scholarly journals The virulence-enhancing factor of mucins. 1. A biological assay of virulence-enhancing activity

1950 ◽  
Vol 46 (3) ◽  
pp. 352-356 ◽  
Author(s):  
H. Smith
Nature ◽  
1955 ◽  
Vol 176 (4479) ◽  
pp. 427-430 ◽  
Author(s):  
R. F. GLASCOCK

1928 ◽  
Vol 78 (2) ◽  
pp. 495-524
Author(s):  
Georgian Adams ◽  
E.V. McCollum

Gene ◽  
1996 ◽  
Vol 177 (1-2) ◽  
pp. 269-270 ◽  
Author(s):  
Takahiko Hayakawa ◽  
Jinhua Xu ◽  
Toshihiko Hukuhara

2006 ◽  
Vol 49 (3) ◽  
pp. 1149-1156 ◽  
Author(s):  
Lourdes Santana ◽  
Eugenio Uriarte ◽  
Humberto González-Díaz ◽  
Giuseppe Zagotto ◽  
Ramón Soto-Otero ◽  
...  

2011 ◽  
Vol 37 (9) ◽  
pp. 1212-1215 ◽  
Author(s):  
Marisa Pascale Quintino ◽  
Mary Uchiyama Nakamura ◽  
Manuel de Jesus Simões ◽  
Edward Araujo Júnior ◽  
Ricardo Martins de Oliveira Filho ◽  
...  

2008 ◽  
Vol 415 (2) ◽  
pp. 207-215 ◽  
Author(s):  
Sivanesan Senthilkumar ◽  
Edwin Chang ◽  
Rajadas Jayakumar

AA (amyloid protein A) amyloidosis in mice is markedly accelerated when the animals are given, in addition to an inflammatory stimulus, an intravenous injection of protein extracted from AA-laden mouse tissue. Previous findings affirm that AA fibrils can enhance the in vivo amyloidogenic process by a nucleation seeding mechanism. Accumulating evidence suggests that globular aggregates rather than fibrils are the toxic entities responsible for cell death. In the present study we report on structural and morphological features of AEF (amyloid-enhancing factor), a compound extracted and partially purified from amyloid-laden spleen. Surprisingly, the chief amyloidogenic material identified in the active AEF was diffusible globular oligomers. This partially purified active extract triggered amyloid deposition in vital organs when injected intravenously into mice. This implies that such a phenomenon could have been inflicted through the nucleation seeding potential of toxic oligomers in association with altered cytokine induction. In the present study we report an apparent relationship between altered cytokine expression and AA accumulation in systemically inflamed tissues. The prevalence of serum AA monomers and proteolytic oligomers in spleen AEF is consistent to suggest that extrahepatic serum AA processing might lead to local accumulation of amyloidogenic proteins at the serum AA production site.


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