4/10/2023 0 Comments Elucidate.![]() ![]() ![]() Approaches that help explain differential effects between populations and context of implementation are especially encouraged. This administrative supplement NOSI is designed to provide support to NIH-funded investigators to add novel analytical approaches to their currently funded project that can illuminate potential new or alternate mechanisms of action, processes, and contextual variables to develop more comprehensive understandings as to why an intervention works or does not work initially and over time. This NOSI should support activities that further the understanding of the “how and why” that are related to the primary outcomes in the parent study. Understanding the “how and why” NIH-funded interventions are (or are not) effective will improve our ability to harness behavior change strategies to improve health outcomes and increase collective knowledge regarding how to facilitate behavior initiation, adoption, maintenance and sustainment during and after interventions. Use of behavior change theories and identification of the underlying MOAs corresponds to OBSSR’s priority to facilitate more cumulative, integrated, and synergistic behavioral and social sciences that can be optimized and translated across conditions based not only on the efficaciousness of the intervention but also on data demonstrating that the intervention influenced a unique human mechanism that led to healthier behavior ( ). When testing theory-based MOAs, operational definitions and measurement approaches with prior evidence of association with behavior change are encouraged. This NOSI encourages use of behavior change theories and models that use variables that can explain individual and interpersonal mechanisms of action (MOA). L.The need to develop a comprehensive understanding of how and why humans initiate, adopt, maintain, and sustain behaviors that impede or promote health and wellbeing is well-documented. 1a) GBD 2017 Pancreatic Cancer Collaborators Lancet Gastroenterol Hepatol 2019, 4, 934 ī) C. ![]() Combining the CD11b agonist ADH-503 with anti-PD-1 immunotherapy and chemotherapy leads to a significant reduction in tumor cell viability, proliferation, metabolic activity, immunomodulation, and secretion of immunosuppressive and tumor growth-promoting cytokines. Human pancreatic cancer cells, cancer-associated fibroblasts, and myeloid cells are grown encapsulated in hydrogels to mimic key components of tumor tissues, and cell responses toward treatment are assessed. To address this limitation and explore the effects of immunotherapy in combination with chemotherapy, a multicellular 3D cancer model using a star-shaped poly(ethylene glycol)–heparin hydrogel matrix is developed. There is a lack of preclinical pancreatic cancer models that reconstruct the extracellular, cellular, and biomechanical elements of tumor tissues to assess responses toward immunotherapy. Resistance to therapy and disease progression are mediated by the tumor microenvironment, which contains excessive amounts of extracellular matrix and stromal cells, acting as a barrier to drug delivery. Standard-of-care therapy, including surgery and chemotherapy, is unsatisfactory, and therapies harnessing the immune system have been unsuccessful in clinical trials. Pancreatic cancer is a devastating malignancy with minimal treatment options. ![]()
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