ライフサイエンスコーパス: acute-phase response

1 under homeostasis conditions and during the acute phase response.

2 etabolic pathways, immune functions, and the acute phase response.

3 transport by HDL during inflammation and the acute phase response.

4 for HNF-4alpha in the control of the liver's acute phase response.

5 1beta (IL-1beta), a central activator of the acute phase response.

6 ubstantial component of the negative hepatic acute phase response.

7 V-1 infection, protein malnutrition, and the acute phase response.

8 gene expression that occurs in the negative acute phase response.

9 ut unexpectedly normal STAT3-dependent liver acute phase response.

10 vitamin C concentration was distorted by the acute phase response.

11 concentration >/=10 mg/L indicated an active acute phase response.

12 human liver, a primary organ involved in the acute phase response.

13 ntent in circulating lipoproteins during the acute phase response.

14 sult in centrally controlled symptoms of the acute phase response.

15 sis, in scavenging free radicals, and in the acute phase response.

16 and that there may also be a blunting of the acute phase response.

17 cklings, even in the absence of induction of acute phase response.

18 of human C-reactive protein (CRP) during the acute phase response.

19 ys associated with complement activation and acute phase response.

20 systemic physiology that is indicative of an acute-phase response.

21 aling, complement, coagulation, and negative acute-phase response.

22 ression of genes in liver associated with an acute-phase response.

23 actin cytoskeleton and cell signaling of the acute-phase response.

24 neration is sufficient to produce a systemic acute-phase response.

25 uces systemic inflammation with an exuberant acute-phase response.

26 IL-1 inhibition of IL-6 activity during the acute-phase response.

27 anges in serum components consistent with an acute-phase response.

28 oduced exclusively by hepatocytes during the acute-phase response.

29 the response to tissue injury-the so-called acute-phase response.

30 ent mice do not show evidence of a deficient acute-phase response.

31 romised mental status may reflect a cerebral acute-phase response.

32 measure of host cell activation and the host acute-phase response.

33 may be an important regulatory factor in the acute-phase response.

34 esis of complement components is part of the acute-phase response.

35 l patients may be partly attributable to the acute-phase response.

36 nse to trauma is associated with the hepatic acute-phase response.

37 is a multifunctional protein associated with acute-phase response.

38 or- and nontumor-bearing mice can produce an acute-phase response.

39 e of iron status, anemic status, and general acute-phase response.

40 tory properties and is a main inducer of the acute-phase response.

41 transcription factors involved in immune and acute phase responses.

42 ctors similar to those involved in mammalian acute phase responses.

43 lifying proinflammatory cytokine release and acute phase responses.

44 ute intercurrent complications causing major acute-phase responses.

45 splenic, hepatic, or brain inflammatory and acute-phase responses.

46 of interaction with the kappaB motif during acute-phase responses.

47 inhibitor, with levels that increase during acute-phase responses.

48 objective was to determine the prevalence of acute phase response activation in a representative samp

49 In conjunction with the acute-phase response, additional biological pathways are

50 The process of inflammation, also called the acute-phase response, additionally causes loss of muscle

51 ed in diverse cellular functions such as the acute phase response, adipocyte differentiation, learnin

52 Response to the burn injury during the acute phase response after burn is substantially differe

53 observed in the development of the systemic acute phase response after turpentine administration bet

54 er binding protein delta (C/EBPdelta) in the acute-phase response after bacterial infection.

55 iratory epithelial cells manifested a local "acute phase response" after stimulation with TLR activat

56 During the acute phase, responses against up to five peptides were

57 trajectories in inflammatory, metabolic, and acute phase responses allowing differentiation of nonsur

58 ate that systemic infections that produce an acute phase response also cause the plasma zinc concentr

59 Infectious diseases that induce the acute-phase response also impair the assessment of vitam

60 tudies have shown that the activation of the acute phase response alters zinc metabolism.

