Biomedical subjects
Publications and source records attributed to J Mathew.
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.
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Two rare cases of pseudohypophosphatasia in two siblings which so far, to best of our knowledge have not been reported.
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Cholesterol, pregnenolone, progesterone, 11-deoxycorticosterone (11-DOC) and corticosterone were quantitated in subcellular fractions isolated from in vivo adrenocorticotropin (ACTH)-stimulated rat adrenal zona fasciculata/reticularis. Six adrenal subcellular fractions separated by discontinuous sucrose gradient centrifugation (lipid, 0.125 M sucrose, cytosolic, microsomal, mitochondrial and nuclear) were extracted with alkaline ether/ethanol and assayed by high pressure liquid chromatography (HPLC). Lipid fractions contained the major cholesterol stores, while most pregnenolone and progesterone was found in lipid, microsomal and mitochondrial fractions. The 0.125 M sucrose and cytosol fractions together contained approximately 75% of the total 11-DOC and corticosterone. The five steroids were only present in small amounts in organelle fractions containing steroidogenic enzymes. Homogenate and lipid fraction cholesterol decreased between 10 and 15 min and again 30 min after ACTH injection. In the homogenate, lipid, microsomal and mitochondrial fractions, pregnenolone and progesterone were increased after ACTH injection; peak pregnenolone and progesterone concentrations were often measured in adrenal gland sucrose, cytosolic, microsomal and mitochondrial fractions 15 to 20 min after rats were injected with ACTH. Although ACTH increased 11-DOC and corticosterone in all but the mitochondrial and nuclear fractions, the sucrose, cytosolic and microsomal 11-DOC, and cytosolic corticosterone increased most dramatically. In many fractions, peak 11-DOC and corticosterone concentrations were most often observed between the 10 and 15 min periods and again at 30 min.
We have reported that single doses of alcohol diminish total sialic acid in rat brain. Recent results indicate that this effect seems to be largely accounted for by alcohol-induced reduction in gangliosides. In these experiments, five replicate groups of mice were injected IP with a single dose of 20% alcohol and saline as control. At 1 hour postinjection, alcohol decreased total brain gangliosides (p less than 0.03) at 1 and 2 g/kg, but not at 3, 4, and 6 g/kg. Free whole-brain sialic acid was increased by 2 g/kg alcohol, which is consistent with the observed decrement in gangliosides at this dose. However, activity of sialidase on the endogenous substrates was not greatly affected by 2 g/kg of alcohol, indicating that ganglioside decrement is probably not attributable to activation of the catabolic enzyme. These results confirm and extend our earlier reports that incriminated gangliosides in the acute action of alcohol. The data also raise the possibility that the effect is due to the "excitatory," rather than the depressive actions of alcohol. Moreover, the action may involve an increased hydrolysis of membrane gangliosides by sialidase.
Acute administration of ethanol reportedly decreases total sialic acid in brain. Here, we tested the hypothesis in brain and liver that the decrement is due to increased hydrolysis of sialoglycoconjugates. Mouse tissue slices were pulse-labeled with N-[3H]acetyl-D-mannosamine, the precursor of sialic acid. Incorporation was linear for up to 4 hr of incubation. When the labeled slices were incubated with three concentrations of ethanol (0.1, 0.5, and 1 M) for 5 hr, labeled liver sialoconjugates were significantly affected only at 0.5 and 1 M ethanol, whereas labeled brain sialoconjugates were markedly decreased even at 100 mM ethanol. Sialidase activity decreased steadily with increasing concentration of ethanol, indicating that the increased hydrolysis was not attributable to an enhanced sialidase activity. n-Propanol and t-butanol had the same degradative effect as ethanol on sialocompounds; and 3 mM pyrazole, an inhibitor of alcohol dehydrogenase (ADH), had no effect on ethanol-induced degradation of sialocompounds. The protein/DNA ratio in liver showed a steady decrease with increasing ethanol. The data thus confirm the in vivo reports of ethanol-enhanced cleavage and rule out any increase in sialidase activity as a major cause.
The functional state of GABAA receptors during physical dependence on ethanol was evaluated in two ways. First, the ability of ethanol dependence to change the convulsant potency of GABAA antagonists microinjected into the inferior colliculus was examined. A second approach evaluated the effects of ethanol dependence on the ability of muscimol or pentobarbital to stimulate chloride uptake in rat brain vesicles. In the studies examining changes in convulsant potency, bilateral microinfusions of GABAA antagonists, bicuculline methiodide and picrotoxinin, as well as the excitatory amino acid agonist, kainic acid (used as a positive control) induced similar dose-related increases in the frequency of wild-running seizures. Ethanol dependence did not significantly change susceptibility to wild-running seizure induction by an of the convulsants, although susceptibility to the more severe, clonic seizures was significantly increased for each convulsant. This suggested that the receptor-blocking effects of GABAA antagonists responsible for inducing wild-running seizures were not selectively increased by ethanol dependence, but that spread of seizure activity responsible for clonic seizures following the initiation of wild running was generally increased. Finally, in studies examining changes in GABAA receptor-mediated chloride uptake, both muscimol and pentobarbital were found to induce concentration-dependent increases in chloride uptake in rat brain vesicles. However, responses to these drugs were not reduced by ethanol dependence suggesting that a generalized adaptive decrease in GABAA receptor function was unlikely. Together these results do not provide support for the hypothesis that the GABAA receptor-chloride channel complex is down-regulated during the development of physical dependence on ethanol.
