Literature DB >> 623207

Spontaneous amyloidosis in LLC mice.

C K Chai.   

Abstract

Practically all low leukocyte count (LLC) mice over 1 year of age develop renal amyloidosis. Renal amyloid is deposited in the glomeruli and in the interstitium between the convoluted as well as collecting tubules, with consequent development of cysts and necrosis. LLC mice die of chronic renal failure. Electron microscopic studies reveal amyloid fibrils in the mesangium, a thickening of the basement membranes, and fusion of the foot processes in the glomeruli. Massive amounts of amyloid fibrils are also present in the interstitium, where intracellular fibrils in the fibroblasts as well as in the tubular epithelium cells are found. Vesicles, which are probably formed from membrane disruption, and amorphous materials are seen along the basement membranes. LLC mouse amyloidosis is discussed with regard to its potential as a model for studies on amyloidosis as well as the etiology and origin of amyloid fibrils.

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Year:  1978        PMID: 623207      PMCID: PMC2018153     

Source DB:  PubMed          Journal:  Am J Pathol        ISSN: 0002-9440            Impact factor:   4.307


  6 in total

1.  Spontaneous amyloidosis of the mouse. 3. Two patterns of amyloid distribution and their pathogenic relationship.

Authors:  W Zschiesche
Journal:  Acta Pathol Microbiol Scand Suppl       Date:  1972

2.  Renal amyloidosis: electron microscopic observations.

Authors:  W Jao; C L Pirani
Journal:  Acta Pathol Microbiol Scand Suppl       Date:  1972

3.  Fine structure of the glomerulus in human and experimental renal amyloidosis.

Authors:  T Shirahama; A S Cohen
Journal:  Am J Pathol       Date:  1967-11       Impact factor: 4.307

4.  Selection for leukocyte counts in mice.

Authors:  C K Chai
Journal:  Genet Res       Date:  1966-10       Impact factor: 1.588

5.  Reticular cell hyperplasia and amyloidosis in a line of mice with low leukocyte counts.

Authors:  C K Chai
Journal:  Am J Pathol       Date:  1976-10       Impact factor: 4.307

6.  The SJL/J mouse: a new model for spontaneous age-associated amyloidosis. I. Morphologic and immunochemical aspects.

Authors:  M A Scheinberg; E S Cathcart; J W Eastcott; M Skinner; M Benson; T Shirahama
Journal:  Lab Invest       Date:  1976-07       Impact factor: 5.662

  6 in total
  1 in total

1.  Systemic amyloidosis in transgenic mice carrying the human mutant transthyretin (Met30) gene. Pathologic similarity to human familial amyloidotic polyneuropathy, type I.

Authors:  S Yi; K Takahashi; M Naito; F Tashiro; S Wakasugi; S Maeda; K Shimada; K Yamamura; S Araki
Journal:  Am J Pathol       Date:  1991-02       Impact factor: 4.307

  1 in total

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