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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.
39                                        Thus, acute-phase protein A1AT is a physiological regulator of
40                                          The acute-phase protein A1AT is an inducer of hepcidin expre
41                            Expression of the acute phase protein alpha(2)-macroglobulin is induced in
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],
44                           The levels of five acute-phase proteins (alpha-2 macroglobulin, haptoglobin
45                We first examined whether the acute-phase protein, alpha-2 macroglobulin (A2M), a majo
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
51                                 Decreases in acute phase protein and proinflammatory cytokine synthes
52 loid cells triggering the release of hepatic acute phase proteins and inducing extravascular manifest
53 y responses, as evidenced by the presence of acute phase proteins and oxidative damage.
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
61 e spleen followed by increased production of acute-phase proteins and proinflammatory cytokines.
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
66         The relations among hyporetinolemia, acute phase proteins, and vitamin A status in children a
67  clusters: interleukins, adhesion molecules, acute-phase proteins, and chemokines.
68 d levels of microbial translocation markers, acute-phase proteins, and inflammatory markers were all
69                  These proteins included the acute-phase proteins apolipoprotein J, fibrinogen, hapto
70                      Nutritional surveys use acute phase protein (APP) biomarkers such as C-reactive
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
73  IL-1, and TNF-alpha) are potent inducers of acute phase proteins (APP).
74                         Whether the positive acute-phase protein (APP) response to infection is affec
75     Fibrinogen-beta (FBG-beta), an important acute-phase protein (APP), is generated by the liver as
76 wing injury or infection, the liver releases acute-phase proteins (APP).
77                                              Acute phase proteins (APPs) are associated with malaria-
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
80                                              Acute phase proteins (APPs), plasma proteins synthesized
81 cids resembles the amino acid composition of acute phase proteins (APPs).
82 in turn exacerbates OS and the expression of acute phase proteins (APPs).
83 the increased or decreased pool sizes of the acute-phase proteins (APPs) during the metabolic respons
84 acterized by increased circulating levels of acute-phase proteins (APPs) generated by the liver.
85 ies of apparently healthy persons by using 2 acute-phase proteins (APPs), C-reactive protein (CRP) an
86  and increased brain and serum cytokines and acute-phase proteins (APPs).
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
94      Moreover, these studies have shown that acute phase protein biosynthesis in enterocytes is regul
95 esis of these cytokines by leukocytes and of acute-phase proteins by HepG2 cells.
96                            Expression of the acute phase protein C-reactive protein (CRP) is tightly
97                        Here we show that the acute phase protein C-reactive protein (CRP), a ligand f
98                                  Because the acute-phase protein C-reactive protein (CRP) is highly u
99        LytA prevented binding of C1q and the acute-phase protein C-reactive protein to S. pneumoniae,
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
103                                          The acute phase protein, C-reactive protein (CRP), can incre
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.
107                                          The acute-phase proteins, C-reactive protein and serum amylo
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
111                                     Elevated acute phase protein concentrations and infectious diseas
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
114                          Many genes encoding acute phase proteins contain HNF-4alpha-binding sites in
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
117                                        Serum acute-phase proteins, cytokines, and insulin-like growth
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
125  a regulator of hepatocyte growth, and three acute phase protein family members.
126 atory process is facilitated by the negative acute-phase protein, fetuin.
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
129                    Northern blot analysis of acute-phase protein gene expression in neonatal mice tre
130                                          For acute phase protein genes, some were increased (TP53, JU
131 ntribute to the transcriptional induction of acute phase protein genes.
132       Unique for Dex was the upregulation of acute phase proteins (Gfap, Cp, Edn2) as well as Plexna2
133  glycan biomarker of N-acetyl side chains of acute-phase proteins (GlycA).
134                                    The human acute phase protein haptoglobin (Hp) protects the host f
135 major difference between Hpr and the soluble acute phase protein haptoglobin (Hp).
136  Recent evidence supports involvement of the acute phase protein haptoglobin in numerous events durin
137                               Fibrinogen, an acute phase protein, has been shown to interact with the
138 ipheral measurement of circulating levels of acute phase proteins have focused attention on Clusterin
139                                Elevations of acute-phase proteins have been associated with an increa
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
144                 C-reactive protein (CRP), an acute phase protein in humans and rabbits, is part of th
145 P component or C-reactive protein, the major acute phase protein in humans, caused a decrease in the
146          C-reactive protein (CRP), the major acute phase protein in humans, was purified free of endo
147         Serum amyloid P component, the major acute phase protein in mice, increased from 27 microg/ml
148 rgy between dysregulated T-cell function and acute phase proteins in acute coronary syndromes.
