Biomedical subjects
Publications and source records attributed to J Mathew.
A rare case of laryngeal tuberculosis in a 15-month-old Indian child is described. The unusual mode of presentation with stridor, suspicious radiological signs and papillomatous nature of the laryngeal lesion are highlighted.
Several reports indicate that acute ethanol promotes the cleavage of brain sialoglycoconjugates (SGC). We attempted to confirm this effect by monitoring cleavage of sialic acid (SA) that had been radiolabeled by pretreatment with the specific precursor of SA, N-[3H]acetyl-D-mannosamine, injected intracerebroventricularly into rats 20 h prior to ethanol injection (2 or 3 g/kg, given four times in a simulated "binge drinking" protocol). Analysis of the residual labeled material revealed a significant reduction of radiolabel (p less than 0.01), as compared to saline controls. A dose of 3 g/kg diminished the total labeled SGC by half. Brain sialidase activity was not affected by the ethanol treatment. Since ethanol intoxication is associated with enhanced SA cleavage, one hypothesis needing testing is that loss of SA might help to cause intoxication. If so, pretreatment with SA might antagonize intoxication, presumably by offsetting loss due to cleavage of SA. Consistent with our earlier results, we found that when sialic acid was given i.p. (25 mg/kg), 1, 6, or 24 h prior to ethanol injection (4 g/kg, i.p.), the sleep time was reduced by 35-40% and the performance on rotorod was significantly enhanced (p less than 0.01). When ethanol was replaced by pentobarbital (40 mg/kg), the sleep time was increased (approximately 30%) at 6 h after injection with either 25 or 100 mg/kg sialic acid, whereas at the 24 h postinjection it was decreased (approximately 20%) at both doses. The results suggest that sialic acid is a key component in mediating ethanol effects and perhaps also, in a different way, anesthetic effects.
Because ethanol elicits a dose-dependent hydrolysis of brain sialogangliosides, we tested the possibility that injected gangliosides might antagonize intoxicating doses of ethanol. Clear anti-intoxication effects were seen at 24 hr post-injection of mixed mouse-brain gangliosides at 125-130 mg/kg, but not at lower or higher doses. Sleep time was reduced on the order of 50%, and roto-rod agility was significantly enhanced. Sialic acid (SA) similarly antagonized ethanol; however, the precursor of SA, N-acetyl-D-mannosamine, as well as ceramide and asialoganglioside did not.
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(S,E)-4-Amino-5-fluoropent-2-enoic acid (6) is synthesized in six steps starting from the known gamma-aminobutyric acid aminotransferase (gamma-Abu-T) inactivator, (S)-4-amino-5-fluoropentanoic acid (1). Compound 6 is a mechanism-based inactivator of gamma-Abu-T: time-dependent inactivation is saturatable and protected by substrate; thiols do not protect the enzyme from inactivation; no enzyme activity returns upon dialysis. This compound (6) binds 50 times more tightly to gamma-Abu-T than does the saturated analogue (1). No transamination of 6 occurs prior to inactivation. However, five molecules of 6 are required to inactivate the enzyme with concomitant release of five fluoride ions. Therefore, four molecules are being converted to product for each inactivation event. (E)-3-(1-Aminocyclopropyl)-2-propenoic acid is synthesized in seven steps from 1-aminocyclopropanecarboxylic acid. It is prepared as a cyclopropyl derivative of the proposed intermediate in the inactivation of gamma-Abu-T by 6. The cyclopropyl derivative, however, is a noncompetitive inhibitor and does not inactivate the enzyme. This study shows the usefulness and hazards of incorporation of a trans double bond into potential gamma-Abu-T inactivators.
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Arylsulphatase C and estrone sulphatase activities of sheep hypothalamus-preoptic area-midbrain were examined for their susceptibility to phospholipase action. Russel's viper phospholipase A could completely inactivate estrone sulphatase without affecting arylsulphatase C. The latter was partially inactivated by S. aureus phospholipase C but not by C. welchi phospholipase C. Both arylsulphatase C and estrone sulphatase were inactivated to different extents by sodium deoxycholate, which is known to activate the intrinsic phospholipases of brain. Hydrophobic interaction chromatography on phenyl-Sepharose resulted in the differential elution of arylsulphatase C and estrone sulphatase. The results suggest that one enzyme is not responsible for arylsulphatase C and estrone sulphatase activities.
A method of measuring flow in a large vessel by using a CT scanner is described. It has been shown that this is a simple, accurate and reproducible method in an experimental model. Possible clinical applications and limitations of this method of measuring flow are briefly considered.