ライフサイエンスコーパス: hypocellularity

1 n patients with pancytopenia and bone marrow hypocellularity.

2 d by tTg-mediated cross-linking and relative hypocellularity.

3 ic disease in the marrow or to severe marrow hypocellularity.

4 marrow failure is typically characterized by hypocellularity.

5 y stimuli, and ultimately led to bone marrow hypocellularity.

6 nounced disruption of the BM vasculature, BM hypocellularity, ablation of HSCs, and pancytopenia in c

7 in thymic differentiation, including thymic hypocellularity, abnormal differentiation of CD3- CD4- C

8 -hypomorphic harlequin (Hq) mice show thymic hypocellularity and a cell-autonomous thymocyte developm

9 the pre-TCR checkpoint, resulting in thymic hypocellularity and a severe reduction in CD4(+)CD8(+) t

10 WT and NQO2(-/-) mice showed hypocellularity and a significant increase in adipocytes

11 sis, and overexpression of Bcl-2 rescued the hypocellularity and associated thymocyte developmental b

12 adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plas

13 f NFAT5/TonEBP function resulted in lymphoid hypocellularity and impaired antigen-specific antibody r

14 mplete looping, lack of chamber demarcation, hypocellularity and lack of trabeculation.

15 pamycin in both models corrected bone marrow hypocellularity and partially restored hematopoietic act

16 ventional DCs display marked lymph node (LN) hypocellularity and reduced frequency of DCs in the same

17 ice was markedly altered, as shown by thymic hypocellularity and reduced numbers of peripheral T cell

18 results in pronounced thymic and bone marrow hypocellularity and the disappearance of c-kit(+) cells.

19 inal neurons into subretinal space to severe hypocellularity and ultrastructural defects in photorece

20 terine fetal growth restriction, fetal liver hypocellularity, and demise.

21 ruption of splenic architecture, bone marrow hypocellularity, and extramedullary hematopoiesis.

22 l fate adoption, lack of fetal angiogenesis, hypocellularity, and poor invasion into maternal tissue.

23 t myeloid dysplasia features and bone marrow hypocellularity are often found in patients with ADA-SCI

24 -treated tissue demonstrated subconjunctival hypocellularity associated with peripheral fibrosis.

25 ) resulting in a profound anterior pituitary hypocellularity due to a general lack of thyrotropes, so

26 ell apoptosis, it failed to improve neonatal hypocellularity due to decreased proliferative capacity

27 atal mice using a Col2-CreER strategy led to hypocellularity in articular cartilage, growth plate dis

28 tributes to defects in cortical layering and hypocellularity in the ventral LGN and amygdala and will

29 EBOV exposure was associated with severe BM hypocellularity, including depletion of myeloid, erythro

30 re described, and a correlation with hepatic hypocellularity is demonstrated.

31 opmentally delayed and accompanied by marked hypocellularity of the bone marrow, elevation of myeloid

32 1 homozygotes was not attributable to global hypocellularity of the paraventricular nucleus (PVN) of

33 .3-34, p < 0.05), and splenic and lymph node hypocellularity (OR, 42, 95% CI, 3.7-473, p < 0.05).

34 ersus multilineage dysplasia, marrow blasts, hypocellularity, or fibrosis.

35 Granule cell hypocellularity persists in 3-month-old Ts65Dn mice befo

36 Despite the hypocellularity, premature cell cycle exit, increased ce

37 Hypocellularity resulting from chondrocyte death in the

38 ther, these findings suggest that the thymic hypocellularity seen in mammary tumor bearers is not due

39 The hypocellularity seen in the trisomic adult hippocampus o

40 ociated with enhanced cartilage degradation, hypocellularity, synovial and cartilage fibrosis, synovi

41 The areas of fibrosis and hypocellularity were associated with increased apoptosis

42 rious defects in many organs associated with hypocellularity, whereas loss of the p18(Ink4c) gene res