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1 mental MI can accelerate atherosclerosis via monocytosis.
2 00a8, or its cognate receptor Rage prevented monocytosis.
3 , with prefibrotic myelofibrosis or reactive monocytosis.
4 levels and subsequent hyperlipidemia-induced monocytosis.
5 am mice, neither diabetes nor MI resulted in monocytosis.
6 morphological features of myelodysplasia or monocytosis.
7 pment of severe anemia with macrocytosis and monocytosis.
8 ype mice with artificially induced Ly-6C(hi) monocytosis.
9 ral infections like Epstein-Barr virus cause monocytosis.
10 and in cDC1s, a mild neutrophilia and a mild monocytosis.
11 characterized by sustained peripheral blood monocytosis.
12 oietic hypocretin-receptor-null mice develop monocytosis and accelerated atherosclerosis, sleep-fragm
13 l monocytosis include clonal cytopenias with monocytosis and acute and chronic myeloid neoplasms.
15 cing panels that effectively identify clonal monocytosis and complement clinical prognostic scoring s
18 nant condition that presents with persistent monocytosis and is often associated with leukocytosis, l
20 oth CCL2 and CCL7 are required for efficient monocytosis and monocyte accumulation in the CNS, only C
21 rom two unrelated kindreds with intermittent monocytosis and mycobacterial disease, including bacillu
22 )/(-) mice fed a chow or Western- type diet, monocytosis and neutrophilia developed in association wi
24 KO) BM-transplanted Ldlr(-/-) mice displayed monocytosis and neutrophilia in the absence of hematopoi
25 ases in IL-23 and IL-17A and proinflammatory monocytosis and neutrophilia that precedes development o
27 ted with a blunting of hyperglycemia-induced monocytosis and reduced monocyte recruitment to the plaq
28 a mouse model of human JMML equally reduces monocytosis and splenomegaly; however, the combined trea
29 phage proinflammatory responses, Ly-6C(high) monocytosis, and atherosclerosis in the settings of hype
31 y via amelioration of hyperlipidemia-induced monocytosis, and can be augmented with a synthetic CXCR7
34 ow myeloid progenitor cell proliferation and monocytosis, as well as reduced atherosclerosis and a st
39 2 mediates highly selective peripheral blood monocytosis during WNV infection of mice and that this i
41 cells revealed an "inflammatory" peripheral monocytosis enriched for the expression of S100A family
43 Defined by a persistent peripheral blood monocytosis >/=1 x 10(9)/L and monocytes accounting for
45 e/monocyte inflammatory activation patterns (monocytosis, high-inflammatory gene expression, raised g
46 reatment-induced resolution of lymphopaenia, monocytosis, hypercytokinaemia, and hyperchemokinaemia.
49 which prompts the question as to whether the monocytosis in childhood obesity contributes to atheroge
50 aim of this study was to test whether blood monocytosis in mice with atherosclerosis affects infarct
51 ) mice induced a strong and highly selective monocytosis in peripheral blood that was absent in Ccr2(
52 nk4b(fl/fl)-LysMcre mice develop nonreactive monocytosis in the peripheral blood accompanied by incre
54 gies of kidney injury associated with clonal monocytosis include direct renal infiltration by monocyt
55 neoplasm characterized by myelodysplasia and monocytosis, including but not limited to, chronic myelo
59 asm (MPN) overlap disorders characterized by monocytosis, myelodysplasia, and a characteristic hypers
60 autonomously to control HSPC proliferation, monocytosis, neutrophilia, and monocyte accumulation in
61 oduction, glomerulonephritis, and the unique monocytosis of BXSB males, were severely reduced or abse
62 feeding prompted mobilization culminating in monocytosis of chronologically older and transcriptional
63 nistic etiologies of kidney injury as clonal monocytosis of renal significance and provide guidance o
64 th healthy donors and patients with reactive monocytosis or another hematologic malignancy, CMML pati
66 verse prognostic impact, whereas response of monocytosis proved to be a positive on-treatment paramet
67 ctional HDL levels in diabetic mice prevents monocytosis, reduces the quantity and inflammation of pl
70 ced frequencies of marginal zone B cells and monocytosis, renal disease, and premature morbidity.
71 atherosclerotic mice with chronic Ly-6C(hi) monocytosis results in impaired healing, underscoring th
73 that WNV infection induces a CCR2-dependent monocytosis that precedes monocyte migration into the CN
77 attributed in part to hyperglycemia-induced monocytosis, which increases monocyte entry into plaques