61 is primarily a response to inflammation (the acute phase response), although it is possible that inad

62 rum retinol decreases transiently during the acute phase response and can thus result in misclassific

63 Inflammation was an acute phase response and chronic inflammation, with litt

64 og[P-value] = 15 vs. 10, respectively) while acute phase response and complement system were affected

65 ription factor known to regulate the hepatic acute phase response and energy homeostasis under stress

66 iptional regulator implicated in the hepatic acute phase response and in adipogenic and myeloid cell

67 cardial infarction induces activation of the acute phase response and infiltration of leukocytes to t

68 Hamp is part of the type II acute phase response and is thought to have a crucial re

69 netic risk factors, its association with the acute phase response and its age of onset and female pre

70 Suppression of the acute phase response and normalization of SAA levels are

71 NF-alpha) is one of the key cytokines of the acute phase response and of many inflammatory processes.

72 ls, 12 proteins some of which participate in acute phase response and platelet activation (APMAP [adi

73 n A status under all conditions, because the acute phase response and protein malnutrition depress RB

74 hepatocytes is important for control of the acute phase response and regulation of liver regeneratio

75 revealed that inflammatory mediators of the acute phase response and the complement cascade were hig

76 vert DIC because the fibrinogen underwent an acute phase response and the platelet count fell and rem

77 Genes associated with the acute phase response and with type I IFN responses were

78 e key regulators of immune, inflammatory and acute phase responses and are also implicated in the con

79 The expression of many acute phase-response and inflammatory markers, including

80 l death, temporally linked with a strong IFN acute-phase response and evidence of gut barrier breakdo

81 are induced minimally, if at all, during the acute-phase response and have only been found in human a

82 ription factor known to regulate the hepatic acute-phase response and lipid homeostasis.

83 ein (C/EBP)-binding elements in the systemic acute-phase response and lung development and the expres

84 ese genes comprise coexpression networks for acute-phase response and pro-inflammatory processes.

85 ing chemokines and molecules involved in the acute-phase response and the antigen-processing and anti

86 availability for bacterial growth during the acute-phase response and the consequences of iron overlo

87 ased expression of genes associated with the acute-phase response and the protein ubiquitination path

88 sceptible to injury, expresses markers of an acute phase response, and displays increased proliferati

89 f genes related to immune cell function, the acute phase response, and glucose metabolism, suggesting

90 g subgroups with HIV-1 infection, a positive acute phase response, and protein malnutrition.

91 ion regulates the unfolded protein response, acute-phase response, and DDR in hepatocytes.

92 site of involvement, serologic abnormality, acute-phase response, and duration of symptoms in the in

93 pression of genes related to retinal stress, acute-phase response, and gliosis, suggesting that IGF-I

94 ent endoplasmic reticulum stress, defects in acute-phase response, and increased hepatocellular damag

95 We analyzed graft function, the acute-phase response, and oxidative stress in the pancre

96 tress and required to activate expression of acute phase response (APR) genes.

97 Lipopolysacharide (LPS) induced acute phase response (APR) in mouse liver leads to eleva

98 The acute phase response (APR) is associated with decreased

99 observed in non-proliferating livers during acute phase response (APR).

100 anscription factor that mediates the hepatic acute phase response (APR).

101 ing liver-specific gene expression during an acute phase response (APR).

102 d in infected and/or injured mice during the acute phase response (APR).

103 kin 1beta and 6 (IL-1beta, IL-6) mediate the acute phase response (APR).

104 delta) has been implicated as a regulator of acute-phase response (APR) genes in hepatocytes.

105 is factor-alpha repressed FBG-beta and other acute-phase response (APR) genes.

106 The acute-phase response (APR) is regulated by TNF-alpha, IL

107 cytoplasmic transcription factors mediating acute-phase response (APR) of the human angiotensinogen

108 The acute-phase response (APR) represents a systemic reactio

109 actors play important roles in mediating the acute-phase response (APR), an inflammatory process resu

110 The acute-phase response (APR), the primary mechanism used b

111 The hepatic acute-phase response (APR), which is largely dependent o

112 Brain injury elicits a systemic acute-phase response (APR), which is responsible for co-

113 a transient deviation from homeostasis, the acute-phase response (APR).

