inhibitors have been shown to block testosterone production in the foetal and neonatal rat selectively at the site of the hydroxylase without other apparent hormonal effects or influence on adrenal size.
The clinical findings and the macroscopic and microscopic lesions in a kitten which died during an outbreak of ulcerative glossitis in a cattery are described. A brief review of the literature is given to support the theory that the virus of feline panleukopenia may well be the aetiological agent in this outbreak.
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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.