5 research outputs found

    Mental Health and Resilience in Adolescent Refugees Resettled in Philadelphia

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    Introduction: Mental health in adolescents has a large impact on physical health, academic achievement, and overall well-being; moreover, refugee youth are at an increased risk for mental health disorders. While growing evidence shows that positive youth development interventions can prevent health risk behaviors, there is need for further evaluation that shows how to tailor interventions to meet population-specific needs. Objective: The aim is to assess how targeted interventions can enhance protective factors and reduce negative adult outcomes in vulnerable refugee adolescents. The goals are to understand the current status of mental health and access to resources among resettled adolescents in Philadelphia, while increasing awareness and discussion of mental health. Methods: Six semi-structured interviews with key informants were conducted to understand the scope of the problem, including social workers and refugee program directors. Individual interviews with 14 adolescents at Southeast by Southeast inquired about living in the US, performance in school, and personal life. The interviews were recorded, transcribed, and analyzed via thematic coding with NVivo12 to identify elements influencing the refugee experience. Results: The major overarching themes identified as key elements of the resettlement experience were identity, vulnerability, resource utilization, responsibility, and resilience. Themes were further split into subthemes distinguished from the key informant and adolescent interviews. Conclusion: Refugee adolescents resettled in Philadelphia high schools face unique experiences that make them vulnerable to adverse outcomes. A deeper understanding of resettlement experiences and protective factors in their personal, social, and cultural contexts can provide avenues for more accessible focused programming

    A Mixed-Methods Refugee Community Health Needs and Assets Assessment

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    Introduction: Many factors may negatively affect the experience of refugees navigating the healthcare system in Philadelphia. These factors include, but are not limited to, lack of familiarity with the healthcare system, language and cultural barriers, limited health literacy, physical and transportation barriers, and fear and/or distrust of the healthcare system. In addition, there are a large proportion of United States refugees in Pennsylvania. According to usnews.com, Pennsylvania was ranked the top 6th state for taking in the most refugees in the year 2017. Objective: The primary objective is to assess the experiences of refugees within the healthcare system since resettlement in Philadelphia. The secondary objective is to use the information gained from our study to implement interventions that may improve navigation of the healthcare system for refugees in Philadelphia. Methods: Quantitative and qualitative survey questions will be administered to participants. These questions will cover experiences directly associated with the healthcare system, as well as participant perceptions of social determinants of health that impact physical and behavioral/mental health such as education, community cohesion/support and employment, community-based services related to food security, housing, and transportation. Quantitative questions will be asked through translated surveys. Qualitative questions are will be administered through 1-on-1 interviews with the assistance of interpreters. The analysis will include a mixed methods approach. Quantitative survey data will use descriptive statistics including frequencies, percentages, and mean values. Data will be entered into EXCEL and analysis will be done through EXCEL and SPSS. Qualitative data will undergo content analysis. Interviews will be taped, transcribed/translated, and coded vis NVIVO software. Results: Pending Conclusion: Pendin

    Hepatocyte growth factor and MET support mouse enteric nervous system development, the peristaltic response, and intestinal epithelial proliferation in response to injury

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    UNLABELLED: Factors providing trophic support to diverse enteric neuron subtypes remain poorly understood. We tested the hypothesis that hepatocyte growth factor (HGF) and the HGF receptor MET might support some types of enteric neurons. HGF and MET are expressed in fetal and adult enteric nervous system. In vitro, HGF increased enteric neuron differentiation and neurite length, but only if vanishingly small amounts (1 pg/ml) of glial cell line-derived neurotrophic factor were included in culture media. HGF effects were blocked by phosphatidylinositol-3 kinase inhibitor and by MET-blocking antibody. Both of these inhibitors and MEK inhibition reduced neurite length. In adult mice, MET was restricted to a subset of calcitonin gene-related peptide-immunoreactive (IR) myenteric plexus neurons thought to be intrinsic primary afferent neurons (IPANs). Conditional MET kinase domain inactivation (Met(fl/fl); Wnt1Cre+) caused a dramatic loss of myenteric plexus MET-IR neurites and 1-1\u27-dioctodecyl-3,3,3\u27,3\u27-tetramethylindocarbocyamine perchlorate (DiI) labeling suggested reduced MET-IR neurite length. In vitro, Met(fl/fl); Wnt1Cre+ mouse bowel had markedly reduced peristalsis in response to mucosal deformation, but normal response to radial muscle stretch. However, whole-bowel transit, small-bowel transit, and colonic-bead expulsion were normal in Met(fl/fl); Wnt1Cre+ mice. Finally, Met(fl/fl); Wnt1Cre+ mice had more bowel injury and reduced epithelial cell proliferation compared with WT animals after dextran sodium sulfate treatment. These results suggest that HGF/MET signaling is important for development and function of a subset IPANs and that these cells regulate intestinal motility and epithelial cell proliferation in response to bowel injury. SIGNIFICANCE STATEMENT: The enteric nervous system has many neuronal subtypes that coordinate and control intestinal activity. Trophic factors that support these neuron types and enhance neurite growth after fetal development are not well understood. We show that a subset of adult calcitonin gene-related peptide (CGRP)-expressing myenteric neurons produce MET, the receptor for hepatocyte growth factor, and that loss of MET activity affects peristalsis in response to mucosal stroking, reduces MET-immunoreactive neurites, and increases susceptibility to dextran sodium sulfate-induced bowel injury. These observations may be relevant for understanding and treating intestinal motility disorders and also suggest that enhancing the activity of MET-expressing CGRP neurons might be a useful strategy to reduce bowel inflammation

    Ibuprofen slows migration and inhibits bowel colonization by enteric nervous system precursors in zebrafish, chick and mouse

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    AbstractHirschsprung Disease (HSCR) is a potentially deadly birth defect characterized by the absence of the enteric nervous system (ENS) in distal bowel. Although HSCR has clear genetic causes, no HSCR-associated mutation is 100% penetrant, suggesting gene–gene and gene-environment interactions determine HSCR occurrence. To test the hypothesis that certain medicines might alter HSCR risk we treated zebrafish with medications commonly used during early human pregnancy and discovered that ibuprofen caused HSCR-like absence of enteric neurons in distal bowel. Using fetal CF-1 mouse gut slice cultures, we found that ibuprofen treated enteric neural crest-derived cells (ENCDC) had reduced migration, fewer lamellipodia and lower levels of active RAC1/CDC42. Additionally, inhibiting ROCK, a RHOA effector and known RAC1 antagonist, reversed ibuprofen effects on migrating mouse ENCDC in culture. Ibuprofen also inhibited colonization of Ret+/− mouse bowel by ENCDC in vivo and dramatically reduced bowel colonization by chick ENCDC in culture. Interestingly, ibuprofen did not affect ENCDC migration until after at least three hours of exposure. Furthermore, mice deficient in Ptgs1 (COX 1) and Ptgs2 (COX 2) had normal bowel colonization by ENCDC and normal ENCDC migration in vitro suggesting COX-independent effects. Consistent with selective and strain specific effects on ENCDC, ibuprofen did not affect migration of gut mesenchymal cells, NIH3T3, or WT C57BL/6 ENCDC, and did not affect dorsal root ganglion cell precursor migration in zebrafish. Thus, ibuprofen inhibits ENCDC migration in vitro and bowel colonization by ENCDC in vivo in zebrafish, mouse and chick, but there are cell type and strain specific responses. These data raise concern that ibuprofen may increase Hirschsprung disease risk in some genetically susceptible children
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