Childhood adversity and parent perceptions of child resilience

Abstract Background Adverse childhood experiences (ACEs) negatively impact health throughout the life course. For children exposed to ACEs, resilience may be particularly important. However, the literature regarding resilience, particularly the self-regulation aspect of resilience, is not often described in children with ACEs. Additionally, family and community factors that might help promote resilience in childhood may be further elucidated. We aimed to describe the relationship between ACEs and parent-perceived resilience in children and examine the child, family, and community-level factors associated with child resilience. Methods Using the US-based, 2011–2012 National Survey of Children’s Health, we examined adverse childhood experiences (NSCH-ACEs) as the main exposure. Affirmative answers to adverse experiences generated a total parent-reported NSCH-ACE score. Bivariate and multivariable logistic regression models were constructed for parent-perceived child resilience and its association with ACEs, controlling for child, family, and neighborhood-level factors. Results Among 62,200 US children 6–17 years old, 47% had 0 ACEs, 26% had 1 ACE, 19% had 2–3 ACEs, and 8% had 4 or more ACEs. Child resilience was associated with ACEs in a dose-dependent relationship: as ACEs increased, the probability of resilience decreased. This relationship persisted after controlling for child, family, and community factors. Specific community factors, such as neighborhood safety (p < .001), neighborhood amenities (e.g., libraries, parks) (p < .01) and mentorship (p < .05), were associated with significantly higher adjusted probabilities of resilience, when compared to peers without these specific community factors. Conclusions While ACEs are common and may be difficult to prevent, there may be opportunities for health care providers, child welfare professionals, and policymakers to strengthen children and families by supporting community-based activities, programs, and policies that promote resilience in vulnerable children and communities in which they live.https://deepblue.lib.umich.edu/bitstream/2027.42/144527/1/12887_2018_Article_1170.pd

European Union’s Arms Embargo on China: Implications and Options for U.S. Policy

Overall, there are two sets of questions for Congress in examining U.S. policy toward the fate of the EU’s arms embargo on China. What are the implications for U.S. interests in trans-Atlantic relations and China? If U.S. interests are adversely affected, what are some options for Congress to discourage the EU from lifting its arms embargo on China and, if it is lifted, to protect U.S. national security interests in both Asia and Europe? Issues raised by these questions are the subject of this CRS Report

Health Insurance Enrollment of Children and Young Adults in Wayne County, Michigan: A Qualitative Evaluation

Since the Affordable Care Act went into effect, community outreach to increase health insurance enrollment of young adults and children in low-income families of color has been a priority in Wayne County, Michigan. Our objective was to inform community efforts for improved outreach, we explored perceptions around the importance of health insurance and barriers to enrollment for children and young adults through a qualitative research study. We conducted a focus group with enrollment assisters and nine focus groups with Arab American, Latino/Hispanic, and African American community members. Several themes emerged about community members’ perceptions and experiences: they believe that children have time sensitive and specific health needs; they appreciate the generous, public health insurance options available for children; they experience frustration with the affordability of enrolling dependents in private insurance; young adults experience frequent denials and failures with insurance enrollment; and they experience confusion about how insurance eligibility changes during the young adulthood. There is a need for community outreach in Wayne County to focus on connecting low-income, working families to affordable health insurance options and tailoring help to young adults to overcome barriers to enrollment in public insurance

An RNA-dependent RNA polymerase gene in bat genomes derived from an ancient negative-strand RNA virus

Endogenous bornavirus-like L (EBLL) elements are inheritable sequences derived from ancient bornavirus L genes that encode a viral RNA-dependent RNA polymerase (RdRp) in many eukaryotic genomes. Here, we demonstrate that bats of the genus Eptesicus have preserved for more than 11.8 million years an EBLL element named eEBLL-1, which has an intact open reading frame of 1,718 codons. The eEBLL-1 coding sequence revealed that functional motifs essential for mononegaviral RdRp activity are well conserved in the EBLL-1 genes. Genetic analyses showed that natural selection operated on eEBLL-1 during the evolution of Eptesicus. Notably, we detected efficient transcription of eEBLL-1 in tissues from Eptesicus bats. To the best of our knowledge, this study is the first report showing that the eukaryotic genome has gained a riboviral polymerase gene from an ancient virus that has the potential to encode a functional RdRp

Biallelic TMEM260 variants cause truncus arteriosus, with or without renal defects

