Sepsis is not only a significant cause of mortality worldwide but has particularly devastating effects on the central nervous system of survivors. It is therefore crucial to understand the molecular structure, physiology, and events involved in the pathogenesis of sepsis-associated encephalopathy, so that potential therapeutic advances can be achieved. A key determinant to the development of this type of encephalopathy is morphological and functional modification of the blood–brain barrier (BBB), whose function is to protect the CNS from pathogens and toxic threats. Key mediators of pathologic sequelae of sepsis in the brain include cytokines, including TNF-α, and sphingolipids, which are biologically active components of cellular membranes that possess diverse functions. Emerging data demonstrated an essential role for sphingolipids in the pulmonary vascular endothelium. This raises the question of whether endothelial stability in other organs systems such as the CNS may also be mediated by sphingolipids and their receptors. In this review, we will model the structure and vulnerability of the BBB and hypothesize mechanisms for therapeutic stabilization and repair following a confrontation with sepsis-induced inflammation.
Coronavirus disease (COVID-19), the clinical syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is currently a global health pandemic with substantial morbidity and mortality. COVID-19 has cast a shadow on nearly every aspect of society, straining health systems and economies across the world. Although it is widely accepted that a close relationship exists between obesity, cardiovascular disease, and metabolic disorders on infection, we are only beginning to understand ways in which the immunological sequelae of obesity functions as a predisposing factor related to poor clinical outcomes in COVID-19. As both the innate and adaptive immune systems are each primed by obesity, the alteration of key pathways results in both an immunosuppressed and hyperinflammatory state. The present review will discuss the cellular and molecular immunology of obesity in the context of its role as a risk factor for severe COVID-19, discuss the role of cytokine storm, and draw parallels to prior viral epidemics such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and 2009 H1N1.
This prospective investigation derived a prediction model for identifying risk of incident lung cancer among patients with visible lung nodules identified on computed tomography (CT). Among 2,924 eligible patients referred for evaluation of a pulmonary nodule to the Stony Brook Lung Cancer Evaluation Center between January 1, 2002 and December 31, 2015, 171 developed incident lung cancer during the observation period. Cox proportional hazard models were used to model time until disease onset. The sample was randomly divided into discovery (n ¼ 1,469) and replication (n ¼ 1,455) samples. In the replication sample, concordance was computed to indicate predictive accuracy and risk scores were calculated using the linear predictions. Youden index was used to identify high-risk versus low-risk patients and cumulative lung cancer incidence was examined for high-risk and
An understanding of thoracic computed tomographic anatomy is vital for procedural planning in bronchoscopy. When reviewing computed tomographic images in preparation for endobronchial ultrasound-directed staging for lung cancer, the presence of fluid in pericardial recesses can often be mistaken for mediastinal lymphadenopathy, potentially causing pitfalls in radiologic interpretation. We describe 2 cases of a high-riding superior aortic recess extending into right paratracheal lymph node station mimicking paratracheal lymphadenopathy. We review the anatomy and imaging characteristics of pericardial recesses with emphasis on differentiating these findings from mediastinal lymphadenopathy.
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