作者: Daniel Gb , McEntee Mf , Johnson Dk , Schultze Ae
DOI:
关键词:
摘要: BACKGROUND AND PURPOSE Previous investigation of fitness1(4226SB) mice revealed growth retardation and microcytic, hypochromic anemia with functional iron deficiency. Serum biochemical analysis suggested protein-losing enteropathy liver dysfunction. METHODS Radiography was done to assess lumbar bone lesions in hemizygous for fitness1 (fit1) [c fit1(4226SB/Df(c Mod2 sh1)26DVT] age-matched sibling controls [c(ch)+/c(ch)+] at 40 or 60 days age. Macroscopic microscopic were evaluated necropsy. Bone marrow examined cytologically evaluate hematopoietic lesions. RESULTS Mice fit1 had radiographically evident vertebral abnormalities, including various degrees body fusion, loss intervertebral disk spaces mild, generalized osteopenia. All mutant scoliosis. Several lordosis and/or kyphosis variable severity mild subluxation the lumbosacral junction. Marked splenomegaly cardiomegaly evident, color ranged from normal slightly pale. The spleen marked extramedullary hematopoiesis; vertebrae contained that corresponded radiographic Cytologic examination normocellular hypocellular status, moderate erythroid hypoplasia characterized by increase myeloid-to-erythroid cell ratio, decreased percentage precursors, slight myeloid precursor cells. CONCLUSIONS Mutations directly indirectly cause alteration(s) blood, organs hematopoiesis (bone marrow, spleen, liver), heart, column, suggest this mouse may be a good model study scoliosis relationships between metabolism growth.