Biomedical subjects

Franco Taroni

Publications and source records attributed to Franco Taroni.

22 records · Page 2Linked to original sources

PubMed2003

How the probability of a false positive affects the value of DNA evidence.

Errors in sample handling or test interpretation may cause false positives in forensic DNA testing. This article uses a Bayesian model to show how the potential for a false positive affects the evidentiary value of DNA evidence and the sufficiency of DNA evidence to meet traditional legal standards for conviction. The Bayesian analysis is contrasted with the "false positive fallacy," an intuitively appealing but erroneous alternative interpretation. The findings show the importance of having accurate information about both the random match probability and the false positive probability when evaluating DNA evidence. It is argued that ignoring or underestimating the potential for a false positive can lead to serious errors of interpretation, particularly when the suspect is identified through a "DNA dragnet" or database search, and that ignorance of the true rate of error creates an important element of uncertainty about the value of DNA evidence.

Bayes Theorem↗

PubMed2002

Evaluation of a simplified method of the conduction system analysis in 110 forensic cases.

A simplified method of the His bundle analysis is evaluated by the study of 110 forensic cases. The atrioventricular node or its part were observed in 96 cases (87.3%), penetrating bundle in 92 cases (83.6%), branching and left bundles branch in 109 cases (99.1%) and right bundle branch in 73 cases (66.4%). The changes such as fibrosis and fatty infiltration show statistically significant differences (P<0.01) between progressive age groups confirming their degenerative and age-related nature. The study included as well nine cases of sudden unexpected death and two cases of sudden infant death syndrome (SIDS), for which the autopsy with histological examination and toxicological analysis resulted negative. For nine of these cases, pathological lesions were found which can even explain the fatal issue. Moreover, in the cases with known cause of death, potentially lethal changes were noticed. This simple, low cost technique could be proposed to forensic pathologists as easy to fit into the routine processing of autopsy material, allowing the detection of major abnormalities with minimal effort. The authors also consider the difficulties related to the interpretation of the pathological findings in the conduction system.

Adipose Tissue↗

PubMed2002

Evaluation of scientific evidence using Bayesian networks.

Bayesian networks provide a valuable aid for representing epistemic relationships in a body of uncertain evidence. The paper proposes some simple Bayesian networks for standard analysis of patterns of inference concerning scientific evidence, with a discussion of the rationale behind the nets, the corresponding probabilistic formulas, and the required probability assessments.

Adult↗

PubMedDate not supplied

Frataxin, iron-sulfur clusters, heme, ROS, and aging.

A deficiency in mitochondrial frataxin causes an increased generation of mitochondrial reactive oxygen species (ROS), which may contribute to the cell degenerative features of Friedreich's ataxia. In this work the authors demonstrate mitochondrial iron-sulfur cluster (ISC) defects and mitochondrial heme defects, and suggest how both may contribute to increased mitochondrial ROS in lymphoblasts from human patients. Mutant cells are deficient in the ISC-requiring mitochondrial enzymes aconitase and succinate dehydrogenase, but not in the non-ISC mitochondrial enzyme citrate synthase; also, the mitochondrial iron-sulfur scaffold protein IscU2 co-immunoprecipitates with frataxin in vivo. Presumably as a consequence of the iron-sulfur cluster defect, cytochrome c heme is deficient in mutants, as well as heme-dependent Complex IV. Mitochondrial superoxide is elevated in mutants, which may be a consequence of cytochrome c deficiency. Hydrogen peroxide, glutathione peroxidase activity, and oxidized glutathione (GSSG) are each elevated in mutants, consistent with activation of the glutathione peroxidase pathway. Mutant status blunted the effects of Complex III and IV inhibitors, but not a Complex I inhibitor, on superoxide production. This suggests that heme defects late in the electron transport chain of mutants are responsible for increased mutant superoxide. The impact of ISC and heme defects on ROS production with age are discussed.

Aging↗