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Acute diseases lung injury

Dr. Douglas J. Weiss is a Professor at the College of Veterinary Medicine at the UrMversity of Minnesota. Over the years, he has been extensively involved in both teaching and research at the College. He has received a number of awards for his teaching. His research interests include platelet activation mechanisms in thrombotic diseases, mechanisms of acute lung injury and mucosal inflammation. He has published extensively on his research. [Pg.379]

Dominici F, Peng RD, Bell ML et al (2006) Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. JAMA 295 1127-1134 Dreher KL, Jaskot RH, Lehmann JR et al (1997) Soluble transition metals mediate residual oil fly ash induced acute lung injury. J Toxicol Environ Health 50 285-305 Dye JA, Lehmann JR, McGee JK et al (2001) Acute pulmonary toxicity of particulate matter filter extracts in rats coherence with epidemiologic studies in Utah Valley residents. Environ Health Perspect 109(Suppl 3) 395-403... [Pg.547]

The hallmark of an inflammatory response in the lung is the presence of infiltrating leukocytes. This process can occur in the context of a variety of disorders, including trauma, infection, autoimmune diseases, idiopathic interstitial pneumonias, asthma, chronic bronchitis, acute respiratory distress syndrome (ARDS), exposure to environmental/occupational noxious agents, cancer, aUograft rejection, and ischemia-reperfusion injury. The course of inflammation in these disease states is defined by the delicate balance and nature of inflammatory mediators expressed in the context of lung inflammation, and the specific leukocyte populations recmited in response to lung injury. [Pg.413]

ANIMAL MODELS OF DISEASE FOR FUTURE TOXICITY PREDICTIONS TABLE 18.6 Models of Acute Lung Injury"... [Pg.284]

Microvasculature [37] peritonitis [38,53] dermal inflammation [28,39,40,53] intestinal inflammation [41,45,54] acute inflammation [42] blood [43] periodontal disease [44,51] airway inflammation [48] glomerulonephritis [35] renal ischemia reperfusion [49,61] bone loss [51] cystic fibrosis [55,56] acute lung injury [57,62] asthma [58] corneal wound heahng [59] vascular inflammation [60] rheumatoid arthritis [63]. [Pg.180]

Evidence for PARP-1 activation during lung disease also exists. For instance, shear forces associated with mechanical ventilation may result in alveolar epithelial cell necrosis, that is, mediated in part by PARP-1 activation (45). Likewise, PARP-1 activation has been implicated in the pathogenesis of septic shock, an important cause of acute lung injury (47). [Pg.344]

Adverse events related to transfusion of blood components have been reported, including febrile non-hemolytic transfusion reactions, mild febrile reactions, acute and delayed hemolytic transfusion reactions, transfusion-related acute lung injury (TRALl), anaphylactic and other allergic reactions, graft-versus-host disease (GvHD), transfusion-associated circulatory overload (TACO), viral infections, post-transfusion bacteremia, transfusion-associated sepsis (TAS), hemosiderosis, post-transfusion purpura, and new allo-antibody formation [18 , 19 ]. Whole blood, erythrocytes, leukocytes, platelets, and plasma for transfusion (fresh frozen plasma, FFP) are involved. Quite a number of these adverse effects, such as TRALl, TACO, TAS, and allergic/anaphylactic reactions can be difficult to evaluate. [Pg.671]


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