114 it systemic inflammation and induce a robust acute-phase response (APR).

115 sure to inescapable tail shock (IS) activate acute phase responses (APRs) that include increases in c

116 ion, suggesting that monocyte activation and acute phase responses are consequences of T-cell activat

117 Two characteristic elements of the acute-phase response are an altered pattern of circulati

118 d to phagocytosis and signaling (IL-6, IL-8, acute phase response) are upregulated in 5xFAD;CD33(-/-)

119 ne disease often present with a debilitating acute phase response as a result of Vgamma9Vdelta2 T cel

120 Lipopolysaccharide caused the expected acute-phase response as judged by the increased expressi

121 ut its effect is adversely influenced by the acute-phase response, as reflected by an elevated CRP le

122 ia, defective B cell memory, and an impaired acute-phase response, as well as skeletal abnormalities

123 The acute-phase response at exacerbation was most strongly r

124 Lipopolysaccharide (LPS), an inducer of the acute phase response, augmented hepatocyte replication i

125 ctivated by natural IgM or components of the acute-phase response bound to bacterial pathogens.

126 r is critical for cytokine signaling and the acute phase response, but its role in allergic asthma is

127 The results show activation of the hepatic acute phase response by 2 hours after TBI, hepatic infla

128 a(des)Arg may provide a control mechanism of acute-phase responses by enhancing IL-6 synthesis in adh

129 The acute-phase response can result in decreased liver-speci

130 Acute phase responses, cellular responses to lipopolysac

131 itis, sensorineural deafness, and an intense acute-phase response characteristic of MWS.

132 fter sepsis had a range of functions such as acute phase response, coagulation, endoplasmic reticulum

133 transcripts associated with inflammatory and acute-phase responses, coagulative activities, and trans

134 er upregulation of interferon signalling and acute phase responses compared to survivors during the a

135 erleukin (IL)-6, in addition to inducing the acute-phase response, contributes to insulin resistance.

136 Severe hypocalcemia and elevated acute-phase response developed in ob/ob mice.

137 Moreover, the acute-phase response diminished significantly with treat

138 ic phenotype of endothelium but also trigger acute phase responses during activation of coagulation i

139 eukin-6 (IL-6) is a critical mediator of the acute-phase response during infections and injuries.

140 Proteins that are part of the acute phase response (e.g. fibrinogen, C-reactive protei

141 the non-specific stressful components of the acute-phase response (e.g. fever, loss of appetite, iron

142 ssion associated with the cytokine-inducible acute-phase response (e.g., SAA1 and CRP) are diminished

143 1 sites at -113 to -107 and -152 to -140, an acute phase response element (APRE (SIE)) at -171 to -16

144 demonstrate specific binding of Stat3 to the acute phase response element in the C/EBPdelta promoter

145 resented with recurrent infections, abnormal acute-phase responses, elevated IgE, eczema, and eosinop

146 alylation of circulatory IgG accompanies the acute phase response elicited by turpentine exposure or

147 al systemic inflammatory biomarkers, but the acute-phase response, enterocyte turnover, monocyte acti

148 high density lipoprotein cholesterol mark an acute phase response even during minor illness.

149 proteins (MxA and p56), complement products, acute-phase response factors, and the STAT and IRF trans

150 r IL-1 effects on another centrally mediated acute phase response (fever) or the anorexia produced by

151 A pronounced activation of the acute-phase response, found to be associated with islet

152 Our recent microarray studies identified an acute phase response gene, 24p3/lipocalin 2, as a novel

153 a1-acid glycoprotein (AGP) promoter, a liver acute-phase response gene, requires receptor-DNA binding

154 a14, involved in fatty acid omega-oxidation, acute phase response genes, and epidermal growth factor

155 STAT3, a transcription factor for acute phase response genes, was found to act as an adapt

156 ne receptor genes, complement components and acute phase response genes.