Polymers capable of recognizing adenine in aqueous medium were developed by the molecular imprinting technique using methacrylic acid and 4(5)-vinylimidazole as comonomers with ethylene glycol dimethacrylate as the cross-linking agent under different polymerization conditions. The affinity of these polymers for adenine and other nucleotide bases was compared. The association constant for the binding of adenine to the polymer is calculated to be 4.3 x 10(3)M(-1). Furthermore, binding of adenosine 5'-triphosphate (ATP) to the polymers was evaluated, and an enhanced binding compared to adenine was observed. The binding of ATP is pH dependent, with the maximum around pH 3. Results have been explained based on the hydrogen bonding and ionic interactions between ATP and the ligands on the polymer matrix. The catalytic effect of these polymers for the hydrolysis of ATP is briefly discussed.
Arylsulfatase A, B and an anionic form of B were separated by DEAE-cellulose column chromatography from the brains of man, monkey, rabbit, rat and chicken. The relative proportion of brain arylsulfatases differed from one species to the other. The anionic form of arylsulfatase B was a minor component as compared to arylsulfatase A or B in human and monkey brains while it was a major component in rat and chicken brains. Anionic arylsulfatase B was found in fetal human brains and in newborn monkey brain. In the rat brain, the activities of arylsulfatases A and anionic B showed an increasing trend during development, reaching a peak around 20 days after birth, without any change in their proportions. Treatment with Escherichia coli alkaline phosphatase resulted in the conversion of a major portion (about 70%) of the anionic arylsulfatase B of human and monkey brains into a less charged form which remained unbound to DEAE-cellulose. This conversion by phosphatase was inhibited by inorganic phosphate. Rat and chicken brain anionic arylsulfatase B was not susceptible to alkaline phosphatase. Vibrio cholerae neuraminidase treatment did not significantly affect the charge on anionic arylsulfatase B from any of the species. The results suggested a phosphorylated form of anionic arylsulfatase B exclusively in the primate brain.
Seeking a solution to bring down the prevalence of simple plantar ulcers in the field, Damien Foundation India Trust (DFIT), Chennai, developed a curriculum to teach the field staff of all its projects. The purpose was to make patients self-reliant in the care of their plantar ulcers in their homes. The strategy used was to make patients take care of their ulcers using tools found in their homes and surroundings and become responsible for the care of their limbs. This strategy was implemented in eight projects of DFIT and the programme was followed regularly for one year. Regular monitoring and evaluation showed that under this strategy the prevalence of plantar ulcers was reduced by about 50%.
BACKGROUND: Intravenous drug use is an increasingly common condition predisposing to infective endocarditis. Data on infective endocarditis in intravenous drug users are limited. OBJECTIVE: To determine the clinical features, bacteriologic findings, site of involvement, complications, and mortality associated with infective endocarditis in intravenous drug users. METHODS: Cohort study of intravenous drug users with native valve infective endocarditis. RESULTS: A total of 125 cases of infective endocarditis occurred in 114 patients (84 cases [67%] in men and 41 cases [32%] in women) with a mean (+/- SD) age of 37 +/- 7 years. The tricuspid valve was involved in 58 cases (46%), the mitral valve in 40 cases (32%), and the aortic valve in 24 cases (19%). The microorganisms identified included Staphylococcus in 82 cases (65.6%) and Streptococcus in 32 cases (25.6%). Twenty-three patients (18%) underwent surgery, and two (9%) of them died. One hundred two patients (82%) were treated medically, and nine (9%) of them died. Fifteen patients (63%) with aortic valve involvement vs 17 patients (17%) without aortic valve involvement underwent surgery or died without surgery (odds ratio, 8.24; 95% confidence interval, 3.1 to 21.8). Among the survivors, at least one major cardiovascular complication occurred in 79 cases (69.3%). CONCLUSIONS: Infective endocarditis in intravenous drug users affects the right and left sides of the heart with approximately equal frequency. At present, more than 90% of cases of infective endocarditis in intravenous drug users in Chicago are caused by staphylococci or streptococci. Involvement of the aortic valve is predictive of increased morbidity and mortality in intravenous drug users with infective endocarditis. With medical treatment, and surgery when medical treatment fails, intravenous drug users with infective endocarditis have an in-hospital survival rate of 91%.
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