| First Author | Coutinho M | Year | 1992 |
| Journal | Eur J Immunogenet | Volume | 19 |
| Issue | 6 | Pages | 419-23 |
| PubMed ID | 1477093 | Mgi Jnum | J:3414 |
| Mgi Id | MGI:51927 | Doi | 10.1111/j.1744-313x.1992.tb00085.x |
| Citation | Coutinho M, et al. (1992) C5 deficiency in A/J mice is not associated with resistance to the development of secondary amyloidosis. Eur J Immunogenet 19(6):419-23 |
| abstractText | The aim of the study was to determine whether C5 deficiency in the mouse is associated with resistance to the development of secondary amyloidosis. 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. Using a restriction fragment length polymorphism generated by digestion of genomic DNA with the restriction enzyme HindIII, C5 sufficient and deficient DNA can be clearly differentiated. Eight mice were found to be C5 sufficient, 32 were heterozygotes and 14 were found to be C5 deficient. Grading of the splenic amyloid load from negative to 4+ was performed after staining tissue squashes with Congo red and viewing them under a polarizing microscope. Seventeen mice were noted to have |
