ライフサイエンスコーパス: SAA

1 SAA added to POBs inhibited PTH-stimulated cAMP response

2 SAA also binds to fibrinogen, as determined with a fluor

3 SAA has been detected within atherosclerotic lesions and

4 SAA increases simultaneously with secretory phospholipas

5 SAA induced inflammatory cytokines and an M1 phenotype i

6 SAA induced the expression of NLRP3, which mediated IL-1

7 SAA instillation into the lungs elicits robust TLR2-, My

8 SAA intake was lower in RTRs compared with controls and

9 SAA is a protein precursor of reactive AA amyloidosis, t

10 SAA is normally associated with the high-density lipopro

11 SAA mRNA expression was positively associated with tissu

12 SAA predominately promoted expression of the TH17 polari

13 SAA promotes expression of IL-17A in gammadelta T cells

14 SAA proteins stimulated the transcription of RANTES (reg

15 SAA solubilized phospholipid bilayers to form lipoprotei

16 SAA supplementation, mTORC1 activation, or chemical/gene

17 SAA was rapidly incorporated into amyloid, acutely reduc

18 SAA was recently shown to be controlled by a rapid syste

19 SAA-enriched HDL colocalized with cell surface-associate

20 SAA-induced inflammation was markedly reduced by a neutr

21 SAAs also offer reduced susceptibility to CO poisoning,

22 SAAs have been shown to catalyze a range of industrially

23 r exhibited increased fecal interleukin 17A, SAA, and SFB levels.

24 The atomic ratio Pt:Cu = 1:125 yielded a SAA which exhibited excellent CO tolerance in H2 activat

25 The fibrillation of Serum Amyloid A (SAA) - a major acute phase protein - is believed to play

26 Serum amyloid A (SAA) 1 and 2 are produced predominantly by the liver and

27 ute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional targets of S100A4 vi

28 of the acute phase protein serum amyloid A (SAA) 1.

29 y C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analysed as inflammatory

30 -associated genes Fizz1 and serum amyloid A (SAA) are significantly up-regulated in M2 macrophages st

31 Here, we identify serum amyloid A (SAA) as a candidate mediator of GC refractory inflammati

32 leads to overproduction of serum amyloid A (SAA) by the liver.

33 Since serum amyloid A (SAA) concentrations in HDL increase with inflammation, w

34 ccharide (LPS) and purified serum amyloid A (SAA) effectively induced the expression and extracellula

35 The fibrillar deposition of serum amyloid A (SAA) has been linked to the disease amyloid A (AA) amylo

36 The acute phase protein serum amyloid A (SAA) has been well characterized as an indicator of infl

37 Serum amyloid A (SAA) is a DAMP that is involved in the development of va

38 Serum amyloid A (SAA) is a family of acute-phase proteins which are shown

39 Serum amyloid A (SAA) is a plasma protein that transports lipids during i

40 Serum amyloid A (SAA) is an acute-phase plasma protein that functions in

41 Serum amyloid A (SAA) is an evolutionally conserved enigmatic biomarker o

42 Serum amyloid A (SAA) is best known for being the main component of amylo

43 Serum amyloid A (SAA) is expressed locally in chronic inflammatory condit

44 The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wh

45 ced histological damage and serum amyloid A (SAA) levels in IL-10(-/-) colitis mice, was efficacious

46 related to high circulating serum amyloid A (SAA) levels, which are linked with inflammation and oxid

47 Serum amyloid A (SAA) promotes neutrophilic inflammation by its interacti

48 Serum amyloid A (SAA) proteins are acute-phase reactant associated with h

49 Serum amyloid A (SAA) proteins are strongly induced in the liver by syste

50 Serum amyloid A (SAA) proteins are strongly induced in the liver by syste

51 n A-dependent expression of serum amyloid A (SAA) proteins by binding directly to Saa promoters.

52 Serum amyloid A (SAA) represents an evolutionarily conserved family of in

53 tion between fibrinogen and serum amyloid A (SAA), a highly fibrillogenic protein that is one of the

54 SP-B), apolipoprotein C-II, serum amyloid A (SAA), and alpha-1-microglobulin/bikunin precursor.

55 g C-reactive protein (CRP), serum amyloid A (SAA), and S100 calcium-binding protein A12 (S100A12).

56 h neonatal sepsis including Serum Amyloid A (SAA), C - reactive protein (CRP), Procalcitonin (PCT) an

57 , C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1 (sICAM-1) and va

58 -reactive protein (hs-CRP), serum amyloid A (SAA), interleukin-6 (IL-6), leukocyte, and neutrophil le

59 Concentrations of HDL-bound serum amyloid A (SAA), lipopolysaccharide binding protein (LBP), apolipop

60 SFB cause an increase in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on

61 -reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in th

62 ury score (HIS), and plasma serum amyloid A (SAA).

