The truth about snitches: an archival analysis of informant testimony.

Informants are witnesses who often testify in exchange for an incentive (i.e. jailhouse informant, cooperating witness). Despite the widespread use of informants, little is known about the circumstances surrounding their use at trial. This study content-analyzed trials from 22 DNA exoneration cases involving 53 informants. Because these defendants were exonerated, the prosecution informant testimony is demonstrably false. Informant characteristics including motivation for testifying, criminal history, relationship with the defendant and testimony were coded. Most informants were prosecution jailhouse informants; however, there were also defence jailhouse informants and prosecution cooperating witnesses. Regardless of informant type, most denied receiving an incentive, had criminal histories, were friends/acquaintances of the defendant and had testimonial inconsistencies. In closing statements, attorneys relied on informant testimony by either emphasizing or questioning its reliability. The impact of informant testimony on jurors' decisions is discussed in terms of truth-default theory (TDT), the fundamental attribution error and prosecutorial vouching.

Abnormal social behavior in mice with tyrosinemia type I is associated with an increase of myelin in the cerebral cortex.

Hereditary tyrosinemia type I (HT1) is caused by mutations in the fumarylacetoacetate hydrolase (FAH) gene, the template for the final enzyme in the tyrosine catabolism pathway. If left untreated this deficiency of functional FAH leads to a buildup of toxic metabolites that can cause liver disease, kidney dysfunction and high mortality. The current treatment with the drug NTBC prevents the production of these metabolites and has consequently increased the survival rate in HT1 children. As a result of this increased survival, long term complications of HT1 are now being observed, including slower learning, impaired cognition and altered social behavior. We studied a mouse model of HT1 to gain insight into the effects of HT1 and treatment with NTBC on social behavior in mice. We showed that mice with HT1 display abnormal social behavior in that they spend more time in the absence of another mouse and do not discriminate between a novel mouse and an already familiar mouse. This altered behavior was due to HT1 and not treatment with NTBC. Quantification of cerebral cortex myelin in mice with HT1 showed a two to threefold increase in myelin expression. Our findings suggest that absence of FAH expression in the brain produces an altered brain biochemistry resulting in increased expression of myelin. This increase in myelination could lead to abnormal action potential velocity and altered neuronal connections that provide a mechanism for the altered learning, social behavior and cognitive issues recently seen in HT1.

Tyrosinemia type I and not treatment with NTBC causes slower learning and altered behavior in mice.

Tyrosinemia type I is a recessive inborn error of metabolism caused by mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme in the metabolism of tyrosine. This renders FAH nonfunctional and without treatment, toxic metabolites accumulate causing liver and kidney damage. Introduction of the drug NTBC in 2002 offered a treatment which inhibits an upstream enzyme, preventing the production of the toxic metabolites. There is now a long-term survival rate of greater than 90 % in children, but there are reports of lower cognitive function and IQ as well as schooling and behavioral problems in these children. We studied a mouse model of tyrosinemia type I to gain insight into the effects of tyrosinemia type I and treatment with NTBC on mouse learning, memory, and behavior. In the Barnes maze, visual and spatial cues can be used by mice to remember the location of a dark escape box. The primary time, distance, and strategy taken by the mice to locate the escape box is a measure of learning and memory. Our findings show that mice with tyrosinemia type I were slower to learn than wild-type mice treated with NTBC and made more mistakes, but were capable of learning and storing long-term memory. After learning the location of the target hole, mice with tyrosinemia type I respond differently to a change in location and were less flexible in learning the new target hole location. Our findings suggest that this slower learning and cognitive difference is caused by tyrosinemia type I and not by the treatment with NTBC.