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In Vivo Models of Inflammation, 2e, Vol. II by Christopher S. Stevenson, Lisa A. Marshall, Douglas W.

By Christopher S. Stevenson, Lisa A. Marshall, Douglas W. Morgan

In Vivo versions of irritation (Vol. 2) presents biomedical researchers in either the pharmaceutical and academia with an outline of the state of the art animal version platforms used to emulate illnesses with elements of irritation. This moment version acts as a supplement to the 1st, describing and updating the traditional versions which are so much applied for particular disorder parts. New types are integrated exploring rising parts of irritation learn.

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Extra resources for In Vivo Models of Inflammation, 2e, Vol. II

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Oxidative damage to HDAC was again the mechanism proposed for the lack of steroid efficacy [66]. Oxidant stress has also been demonstrated to play a key role in mediating the chronic effects of smoke-induced lung damage. , p38 MAP kinase and NF-gB activation), oxidants can also inactivate endogenous protease inhibitors, and thereby potentiate the proteolytic activity in the lung that contributes to airspace enlargement. Similar to the elastase model, Nrf2-deficient mice had greater lung inflammation and emphysematous destruction in response to 6 months of smoke exposures [103].

COPD is a smoking-related disorder that is a major cause of morbidity and mortality throughout the world. It comprises a group of lung conditions commonly described clinically as chronic bronchitis, small airways disease, and emphysema. While no single animal model replicates the degree of lung destruction observed in the human disease condition, there are models that can mimic many of the same types of pathologies using disease-relevant agents. Several modeling systems have been developed over the years to mimic aspects of COPD, and it is therefore beyond the scope of this chapter to be a comprehensive review of all them; however, where possible, tables citing the relevant publications on these diverse models have been included for the readers’ reference.

J Allergy Clin Immunol 116: 94–101 Grunstein MM, Hakonarson H, Maskeri N, Chuang S (2000) Autocrine cytokine signaling mediates effects of rhinovirus on airway responsiveness. Am J Physiol Lung Cell Mol Physiol 278: L1146–1153 Whelan R, Kim C, Chen M, Leiter J, Grunstein MM, Hakonarson H (2004) Role and regulation of interleukin-1 molecules in pro-asthmatic sensitised airway smooth muscle. Eur Respir J 24: 559–567 Gascoigne MH, Holland K, Page CP, Shock A, Robinson M, Foulkes R, Gozzard N (2003) The effect of anti-integrin monoclonal antibodies on antigen-induced pulmonary inflammation in allergic rabbits.

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