Transactions of the American Clinical and Climatological Association最新文献

Traditionally, the islet hormone glucagon has been considered as a counterbalance to insulin, preventing hypoglycemia by promoting glucose release from the liver. This model is compatible both with clinical studies demonstrating that one of the initial endocrine responses to insulin-induced hypoglycemia is a rise in glucagon and with in vitro work demonstrating that glucagon signaling activates glycogenolysis in hepatocytes. This model has been extended to implicate glucagon in diabetogenesis, positing that the increased secretion of glucagon acts as a primary driver of hyperglycemia. However, recent work suggests an alternative set of actions for glucagon, including stimulation of insulin secretion and enhancement of hepatic insulin action. These recent findings align with the results of clinical trials using novel drugs that activate the glucagon receptor as part of a multi-receptor mechanism of action. Taken together, it appears that glucagon has distinct actions in the fed and fasted states, and glucagon receptor agonism has potential as a therapeutic approach to the treatment of diabetes.

Treating breast cancer is both a success story and a lesson in the challenges of tailoring treatment to need. Beginning in the 1980s, multiple initiatives minimized surgical intervention and toxicity, integrated radiation therapy, and began to incorporate increasingly targeted medical therapy. Because of advances in treatment and screening, the U.S. mortality from breast cancer has dropped over 40%. However, these advances have come at a financial, physical, and social cost. It costs nearly $30 billion per year in the United States to achieve these improved outcomes in treating breast cancer, and we know that we overtreat many patients. Moreover, racial disparities in outcome persist, and many patients cannot access modern treatments. Ensuring that we give the right treatment to the right patient, and that we omit therapy when it is safe to do so, will require new strategies.

Cancer remains a leading cause of mortality in the United States, with significant inequities across racial and ethnic groups. Evidence-based cancer screening and prevention offers one pathway to reducing cancer mortality but can be challenging to implement with high fidelity and equity. In this paper, we describe the development of equitable, evidence-based cancer screening programs in Central Texas as a potential model for other regions and for other conditions for which evidence-based clinical preventive services exist but are not well-implemented or have not been implemented equitably. Key features include basing the program in Federally Qualified Health Centers (FQHCs); developing proactive outreach along with opportunistic in-reach; bilingual, bicultural social work-trained patient navigators for follow-up of abnormal screening; virtual multi-disciplinary conferences for challenging diagnostic and management decisions; and advocacy work to improve the entire screening process, including treatment.

Pericytes are specialized, mural cells essential to vascular integrity and homeostasis, with emerging roles in lung injury, fibrosis, and viral pathology. Situated around capillaries, pericytes can transition into myofibroblast-like cells and contribute to extracellular matrix (ECM) deposition following lung injury. This review delves into pericyte biology in the lung, highlighting their contributions to fibrotic processes, immune response mediation, and potential as viral reservoirs. Experimental insights from murine models and human lung pericytes underscore their dual function in structural repair and immune signaling. Here, we explore the impact of pericyte plasticity on fibrosis and immune dynamics, evaluate their interactions with viruses, and discuss their potential as therapeutic targets in lung disease. A comprehensive understanding of pericyte plasticity and heterogeneity could pave the way for novel treatments targeting fibrosis and virus-induced lung pathology.