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1 d by tTg-mediated cross-linking and relative hypocellularity.
2 ic disease in the marrow or to severe marrow hypocellularity.
3 nounced disruption of the BM vasculature, BM hypocellularity, ablation of HSCs, and pancytopenia in c
4 in thymic differentiation, including thymic hypocellularity, abnormal differentiation of CD3- CD4- C
5 -hypomorphic harlequin (Hq) mice show thymic hypocellularity and a cell-autonomous thymocyte developm
6 the pre-TCR checkpoint, resulting in thymic hypocellularity and a severe reduction in CD4(+)CD8(+) t
8 sis, and overexpression of Bcl-2 rescued the hypocellularity and associated thymocyte developmental b
9 adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plas
10 f NFAT5/TonEBP function resulted in lymphoid hypocellularity and impaired antigen-specific antibody r
12 pamycin in both models corrected bone marrow hypocellularity and partially restored hematopoietic act
13 ventional DCs display marked lymph node (LN) hypocellularity and reduced frequency of DCs in the same
14 ice was markedly altered, as shown by thymic hypocellularity and reduced numbers of peripheral T cell
15 results in pronounced thymic and bone marrow hypocellularity and the disappearance of c-kit(+) cells.
18 l fate adoption, lack of fetal angiogenesis, hypocellularity, and poor invasion into maternal tissue.
19 t myeloid dysplasia features and bone marrow hypocellularity are often found in patients with ADA-SCI
20 -treated tissue demonstrated subconjunctival hypocellularity associated with peripheral fibrosis.
21 ) resulting in a profound anterior pituitary hypocellularity due to a general lack of thyrotropes, so
22 ell apoptosis, it failed to improve neonatal hypocellularity due to decreased proliferative capacity
23 atal mice using a Col2-CreER strategy led to hypocellularity in articular cartilage, growth plate dis
24 tributes to defects in cortical layering and hypocellularity in the ventral LGN and amygdala and will
26 opmentally delayed and accompanied by marked hypocellularity of the bone marrow, elevation of myeloid
27 1 homozygotes was not attributable to global hypocellularity of the paraventricular nucleus (PVN) of
28 .3-34, p < 0.05), and splenic and lymph node hypocellularity (OR, 42, 95% CI, 3.7-473, p < 0.05).
32 ther, these findings suggest that the thymic hypocellularity seen in mammary tumor bearers is not due
34 ociated with enhanced cartilage degradation, hypocellularity, synovial and cartilage fibrosis, synovi
36 rious defects in many organs associated with hypocellularity, whereas loss of the p18(Ink4c) gene res
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