157 flammation-related liver transcripts, mostly acute phase response genes.

158 hepatic injury or stress, gluconeogenic and acute-phase response genes are rapidly upregulated to re

159 embers important in hormonal homeostasis and acute-phase response genes important in inflammatory res

160 ation was induced in male rats, two positive acute-phase response genes, alpha1-acid glycoprotein and

161 roliferation, apoptosis, or the induction of acute-phase response genes.

162 The acute phase response has been suggested to be a contribu

163 Fever, a nonspecific acute-phase response, has been associated with improved

164 marker of inflammation and a hallmark of the acute-phase response, has been shown to be a powerful an

165 and determine whether persons with an active acute phase response have lower serum retinol concentrat

166 Additionally, we show that platelet-driven acute-phase responses have a major role in protecting mi

167 lating levels of 43 proteins involved in the acute-phase response, hepatic signaling, the complement

168 iological ER stress-induced inflammatory and acute phase response in adipocytes, leading to lower cir

169 We demonstrate that the lack of acute phase response in C/EBPalpha knock-out mice is bec

170 he IL1B regulator induces a highly conserved acute phase response in each organ assessed for all of b

171 Utilizing a cytokine induced acute phase response in HepG2 cells, we investigated the

172 irculating Lp-PLA(2) did not increase during acute phase response in humans, whereas inflammatory mac

173 tocytes with IL-6, the major mediator of the acute phase response in liver, and characterized acute p

174 lood cells, a process that is similar to the acute phase response in mammals.

175 examine the effects of exogenous rHGH on the acute phase response in pediatric bum patients.

176 r necrosis factor (TNF) is a mediator of the acute phase response in the liver and can initiate proli

177 Current data support a model for the acute phase response in which serum amyloid A and sPLA2-

178 Acute phase responses in immunocompetent donors appear t

179 verity, and progression on components of the acute-phase response in an urban minority population.

180 esponse in immune cells) participates in the acute-phase response in hepatocytes is not known.

181 oprotein, induced at the early stages of the acute-phase response in liver and plasma.

182 le, whereas activin A curbed the IL6-induced acute-phase response in liver.

183 insulin requirement, or an activation of the acute-phase response in older individuals with type 2 di

184 examines the effects of exogenous HGF on the acute-phase response in thermally injured rats.

185 the brain; however, induction of a systemic acute-phase response in transgenic mice enhanced amyloid

186 factor (HGF) has been shown to modulate the acute-phase response in vitro.

187 hese findings suggest that HGF modulates the acute-phase response in vivo after burn and causes chang

188 is available about the development of innate acute-phase responses in Lyme disease.

189 ia and body weight with SAP, a marker of the acute-phase response, in hyperlipidemic apoE(-/-) mice a

190 nes, including CXCL16, and regulators of the acute-phase response, including interleukin-1alpha (IL-1

191 Moreover, this interruption of the acute phase response increased mortality and exacerbated

192 ly attenuated the type I and type II hepatic acute phase response, increased serum levels of constitu

193 r hormone receptors are repressed during the acute phase response induced by lipopolysaccharide (LPS)

194 n of a heat-shock response after exposure to acute-phase response inducers (cytokines and LPS) may re

195 T3 target genes that are associated with the acute-phase response, inflammation, and wound healing.

196 ional rate of a variety of genes involved in acute-phase response, inflammation, lymphocytic activati

197 During an acute phase response, interleukin-6 (IL-6) and glucocort

198 The acute-phase response involves molecules including tumor

199 The hepatic acute phase response is a cascade of events initiated to

200 The hepatic acute phase response is a cascade of events initiated to

201 ost bacteria and hypoferremia induced by the acute phase response is a key element of innate immunity

202 The acute phase response is an evolutionarily conserved reac

203 The acute phase response is an evolutionarily conserved resp

204 The acute phase response is associated with changes in the h

205 iver regeneration, its effect on the hepatic acute phase response is not known.

