271 research outputs found

    Family-centered caregiving from hospital to home: Coping with trauma and building capacity with the HOPE for Families model

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    Informal caregivers and families play a significant role in the recovery process of trauma survivors. However, the needs and outcomes of orthopedic caregiving family members in the months following traumatic injury have received almost no attention in the literature. Our study sought to understand the factors impacting orthopedic trauma families’ experience and their ability to cope and provide care post-acute hospitalization. Based on these findings, we designed a hospital-based program to enhance family coping and adjustment post-discharge. Caregivers (N=12) of patients with orthopedic trauma injury engaged in three in-depth semi-structured face-to-face interviews to identify their most salient concerns. Once home, subjects described caregiving life at home, their coping strategies for managing the patient’s recovery, and help they received from formal and informal sources. Analysis of the qualitative data found that trauma care lacks a unified system of coordination after the patient’s return home. Thus, the role of “secondary caregivers” - longtime friends, family members, church groups, neighbors - was significant. Without an organized system of support and information, the caregivers in our study turned to their established communities for comfort and assistance. Conclusions: Based on these findings, we designed a family caregiver program, Holistic Orthopedic Patient-centered Engagement (HOPE for Families), to support families in this early transition, and to enhance collective and continuous caregiving capacity. HOPE for Families uses peer mentors as “central care organizers” to identify and engage the family’s secondary caregivers system, using the HOPE Care Planning tool to identify stressor/demands and caregiver resources to meet anticipated needs

    A novel mobile biobehavioral regulation system for personalized trauma recovery support

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    Even years after experiencing a physical trauma, individuals describe trauma-specific distress, as trauma triggers present as sensory reminders that initiate physiological reactions at time of exposure. Mobile technologies offer tremendous potential in helping individuals who have experienced trauma manage symptoms as they transition out of hospital care and move back into their communities where they are at risk of trauma trigger exposure. A personalized wearable device, tailored to a patient-specific diagnosis (e.g., PTSD) with programmable neurophysiological behavioral risk set-points, could be a useful tool in helping individuals monitor symptomology. When this type of monitoring device is also connected to a personalized recovery cue intervention on a smartwatch or phone, and activated when the wearable sensor detects heightened risk, there is the opportunity for in-the-moment symptom management. In this study we sought to understand the value for trauma survivors of using this type of personalized mobile recovery support system. Study participants were all trauma survivors or family members of survivors who were involved in the Trauma Survivors Network. A semi-structured interview was conducted with participants to understand perceptions on the utility, sensory experiences, and innovation insights of a mobile recovery sensory support system overall, and about the recovery cue intervention most specifically. Results from participant interviews inform the further development of our mobile recovery support system model in significant ways, suggesting that three components must be included: 1) Recovery cues; 2) Relationships (connecting to supportive network); and 3) Regulation (neurophysiological regulation and behavioral risk reduction). Experience Framework This article is associated with the Innovation & Technology lens of The Beryl Institute Experience Framework. (http://bit.ly/ExperienceFramework) Access other PXJ articles related to this lens. Access other resources related to this len

    BRAF Mutation Status and Survival after Colorectal Cancer Diagnosis According to Patient and Tumor Characteristics

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    BRAF mutations in colorectal cancer (CRC) are disproportionately observed in tumors exhibiting microsatellite instability (MSI), and are associated with other prognostic factors. The independent association between BRAF-mutation status and CRC survival, however, remains unclear

    Immature myeloid cells directly contribute to skin tumor development by recruiting IL-17-producing CD4(+) T cells

