Uninsured Veterans and Family Members: Who Are They and Where Do They Live?

Examines uninsurance rates and access to health care among veterans and family members by state, time of service, age, education, and marital and employment status. Points to high uninsurance in states that have been slow to implement federal reform

Uninsured Veterans and Family Members: State and National Estimates of Expanded Medicaid Eligibility Under the ACA

Analysis of the 2008-2010 American Community Survey indicates that 535,000 uninsured veterans and 174,000 uninsured spouses of veterans -- or 4 in 10 uninsured veterans and 1 in 4 uninsured spouses -- have incomes below 138 percent of poverty and could qualify for Medicaid or new subsidies for coverage under the Affordable Care Act. Most have incomes below 100 percent of poverty and will only have new coverage options if their state expands Medicaid. Since uninsurance is related to greater problems accessing care, increased Medicaid enrollment could improve the likelihood that their health care needs are being met

Empowering Non-Traditional Students to Succeed in Online Programs

In their research on student learning Rieh and Hilligoss (2008) study the proximal factors of today’s students and how they interact with technology, in their pursuit of information. This paper looks at how race, age and job status are related to students’ perception of their in

Nutrition and \u3ci\u3eHelicobacter pylori\u3c/i\u3e: Host Diet and Nutritional Immunity Influence Bacterial Virulence and Disease Outcome

Helicobacter pylori colonizes the stomachs of greater than 50% of the world’s human population making it arguably one of the most successful bacterial pathogens. Chronic H. pylori colonization results in gastritis in nearly all patients; however in a subset of people, persistent infection with H. pylori is associated with an increased risk for more severe disease outcomes including B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma) and invasive adenocarcinoma. Research aimed at elucidating determinants that mediate disease progression has revealed genetic differences in both humans and H. pylori which increase the risk for developing gastric cancer. Furthermore, host diet and nutrition status have been shown to influence H. pylori-associated disease outcomes. In this review we will discuss how H. pylori is able to create a replicative niche within the hostile host environment by subverting and modifying the host-generated immune response as well as successfully competing for limited nutrients such as transition metals by deploying an arsenal of metal acquisition proteins and virulence factors. Lastly, we will discuss how micronutrient availability or alterations in the gastric microbiome may exacerbate negative disease outcomes associated with H. pylori colonization

Changes in SEBT Scores in College Basketball Players Participating in a Preventative Ankle Program

In volume 4, Issue 1 of the JSMAHS you will find Professional Research Abstracts, as well as Bachelor Student Research Abstracts and Case Reports. Thank you for viewing this 4th Annual OATA Special Editio

\u3ci\u3eHelicobacter pylori\u3c/i\u3e: Genomic Insight into the Host-Pathogen Interaction

The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen, Helicobacter pylori, has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host and H. pylori. Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship of H. pylori with the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools

XFEB, A Direct Target of ZIC1, is Involved in Neural Crest Development

The peripheral nervous system, melanocytes and craniofacial cartilage and bone arise from neural crest cells that develop during early embryonic neural development. Transcription and signaling factors form a network to regulate this development. For example, it has been shown that Zic1 and Pax3 in conjunction are able to induce full neural crest cell development (Monsoro-Burq et al., 2005). Xfeb and Gbx2 also play roles during neural crest cell development as they are present in the same regions and developmental stages as the neural crest (Plouhinec et al., 2014; Li et al., 2009). A microarray identified Xfeb as a direct, downstream target of Zic1 (Li et al., 2006). An additional lab also identified Xfeb as a neural crest gene induced by Zic1 (Plouhinec et al., 2014). We hypothesize that Pax3, Xfeb, Gbx2 and Zic1 are all part of the same gene regulatory network controlling neural crest development. To investigate the relationship between the Xfeb, Pax3, Gbx2, and Zic1 genes, we first upregulated Xfeb gene expression with sense RNA and down regulated Xfeb gene expression with morpholino oligonucleotides (MO). We used in situ hybridization to visualize neural crest induction by staining for Slug RNA expression, a known neural crest marker. Our results showed that embryos injected with Xfeb sense RNA expanded Slug expression while those injected with Xfeb MO diminished Slug expression. Given other labs’ results suggesting that Zic1 plus Pax3 or Zic1 plus Gbx2 induced ectopic Slug expression, we will determine whether Xfeb plus Pax3 or Xfeb plus Gbx2 genes can induce ectopic Slug expression. These experiments will allow us to determine whether Xfeb acts in neural crest induction and will allow us to place Xfeb into the gene regulatory network that drives neural crest development

Children's Uninsurance Fell between 2019 and 2021, but Progress Could Stall When Pandemic Protections Expire

The pandemic and associated job losses threatened to reduce employer-sponsored health insurance coverage and increase uninsurance among American families. Though such risks were higher for adults because of the long-standing generosity of public coverage policies for children, the severity and novelty of the pandemic also had the potential to exacerbate children's coverage losses that had occurred between 2016 and 2019 and to jeopardize decades of progress in reducing their uninsurance rate. In this brief, we explore changes in coverage status and type among children from birth to age 17 from 2019 to 2021. To do so, we use data from the National Health Interview Survey (NHIS) and the Current Population Survey (CPS) Annual Social and Economic Supplement and administrative data on children's enrollment in Medicaid and the Children's Health Insurance Program (CHIP) and Marketplace coverage through early 2022. We examine (1) changes between early 2019 and early 2021 to reflect the first year of the pandemic and the first round of pandemic recovery legislation passed in March 2020 and (2) changes from early 2021 through late 2021 and early 2022 to reflect continuing trends and initial responses to the second major federal recovery effort in March 2021

Factors Impacting Psychological and Health Outcomes in Mothers and Infants Following NICU Hospitalization of the Infant

Purpose: There is evidence that mothers of infants hospitalized in the Neonatal Intensive Care Unit (NICU) experience elevated rates of psychopathology. However, most studies have focused on very preterm infants, with little attention to mothers of moderate- to late-preterm infants. In addition, the majority of previous research has been cross-sectional, which does not allow for the examination of symptoms over time. Method: The current study investigated whether rates of psychopathology are elevated in mothers of moderate- to late-preterm infants during/following infant hospitalization in the NICU, and associated protective and risk factors. Mothers completed self-report questionnaires during the infant’s hospitalization and six months later. Results: Mothers of moderate- to late-preterm infants hospitalized in the NICU showed elevated rates of depression, anxiety, and PTSD compared to mothers of term infants at both baseline and six months post-birth. Importantly, no differences in psychopathology between mothers of moderate-preterm and late-preterm infants were found at either time point. A number of important risk factors were identified, including previous maternal mental illness, more severe infant health problems, and a lack of coping skills. Potential protective factors were also identified, including mother-infant contact, maternal optimism, and expectations about the infants potential for recovery. Limitations: The current study did not include mothers who were unable to visit the NICU or fathers/siblings, and future studies might include these groups to better understand familial adjustment to the NICU hospitalization of an infant. In addition, research in the future should examine a larger sample of NICU mothers in order to conduct more in-depth longitudinal analyses of risk and protective factors. Finally, future studies will need to pilot and test the efficacy of the proposed screening and programmatic components in order to assess feasibility, acceptability, and effectiveness with the target population. Conclusions: These results may inform the development of NICU programming aimed at buffering the development of psychopathology in mothers. Identified risk and protective factors could help in effectively targeting intervention programs to mothers most in need while the infant is in the hospital and over time