ライフサイエンスコーパス: osteosclerosis

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1 fibrosis, increased microvessel density, and osteosclerosis).

2 associated with a splenomegaly and a marked osteosclerosis.

3 al cell-derived osteoprotegerin in promoting osteosclerosis.

4 al osteoclasts resulting in osteopetrosis or osteosclerosis.

5 elopmental increase in bone mass, leading to osteosclerosis.

6 mice represent a model for myelofibrosis and osteosclerosis.

7 marrow (BM) cells develop myelofibrosis and osteosclerosis.

8 hematopoiesis, and bone marrow fibrosis and osteosclerosis.

9 In the latter case, diffuse osteosclerosis and H-shaped vertebrae are most typical.

10 and 9 mo of age, mutant animals also develop osteosclerosis and osteoarthritis.

11 ic bone lesions that consist of a mixture of osteosclerosis and osteolysis.

12 re the underlying cause of myelofibrosis and osteosclerosis and potential treatments for these diseas

13 ssive osteochondrodysplasia characterized by osteosclerosis and short stature, maps to chromosome 1q2

14 secondary intramedullary collagen fibrosis, osteosclerosis, angiogenesis, and extramedullary hematop

15 BMP-6 contributes to prostate cancer-induced osteosclerosis at bone metastatic sites.

16 Hepatitis C-associated osteosclerosis (HCAO) is a rare disorder characterized b

17 peractive WNT signaling mouse model of human osteosclerosis, inhibition of glutamine catabolism or Gc

18 Intramedullary osteosclerosis is a distinct disorder that typically aff

19 osteoporosis (bone loss) together with focal osteosclerosis (localized bone formation).

20 The phenotype of mice homozygous for the osteosclerosis (oc) mutation includes osteopetrosis, and

21 pe is similar to that of the murine mutation osteosclerosis (oc), which is localized to proximal mous

22 and no pathologic bone abnormalities such as osteosclerosis or myelofibrosis.

23 pecific gain of Notch function causes severe osteosclerosis owing to increased proliferation of immat

24 hese observations indicate that BMPs promote osteosclerosis through VEGF in prostate cancer metastase

25 d to normal levels and the myelofibrosis and osteosclerosis were completely corrected.

26 tal stromal changes, such as BM fibrosis and osteosclerosis, whose occurrence is harbinger of a disma

27 histologically and radiographically evident osteosclerosis with age.

28 Mice lacking Shn3 display adult-onset osteosclerosis with increased bone mass due to augmented

29 essive disorder characterized by generalized osteosclerosis with periosteal bone formation and a dist

30 cular atrophy, platyspondyly and metaphyseal osteosclerosis with relative radiolucency of widened dia

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