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    Evidence links chronic inflammation with cancer, but cellular mechanisms involved in this process remain unclear. We have demonstrated that in humans, inflammatory conditions that predispose to development of skin and colon tumors are associated with accumulation in tissues of CD33(+)S100A9(+) cells, the phenotype typical for myeloid-derived suppressor cells in cancer or immature myeloid cells (IMCs) in tumor-free hosts. To identify the direct role of these cells in tumor development, we used S100A9 transgenic mice to create the conditions for topical accumulation of these cells in the skin in the absence of infection or tissue damage. These mice demonstrated accumulation of granulocytic IMCs in the skin upon topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA), resulting in a dramatic increase in the formation of papillomas during epidermal carcinogenesis. The effect of IMCs on tumorigenesis was not associated with immune suppression, but with CCL4 (chemokine [C-C motif] ligand 4)-mediated recruitment of IL-17–producing CD4(+) T cells. This chemokine was released by activated IMCs. Elimination of CD4(+) T cells or blockade of CCL4 or IL-17 abrogated the increase in tumor formation caused by myeloid cells. Thus, this study implicates accumulation of IMCs as an initial step in facilitation of tumor formation, followed by the recruitment of CD4(+) T cells

    Breast cancer risk factors in relation to breast density (United States)

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    OBJECTIVES: Evaluate known breast cancer risk factors in relation to breast density. METHODS: We examined factors in relation to breast density in 144,018 New Hampshire (NH) women with at least one mammogram recorded in a statewide mammography registry. Mammographic breast density was measured by radiologists using the BI-RADS classification; risk factors of interest were obtained from patient intake forms and questionnaires. RESULTS: Initial analyses showed a strong inverse influence of age and body mass index (BMI) on breast density. In addition, women with late age at menarche, late age at first birth, premenopausal women, and those currently using hormone therapy (HT) tended to have higher breast density, while those with greater parity tended to have less dense breasts. Analyses stratified on age and BMI suggested interactions, which were formally assessed in a multivariable model. The impact of current HT use, relative to nonuse, differed across age groups, with an inverse association in younger women, and a positive association in older women (p < 0.0001 for the interaction). The positive effects of age at menarche and age at first birth, and the inverse influence of parity were less apparent in women with low BMI than in those with high BMI (p = 0.04, p < 0.0001 and p = 0.01, respectively, for the interactions). We also noted stronger positive effects for age at first birth in postmenopausal women (p = 0.004 for the interaction). The multivariable model indicated a slight positive influence of family history of breast cancer. CONCLUSIONS: The influence of age at menarche and reproductive factors on breast density is less evident in women with high BMI. Density is reduced in young women using HT, but increased in HT users of age 50 or more

    Systematic meta-analyses, field synopsis and global assessment of the evidence of genetic association studies in colorectal cancer

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    Objective: To provide an understanding of the role of common genetic variations in colorectal cancer (CRC) risk, we report an updated field synopsis and comprehensive assessment of evidence to catalogue all genetic markers for CRC (CRCgene2). Design: We included 869 publications after parallel literature review and extracted data for 1063 polymorphisms in 303 different genes. Meta-Analyses were performed for 308 single nucleotide polymorphisms (SNPs) in 158 different genes with at least three independent studies available for analysis. Scottish, Canadian and Spanish data from genome-wide association studies (GWASs) were incorporated for the meta-Analyses of 132 SNPs. To assess and classify the credibility of the associations, we applied the Venice criteria and Bayesian False-Discovery Probability (BFDP). Genetic associations classified as â € positive' and â € less-credible positive' were further validated in three large GWAS consortia conducted in populations of European origin. Results: We initially identified 18 independent variants at 16 loci that were classified as â € positive' polymorphisms for their highly credible associations with CRC risk and 59 variants at 49 loci that were classified as â € less-credible positive' SNPs; 72.2% of the â € positive' SNPs were successfully replicated in three large GWASs and the ones that were not replicated were downgraded to â € less-credible' positive (reducing the â € positive' variants to 14 at 11 loci). For the remaining 231 variants, which were previously reported, our meta-Analyses found no evidence to support their associations with CRC risk. Conclusion: The CRCgene2 database provides an updated list of genetic variants related to CRC risk by using harmonised methods to assess their credibility.</p
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