245 research outputs found

    Advancing trauma informed practices in schools using the Consolidated Framework for Implementation Research

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    As the world becomes more aware of the prevalence and consequences of trauma for young people, the education sector is increasingly responsible for supporting students emotionally and academically. School-based mental health supports for students who have experienced trauma are crucial, as schools are often the only access point for intervention for many children and families. Given that over two-thirds of children in the U.S. will experience a traumatic event by age 16, it is imperative to better understand the mechanisms of implementing mental health support in schools. Despite the increasing need for trauma-informed practices in schools (TIPS), schools often struggle to provide them due to a myriad of barriers. More research is needed to understand how to implement and sustain TIPS. Researchers have begun exploring these questions, but there is still a shortage of research about how to best implement TIPS. We argue that the Consolidated Framework for Implementation Research (CFIR) is useful for organizing and advancing the implementation of TIPS. By consolidating findings from existing scholarship on TIPS, we identify themes and future directions within the CFIR framework. Based on our review, we also provide practical suggestions for schools seeking to implement TIPS

    The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins

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    Insulin-like growth factors elicit many responses through activation of phosphoinositide 3-OH kinase (PI3K). The tuberous sclerosis complex (TSC1-2) suppresses cell growth by negatively regulating a protein kinase, p70S6K (S6K1), which generally requires PI3K signals for its activation. Here, we show that TSC1-2 is required for insulin signaling to PI3K. TSC1-2 maintains insulin signaling to PI3K by restraining the activity of S6K, which when activated inactivates insulin receptor substrate (IRS) function, via repression of IRS-1 gene expression and via direct phosphorylation of IRS-1. Our results argue that the low malignant potential of tumors arising from TSC1-2 dysfunction may be explained by the failure of TSC mutant cells to activate PI3K and its downstream effectors

    Family History of Cancer in Benign Brain Tumor Subtypes Versus Gliomas

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    Purpose: Family history is associated with gliomas, but this association has not been established for benign brain tumors. Using information from newly diagnosed primary brain tumor patients, we describe patterns of family cancer histories in patients with benign brain tumors and compare those to patients with gliomas. Methods: Newly diagnosed primary brain tumor patients were identified as part of the Ohio Brain Tumor Study. Each patient was asked to participate in a telephone interview about personal medical history, family history of cancer, and other exposures. Information was available from 33 acoustic neuroma (65%), 78 meningioma (65%), 49 pituitary adenoma (73.1%), and 152 glioma patients (58.2%). The association between family history of cancer and each subtype was compared with gliomas using unconditional logistic regression models generating odds ratios (ORs) and 95% confidence intervals. Results: There was no significant difference in family history of cancer between patients with glioma and benign subtypes. Conclusion: The results suggest that benign brain tumor may have an association with family history of cancer. More studies are warranted to disentangle the potential genetic and/or environmental causes for these diseases
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