Carle Foundation Hospital is a 433-bed regional care hospital in Urbana, Illinois, United States, that has achieved Magnet designation. It is owned by the not-for-profit Carle Foundation, which also consists of Carle Physician Group and Health Alliance Medical Plans. It is the area's only level 1 trauma center.The Carle system also includes Carle BroMenn Medical Center, Carle Eureka Hospital, Carle Hoopeston Regional Health Center and Carle Richland Memorial Hospital.Carle is a vertically integrated system led by James Leonard, President and CEO since 2000. He has served Carle since the early 1980s. The hospital is the primary teaching hospital for the Carle-Illinois College of Medicine, the medical school at the University of Illinois at Urbana-Champaign.
Abstract Secondary injury following ischemic traumatic brain injury (TBI) is heavily driven by neurovascular dysfunction involving endothelial damage, astrocyte reactivity, inflammation, and hypoxic stress, among other contributing pathophysiological processes. Here, we establish a mechanistically informative in vitro ischemic TBI model that isolates endothelial-astrocyte crosstalk using human brain microvascular endothelial cells (HBMECs) and astrocytes. Using this platform, we evaluated melatonin and oxygen nanobubbles (ONBs) as a combinatorial therapeutic strategy. Fabricated ONBs exhibited a mean hydrodynamic diameter of 78.35 ± 0.42 nm, a negative surface charge of −37.86 ± 1.32 mV, and sustained oxygen retention (56.38 ± 0.86 mg/L initially). Mechanical needle-scratch injury combined with hypoxia induced primary endothelial injury characterized by reduced viability and increased expression of inflammatory and hypoxia-associated markers, quantified by quantitative real-time PCR (qRT-PCR). Injured HBMECs subsequently triggered astrocyte reactivity marked by elevated GFAP (1.93-fold; p < 0.0001), NLRP3 (3.21-fold; p < 0.0001), NF-κβ signaling (1.62-fold; p < 0.0001), and HIF-1α (2.28-fold; p < 0.0001), while reactive astrocytes propagated a secondary wave of endothelial degeneration, establishing a bidirectional injury loop. Melatonin alone only partially mitigated injury-associated signaling, whereas the melatonin-ONBs combination restored astrocytic and endothelial gene expression to near-baseline levels. These findings highlight a multimodal therapeutic approach that effectively suppresses inflammatory, apoptotic, and hypoxic signaling in ischemic TBI.
A BSTRACT Coronary artery calcium (CAC) scoring is an established tool for cardiovascular risk stratification and is primarily recommended when preventive treatment decisions remain uncertain. Current guidelines do not routinely support CAC screening in asymptomatic individuals already receiving guideline-directed medical therapy. We present a case in which a significant vascular calcification was incidentally identified on a knee X-ray, leading to CAC scoring that identified severe multivessel coronary artery disease (CAD) in an asymptomatic patient with controlled cardiovascular risk factors. Clinical history, diagnostic imaging, operative management, and follow-up data were reviewed for an asymptomatic 77-year-old man who underwent CAC scoring after incidental vascular calcification was identified on knee radiography. A physically active 77-year-old man with multiple cardiovascular risk factors was referred for CAC scoring after popliteal artery atherosclerosis was incidentally noted on knee radiography. He denied chest pain, dyspnea, and claudication. Despite well-controlled medically managed comorbidities, CAC scoring demonstrated an Agatston score of 4011. Subsequent stress myocardial perfusion imaging revealed a large partially reversible perfusion defect in the right coronary artery (RCA) territory. Coronary angiography demonstrated chronic total occlusion of the RCA and approximately 80% stenoses of the left anterior descending and left circumflex arteries. The patient subsequently underwent successful quadruple coronary artery bypass grafting with good postoperative recovery. This case highlights the potential diagnostic and prognostic value of CAC scoring in selected asymptomatic patients. Significant obstructive CAD may remain clinically silent despite good functional status and optimized medical therapy. In carefully selected contexts, CAC scoring may facilitate earlier identification of advanced coronary disease that might otherwise remain undetected.
