ABSTRACT
The US healthcare sector is undergoing significant payment reforms, leading to the emergence of Alternative Payment Models (APMs) aimed at improving clinical outcomes and patient experiences while reducing costs. This scoping review provides an overview of the involvement of anesthesiologists in APMs as found in published literature. It specifically aims to categorize and understand the breadth and depth of their participation, revolving around 3 main axes or "Aims": (1) shaping APMs through design and implementation, (2) gauging the value and quality of care provided by anesthesiologists within these models, and (3) enhancing nonclinical abilities of anesthesiologists for promoting more value in care. To map out the existing literature, a comprehensive search of relevant electronic databases was conducted, yielding a total of 2173 articles, of which 24 met the inclusion criteria, comprising 21 prospective or retrospective cohort studies, 2 surveys, and 1 case-control cohort study. Eleven publications (45%) discussed value-based, bundled, or episode-based payments, whereas the rest discussed non-payment-based models, such as Enhanced Recovery After Surgery (7 articles, 29%), Perioperative Surgical Home (4 articles, 17%), or other models (3 articles, 13%).The review identified key themes related to each aim. The most prominent themes for aim 1 included protocol standardization (16 articles, 67%), design and implementation leadership (8 articles, 33%), multidisciplinary collaboration (7 articles, 29%), and role expansion (5 articles, 21%). For aim 2, the common themes were Process-Based & Patient-Centric Metrics (1 article, 4%), Shared Accountability (3 articles, 13%), and Time-Driven Activity-Based Costing (TDABC) (3 articles, 13%). Furthermore, we identified a wide range of quality metrics, spanning 8 domains that were used in these studies to evaluate anesthesiologists' performance. For aim 3, the main extracted themes included Education on Healthcare Transformation and Policies (3 articles, 13%), Exploring Collaborative Leadership Skills (5 articles, 21%), and Embracing Advanced Analytics and Data Transparency (4 articles, 17%).Findings revealed the pivotal role of anesthesiologists in the design, implementation, and refinement of these emerging delivery and payment models. Our results highlight that while payment models are shifting toward value, patient-centered metrics have yet to be widely accepted for use in measuring quality and affecting payment for anesthesiologists. Gaps remain in understanding how anesthesiologists assess their direct impact and strategies for enhancing the sustainability of anesthesia practices. This review underscores the need for future research contributing to the successful adaptation of clinical practices in this new era of healthcare delivery.
ABSTRACT
Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific Interleukin 20 receptors in the plasma membrane and subsequent cytoplasmic Janus protein tyrosine kinases (JAK)/signal transducer and activator of the transcription (STAT) activation. The identification of noncanonical JAK/STAT-independent signaling pathways downstream of IL-24 relies on the interaction of IL-24 with protein kinase R in the cytosol, respiratory chain proteins in the inner mitochondrial membrane, and chaperones such as Sigma 1 Receptor in the endoplasmic reticulum. Numerous studies have shown that enhancing or inhibiting the expression of Interleukin 24 has a therapeutic effect in animal models and clinical trials in different pathologies. Successful drug targeting will require a deeper understanding of the downstream signaling pathways. In this review, we discuss the signaling pathway triggered by IL-24.
ABSTRACT
STAT3 transcription factor induces differentiation of naïve T cells into Th17 cells and loss of STAT3 in T cell prevents development of CNS autoimmune diseases. However, function of STAT3 in the B lymphocyte subset is not well understood. In this study, we have generated mice lacking STAT3 in CD19+ B cells (CD19-STAT3KO) and investigated intrinsic and extrinsic functions of STAT3 in B cells and its potential role in resistance or pathogenesis of organ-specific autoimmune diseases. We show that STAT3 regulates metabolic mechanisms in B cells with implications for bioenergetic and metabolic pathways that control cellular homeostasis in B cells. Thus, loss of STAT3 in CD19-STAT3KO cells perturbed growth and apoptosis by inducing rapid entry of B cells into the S-phase of the cell cycle, decreasing expression of cyclin-dependent kinase inhibitors and upregulating pro-apoptotic proteins. We further show that the CD19-STAT3KO mice develop severe experimental autoimmune uveitis (EAU), an animal model of human uveitis. Exacerbated uveitis in CD19-STAT3KO mice derived in part from enhanced expression of costimulatory molecules on B cells, marked increase of Th17 responses and increased recruitment of granulocytes into the neuroretina. The enhanced autoimmunity upon deletion of STAT3 in B cells is also recapitulated in experimental autoimmune encephalitis, a mouse model of multiple sclerosis and thus support our conclusion that STAT3 deletion in B cells enhanced inflammation and the effects observed are not model specific. Our data further indicate that STAT3 pathway modulates interactions between B and T cells during EAU resulting in alteration of lymphocyte repertoire by increasing levels of autoreactive pathogenic T cells while suppressing development and/or expansion of immune-suppressive lymphocytes (Bregs and Tregs). Taken together, STAT3 exerts diametrically opposite effects in lymphocytes, with loss of STAT3 in B cells exacerbating uveitis whereas Stat3 deletion in T cells confers protection.
