Biomedical subjects

S Cornelius

Publications and source records attributed to S Cornelius.

4 recordsLinked to original sources

PubMed2001

COMKAT: compartment model kinetic analysis tool.

UNLABELLED: Compartment models are the basis for most physiologically based quantification of nuclear medicine data. Although some software packages are available for this purpose, many are expensive, run on relatively few types of computers or are of limited capability, and cannot be extended because of the unavailability of source code. Consequently, institutions with modeling expertise often develop software for themselves, which has the disadvantages of lack of standardization and possible replication of effort. Therefore, general-purpose compartment-modeling software distributed with source code would be a welcome resource for the nuclear medicine community. METHODS: We formulated a mathematic framework within which compartment models containing unimolecular and bimolecular (receptor saturation) kinetics can be described. We implemented this framework within MATLAB and call the resultant software COMKAT (Compartment Model Kinetic Analysis Tool). RESULTS: COMKAT simplifies the process of defining and solving standard blood flow, 18F-FDG, and receptor models as well as models of a user's own design. In particular, COMKAT automatically defines and implements state, analytic sensitivity, and Jacobian equations. Given these, COMKAT can perform simulations in which model outputs are solved for specified parameter values, thereby allowing the user to predict how sensitive data are to these parameters. In addition, COMKAT can be used to estimate values for the parameters by fitting model output to experimental data. COMKAT is equipped with command-line and graphic user interfaces from which the user can access these features. Examples of these applications are presented along with validation and performance summaries. CONCLUSION: COMKAT is a useful software tool and is available without cost to researchers, at www.nuclear.uhrad.com/comkat.

Computer Simulation↗

PubMed1997

Analysis of low and high grade B-cell lymphoma subtypes using semi-nested PCR and two primer sets.

Immunoglobulin gene rearrangements in B-cell lymphoma subtypes may not always be detected by PCR if only one primer set is applied. We therefore analysed a range of low and high grade B-cell lymphoma subtypes for monoclonality using PCR, to determine appropriate primer selection strategies for routine diagnostic use. Semi-nested PCR was performed on 70 unequivocal B-cell lymphoma cases using paraffin-embedded tissue (PET). Consensus primers directed at the framework 3 (Fr3) and framework 2 (Fr2) regions of the immunoglobulin heavy chain (IgH) gene were used to detect monoclonality. Monoclonality was found in 77% of cases using primer Fr3, 58% using Fr2, and in 93% of cases when data were combined for both primers. In 89% of the 38 low grade and 97% of the 31 high grade B-cell lymphomas monoclonality could be detected when combining both primers. Fr3 gave superior results in most of the lymphoma subtypes analysed. We conclude that both Fr3 and Fr2 are useful, in a routine histopathology laboratory, for detecting monoclonality in most B-cell lymphoma subtypes. Certain subtypes, however, are sometimes not targeted by these primers and therefore require additional analyses.

Clone Cells↗

PubMed1986

Ferrous ion supported in vivo lipid peroxidation induced by paracetamol--its relation to hepatotoxicity.

Treatment of mice with 400 mg/kg paracetamol or 20 mg/kg Fe2+ did not evoke in vivo lipid peroxidation as evidenced by the rate of ethane exhalation. The combined treatment with both, however, led to a more than ninefold enhancement of lipid peroxidation. In glutathione-depleted mice treatment by either agent alone almost doubled the rate of ethane exhalation as compared to the respective control group. Here, again, treatment with both led to an even 26-fold increase in in vivo-lipid peroxidation. These results indicate that iron ions are needed to initiate lipid peroxidation by a redox-cycling metabolite of paracetamol. Marked hepatotoxicity was seen in both groups of mice treated with both Fe2+ and paracetamol as well as in glutathione-depleted mice treated with paracetamol only, the degree of liver damage being identical in all three groups despite of the different rates of lipid peroxidation. This dissociation of hepatotoxic response from ethane exhalation indicates that lipid peroxidation is at least not the sole mechanism by which paracetamol exerts its toxicity towards liver cells.

Acetaminophen↗

PubMed1985

Fe2+-supported in vivo lipid peroxidation induced by compounds undergoing redox cycling.

Treatment of male mice with the redox cycling compounds nitrofurantoin, paraquat, diquat or menadione failed to elicit in vivo lipid peroxidation as evidenced by ethane exhalation. The first three led to an enhanced ethane production, however, when the animals were pretreated with a low dose of Fe2+. While GSH-depletion by phorone pretreatment alone had no influence on the in vivo lipid peroxidation as evidenced by ethane expiration in the presence of either compound, the combined treatment with phorone, Fe2+ and nitrofurantoin, paraquat or diquat led to a further enhancement of ethane exhalation. These results indicate that redox cycling compounds do not initiate lipid peroxidation by themselves, but are well capable of stimulating the iron-induced LPO.

Animals↗