An experimental investigation of the misinformation effect in crime-related amnesia claims

Research suggests that both internal (i.e., lying) and external (i.e., misinformation) factors can affect memory for a crime. We aimed to explore the effects of post-event misinformation on crime-related amnesia claims. We showed participants a mock crime and asked them to either simulate amnesia (simulators) or confess to it (confessors). Next, some participants were provided with misinformation. Finally, all participants were requested to genuinely recollect the crime. Overall, simulators reported less correct information than confessors. Moreover, these two groups were equally vulnerable to misinformation. In addition, exploratory analyses on strategies adopted by simulators revealed that those who previously, mostly omitted information while simulating amnesia exhibited the lowest amount of correct details. Simulators who instead used a mixed strategy disclosed more fabricated memory errors. Findings suggest that legal professionals and jurors should take into account that even offenders, irrespective of confessing or simulating memory loss for a crime, can be susceptible to post-event misinformation

The Impact of False Denials on Forgetting and False Memory

People sometimes falsely deny having experienced an event. In the current experiments, we examined the effect of false denials on forgetting and false memory formation. In Experiment 1, participants were presented with emotionally-negative and neutral associatively related word lists known to engender false memories. After encoding, half of the participants had to falsely deny having seen the words while the other half had to tell the truth. During a final memory test (recall or source monitoring task), participants who falsely denied forgot that they discussed certain words with an experimenter. Furthermore, the act of falsely denying reduced the formation of false memories. These results were partially replicated in Experiment 2 where participants also had to re-learn several words and received a second memory task. This latter design feature diminished the effect of false denials on false memory creation. Our experiments suggest that false denials not only have negative consequences (forgetting), but can have positive ones too (reduction in false memories)

Crime-Related Scenarios Do not Lead to Superior Memory Performance in the Survival Processing Paradigm

The survival processing advantage refers to the finding that processing information according to its survival value improves memory retention. We used mass-testing across three experiments to examine whether the survival processing advantage could be extended to crime-related contexts when adopting both offender’s (Experiment 1 and 2) and victim’s (Experiment 3) perspectives. Interestingly, crime-related scenarios produced the lowest memory retention in Experiments 2 and 3, indicating no mnemonic benefit resulting from crimerelated processing. Furthermore, in Experiments 1 and 2, we failed to replicate the standard survival processing effect, while in Experiment 3 the superior survival memory retention emerged in comparison with the standard control conditions (i.e., moving and pleasantness). Overall, our experiments showed that crime-related contexts did not lead to superior memory retention. Moreover, although we detected some failures to replicate the survival processing effect, this evidence is not sufficiently compelling to argue that there was a general absence of the survival processing advantage

External and Internal Influences Yield Similar Memory Effects: The Role of Deception and Suggestion

In legal cases, testimonies can become contaminated because of an amalgam of external and internal influences on memory. It is well-established that external influences can hurt memory (e.g., suggestive interviews). However, less focus has been placed on the impact of internal influences (e.g., lying) on memory. In the current review, we show that the available evidence suggests that both external and internal influences exert similar effects on memory. That is, we review studies showing that suggesting non-occurrences and suggesting non-experiences can lead to omission errors and false memories, respectively. Likewise, these memory effects are also observed when focusing on internal influences. That is, false denials, feigning amnesia, and fabrication have been shown to affect memory in terms of forgetting (i.e., omissions) and false memories (i.e., commissions). Also, we show that both external and internal influences can lead to changes in the belief that an event occurred. We argue that in legal cases, triers of fact should concentrate on whether both types of influences might have affected testimonial accuracy in witnesses, victims, and suspects

reduction in heart rate variability in autosomal dominant polycystic kidney disease

Introduction: Cardiovascular disease is one of the main causes of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Autonomic dysfunction is associated with an increased risk for all cardiovascular events in the general population and can be evaluated with heart rate variability (HRV). Objective: To evaluate HRV in ADPKD patients with mild hypertension versus hypertensive patients with organ damage and healthy controls (HC). Materials and Methods: We have enrolled 65 patients: 21 ADPKD patients (10 males), 20 patients with hypertension (14 males), and 24 HC (10 males). Biochemical analysis, clinical evaluation, anthropometric data, intima-media thickness, 24-h ECG Holter recording, and echocardiography were investigated at the time of enrollment. Results: No significant differences in HRV parameters were found between ADPKD with mild hypertension and hypertensive patients with organ damage. The median of HRV variables in time domain as SDNN (global autonomic activity) was significantly lower in ADPKD and hypertensive patients than HC (p < 0.05). In the frequency domain analysis, low frequency (LF), which mainly reflects the sympathetic component, showed higher values in ADPKD and hypertensive patients than HC during the night (p < 0.01). During the night, the sympathovagal balance, LF/high frequency (HF), showed higher values in ADPKD and hypertensive patients than HC (p < 0.0001). Conversely, LF day was lower in ADPKD and hypertensive patients than HC (p < 0.01). HF, which mainly reflects the parasympathetic component, was lower in ADPKD and hypertensive patients during the night than HC (p < 0.0001). Conclusions: HRV reduction is present in ADPKD patients with mild hypertension in the absence of organ damage. The evaluation of sympathovagal balance can provide novel information on the cardiovascular risk in ADPKD patients in addition to classical risk factors

p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis.