149 tudies have shown that there is synthesis of acute phase proteins in enterocytes.
150 ME7 animals allow independent measurement of acute phase proteins in the brain and circulation, we ex
151 f p19 resulted in constitutive expression of acute phase proteins in the liver.
152          Because CRP, the most commonly used acute-phase protein in clinical practice, is very stable
153           C-reactive protein (CRP) is not an acute-phase protein in mice, and therefore, mice are wid
154 IL-1 receptor antagonist anakinra suppressed acute-phase proteins in a patient with FMF and amyloidos
155 re accompanied by rises in concentrations of acute-phase proteins in plasma.
156 ables, peak values of 15 cytokines, and nine acute-phase proteins in serum were evaluated as potentia
157         Here, we posit that inflammatory and acute-phase proteins in the circulation increase after O
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
160                          The upregulation of acute-phase proteins in the retina of diabetic rats was
161                                              Acute-phase proteins increased with treatment at all dos
162                         Elevated circulating acute phase proteins indicate disease risk.
163                                              Acute phase proteins indicated no evidence of an inflamm
164                     Elevated serum levels of acute-phase proteins, indicating chronic subclinical inf
165 to the endogenous Foxp3 locus, that IL-6, an acute phase protein induced during inflammation, complet
166                  Serum amyloid A (SAA) is an acute-phase protein induced by a variety of inflammatory
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
172             Serum amyloid A (SAA) is a major acute phase protein involved in multiple physiological a
173                          A major activity of acute phase proteins is to limit the inflammatory respon
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
176           Here, we show that haptoglobin, an acute phase protein, is an initiator of this MyD88-depen
177                                YKL-40, a new acute-phase protein, is shown to be elevated in inflamma
178 ly characterised patient cohort revealed the acute phase protein lactoferrin (Lf) as the key predicto
179 kines CCL2, CXCL1 and IL-6 together with the acute phase protein Lcn2.
180 ortality, incidence of infection and sepsis, acute phase protein levels, and muscle fractional synthe
181                                              Acute-phase protein levels on HDL may serve as novel bio
182 ost significantly upregulated factors is the acute phase protein lipocalin-2 (LCN2).
183                                         This acute phase protein may have a role in the progression o
184 sclerosis since C-reactive protein (CRP), an acute-phase protein monitored as a marker of inflammator
185                          In response to LPS, acute phase protein mRNA induction are equivalent in typ
186         C-reactive protein (CRP) is a plasma acute-phase protein, normally not found in the brain.
187 n C-reactive protein (CRP), a homopentameric acute-phase protein of the innate immune system, and a s
188         More than half of these ligands were acute phase proteins or members of the complement or coa
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.
191               C-reactive protein (CRP) is an acute phase protein produced by hepatocytes.
192               C-reactive protein (CRP) is an acute-phase protein produced in high quantities by the l
193 ury, mortality, serum constitutive proteins, acute phase proteins, proinflammatory cytokines and insu
194                           Fetuin, a negative acute-phase protein, recently was implicated as an anti-
195         C1-esterase inhibitor, an endogenous acute-phase protein, regulates various inflammatory and
196 ing a major modification of the mechanism of acute-phase protein regulation at 40 degreesC.
197 examined the association among elevations in acute phase proteins, reported illness, and hyporetinole
198  also reduced the lipopolysaccharide-induced acute phase protein response (C-reactive protein).
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
202 d by fever, anorexia, behavioral withdrawal, acute-phase protein responses, and inflammation.
203                         We conclude that the acute phase protein SAA plays an important role in HDL c
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
206 ntified as a carboxy-terminal peptide of the acute phase protein serum amyloid A (SAA) 1.
207                                          The acute phase protein serum amyloid A (SAA) has been well
208         We have previously reported that the acute phase protein serum amyloid A (SAA) is a potent ch
209       Metabolic hormones, cytokines, and the acute phase protein serum amyloid a (SAA) were then meas
210 om the formation of amyloid fibrils from the acute phase protein serum amyloid A.