63 of the acute-phase reactant serum amyloid A (SAA).

64 ], haptoglobin, and serum amyloid protein A [SAA]), inflammatory markers (matrix metalloproteinase 1

65 A-SAA in blood correlated with total leukocytes, macrophag

66 A-SAA mRNA and protein were increased in the liver.

67 The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reac

68 Serum amyloid A (A-SAA/Saa3) was shown before to affect osteoblastic metabo

69 Finally, A-SAA protein, but not mRNA, was increased in the CNS 24 h

70 We found that both isoforms of A-SAA completely crossed the intact blood-brain barrier, a

71 ammation in our O3 exposure model and that A-SAA could be an important systemic signal of O3 exposure

72 Our findings suggest that A-SAA is functionally linked to pulmonary inflammation in

73 signaling and systemic acquired acclimation (SAA) are essential for plant survival during episodes of

74 Systemic acquired acclimation (SAA) is a key biological process essential for plant sur

75 Systemic acquired acclimation (SAA) plays a key role in optimizing growth and preventin

76 on and distal systemic acquired acclimation (SAA).

77 tress (termed systemic acquired acclimation [SAA]).

78 We show that hepatic sulfur amino acid (SAA) metabolism is under transcriptional control of HNF4

79 resistance, we found that sulfur amino acid (SAA) restriction increased expression of the transsulfur

80 mounts of acid-producing sulfur amino acids (SAA) and examined how this adaption requires the RhCG am

81 nd product of sulfur-containing amino acids (SAAs), contributes to metabolic acid load and may advers

82 The etiology of acquired SAA is not understood but is likely related to abnormal

83 To determine its direct actions, SAA was administered into murine lung, leading to induct

84 nosensitive single-unit afferent activities (SAAs) in rats with a bladder outlet obstruction (BOO) an

85 tients with COPD and in vivo using an airway SAA challenge model in BALB/c mice.

86 Unlike albumin, SAA effectively removed free fatty acids under acidic co

87 entity among different SAA isoforms, not all SAA proteins are pathogenic.

88 e we demonstrate that the single-atom alloy (SAA) strategy applied to Pt reduces the binding strength

89 Single-atom alloys (SAAs) play an increasingly significant role in the field

90 Although SAA is thought to play a key role in plant survival duri

91 inus of SAA, which is highly conserved among SAA sequences in all vertebrates, might play important s

92 s rarely involves the heart, but amyloidotic SAA transgenic mice consistently had minor cardiac amylo

93 lantation (HSCT) in severe aplastic anaemia (SAA) have improved steadily over the past decades, large

94 In WB scanning electron microscopy analysis, SAA mediated red blood cell (RBC) agglutination, platele

95 ular inflammation (CRP, ICAM-1, VCAM-1), and SAA (all P < .001).

96 Circulating concentrations of CRP and SAA in patients with a range of early to late objective

97 e findings indicate that circulating CRP and SAA levels are highest when the concentration of spiroch

98 CRP and SAA levels were significantly elevated in early localize

99 ch were accompanied by reductions in CRP and SAA, continued over the treatment duration.

100 radiation-induced cytokines EPO, G-CSF, and SAA in the plasma.

101 c stress-response transcript expression, and SAA to a local treatment of light stress.

102 ignaling in mediating systemic responses and SAA during light stress in Arabidopsis (Arabidopsis thal

103 hermore, coordinate expression of S100A4 and SAA in tumor samples from colorectal carcinoma patients

104 function of MYB30 in systemic signaling and SAA is unknown.

105 light stress-induced systemic signaling and SAA.

106 transplantation for severe aplastic anemia (SAA) has improved, with survival rates now approximately

107 Survival in severe aplastic anemia (SAA) has markedly improved in the past 4 decades because

108 Severe aplastic anemia (SAA) is a rare disorder characterized by hypoplastic bon

109 Acquired severe aplastic anemia (SAA) is a rare hematologic disease associated with signi

110 irst-line therapy of severe aplastic anemia (SAA) with high-dose cyclophosphamide causes toxicity and

111 ing hematopoiesis in severe aplastic anemia (SAA).

112 in HSCT for acquired severe aplastic anemia (SAA).

113 Although splenic artery aneurysms (SAAs) are common, their giant forms (more than 10 cm in

114 proved small-angle scattering approximation (SAA) to radiative transfer for sub-diffusive light refle

115 yloid A1 and A2 (referred to collectively as SAA).

116 "Surface-associated astrocytes" (SAAs) in posterior piriform cortex (PPC) are unique by v

117 We then review all available SAA literature on a per reaction basis before concluding

118 The relationship between SAA and neutrophils was investigated in lung sections fr

119 alizing antibody to IL-17A was used to block SAA responses in vivo, and a cell-sorting strategy was u

120 During acute exacerbation, peripheral blood SAA levels increased dramatically and were disproportion

121 e SAAs of Adelta-fibers were attenuated, but SAAs of both Adelta- and C-fibers were intermittently en

122 Cellular sources of IL-17A induced by SAA include CD4(+) T cells, gammadelta T cells, and an E

123 the molecular basis for retinol transport by SAA proteins during infection.

