Justice Efficacy and Argument Strength in Mock Juror Decision-Making in a Civil Trial

In 2005, 48,300 state and federal civil jury trials occurred in the United States (National Center for State Courts, 2009). Approximately 15% of the verdicts juries render are inaccurate (Spencer, 2007). Therefore, it is of utmost important to increase juror accuracy. The current thesis investigated jurors\u27 justice efficacy as it relates to persuasion. Mock jurors\u27 levels of justice efficacy were manipulated by giving them false feedback on a moral reasoning task. Participants read a civil trial summary, and received weak or strong statements by potential other jurors. The relation between argument strength and verdict did not depend on the feedback condition. There was a marginally significant Feedback x Initial liability judgment interaction. Participants who received positive feedback were more influenced by the arguments than participants who received negative or no feedback

The Influence of Racial and Crime Stereotypes on Jurors\u27 Representations of Trial Evidence and Verdict Decisions

Past research has shown that jurors tend to make more severe culpability judgments when defendants are charged with crimes that are associated with their racial group (e.g., Jones & Kaplan, 2013). Although the Story Model (e.g., Pennington & Hastie, 1988) has received much empirical support and currently is the most prominent model in the juror decision making literature, it has not been applied to cases where racially stereotypical crimes might bias verdict decisions. The present research investigated whether the narrative believability of the stories that are suggested at trial, especially story coherence, would explain the effect of race-crime congruence on verdict decisions. Specifically, I attempted to answer the question of whether race-crime congruence affects biased verdict judgments because it leads to an increase in the coherence of the stories jurors form from the evidence. In addition, my goal was to assess whether motivation to control prejudice and stereotype suppression instructions serve as two potential moderating variables. In Study 1 I developed a scale that fully captures the certainty principles affecting acceptance of and confidence in a story (i.e., interpretation of the evidence leading to trial) in the specific context of juror decision making. Specifically, I examined the factor structure underlying a modified version of Yale\u27s (2013) Narrative Believability Scale-12. Study 2 investigated whether the coherence of the prosecution story (and/or the defense story) mediates the relationship between race-crime congruence and verdict judgments in a diverse online sample. In addition, I planned to assess whether high levels of motivation to control prejudice and the presence of stereotype suppression instructions independently reduce this effect. Moreover, with study 3, I attempted to replicate the results in study 2 with a student sample in the laboratory, using the stories that were actually created by the mock jurors as the mediating mechanisms. Based on the findings of Study 2 and Study 3, an additional study was conducted to investigate whether those null effects that emerged in the other studies were due to order effects. No race-crime congruence effects emerged. Findings and implications were discussed

Understanding the Processes that Regulate Positive Emotional Experience: Unsolved Problems and Future Directions for Theory and Research on Savoring

In this paper, we focus on unanswered questions and future directions in positive psychology, with a special emphasis on savoring processes that regulate positive emotions. To advance our understanding of the savoring processes underlying positive experience, we highlight three unresolved issues that must be addressed: (1) discriminating the distinctive neuropsychological profiles associated with different savoring processes; (2) developing viable methods of measuring and analyzing the mediational mechanisms involved in real-time savoring; and (3) clarifying the developmental processes through which people acquire different strategies to savor positive experiences across the life span. We propose several potentially fruitful lines of attack aimed at addressing these unsolved problems, each of which requires new methods of assessment to advance theory and refine our conceptual understanding of savoring

Good and Bad Group Performance: Same Process—Different Outcomes

Much of the research on small group performance shows that groups tend to outperform individuals in most task domains. However, there is also evidence that groups sometimes perform worse than individuals, occasionally with severe negative consequences. Theoretical attempts to explain such negative performance events have tended to point to characteristics of the group or the group process that were different than those found for better performing groups. We argue that typical group processes can be used to explain both good and bad group performance in many instances. Results from a pair of experiments focusing on two different task domains are reported and used to support our arguments

Mechanisms of loss of heterozygosity in neurofibromatosis type 1-associated plexiform neurofibromas

