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1 sic PFV was similar to the latter aside from hypercellularity.
2 rtic valve leaflet edema without evidence of hypercellularity.
3 early postnatal period, resulting in cardiac hypercellularity.
4 rescents and marked reductions in glomerular hypercellularity.
5 seudopalisading cells and cannot account for hypercellularity.
6 e only group to exhibit glomerular mesangial hypercellularity.
7 without (WHO Va) or with (WHO Vb) mesangial hypercellularity.
8 mild, with 2 showing segmental endocapillary hypercellularity, 1 focal glomerular microangiopathy, an
9 and more commonly associated with mesangial hypercellularity (30 vs. 5%), electron dense deposits (6
10 n of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secret
12 ctive glomerular inflammation, endocapillary hypercellularity and crescents, also have been found to
15 Ebf1-deficient hearts display myocardial hypercellularity and reduced cardiomyocyte size, ventric
17 f apoptosis has been postulated to cause the hypercellularity and thus excess scar-tissue formation o
18 p laminar cell loss, microgyri, white matter hypercellularity, and blurring of the white and gray mat
19 y: mesangial hypercellularity, endocapillary hypercellularity, and cellular/fibrocellular crescents.
20 nal to T(1) relaxation time, capturing early hypercellularity, and elevated astrocytic and ependymal
21 owed an increase in neutrophils, bone marrow hypercellularity, and enlarged lymph nodes and spleen.
22 s including anemia, neutropenia, bone marrow hypercellularity, and splenomegaly with myeloid infiltra
23 re clearly demarcated borders and tumor core hypercellularity as compared with controls, suggesting a
24 ified segmental sclerosis and extracapillary hypercellularity as novel, poor prognostic indicators of
25 mmation, mesangial [M] and endocapillary [E] hypercellularity as well as cellular or fibrocellular cr
26 y capillary collapse and visceral epithelial hypercellularity associated with nephrotic range protein
27 the 10 specimens contained extensive foci of hypercellularity composed predominantly of SMCs (mean+/-
28 , the hyaloid vascular system showed hyaloid hypercellularity consisting of aberrant vasculature, whi
29 IFNAR(-/-) mice, proteinuria and glomerular hypercellularity did not develop, whereas these features
30 tures of active glomerular injury: mesangial hypercellularity, endocapillary hypercellularity, and ce
31 te of eGFR loss, combined with the mesangial hypercellularity, endocapillary hypercellularity, segmen
32 roduction of mature blood cells, bone marrow hypercellularity, extramedullary hematopoiesis, a tenden
33 R 2.48, 95% CI 1.40-4.37) and extracapillary hypercellularity (HR 2.68, 95% CI 1.55-4.62) were identi
34 tokine, interleukin-1 (IL-1), contributes to hypercellularity in human and experimental proliferative
35 y tissue has epithelial hyperplasia, stromal hypercellularity, increased collagen, and increased oxid
36 so were the single components endocapillary hypercellularity, interstitial fibrosis/tubular atrophy,
37 ally obsolescent glomeruli or mild mesangial hypercellularity may be associated with greater difficul
38 rain tumors are classically characterized by hypercellularity of glioma and vascular endothelial cell
41 opoietic stem cell disorder characterized by hypercellularity of the bone marrow with an increase in
42 o tumors, inflammation, vascular disease, or hypercellularity of the cerebrospinal fluid or hematic c
44 ssive collagen I and elastin deposition, and hypercellularity of the mesenchyme occurred independentl
45 apse of glomerular capillaries, swelling and hypercellularity of the visceral epithelium, hyaline art
48 dified glomerulosclerosis and extracapillary hypercellularity predict diabetic ESRD in Chinese patien
49 he mesangial hypercellularity, endocapillary hypercellularity, segmental glomerulosclerosis, tubular
50 d classification mesangial and endocapillary hypercellularity, segmental sclerosis, interstitial fibr
51 luded segmental sclerosis and extracapillary hypercellularity (subdistribution HR, 2.04; 95% confiden
52 ncluding expanded capillary lumen, mesangial hypercellularity, synechiae formation, and podocyte loss
54 d by splenomegaly, leukocytosis, and myeloid hypercellularity, which progressed to mortality by 6 to
55 nexplained feature of WHIM is myelokathexis (hypercellularity with apoptosis of mature myeloid cells
56 arenchyma (an endothelial-rich tissue) shows hypercellularity with thickened alveolar septa and an in
58 ucosa showed striking stromal and epithelial hypercellularity, with increased epithelial proliferatio
59 system, the Cav-2-null lung parenchyma shows hypercellularity, with thickened alveolar septa and an i
60 ts in a significant leukocytosis, leading to hypercellularity within the CNS, where monocytes/macroph