@article{SmithBrayHoffmanetal.2015,
  author    = {Smith, Craig J. and Bray, Benjamin D. and Hoffman, Alex and Meisel, Andreas and Heuschmann, Peter U. and Wolfe, Charles D. A. and Tyrrell, Pippa J. and Rudd, Anthony G.},
  title     = {Can a novel clinical risk score improve pneumonia prediction in acute stroke care? A UK multicenter cohort study},
  series = {Journal of the American Heart Association},
  volume    = {4},
  journal   = {Journal of the American Heart Association},
  number    = {1},
  doi       = {10.1161/JAHA.114.001307},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-144602},
  pages     = {e001307},
  year      = {2015},
  abstract  = {Background Pneumonia frequently complicates stroke and has amajor impact on outcome. We derived and internally validated a simple clinical risk score for predicting stroke-associated pneumonia (SAP), and compared the performance with an existing score (A\(^{2}\)DS\(^{2}\)). Methods and Results We extracted data for patients with ischemic stroke or intracerebral hemorrhage from the Sentinel Stroke National Audit Programme multicenter UK registry. The data were randomly allocated into derivation (n=11 551) and validation (n=11 648) samples. A multivariable logistic regression model was fitted to the derivation data to predict SAP in the first 7 days of admission. The characteristics of the score were evaluated using receiver operating characteristics (discrimination) and by plotting predicted versus observed SAP frequency in deciles of risk (calibration). Prevalence of SAP was 6.7\% overall. The final 22-point score (ISAN: prestroke Independence [modified Rankin scale], Sex, Age, National Institutes of Health Stroke Scale) exhibited good discrimination in the ischemic stroke derivation (C-statistic 0.79; 95\% CI 0.77 to 0.81) and validation (C-statistic 0.78; 95\% CI 0.76 to 0.80) samples. It was well calibrated in ischemic stroke and was further classified into meaningful risk groups (low 0 to 5, medium6 to 10, high 11 to 14, and very high >= 15) associated with SAP frequencies of 1.6\%, 4.9\%, 12.6\%, and 26.4\%, respectively, in the validation sample. Discrimination for both scores was similar, although they performed less well in the intracerebral hemorrhage patients with an apparent ceiling effect. Conclusions The ISAN score is a simple tool for predicting SAP in clinical practice. External validation is required in ischemic and hemorrhagic stroke cohorts.},
  language  = {en}
}
@article{RommelMildeEberleetal.2020,
  author    = {Rommel, Marcel G. E. and Milde, Christian and Eberle, Regina and Schulze, Harald and Modlich, Ute},
  title     = {Endothelial-platelet interactions in influenza-induced pneumonia: A potential therapeutic target},
  series = {Anatomia, Histologia, Embryologia},
  volume    = {49},
  journal   = {Anatomia, Histologia, Embryologia},
  number    = {5},
  doi       = {10.1111/ahe.12521},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-213610},
  pages     = {606 -- 619},
  year      = {2020},
  abstract  = {Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro-thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza-mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza-induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.},
  language  = {en}
}