206 As the acute phase response is stimulated by diverse cytokines

207 that transcriptional activity not linked to acute phase responses is an important determinant of out

208 An elevated acute-phase response is associated with increased radiol

209 The acute-phase response is characteristic of perhaps all in

210 The acute-phase response is characterized by increased circu

211 ionships between biomarkers suggest that the acute-phase response is related, separately, to monocyti

212 BRINDA investigators found that the acute-phase response is so prevalent that it must be ass

213 Thus, a significant component of the hepatic acute-phase response is the release of chemokines by the

214 gest that a major function of CRP during the acute-phase response is to limit tissue damage and modul

215 rate (ESR), a commonly performed test of the acute phase response, is the rate at which erythrocytes

216 SAF-1 transgenic mice exhibited a prolonged acute phase response, leading to an extended period of S

217 es that cause hypermetabolism/catabolism via acute phase response, leading to increased morbidity and

218 GAD65 and IA-2 autoantibodies along with the acute-phase response markers fibrinogen and C-reactive p

219 CRP values present the possibility that the acute-phase response may link these 2 disease processes.

220 y analysis suggests that cerebral immune and acute-phase response may play a role in mediating PaO2 o

221 and STAT3, but neither alone, abrogated all acute phase responses measured.

222 set of genes implicated in proteostasis, the acute-phase response, metabolism, and the DNA damage res

223 this cytokine as a possible mediator of the acute-phase response mounted by Muller cells in diabetes

224 dentify a novel function of STAT3 during the acute-phase response, namely, the induction of secretory

225 roximal pain, morning stiffness <30 minutes, acute-phase response not elevated), relapses, QOL as mea

226 The acute phase response of AAT (alpha-1 antitrypsin) to COV

227 cently reported in this journal to induce an acute phase response of serum amyloid A protein (SAA) an

228 This study identifies a strong acute phase response of the kidney that is characterized

229 NF4alpha in having a role in controlling the acute phase response of the liver induced by ER stress b

230 tor of transcription 3 (STAT3) as part of an acute-phase response of infection.

231 The acute-phase response of Muller cells in diabetes was ass

232 acterize the effects of inflammation and the acute-phase response on nutrient biomarkers.

233 drug-metabolizing enzymes, the effect of the acute-phase response on the expression of glutathione S-

234 resent because of confounding effects of the acute-phase response on the interpretation of most iron

235 lly, the up-regulated genes were enriched in acute phase response (P < 0.01), pyruvate metabolic proc

236 implicated in nuclear receptor activations, acute phase response pathway, glutaryl-CoA/tryptophan de

237 bial defense, tissue healing and remodeling, acute phase response, pattern recognition, protease/anti

238 he aim of this study was to determine if the acute phase response post burn injury is significantly d

239 ur study indicates that haptoglobin (Hp), an acute-phase response protein primarily synthesized in th

240 Serum amyloid P-component (SAP), an acute-phase response protein with 60% to 70% sequence ho

241 ne encoding the interleukin-6 (IL-6)-induced acute-phase response protein, alpha(2)-macroglobulin.

242 regulation in the concentration of specific acute phase response proteins at the time of bone marrow

243 more, circulating TNFalpha and expression of acute phase response proteins CRP and SAP were significa

244 The high-levels and representation of acute phase response proteins suggests a functional role

245 ng those encoding cytokines, growth factors, acute phase response proteins, cell adhesion molecules,

246 These included transcripts encoding acute phase response proteins, IER2 and JUNB, and regula

247 ng those encoding cytokines, growth factors, acute phase response proteins, immunoreceptors, other tr

248 bH(-/-) mice displayed reduced expression of acute phase response proteins.

