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1 hepatic cells with the characteristics of an acute phase protein.
2 iron homeostasis, in addition it acts as an acute phase protein.
3 egulation of inflammation and immunity by an acute-phase protein.
4 EIU), which suggests that PEDF is a negative acute-phase protein.
5 ed by hepatocytes with characteristics of an acute-phase protein.
6 regulated by proinflammatory cytokines as an acute-phase protein.
7 physiological regulator of angptl4, another acute-phase protein.
8 n-6 is also responsible for the synthesis of acute phase proteins.
9 nd type II (haptoglobin, alpha1-antitrypsin) acute phase proteins.
10 that this effect may limit the synthesis of acute phase proteins.
11 rs, proinflammatory cytokine production, and acute phase proteins.
12 d no significant effect on concentrations of acute phase proteins.
13 and induction of a characteristic pattern of acute phase proteins.
14 IGF-I/ BP-3 had no effect on type II acute phase proteins.
15 ctor alpha, followed by a decrease in type I acute phase proteins.
16 The complex had no effect on type II acute phase proteins.
17 amination were each associated with elevated acute phase proteins.
18 3 had no effect on interleukin 6 and type II acute phase proteins.
19 e production of IL-6 and the upregulation of acute phase proteins.
20 presence of numerous activated microglia and acute phase proteins.
21 In liver, they regulate the secretion of acute phase proteins.
22 any increase in proinflammatory cytokines or acute phase proteins.
23 ecules and chemokines, oxidative markers and acute phase proteins.
24 s responsible for induction of CRP and other acute phase proteins.
25 the down-regulation of many coagulation and acute-phase proteins.
26 ion correlated with the genomic induction of acute-phase proteins.
27 inol concentrations in the whole group using acute-phase proteins.
28 with none and those with one or more raised acute-phase proteins.
29 f a set of liver-specific proteins named the acute-phase proteins.
30 ear relation of ferritin concentrations with acute-phase proteins.
31 d IL-6 mRNA, which induces the production of acute-phase proteins.
32 he spleen, or cytokine-mediated induction of acute-phase proteins.
33 ositive and decreased expression of negative acute-phase proteins.
34 tenidap decreased plasma levels of IL-6 and acute-phase proteins.
35 hyl groups of N-glycans covalently linked to acute-phase proteins.
36 lutionarily conserved family of inflammatory acute-phase proteins.
37 d with a transient rise in interleukin-6 and acute-phase proteins.
38 onse genes, including those encoding several acute-phase proteins.
42 8 g/L), ferritin (3.7 micrograms/L), and the acute-phase protein alpha 1-antichymotrypsin (ACT; 0.06
43 and endotoxin core IgG antibody [EndoCAb]), acute-phase proteins (alpha-2 macroglobulin [alpha-2M],
46 relationships between concentrations of two acute-phase proteins, alpha 1-antichymotrypsin (ACT) and
47 okines-CCL2, CCL11, CXCL1, CXCL8 and CXCL10, acute phase proteins-alpha-2M, CRP, growth factors VEGF
48 entrations of plasma retinol and one or more acute-phase proteins (alpha1-acid-glycoprotein, alpha1-a
49 solution; the same ratio to Abeta of another acute phase protein, alpha1-antichymotrypsin, was not ac
50 to the serum concentration of one potential acute phase protein (alpha2 macroglobulin), and albumin
52 loid cells triggering the release of hepatic acute phase proteins and inducing extravascular manifest
54 jective was to examine the relations between acute phase proteins and plasma retinol concentrations i
55 chemokines, oxidation markers, apoptosis and acute phase proteins and the levels of CD68 positive mac
56 lso support the idea that soluble CD14 is an acute-phase protein and that hepatocytes could be a sour
57 Decreases in circulating plasma markers and acute-phase proteins and an increased baseline effector
58 talyze fluctuations in the concentrations of acute-phase proteins and certain micronutrient biomarker
59 infiltrating Ly6C(pos) macrophages expressed acute-phase proteins and exhibited an inflammatory profi
60 tion and accompanying increases in levels of acute-phase proteins and markers of inflammation and pro
62 red proteome, including increased amounts of acute-phase proteins and proteins involved in the comple
63 ese data show that GSTs and GCS are negative acute-phase proteins and that decreased GCS activity res
64 aken for serum hepatic constitutive protein, acute phase protein, and proinflammatory cytokine analys
65 n, alpha 1 acid glycoprotein and albumin, an acute phase protein, and subsequent risk of myocardial i
68 d levels of microbial translocation markers, acute-phase proteins, and inflammatory markers were all