211 ing factor beta, inflammatory mediators, the acute phase protein serum amyloid P, vascular endothelia
212                                          The acute-phase protein serum amyloid A (A-SAA) was signific
213                                          The acute-phase protein serum amyloid A (SAA) is commonly co
214                                          The acute-phase protein serum amyloid A (SAA) is highly indu
215 e, all the six cytokines studied induced the acute-phase protein serum amyloid A when administered al
216                               The endogenous acute-phase protein serum amyloid P (SAP) was expressed
217             HDL particles were enriched with acute-phase proteins (serum amyloid A, haptoglobin, and
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
220 ure supernatants and increased levels of the acute-phase protein, serum amyloid A (SAA).
221 ly are sensed by an evolutionarily conserved acute-phase protein, serum amyloid A1 (SAA1), that promo
222              Levels of several cytokines and acute-phase proteins significantly changed after treatme
223 oned medium increased mRNA levels of various acute-phase proteins such as albumin, fibrinogen, transf
224                             In this context, acute-phase proteins such as Pentraxin-3 (PTX3) are rele
225  accompanied by a rapid rise in the blood of acute-phase proteins such as serum amyloid A (SAA).
226                                              Acute-phase proteins, such as C-reactive protein and alb
227               The detection of liver-derived acute-phase proteins suggests that BNB disruption facili
228 measuring cell proliferation or induction of acute phase protein synthesis.
229 terleukin-6 (IL-6) is the major regulator of acute-phase protein synthesis and one of the most studie
230 tuitary-adrenal axis and the potentiation of acute-phase protein synthesis.
231             Serum amyloid A (SAA) is a major acute-phase protein synthesized and secreted mainly by t
232                         Hemopexin (Hx) is an acute-phase protein synthesized by hepatocytes in respon
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
236               C-reactive protein (CRP) is an acute phase protein that binds phosphocholine residues o
237         Human C-reactive protein (CRP) is an acute phase protein that binds to receptors on human and
238 t secretory phospholipase A(2) (sPLA(2)), an acute phase protein that has been found in association w
239                        Serum amyloid A is an acute phase protein that is carried in the plasma largel
240                                   A1AT is an acute phase protein that is expressed and secreted from
241              Alpha-1 antitrypsin (AAT) is an acute phase protein that possesses immune-regulatory and
242                             Fibrinogen is an acute phase protein that will protect exposed cells from
243 d TNF-alpha followed by a decrease in type I acute phase proteins that was associated with a concomit
244               C-reactive protein (CRP) is an acute-phase protein that binds specifically to phosphory
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
247               C-reactive protein (CRP) is an acute-phase protein that plays an important defensive ro
248                               Pentraxins are acute-phase proteins that belong to a family of evolutio
249         WAT also secretes many cytokines and acute-phase proteins that contribute to insulin resistan
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
252                               rHGH decreased acute phase proteins, tumor necrosis factor-alpha, and I
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)
255        Analyses were performed on cytokines, acute-phase proteins, virus load, and CD4 cell counts.
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
258              Levels of 13 cytokines and nine acute-phase proteins were measured using a bead-based mu
259                                         Many acute-phase proteins were up-regulated early in murine c
260 ent, genes related to cellular effectors and acute-phase proteins were up-regulated, whereas genes la
261         Serum amyloid A (SAA) is a family of acute-phase proteins which are shown to correlate with c
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
264                                 Preoperative acute phase proteins (white cell count, C-reactive prote
265                  Serum amyloid A (SAA) is an acute phase protein whose expression is markedly up-regu
266                            Haptoglobin is an acute phase protein whose level increases severalfold du
267               C-reactive protein (CRP) is an acute phase protein whose levels are increased in many d
268                     Fibrinogen is one of the acute-phase proteins whose levels are elevated during pe
269                            Information about acute-phase proteins will enable plasma retinol concentr
270               C-reactive protein (CRP) is an acute-phase protein with a well-known association with i
271                     Ceruloplasmin (Cp) is an acute-phase protein with ferroxidase, amine oxidase, and
272               C-reactive protein (CRP) is an acute-phase protein with therapeutic activity in mouse m

 
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