Only two families have been reported with biallelic TMEM260 variants segregating with structural heart defects and renal anomalies syndrome (SHDRA). With a combination of genome, exome sequencing and RNA studies, we identified eight individuals from five families with biallelic TMEM260 variants. Variants included one multi-exon deletion, four nonsense/frameshifts, two splicing changes and one missense change. Together with the published cases, analysis of clinical data revealed ventricular septal defects (12/12), mostly secondary to truncus arteriosus (10/12), elevated creatinine levels (6/12), horse-shoe kidneys (1/12) and renal cysts (1/12) in patients. Three pregnancies were terminated on detection of severe congenital anomalies. Six patients died between the ages of 6 weeks and 5 years. Using a range of stringencies, carrier frequency for SHDRA was estimated at 0.0007–0.007 across ancestries. In conclusion, this study confirms the genetic basis of SHDRA, expands its known mutational spectrum and clarifies its clinical features. We demonstrate that SHDRA is a severe condition associated with substantial mortality in early childhood and characterised by congenital cardiac malformations with a variable renal phenotype

Biallelic TMEM260 variants cause truncus arteriosus, with or without renal defects

From Wiley via Jisc Publications RouterHistory: received 2021-08-18, rev-recd 2021-09-22, accepted 2021-10-02, pub-electronic 2021-10-11Article version: VoRPublication status: PublishedFunder: Cancer Research UK; Id: http://dx.doi.org/10.13039/501100000289Funder: European Union's Horizon 2020; Grant(s): 779257Funder: Medical Research Council; Id: http://dx.doi.org/10.13039/501100007155Funder: NHS EnglandFunder: NIHR Oxford Biomedical Research Centre ProgrammeFunder: Society for the Relief of Disabled Children, Hong KongFunder: Wellcome Trust; Id: http://dx.doi.org/10.13039/100010269; Grant(s): 203141/Z/16/ZAbstract: Only two families have been reported with biallelic TMEM260 variants segregating with structural heart defects and renal anomalies syndrome (SHDRA). With a combination of genome, exome sequencing and RNA studies, we identified eight individuals from five families with biallelic TMEM260 variants. Variants included one multi‐exon deletion, four nonsense/frameshifts, two splicing changes and one missense change. Together with the published cases, analysis of clinical data revealed ventricular septal defects (12/12), mostly secondary to truncus arteriosus (10/12), elevated creatinine levels (6/12), horse‐shoe kidneys (1/12) and renal cysts (1/12) in patients. Three pregnancies were terminated on detection of severe congenital anomalies. Six patients died between the ages of 6 weeks and 5 years. Using a range of stringencies, carrier frequency for SHDRA was estimated at 0.0007–0.007 across ancestries. In conclusion, this study confirms the genetic basis of SHDRA, expands its known mutational spectrum and clarifies its clinical features. We demonstrate that SHDRA is a severe condition associated with substantial mortality in early childhood and characterised by congenital cardiac malformations with a variable renal phenotype

Somatic Mutagenesis with a Sleeping Beauty Transposon System Leads to Solid Tumor Formation in Zebrafish

Large-scale sequencing of human cancer genomes and mouse transposon-induced tumors has identified a vast number of genes mutated in different cancers. One of the outstanding challenges in this field is to determine which genes, when mutated, contribute to cellular transformation and tumor progression. To identify new and conserved genes that drive tumorigenesis we have developed a novel cancer model in a distantly related vertebrate species, the zebrafish, Danio rerio. The Sleeping Beauty (SB) T2/Onc transposon system was adapted for somatic mutagenesis in zebrafish. The carp ß-actin promoter was cloned into T2/Onc to create T2/OncZ. Two transgenic zebrafish lines that contain large concatemers of T2/OncZ were isolated by injection of linear DNA into the zebrafish embryo. The T2/OncZ transposons were mobilized throughout the zebrafish genome from the transgene array by injecting SB11 transposase RNA at the 1-cell stage. Alternatively, the T2/OncZ zebrafish were crossed to a transgenic line that constitutively expresses SB11 transposase. T2/OncZ transposon integration sites were cloned by ligation-mediated PCR and sequenced on a Genome Analyzer II. Between 700–6800 unique integration events in individual fish were mapped to the zebrafish genome. The data show that introduction of transposase by transgene expression or RNA injection results in an even distribution of transposon re-integration events across the zebrafish genome. SB11 mRNA injection resulted in neoplasms in 10% of adult fish at ∼10 months of age. T2/OncZ-induced zebrafish tumors contain many mutated genes in common with human and mouse cancer genes. These analyses validate our mutagenesis approach and provide additional support for the involvement of these genes in human cancers. The zebrafish T2/OncZ cancer model will be useful for identifying novel and conserved genetic drivers of human cancers