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J Gyorkos

Publications and source records attributed to J Gyorkos.

4 recordsLinked to original sources

Diagnostics and a qualitative model.

First generation expert systems were using shallow knowledge based on heuristic information to solve a diagnostic problem. This approach has many disadvantages, which can be avoided by using deep knowledge. Diagnostic reasoning based on deep knowledge is called model-based diagnostics. Recently, the use of qualitative modeling in relation to deep knowledge in expert systems has become increasingly important. The main purpose of our contribution is to present the model-based diagnostic approach at a formal level. The originality of the presented formalization is the concept of the diagnostic space, the characterization of the minimal diagnoses, and the measurement. The formalization serves as the theoretical background to prove our view to the design of qualitative system models and to establish the diagnostic architecture called DISY. The qualitative system model in our diagnostic approach needs not to be specially adopted for use in the diagnostic domain. The only requirement is that it must simulate the system behavior expressed by normal or abnormal functioning of its components. Proposed DISY architecture is not complex and simply takes into an account the previous diagnostic result to obtain a new one from the additional observation-measurement (medical tests or examinations) of the system.

Decision Support Techniques↗

Reconstituted halogenated hydrocarbon pesticide and pollutant mixtures found in human tissues: effects on the immature male Wistar rat after short-term exposure.

Halogenated hydrocarbon insecticides and polychlorinated biphenyl (PCB) mixtures are routinely detected as residues in human adipose tissue, serum, and milk. Based on average values observed in analytical studies, reconstituted halogenated hydrocarbon pesticide mixtures and PCB mixtures were prepared and administered to immature male Wistar rats. The mixtures were administered at dose levels which approximate the concentrations which would be absorbed by an infant suckling for 180 days (low dose, L), and at three higher dose levels (2 X L, 10 X L, and 100 X L). The pesticide mixture contained isomeric hexachlorocyclohexanes, dieldrin, heptachlor epoxide, oxychlordane, trans-nonachlor, hexachlorobenzene, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane, and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene; the reconstituted PCB mixture contained 13 of the major congeners which have been identified in human milk samples. Administration of the L dose level of the pesticide (0.95 mg/kg), PCB (0.45 mg/kg), and pesticide plus PCB mixture (0.95 + 0.45 mg/kg, respectively) in corn oil on days 1 and 3 did not significantly alter hepatic drug-metabolizing enzyme activities or elicit any observable pathological damage 6 days after the first exposure. In contrast, administration of the higher dose levels of this mixture elicited a dose-dependent induction of several hepatic drug-metabolizing enzymes. Moreover, despite the short duration of exposure to these chemicals, the rats treated with the higher doses (10 X L and 100 X L) of these mixtures exhibited mild alterations in thyroid architecture, changes in hepatocellular nuclei including variations in chromatin distribution, vesiculation of larger nuclei, and frequent appearance of pyknotic shrunken nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The effects of twenty-two organochlorine pesticides as inducers of the hepatic drug-metabolizing enzymes.

The effects of 22 organohalogen pesticides as inducers of hepatic drug-metabolizing enzymes in the immature male Wistar rat have been determined, this group includes four isomeric hexachlorocyclohexanes, technical chlordane, alpha-chlordane, gamma-chlordane, oxychlordane, trans-nonachlor, heptachlor, heptachlor epoxide, aldrin, dieldrin, kepone, toxaphene, mirex, hexachlorobenzene (HCB) and several DDT analogs. With the exception of HCB, all of the pesticides induced microsomal dimethylaminoantipyrine, N-demethylase and aldrin epoxidase activities and the cytochrome P-450 content of microsomes from animals pretreated with most of the compounds was also increased compared to control rats. These pesticides all resembled phenobarbitone in their mode of induction. The effects of HCB as a microsomal enzyme inducer resembled those observed after coadministration of phenobarbitone plus 3-methylcholanthrene.

Animals↗

Polychlorinated benzene and phenol congeners as inducers of rat hepatic drug-metabolizing enzymes in immature male Wistar rats.

The effects of the higher chlorinated benzene and phenol congeners as inducers of the hepatic microsomal drug-metabolizing enzymes have been determined in the immature male Wistar rat by comparing the enzymic, electrophoretic, and spectral properties of the microsomes. 3,4,5-Trichlorophenol, 1,2,4,5-tetrachlorobenzene, 1,2,3,5-tetrachlorobenzene, 1,2,4-trichlorobenzene, and pentachlorobenzene induced 4-dimethylaminoantipyrine (DMAP) N-demethylase, an enzyme induced by phenobarbitone (PB) and several PB-type inducers. Hexachlorobenzene induced DMAP N-demethylase and aldrin epoxidase, two PB-inducible enzymes, and benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase, two enzymes induced by 3-methylcholanthrene (MC). This mixed-type induction pattern has been previously reported for hexachlorobenzene. The remaining higher chlorinated benzene and phenol congeners were inactive as inducers of the drug-metabolizing enzymes in the immature male Wistar rats.

Animals↗