Community engagement is important for research, yet many researchers do not routinely seek feedback from people with lived experience. A key barrier to this engagement is that the resources required to create an advisory board may be unavailable to individual investigators, and creating an advisory board for a single study may often be impractical. In this column, the authors describe how to create a standing research advisory board that can serve as a shared resource for researchers and community members and provide a psychosis research advisory board example to aid discussion.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10984771 | PMC |
| http://dx.doi.org/10.1176/appi.ps.20230328 | DOI Listing |
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Department of Biochemistry, McGill University, Montreal, QC, Canada.
Proteostasis is maintained through regulated protein synthesis and degradation and chaperone-assisted protein folding. However, this is challenging in neuronal projections because of their polarized morphology and constant synaptic proteome remodeling. Using high-resolution fluorescence microscopy, we discover that hippocampal and spinal cord motor neurons of mouse and human origin localize a subset of chaperone mRNAs to their dendrites and use microtubule-based transport to increase this asymmetric localization following proteotoxic stress.
View Article and Find Full Text PDFCancer-specific innate and adaptive immune rewiring drives resistance to PD-1 blockade in classic Hodgkin lymphoma.
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December 2024
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Hodgkin Reed-Sternberg (HRS) cells of classic Hodgkin lymphoma (cHL), like many solid tumors, elicit ineffective immune responses. However, patients with cHL are highly responsive to PD-1 blockade, which largely depends on HRS cell-specific retention of MHC class II and implicates CD4 T cells and additional MHC class I-independent immune effectors. Here, we utilize single-cell RNA sequencing and spatial analysis to define shared circulating and microenvironmental features of the immune response to PD-1 blockade in cHL.
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View Article and Find Full Text PDFNeoadjuvant anti-PD1 immunotherapy for surgically accessible recurrent glioblastoma: clinical and molecular outcomes of a stage 2 single-arm expansion cohort.
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Center for Neuro-Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
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View Article and Find Full Text PDFJAK inhibition decreases the autoimmune burden in Down syndrome.
Elife
December 2024
Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, United States.
Background: Individuals with Down syndrome (DS), the genetic condition caused by trisomy 21 (T21), display clear signs of immune dysregulation, including high rates of autoimmunity and severe complications from infections. Although it is well established that T21 causes increased interferon responses and JAK/STAT signaling, elevated autoantibodies, global immune remodeling, and hypercytokinemia, the interplay between these processes, the clinical manifestations of DS, and potential therapeutic interventions remain ill defined.
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