71 C/EBPalpha) is required for the induction of acute phase protein (APP) genes in newborn mice in respo
72 tory reactions, interleukin 6 (IL-6) induces acute phase protein (APP) genes through the Janus kinase
78 ne parameters such as cytokines, chemokines, acute phase proteins (APPs), growth factors, microbial t
79 isk of ASD in relation to levels of neonatal acute phase proteins (APPs), key components of innate im
83 the increased or decreased pool sizes of the acute-phase proteins (APPs) during the metabolic respons
85 ies of apparently healthy persons by using 2 acute-phase proteins (APPs), C-reactive protein (CRP) an
87 t fevers, leukocytosis, anemia, and elevated acute phase proteins are linked to interleukin (IL)-1 ac
88 ction in edematous malnutrition implies that acute phase proteins are made with a corresponding deple
89 lammation such as inflammatory cytokines and acute-phase proteins are reliably elevated in a signific
90 ytokines, proteases, adhesion molecules, and acute phase proteins as participants in the generation o
91 by cytokines, which signal the synthesis of acute-phase proteins as well as changes in intermediary
92 anifestations of disease, including elevated acute-phase proteins, as well as the local consequences
93 y by measuring changes in plasma retinol and acute-phase proteins associated with subclinical infecti
100 m, longitudinal within-individual changes in acute phase proteins (C-reactive protein [CRP], alpha-1-
101 ed with IGF-I/BP-3, whereas levels of type I acute phase proteins (C-reactive protein, alpha1-acid gl
102 leukin-6 and tumor necrosis factor alpha) or acute-phase proteins (C-reactive protein and serum amylo
104 ssed interleukin 1beta-induced expression of acute phase proteins, C-reactive protein, and haptoglobi
105 correlated with plasma concentrations of the acute-phase protein, C-reactive protein (CRP), and the a
106 oclonal antibody immunoassay for the classic acute-phase protein, C-reactive protein (CRP), in serum.
108 -4, IL-7, IL-9; myeloid growth-factor: IL-5; acute phase protein: C-Reactive Protein (CRP); immune ce
109 higher levels of proinflammatory cytokines, acute phase proteins, chemokines and cellular adhesion m
110 significant changes in several cytokines and acute-phase proteins: Compared with baseline, levels of
112 ations as a biomarker for sleep restriction, acute phase protein concentrations and malaria infection
113 The study was a nonconcurrent analysis of acute phase protein concentrations and other data from a
115 t activation contributes to induction of the acute-phase proteins CRP and serum amyloid P-component (
116 ial expression of chemokines, cytokines, and acute-phase proteins, cytokeratin(+) epidermal cells upr
118 indicates that soluble CD14 in plasma is an acute-phase protein derived, among other sources, from l
119 with brief increase in body temperature and acute phase proteins during first infusion but no signs
120 abolites (e.g., propionate and isobutyrate), acute phase proteins (e.g., calprotectin and C-reactive
121 ells, elevated body temperatures and induced acute phase proteins, each indicative of infection, were
122 g and delivery of newly synthesized loads of acute-phase proteins, enhancing innate immunity and prev
123 y reduced levels of circulating and airspace acute-phase proteins, exhibited significantly elevated l
124 ck can significantly modulate the pattern of acute-phase protein expression and that fever may be an
127 tudies are needed to assess the potential of acute-phase proteins for inclusion in prediction models
128 rotein in hepatocytes resulting in a lack of acute phase protein gene induction in newborn C/EBPalpha
136 Recent evidence supports involvement of the acute phase protein haptoglobin in numerous events durin
138 ipheral measurement of circulating levels of acute phase proteins have focused attention on Clusterin
140 mation, including inflammatory cytokines and acute-phase proteins, have been found in depressed patie
141 n A deficiency in individuals with no raised acute-phase proteins (healthy group) were much the same
142 eripheral inflammatory markers including the acute phase protein high-sensitivity C-reactive protein
143 ver cells with characteristics resembling an acute-phase protein, human primary hepatocytes isolated
145 P component or C-reactive protein, the major acute phase protein in humans, caused a decrease in the
150 ME7 animals allow independent measurement of acute phase proteins in the brain and circulation, we ex
154 IL-1 receptor antagonist anakinra suppressed acute-phase proteins in a patient with FMF and amyloidos
156 ables, peak values of 15 cytokines, and nine acute-phase proteins in serum were evaluated as potentia
