Breaking the Cycle: Interrupting Generational Incarceration in Maine

Parental incarceration is a known Adverse Childhood Experience (ACE) which affects a large number of children nationwide. Research shows that children who experience parental incarceration are more at risk for trauma, mental health problems, and juvenile justice system involvement. The goal of this report was to further our understanding of the scale of parental incarceration and the impact on the children in Maine. This report provides a snapshot of the number of children who were impacted by parental incarceration in the state system over a 5-year period (2015-2020). The findings show that for the majority of these parents, there is no legal factor prohibiting contact with their children. Therefore, continuing to nurture the parent-child relationship while the parent is incarcerated is possible and important to minimize the trauma and associated risks. While more research is needed to better understand the nuances of parental incarceration in Maine, this research supports the implementation of policies and programs to help put Maine families and children first. By ensuring Maine families have access to appropriate services and a community-based network of support we can stop the cycle of intergenerational incarceration and improve outcomes for Maine’s children

The Politics of the Presidential Medal of Freedom: A Fifty Year Analysis, 1963-2013

Established in 1963, the Presidential Medal of Freedom (PMOF) is the nation’s highest civilian honor. Presidents award the Medal at their discretion to “any person who has made an especially meritorious contribution to (1) the security or national interests of the United States, or (2) world peace, or (3) cultural or other significant public or private endeavors” (Executive Order 11085). Using an original database of all 1963-2013 PMOF recipients, we analyze how presidents exercise this symbolic unilateral power. In particular, we find that Democratic and Republican presidents differ in their recognition of various categories of achievement. Also, presidents have awarded a greater number of PMOFs annually in recent years, and it has become increasingly common to honor a large number of recipients in a single ceremony. While a strategic objective may be to attract positive media attention, our analysis indicates that PMOF ceremonies do not increase presidential approval ratings

ACAS-Xu Run 5 HITL (June 2019) SC-228 WG 1.3 Results Outbrief

This presentation provides an overview of a recently completed human-in-the-loop simulation, conducted as part of the Unmanned Aircraft Systems (UAS) Integration in the National Airspace System (NAS) Project. This study examined how to present resolution advisories (RAs) issued by Airborne Collision Avoidance System (ACAS) Xu, which can be in the vertical dimension, the horizontal dimension, or both (i.e., blended). The study varied the location of the ACAS Xu traffic information - it was either presented within an 'integrated' display or a 'standalone' display, where the traffic information was separated from the vehicle control interfaces and navigational information. Results revealed generally positive feedback on the visual and aural presentation of RAs, with special considerations and performance implications noted throughout

‘The smell of death and the smell of life’: authenticity, anxiety and perceptions of death at Varanasi’s cremation grounds

This paper contributes to an understanding of existential authenticity and existential anxiety in tourism studies through an investigation of tourists' perceptions of death, the Self, and "others" at the Hindu cremation grounds in Varanasi, India. Encounters with death at dark tourism sites serve as reminders of one's own mortality affecting one's attitude towards death, perception of self, and even challenging one's personal values. Existentialists assert that anxiety is a condition of existential authenticity, and therefore moments of the existentially authentic experience are not always pleasurable. This paper argues that confrontation with death, as exemplified by the Aghori rituals and the cremation grounds in Varanasi, offers tourists an opportunity to examine the inevitability that life will end and to engage with this existential predicament and anxiety in an embodied sense, thereby pushing some of them towards life changes in the pursuit of existential authenticity

Individual common variants exert weak effects on the risk for autism spectrum disorders.

While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest

Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders.

International audienceRare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation

The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism.

International audienceAlthough multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions

Individual common variants exert weak effects on the risk for autism spectrum disorders

While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASD), the contribution of common variation to ASD risk is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating association of individual SNPs, we also sought evidence that common variants, en masse, might affect risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest p-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. By contrast, allele-scores derived from the transmission of common alleles to Stage 1 cases significantly predict case-status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele-score results, it is reasonable to conclude that common variants affect ASD risk but their individual effects are modest