249 n diabetes characterized by the induction of acute-phase response proteins and other inflammation-rel

250 We found that the acute-phase response proteins serum amyloid A (SAA) 1 an

251 Many acute-phase response proteins were also detected, suppor

252 RP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in the context of the var

253 8% of the differentially expressed genes) of acute-phase response proteins: alpha2-macroglobulin, cer

254 ne defense, the net biological effect of the acute phase response remains unknown.

255 It is unclear whether the reported systemic acute-phase response represents a systemic inflammatory

256 ed serum amyloid A content in HDL during the acute phase response result from reciprocal and coordina

257 charide (LPS), an endotoxin that induces the acute-phase response, results in a marked decrease in th

258 In the acute-phase response SAA is synthesized by the liver and

259 o its production by the liver as part of the acute phase response, SAA is also expressed by several p

260 ics, clinical outcomes, and inflammatory and acute-phase responses (serum cytokines, hormones, and pr

261 After adjusting for the acute-phase response, serum ferritin and RBP concentrati

262 ession through Janus kinase 2 (JAK2) and the acute phase response signal transducer and activator of

263 y and repair such as coagulation/thrombosis, acute phase response signaling and complement activation

264 al antiviral factors and pathways (including acute-phase response signaling and complement system) we

265 Proteins involved in the acute-phase response signaling pathway, the complement p

266 ys were identified among these proteins: the acute-phase response signaling pathway, the complement p

267 an association between calcification events, acute-phase response signaling, and coagulation and gluc

268 ing enzymes known to be decreased during the acute-phase response, some phase II enzymes involved in

269 -type females, the duration of the human CRP acute phase response that accompanies the inductive phas

270 s during septic shock and for STAT3-mediated acute phase responses that promote survival during septi

271 During acute-phase responses, the CL-L1 levels display only min

272 The acute-phase responses then were compared in the two grou

273 tations did not show altered kinetics of the acute phase response to administered ligand.

274 The acute phase response to infection and inflammation induc

275 reactive protein (CRP) is a component of the acute phase response to infection, inflammation, and tra

276 omponent of the innate immune system and the acute phase response to infection.

277 roles in the production of a fever during an acute phase response to infection.

278 STAT3 regulates the acute phase response to innate immune stimuli such as li

279 merged as the hormone that links the type II acute phase response to iron handling and erythropoiesis

280 Initially, NTIS is a consequence of the acute phase response to systemic illness and macronutrie

281 nt mice, IL-1RI-deficient mice had a reduced acute phase response to turpentine.

282 and have a central role in initiation of the acute-phase response to blood-stage infection.

283 During the acute-phase response to infection and inflammation, cyto

284 as a result of iron sequestration during the acute-phase response to infection, and the severity of d

285 nsible for hypozincemia that accompanies the acute-phase response to inflammation and infection.

286 factor Relish performs a central role in the acute-phase response to microbial challenge by activatin

287 arly hypoferremia suggested a dose-dependent acute-phase response to the vector.

288 ent the induction of normally immunodominant acute-phase responses to both epitopes.

289 Notably, hypoxia increased expression of the acute phase response transcription factor C/EBPdelta whi

290 may be a factor in induction of an excessive acute-phase response triggered by T cell activation.

291 provides an additional means to modulate the acute-phase response upon stimulation with inflammatory

292 d to neurological disease, oxidative-stress, acute-phase response, vitamin/mineral metabolism and ske

293 n SAA, in concentrations resembling a modest acute phase response, was added to platelet-poor plasma

294 cause RBP concentrations decrease during the acute-phase response.We aimed to assess the relation bet

295 Protein malnutrition and a positive acute phase response were common, especially among HIV-1

296 pe controls, either at baseline or during an acute phase response when the demand for sialylation is

297 une function, inflammatory processes and the acute phase response, which are an orchestrated attempt

298 t increase HNF-4 alpha protein levels in the acute-phase response, which could result in increased li

299 n systemic immunity, they are central in the acute-phase response, which floods the circulation with

300 e liver and the subsequent activation of the acute phase response, whose functional role includes com