The role of apoptosis in melanoma pathogenesis and chemoresistance is poorly characterized. Mutations in TP53 occur infrequently, yet the TP53 apoptotic pathway is often abrogated. This may result from alterations in TP53 family members, including the TP53 homologue TP63. Here we demonstrate that TP63 has an antiapoptotic role in melanoma and is responsible for mediating chemoresistance. Although p63 was not expressed in primary melanocytes, up-regulation of p63 mRNA and protein was observed in melanoma cell lines and clinical samples, providing the first evidence of significant p63 expression in this lineage. Upon genotoxic stress, endogenous p63 isoforms were stabilized in both nuclear and mitochondrial subcellular compartments. Our data provide evidence of a physiological interaction between p63 with p53 whereby translocation of p63 to the mitochondria occurred through a codependent process with p53, whereas accumulation of p53 in the nucleus was prevented by p63. Using RNA interference technology, both isoforms of p63 (TA and ΔNp63) were demonstrated to confer chemoresistance, revealing a novel oncogenic role for p63 in melanoma cells. Furthermore, expression of p63 in both primary and metastatic melanoma clinical samples significantly correlated with melanoma-specific deaths in these patients. Ultimately, these observations provide a possible explanation for abrogation of the p53-mediated apoptotic pathway in melanoma, implicating novel approaches aimed at sensitizing melanoma to therapeutic agents

ASPicDB: a database of annotated transcript and protein variants generated by alternative splicing

Alternative splicing is emerging as a major mechanism for the expansion of the transcriptome and proteome diversity, particularly in human and other vertebrates. However, the proportion of alternative transcripts and proteins actually endowed with functional activity is currently highly debated. We present here a new release of ASPicDB which now provides a unique annotation resource of human protein variants generated by alternative splicing. A total of 256 939 protein variants from 17 191 multi-exon genes have been extensively annotated through state of the art machine learning tools providing information of the protein type (globular and transmembrane), localization, presence of PFAM domains, signal peptides, GPI-anchor propeptides, transmembrane and coiled-coil segments. Furthermore, full-length variants can be now specifically selected based on the annotation of CAGE-tags and polyA signal and/or polyA sites, marking transcription initiation and termination sites, respectively. The retrieval can be carried out at gene, transcript, exon, protein or splice site level allowing the selection of data sets fulfilling one or more features settled by the user. The retrieval interface also enables the selection of protein variants showing specific differences in the annotated features. ASPicDB is available at http://www.caspur.it/ASPicDB/

Assessment of orthologous splicing isoforms in human and mouse orthologous genes

<p>Abstract</p> <p>Background</p> <p>Recent discoveries have highlighted the fact that alternative splicing and alternative transcripts are the rule, rather than the exception, in metazoan genes. Since multiple transcript and protein variants expressed by the same gene are, by definition, structurally distinct and need not to be functionally equivalent, the concept of gene orthology should be extended to the transcript level in order to describe evolutionary relationships between structurally similar transcript variants. In other words, the identification of true orthology relationships between gene products now should progress beyond primary sequence and "splicing orthology", consisting in ancestrally shared exon-intron structures, is required to define orthologous isoforms at transcript level.</p> <p>Results</p> <p>As a starting step in this direction, in this work we performed a large scale human- mouse gene comparison with a twofold goal: first, to assess if and to which extent traditional gene annotations such as RefSeq capture genuine splicing orthology; second, to provide a more detailed annotation and quantification of true human-mouse orthologous transcripts defined as transcripts of orthologous genes exhibiting the same splicing patterns.</p> <p>Conclusions</p> <p>We observed an identical exon/intron structure for 32% of human and mouse orthologous genes. This figure increases to 87% using less stringent criteria for gene structure similarity, thus implying that for about 13% of the human RefSeq annotated genes (and about 25% of the corresponding transcripts) we could not identify any mouse transcript showing sufficient similarity to be confidently assigned as a splicing ortholog. Our data suggest that current gene and transcript data may still be rather incomplete - with several splicing variants still unknown. The observation that alternative splicing produces large numbers of alternative transcripts and proteins, some of them conserved across species and others truly species-specific, suggests that, still maintaining the conventional definition of gene orthology, a new concept of "splicing orthology" can be defined at transcript level.</p