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1 e only group to exhibit glomerular mesangial hypercellularity.
2 early postnatal period, resulting in cardiac hypercellularity.
3 rescents and marked reductions in glomerular hypercellularity.
4 seudopalisading cells and cannot account for hypercellularity.
5  without (WHO Va) or with (WHO Vb) mesangial hypercellularity.
6 sic PFV was similar to the latter aside from hypercellularity.
7 rtic valve leaflet edema without evidence of hypercellularity.
8 n of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secret
9  degrees of overall glomerular endocapillary hypercellularity and crescent formation.
10 eases in marrow angiogenesis correlated with hypercellularity and megakaryocyte clumping.
11 ar abnormalities, including focal to diffuse hypercellularity and segmental sclerosis.
12 f apoptosis has been postulated to cause the hypercellularity and thus excess scar-tissue formation o
13 p laminar cell loss, microgyri, white matter hypercellularity, and blurring of the white and gray mat
14 owed an increase in neutrophils, bone marrow hypercellularity, and enlarged lymph nodes and spleen.
15 s including anemia, neutropenia, bone marrow hypercellularity, and splenomegaly with myeloid infiltra
16 ified segmental sclerosis and extracapillary hypercellularity as novel, poor prognostic indicators of
17 y capillary collapse and visceral epithelial hypercellularity associated with nephrotic range protein
18 the 10 specimens contained extensive foci of hypercellularity composed predominantly of SMCs (mean+/-
19 , the hyaloid vascular system showed hyaloid hypercellularity consisting of aberrant vasculature, whi
20  IFNAR(-/-) mice, proteinuria and glomerular hypercellularity did not develop, whereas these features
21 roduction of mature blood cells, bone marrow hypercellularity, extramedullary hematopoiesis, a tenden
22 y tissue has epithelial hyperplasia, stromal hypercellularity, increased collagen, and increased oxid
23 ally obsolescent glomeruli or mild mesangial hypercellularity may be associated with greater difficul
24        The above-described changes involving hypercellularity of the adventitia, myofibroblast format
25                                          The hypercellularity of the adventitial layer, proliferation
26 opoietic stem cell disorder characterized by hypercellularity of the bone marrow with an increase in
27 nied with marked thickening, remodeling, and hypercellularity of the fibromuscular stroma.
28 ssive collagen I and elastin deposition, and hypercellularity of the mesenchyme occurred independentl
29 apse of glomerular capillaries, swelling and hypercellularity of the visceral epithelium, hyaline art
30 y, along with reversal of the intense tissue hypercellularity of untreated lymphedema.
31 asts (P = .01), and age-adjusted bone marrow hypercellularity (P = .04).
32 luded segmental sclerosis and extracapillary hypercellularity (subdistribution HR, 2.04; 95% confiden
33 apillary fibrinogen deposits, and glomerular hypercellularity than IL-4+/+ mice.
34 d by splenomegaly, leukocytosis, and myeloid hypercellularity, which progressed to mortality by 6 to
35 nexplained feature of WHIM is myelokathexis (hypercellularity with apoptosis of mature myeloid cells
36 arenchyma (an endothelial-rich tissue) shows hypercellularity with thickened alveolar septa and an in
37 ged extramedullary hematopoiesis, and portal hypercellularity with thickening and fibrosis.
38 ucosa showed striking stromal and epithelial hypercellularity, with increased epithelial proliferatio
39 system, the Cav-2-null lung parenchyma shows hypercellularity, with thickened alveolar septa and an i
40 ts in a significant leukocytosis, leading to hypercellularity within the CNS, where monocytes/macroph

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