Influence of Poverty Simulation on Educators\u27 Social Empathy and Education Practices

A capstone submitted in partial fulfillment of the requirements for the degree of Doctor of Education in the Ernst and Sara Lane Volgenau College of Education at Morehead State University by Rebecca K. Davison on March 31, 2023

Maternal depression and childhood obesity: A systematic review

Objective. Maternal depression is prevalent and has been associated with parenting practices that influence child weight. In this systematic review we aimed to examine the prospective association between maternal depression and child overweight.Methods. We searched four databases (PsycINFO, PubMed, Embase, and Academic Search Premier) to identify studies for inclusion. We included studies with a prospective design with at least one year follow-up, measuring maternal depression at any stage after childbirth, and examining child overweight or obesity status, body mass index z-score or percentile, or adiposity. Two authors extracted data independently and findingswere qualitatively synthesized.Results. We identified nine prospective studies for inclusion. Results were examined separately for episodic depression (depression at a single measurement occasion) and chronic depression (depression on multiple measurement occasions). Mixed results were observed for the relationship between episodic depression and indicators of child adiposity. Chronic depression, but not episodic depression,was associated with greater risk for child overweight.Conclusions.While chronic depression may be associated with child overweight, further research is needed. Research is also needed to determine whether maternal depression influences child weight outcomes in adolescence and to investigate elements of the family ecology that may moderate the effect of maternal depression on child overweight

Two novel human cytomegalovirus NK cell evasion functions target MICA for lysosomal degradation

NKG2D plays a major role in controlling immune responses through the regulation of natural killer (NK) cells, αβ and γδ T-cell function. This activating receptor recognizes eight distinct ligands (the MHC Class I polypeptide-related sequences (MIC) A andB, and UL16-binding proteins (ULBP)1–6) induced by cellular stress to promote recognition cells perturbed by malignant transformation or microbial infection. Studies into human cytomegalovirus (HCMV) have aided both the identification and characterization of NKG2D ligands (NKG2DLs). HCMV immediate early (IE) gene up regulates NKGDLs, and we now describe the differential activation of ULBP2 and MICA/B by IE1 and IE2 respectively. Despite activation by IE functions, HCMV effectively suppressed cell surface expression of NKGDLs through both the early and late phases of infection. The immune evasion functions UL16, UL142, and microRNA(miR)-UL112 are known to target NKG2DLs. While infection with a UL16 deletion mutant caused the expected increase in MICB and ULBP2 cell surface expression, deletion of UL142 did not have a similar impact on its target, MICA. We therefore performed a systematic screen of the viral genome to search of addition functions that targeted MICA. US18 and US20 were identified as novel NK cell evasion functions capable of acting independently to promote MICA degradation by lysosomal degradation. The most dramatic effect on MICA expression was achieved when US18 and US20 acted in concert. US18 and US20 are the first members of the US12 gene family to have been assigned a function. The US12 family has 10 members encoded sequentially through US12–US21; a genetic arrangement, which is suggestive of an ‘accordion’ expansion of an ancestral gene in response to a selective pressure. This expansion must have be an ancient event as the whole family is conserved across simian cytomegaloviruses from old world monkeys. The evolutionary benefit bestowed by the combinatorial effect of US18 and US20 on MICA may have contributed to sustaining the US12 gene family

Television viewing and sleep are associated with overweight among urban and semi-urban South Indian children

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Using School Staff Members to Implement a Childhood Obesity Prevention Intervention in Low-Income School Districts: the Massachusetts Childhood Obesity Research Demonstration (MA-CORD Project), 2012–2014