Plexiform neurofibromas constitute a serious burden for patients with neurofibromatosis type 1 (NF1), a common autosomal dominant disorder characterized by pigmentary changes and tumorous skin lesions (neurofibromas). Despite the prominence of these benign tumors in NF1 patients, the mechanisms underlying the tumor-associated loss of heterozygosity (LOH) in plexiform neurofibromas have not been extensively studied. We performed LOH analysis on 43 plexiform neurofibromas from 31 NF1 patients, the largest study of its kind to date. A total of 13 (30%) plexiform neurofibromas exhibited LOH involving 17q markers. In three tumors, LOH was found to be confined to the NF1 gene region. However, in none of the tumors was a somatic NF1 microdeletion, mediated by non-allelic homologous recombination between either NF1-REPs or SUZ12 genes, detected. Thus, NF1 microdeletions do not appear to be frequent somatic events in plexiform neurofibromas. Determination of NF1 gene copy number by multiplex ligation-dependent probe amplification indicated that although tumors with smaller regions of LOH were characterized by 17q deletions, no NF1 gene copy number changes were detected in six plexiform neurofibromas with more extensive LOH. To our knowledge, mitotic recombination has not previously been reported to be a frequent cause of LOH in plexiform neurofibromas

A novel third type of recurrent NF1 microdeletion mediated by non-allelic homologous recombination between LRRC37B-containing low-copy repeats in 17q11.2

Large microdeletions encompassing the neurofibromatosis type-1 (NF1) gene and its flanking regions at 17q11.2 belong to the group of genomic disorders caused by aberrant recombination between segmental duplications. The most common NF1 microdeletions (type-1) span 1.4-Mb and have breakpoints located within NF1-REPs A and C, low-copy repeats (LCRs) containing LRRC37-core duplicons. We have identified a novel type of recurrent NF1 deletion mediated by nonallelic homologous recombination (NAHR) between the highly homologous NF1-REPs B and C. The breakpoints of these ∼1.0-Mb (“type-3”) NF1 deletions were characterized at the DNA sequence level in three unrelated patients. Recombination regions, spanning 275, 180, and 109-bp, respectively, were identified within the LRRC37B-P paralogues of NF1-REPs B and C, and were found to contain sequences capable of non-B DNA formation. Both LCRs contain LRRC37-core duplicons, abundant and highly dynamic sequences in the human genome. NAHR between LRRC37-containing LCRs at 17q21.31 is known to have mediated the 970-kb polymorphic inversions of the MAPT-locus that occurred independently in different primate species, but also underlies the syndromes associated with recurrent 17q21.31 microdeletions and reciprocal microduplications. The novel NF1 microdeletions reported here provide further evidence for the unusually high recombinogenic potential of LRRC37-containing LCRs in the human genome

Type 2 NF1 Deletions Are Highly Unusual by Virtue of the Absence of Nonallelic Homologous Recombination Hotspots and an Apparent Preference for Female Mitotic Recombination

Approximately 5% of patients with neurofibromatosis type 1 (NF1) exhibit gross deletions that encompass the NF1 gene and its flanking regions. The breakpoints of the common 1.4-Mb (type 1) deletions are located within low-copy repeats (NF1-REPs) and cluster within a 3.4-kb hotspot of nonallelic homologous recombination (NAHR). Here, we present the first comprehensive breakpoint analysis of type 2 deletions, which are a second type of recurring NF1 gene deletion. Type 2 deletions span 1.2 Mb and are characterized by breakpoints located within the SUZ12 gene and its pseudogene, which closely flank the NF1-REPs. Breakpoint analysis of 13 independent type 2 deletions did not reveal any obvious hotspots of NAHR. However, an overrepresentation of polypyrimidine/polypurine tracts and triplex-forming sequences was noted in the breakpoint regions that could have facilitated NAHR. Intriguingly, all 13 type 2 deletions identified so far are characterized by somatic mosaicism, which indicates a positional preference for mitotic NAHR within the NF1 gene region. Indeed, whereas interchromosomal meiotic NAHR occurs between the NF1-REPs giving rise to type 1 deletions, NAHR during mitosis appears to occur intrachromosomally between the SUZ12 gene and its pseudogene, thereby generating type 2 deletions. Such a clear distinction between the preferred sites of mitotic versus meiotic NAHR is unprecedented in any other genomic disorder induced by the local genomic architecture. Additionally, 12 of the 13 mosaic type 2 deletions were found in females. The marked female preponderance among mosaic type 2 deletions contrasts with the equal sex distribution noted for type 1 and/or atypical NF1 deletions. Although an influence of chromatin structure was strongly suspected, no sex-specific differences in the methylation pattern exhibited by the SUZ12 gene were apparent that could explain the higher rate of mitotic recombination in females

Extended runs of homozygosity at 17q11.2: an association with type-2NF1 deletions?

