|1.||Benjumea, Dora María: 1 article (09/2013)|
|2.||Pereañez, Jaime Andrés: 1 article (09/2013)|
|3.||Patiño, Arley Camilo: 1 article (09/2013)|
|4.||Bao, Juan: 1 article (12/2010)|
|5.||Sun, Qian-Yun: 1 article (12/2010)|
|6.||Tavares, Flávio L: 1 article (07/2009)|
|7.||Breno, María C: 1 article (07/2009)|
|8.||Peichoto, María E: 1 article (07/2009)|
|9.||Teibler, Pamela: 1 article (07/2009)|
|10.||Acosta, Ofelia: 1 article (07/2009)|
|1.||Pemphigus (Pemphigus Vulgaris)
11/01/1993 - "Inbred CE/J mice have been identified as extremely resistant to azocasein-induced amyloidosis relative to five commonly used inbred strains, A/J, CBA/J, C57BL/6J, C3H/HeN, and SJL/J. "
06/01/1980 - "Amyloidosis was accelerated by A/J spleen homogenates only when the donors were given a prolonged course of azocasein. "
09/01/1981 - "A/J mice are highly resistant to induction of amyloidosis with serial injections of azocasein, compared to the CBA/J strain. "
06/01/1980 - "Both strains developed amyloidosis after three or four azocasein injections, following sublethal irradiation and intravenous administration of spleen homogenates from azocasein-treated CBA donors. "
06/01/1980 - "A/J mice required over 3 times as many injections of azocasein to develop splenic amyloidosis as the CBA/J strain. "
08/15/2006 - "Furthermore, SAF-1 transgenic mice rapidly developed severe AA amyloidosis in response to azocasein injection, indicating increased susceptibility to inflammation. "
11/01/1989 - "SAP mRNA levels were correlated with other parameters of inflammation: infiltration of peritoneal exudate cells (PEC) into the peritoneum after thioglycollate injection, and serum concentrations of SAP after azocasein injection. "
12/01/1992 - "Chronic inflammation was induced in the F2 progeny, derived from matings between amyloid-susceptible and amyloid-resistance mice, by daily injections of azocasein for thirty days. "
02/01/1991 - "Hepatic levels of mRNA specific for total serum amyloid A (SAA), the SAA1 and SAA2 isotypes, serum amyloid P (SAP), C-reactive protein (CRP), and fibronectin, as well as the plasma concentrations of SAA and SAP were examined in amyloid-resistant (A/J) and amyloid-susceptible (CBA/J) mice during azocasein-induced chronic inflammation. "
09/16/2013 - "The protocols investigated included inhibition of proteolytic activity on azocasein, inhibition of proteolytic activity on fibrinogen, inhibition of pro-coagulant activity, inhibition of hemorrhagic activity and inhibition of edema-forming activity. "
07/01/2009 - "The purified protein hydrolyzed neither azocasein nor fibrinogen, and it could induce no edema, hemorrhage or inhibition of platelet adhesion and aggregation. "
12/01/2010 - "It also exhibits edema-inducing activity, but has no hemorrhagic activity and proteolytic activity against fibrin, azocasein, and N-benzoyl-l-arginine ethyl ester. "
|1.||Serum Amyloid A Protein (Serum Amyloid A)
|2.||Amyloid (Amyloid Fibrils)
|3.||Messenger RNA (mRNA)
|4.||Plasminogen Activators (Plasminogen Activator)
|5.||Fibrinogen (Factor I)
|7.||Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)
|8.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|10.||Peptide Hydrolases (Proteases)