Introduction: Although evidence-based interventions to prevent childhood obesity in school settings exist, few studies have identified factors that enhance school districts’ capacity to undertake such efforts. We describe the implementation of a school-based intervention using classroom lessons based on existing “Eat Well and Keep Moving” and “Planet Health” behavior change interventions and schoolwide activities to target 5,144 children in 4th through 7th grade in 2 low-income school districts. Methods: The intervention was part of the Massachusetts Childhood Obesity Research Demonstration (MA-CORD) project, a multisector community-based intervention implemented from 2012 through 2014. Using mixed methods, we operationalized key implementation outcomes, including acceptability, adoption, appropriateness, feasibility, implementation fidelity, perceived implementation cost, reach, and sustainability. Results: MA-CORD was adopted in 2 school districts that were facing resource limitations and competing priorities. Although strong leadership support existed in both communities at baseline, one district’s staff reported less schoolwide readiness and commitment. Consequently, fewer teachers reported engaging in training, teaching lessons, or planning to sustain the lessons after MA-CORD. Interviews showed that principal and superintendent turnover, statewide testing, and teacher burnout limited implementation; passionate wellness champions in schools appeared to offset implementation barriers. Conclusion: Future interventions should assess adoption readiness at both leadership and staff levels, offer curriculum training sessions during school hours, use school nurses or health teachers as wellness champions to support teachers, and offer incentives such as staff stipends or play equipment to encourage school participation and sustained intervention activities

Severe Community-acquired Pneumonia Due to Staphylococcus aureus, 2003–04 Influenza Season

S. aureus community-acquired pneumonia has been reported from 9 states

Isolation and Characterization of Adenoviruses Persistently Shed from the Gastrointestinal Tract of Non-Human Primates

Adenoviruses are important human pathogens that have been developed as vectors for gene therapies and genetic vaccines. Previous studies indicated that human infections with adenoviruses are self-limiting in immunocompetent hosts with evidence of some persistence in adenoid tissue. We sought to better understand the natural history of adenovirus infections in various non-human primates and discovered that healthy populations of great apes (chimpanzees, bonobos, gorillas, and orangutans) and macaques shed substantial quantities of infectious adenoviruses in stool. Shedding in stools from asymptomatic humans was found to be much less frequent, comparable to frequencies reported before. We purified and fully sequenced 30 novel adenoviruses from apes and 3 novel adenoviruses from macaques. Analyses of the new ape adenovirus sequences (as well as the 4 chimpanzee adenovirus sequences we have previously reported) together with 22 complete adenovirus genomes available from GenBank revealed that (a) the ape adenoviruses could clearly be classified into species corresponding to human adenovirus species B, C, and E, (b) there was evidence for intraspecies recombination between adenoviruses, and (c) the high degree of phylogenetic relatedness of adenoviruses across their various primate hosts provided evidence for cross species transmission events to have occurred in the natural history of B and E viruses. The high degree of asymptomatic shedding of live adenovirus in non-human primates and evidence for zoonotic transmissions warrants caution for primate handling and housing. Furthermore, the presence of persistent and/or latent adenovirus infections in the gut should be considered in the design and interpretation of human and non-human primate studies with adenovirus vectors

Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A

The major histocompatibility complex (MHC) on chromosome 6 is associated with susceptibility to more common diseases than any other region of the human genome, including almost all disorders classified as autoimmune. In type 1 diabetes the major genetic susceptibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1 (refs 1-3), but these genes cannot completely explain the association between type 1 diabetes and the MHC region. Owing to the region's extreme gene density, the multiplicity of disease-associated alleles, strong associations between alleles, limited genotyping capability, and inadequate statistical approaches and sample sizes, which, and how many, loci within the MHC determine susceptibility remains unclear. Here, in several large type 1 diabetes data sets, we analyse a combined total of 1,729 polymorphisms, and apply statistical methods - recursive partitioning and regression - to pinpoint disease susceptibility to the MHC class I genes HLA-B and HLA-A (risk ratios >1.5; Pcombined = 2.01 × 10-19 and 2.35 × 10-13, respectively) in addition to the established associations of the MHC class II genes. Other loci with smaller and/or rarer effects might also be involved, but to find these, future searches must take into account both the HLA class II and class I genes and use even larger samples. Taken together with previous studies, we conclude that MHC-class-I-mediated events, principally involving HLA-B*39, contribute to the aetiology of type 1 diabetes. ©2007 Nature Publishing Group