Publications by authors named "Mark T Kearns"

Introduction: Graduate medical education on social determinants of health (SDOH) is limited. Residents often directly care for vulnerable populations at safety-net hospitals, yet curricula thus far are based in the ambulatory setting.

Methods: We developed a case-based curriculum integrating SDOH with critical care topics to standardize knowledge and improve skills and attitudes of internal medicine residents working with these patients.

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Article Synopsis
  • - Exposure to Schistosoma mansoni can cause pulmonary arterial hypertension (PAH) through type-2 inflammation, specifically involving IL-4 and IL-13, leading to changes in blood vessel structure.
  • - In experiments, mice lacking both IL-4 and IL-13 (IL-4(-/-)IL-13(-/-)) were protected from Schistosoma-induced PAH, showing lower pressure and less vascular damage compared to other mice.
  • - Analysis of human lung tissues confirmed that type-2 inflammation is present in cases of schistosomiasis-associated PAH, suggesting a similar mechanism might occur in humans.
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Purpose/aim: Angiogenesis is a central component of normal wound healing but it has not been fully characterized in lung repair following acute inflammatory injury. The current literature lacks vital information pertaining to the extent, timing, and location of this process. This information is necessary for examining mechanisms that drive normal lung repair in resolving acute inflammatory injury.

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Apoptosis of alveolar macrophages and their subsequent clearance by neighboring phagocytes are necessary steps in the resolution of acute pulmonary inflammation. We have recently identified that activation of the Fas death receptor on the cell surface of macrophages drives macrophage apoptosis. However, the source of the cognate ligand for Fas (FasL) responsible for induction of alveolar macrophage apoptosis is not defined.

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Rationale: Bone marrow derived progenitor cells participate in the repair of injured vessels. The lungs of individuals with emphysema have reduced alveolar capillary density and increased endothelial apoptosis. We hypothesized that circulating levels of endothelial and hematopoietic progenitor cells would be reduced in this group of patients.

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Efficient clearance of apoptotic cells from the lung by alveolar macrophages is important for the maintenance of tissue structure and function. Lung tissue from humans with emphysema contains increased numbers of apoptotic cells and decreased levels of vascular endothelial growth factor (VEGF). Mice treated with VEGF receptor inhibitors have increased numbers of apoptotic cells and develop emphysema.

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Rationale: During acute lung injury (ALI) the macrophage pool expands markedly as inflammatory monocytes migrate from the circulation to the airspaces. As inflammation resolves, macrophage numbers return to preinjury levels and normal tissue structure and function are restored.

Objectives: To determine the fate of resident and recruited macrophages during the resolution of ALI in mice and to elucidate the mechanisms responsible for macrophage removal.

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Allogeneic bone marrow transplantation is a common method used to study the contribution of myeloid and lymphoid cell populations in murine models of disease. The method requires lethal doses of radiation to ablate the bone marrow. Unintended consequences of radiation include organ injury and inflammatory cell activation.

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