Large deletions in the NF1 gene region at 17q11.2 are caused by nonallelic homologous recombination (NAHR). The recurrent type-2 NF1 deletions span 1.2 Mb, with breakpoints in the SUZ12 gene and SUZ12P. Type-2 NF1 deletions occur preferentially during mitosis and are associated with somatic mosaicism. A panel of 16 type-2 NF1 deletions was used as a model system in which to investigate whether extended homozygosity across 17q11.2 might be associated with somatic deletion. Using SNP arrays, a 3.2Mb interval encompassing the NF1 deletion region was found to harbor runs of homozygosity (ROHs) in different human populations. However, ROHs Z500 kb directly flanking the NF1 deletion region on both sides were not found to occur disproportionately in NF1 patients harboring type- 2 deletions compared to controls. Although low allelic diversity in 17q11.2 is unlikely to be a key factor in promoting NAHR-mediated somatic type-2 deletions, a specific ROH of 588 kb (roh1), located some 525 kb proximal to the deletion interval, was found to occur more frequently (P50.012) in the type-2 deletion patients compared with controls. We postulate that roh1 may act remotely, via an as yet unknown mechanism, to increase the frequency of somatic recombination between the distally duplicated SUZ12 sequences

Copy number variations in the NF1 gene region are infrequent and do not predispose to recurrent type-1 deletions

Gross deletions of the NF1 gene at 17q11.2 belong to the group of ‘genomic disorders’ characterized by local sequence architecture that predisposes to genomic rearrangements. Segmental duplications within regions associated with genomic disorders are prone to non-allelic homologous recombination (NAHR), which mediates gross rearrangements. Copy number variants (CNVs) without obvious phenotypic consequences also occur frequently in regions of genomic disorders. In the NF1 gene region, putative CNVs have been reportedly detected by array comparative genomic hybridization (array CGH). These variants include duplications and deletions within the NF1 gene itself (CNV1) and a duplication that encompasses the SUZ12 gene, the distal NF1-REPc repeat and the RHOT1 gene (CNV2). To explore the possibility that these CNVs could have played a role in promoting deletion mutagenesis in type-1 deletions (the most common type of gross NF1 deletion), non-affected transmitting parents of patients with type-1 NF1 deletions were investigated by multiplex ligation-dependent probe amplification (MLPA). However, neither CNV1 nor CNV2 were detected. This would appear to exclude these variants as frequent mediators of NAHR giving rise to type-1 deletions. Using MLPA, we were also unable to confirm CNV1 in healthy controls as previously reported. We conclude that locus-specific techniques should be used to independently confirm putative CNVs, originally detected by array CGH, to avoid false-positive results. In one patient with an atypical deletion, a duplication in the region of CNV2 was noted. This duplication could have occurred concomitantly with the deletion as part of a complex rearrangement or may alternatively have preceded the deletion

Tissue-specific differences in the proportion of mosaic large NF1 deletions are suggestive of a selective growth advantage of hematopoietic del(+/-) stem cells

Type-2 NF1 deletions spanning 1.2 Mb are frequently of postzygotic origin and hence tend to be associated with mosaicism for normal cells and those harboring the deletion (del(+/−) cells). Eleven patients with mosaic type-2 deletions were investigated by FISH and high proportions (94–99%) of del(+/−) cells were detected both in whole blood and in isolated CD3+, CD14+, CD15+, and CD19+ leukocytes. Significantly lower proportions of del(+/−) cells (24-82%) were however noted in urine-derived epithelial cells. A patient harboring an atypical large NF1 deletion with nonrecurrent breakpoints was also found to have a much higher proportion of del(+/−) cells in blood (96%) than in urine (51%). The tissue-specific differences in the proportions of del(+/−) cells as well as the X chromosome inactivation (XCI) patterns observed in these mosaic patients suggest that the majority of the deletions had occurred before or during the preimplantation blastocyst stage before the onset of XCI. We postulate that hematopoietic del(+/−) stem cells present at an early developmental stage are characterized by a selective growth advantage over normal cells lacking the deletion, leading to a high proportion of del(+/−) cells in peripheral blood from the affected patients