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1 y induced by carrageenan in a mouse model of pleurisy.
2 established guinea pig model of tuberculous pleurisy.
3 mg/kg, i.p.) in a mouse model of CAR-induced pleurisy.
4 biopsy sections of patients with tuberculous pleurisy.
5 el of lipopolysaccharide (LPS)-induced mouse pleurisy.
6 ritical role of TNF to control mycobacterial pleurisy.
7 sion increased during resolving phase of the pleurisy.
8 ing more common in patients with tuberculous pleurisy (92%) in comparison with healthy M. tuberculosi
9 niae, ApUT, the pathogen that causes porcine pleurisy and pneumonia, was expressed in Escherichia col
10 t inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively i
11 ing the early phase of a carrageenin-induced pleurisy, dominated by polymorphonuclear leucocytes, but
12 d during the resolution phase of LPS-induced pleurisy, especially in macrophages with resolving pheno
15 ecruitment in a murine model of experimental pleurisy induced by the administration of carrageenan an
17 is of cytokine expression during tuberculous pleurisy may lead to a better understanding of the self-
18 had superior oral activity in vivo, in a rat pleurisy model (ED(50) = 0.14 mg/kg) and rat anaphylaxis
24 that type VI iPLA2 drives the onset of acute pleurisy through the synthesis of PGE2, LTB4, PAF, and I
25 ave used the guinea pig model of tuberculous pleurisy to examine several aspects of the immune respon
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