158 oteins that are homologous to C-reactive and acute-phase proteins in the immune system and have been
159 at shock response could affect expression of acute-phase proteins in the liver, the effects of a mode
165 to the endogenous Foxp3 locus, that IL-6, an acute phase protein induced during inflammation, complet
167 ther increases in cytokine production and in acute phase protein-inducing ability in both patient gro
168 ared with FMF reflects greater production of acute phase protein-inducing cytokines in the former pat
169 could be due to differences in production of acute phase protein-inducing mediators, we studied PBMC
170 S and other microbial translocation markers, acute-phase proteins, inflammatory markers, and proinfla
171 e-rich alpha-2 glycoprotein (LRG) is a novel acute phase protein involved in inflammation-associated
174 rillation of Serum Amyloid A (SAA) - a major acute phase protein - is believed to play a role in the
175 active protein (CRP), the prototypical human acute phase protein, is an independent risk predictor of
178 ly characterised patient cohort revealed the acute phase protein lactoferrin (Lf) as the key predicto
180 ortality, incidence of infection and sepsis, acute phase protein levels, and muscle fractional synthe
184 sclerosis since C-reactive protein (CRP), an acute-phase protein monitored as a marker of inflammator
187 n C-reactive protein (CRP), a homopentameric acute-phase protein of the innate immune system, and a s
189 e towards understanding how inflammation and acute phase proteins, particularly serum amyloid A and g
190 y pathways including marked increases in the acute phase proteins pentraxin-3 and chitinase-3-like-1.
193 ury, mortality, serum constitutive proteins, acute phase proteins, proinflammatory cytokines and insu
197 examined the association among elevations in acute phase proteins, reported illness, and hyporetinole
199 nergy, glucose, and lipid metabolism and the acute phase protein response; (3) the mechanisms by whic
200 ts is associated with induction of a hepatic acute-phase protein response and altered host energy and
201 higher in IL-6-/- mice (P < .05), while the acute-phase protein response was strongly attenuated (P
204 the chemokines CXCL1, CXCL2, and S100A8; the acute-phase protein SAA3; and the LPS binding protein CD
205 ember of the serpin family (SERPINA3), is an acute-phase protein secreted by hepatocytes in response
211 ing factor beta, inflammatory mediators, the acute phase protein serum amyloid P, vascular endothelia
215 e, all the six cytokines studied induced the acute-phase protein serum amyloid A when administered al
218 showed comparable rises in the levels of two acute-phase proteins (serum amyloid P and C3) at 24, 48,
219 rkedly potentiated circulating levels of the acute phase proteins, serum amyloid A and IL-6, and the
221 ly are sensed by an evolutionarily conserved acute-phase protein, serum amyloid A1 (SAA1), that promo
223 oned medium increased mRNA levels of various acute-phase proteins such as albumin, fibrinogen, transf
229 terleukin-6 (IL-6) is the major regulator of acute-phase protein synthesis and one of the most studie
233 sin (AAT) encoded by the SERPINA1 gene is an acute-phase protein synthesized in the liver and secrete
234 and C-reactive protein, which are two of the acute-phase proteins synthesized in response to infectio
235 ch less serum amyloid A and haptoglobin (two acute-phase proteins) than WT mice, there were no other
238 t secretory phospholipase A(2) (sPLA(2)), an acute phase protein that has been found in association w
243 d TNF-alpha followed by a decrease in type I acute phase proteins that was associated with a concomit
245 uman C-reactive protein (CRP), the classical acute-phase protein that binds to ligands exposed in dam
246 ata suggest that shrimp LGBP is an inducible acute-phase protein that may play a critical role in shr
250 ar weight components (e.g., lipoproteins and acute phase proteins) that are closely associated with g
251 P) is well characterized as one of the serum acute phase proteins, the levels of which increase drama
253 ultiple chemokines, cell adhesion molecules, acute-phase proteins, type I IL-1 receptor, and multiple
254 er is the primary site for the production of acute phase proteins, typically serum amyloid A1 (SAA1)
256 , hepatic mRNA of inflammatory cytokines and acute phase proteins was upregulated, and liver-infiltra
257 globulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all
260 ent, genes related to cellular effectors and acute-phase proteins were up-regulated, whereas genes la
262 plasma proteomics analyses we observed that acute phase proteins - which are usually involved in the
263 ciated lipocalin (NGAL) is a 25-kDa secreted acute phase protein, which is also up-regulated in multi