124 ing HGA, body mass index, total cholesterol, SAA, and chitotriosidase.

125 static disease show increases in circulating SAA.

126 Most circulating SAA is protected from proteolysis and misfolding by bind

127 d into amyloid, acutely reducing circulating SAA concentrations by up to 90%.

128 deposition is determined by the circulating SAA concentration.

129 Consequently, SAA and sPLA(2) can act synergistically to remove cellul

130 In contrast, SAAs of C-fibers were not significantly different betwee

131 peared-because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 responses to the sunflower oil

132 oss reduced inflammatory biomarkers (hs-CRP, SAA, and IL-6) compared with controls.

133 Immunohistochemistry detected SAA was in close proximity to airway epithelium, and in

134 e the high sequence identity among different SAA isoforms, not all SAA proteins are pathogenic.

135 This study reports that HS dissociates SAA from HDLs isolated from inflamed mouse plasma.

136 n of Jmjd3 H3K27 demethylase activity during SAA treatment or blockade of granulocyte-macrophage colo

137 ome acclimated to a particular stress during SAA involves thousands of transcripts that display a rap

138 To be effective, SAA has to occur at a rapid rate and depend on rapid sig

139 flammation, we investigated whether elevated SAA is a causal factor in HDL dysfunction.

140 which secreted IL-22 that induced epithelial SAA production in a Stat3-dependent manner.

141 To explore SAA solution conformations and lipid-binding mechanism,

142 Extrahepatic SAA was detected locally in COPD bronchoalveolar lavage

143 Diet was assessed for SAA content and various risk factors were measured.

144 use of an alemtuzumab-based HSCT regimen for SAA results in durable engraftment with a low incidence

145 nor (MSD) HSCT remains the gold standard for SAA patients younger than 40-50 years, with HLA-matched

146 ithout binding to HDL, thus identifying free SAA as the predominant retinol-binding form in vivo.

147 Furthermore, SAA levels in ESRD-HDL inversely correlated with its ant

148 Furthermore, SAA-differentiated macrophages stimulated with lipopolys

149 year-old male patient with symptomatic giant SAA (13 cm) was urgently admitted to our hospital for th

150 an be an efficient method to treat the giant SAA.

151 se of this method of treatment of true giant SAA.

152 neously binds to two apolipoproteins of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.

153 entifies HNF4alpha as a regulator of hepatic SAA metabolism that regulates the sensitivity of liver c

154 2) (sPLA(2)), compelling us to determine how SAA influences sPLA(2) hydrolysis of lipoproteins.

155 ion of a disease-associated isoform of human SAA - human SAA1.1 (hSAA1.1) - using techniques ranging

156 eriments were performed where purified human SAA, in concentrations resembling a modest acute phase r

157 Here we show that mouse and human SAAs are retinol binding proteins.

158 Mouse and human SAAs bound retinol with nanomolar affinity, were associa

159 Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate

160 Our results thus identify SAAs as a family of microbe-inducible retinol binding pr

161 TSP4, TIMP-2, SEPR, MRC-2, Antithrombin III, SAA, CRP, NPS-PLA2, LEAP-1, and LBP.

162 sitive epithelial liver cancer lines impairs SAA metabolism, increases resistance to methionine restr

163 rapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that

164 Recent studies have implicated SAAs in innate immunity and various disorders; however,

165 anti-CD52 mAb alemtuzumab might be active in SAA because of its lymphocytotoxic properties.

166 Although cyclophosphamide has activity in SAA, its toxicity is not justified when far less dangero

167 cal surgical specimens and mice deficient in SAA and Toll-like receptors (TLR).

168 ted to the HL stress, they were deficient in SAA to HL stress.

169 We conclude that alemtuzumab is effective in SAA, but best results are obtained in the relapsed and r

170 that HDL from HD+ patients were enriched in SAA but had lower levels of sialylation across glycoprot

171 HDL from HD patients were enriched in SAA, LBP, ApoC-III, di-sialylated ApoC-III (ApoC-III2) a

172 nd apex of the hexamer, that are involved in SAA association with heparin.

173 storation of the transsulfuration pathway in SAA metabolism significantly alleviates the outcomes ind

174 nderstanding of the role HSCT has to play in SAA with particular emphasis on alternative donor source

175 Diets rich in SAA stimulated expression of enzymes and transporters in

176 ligands via a concave hydrophobic surface in SAA oligomers.

177 ource for unrelated donor transplantation in SAA.

178 ocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(50) 43 nM).

179 s of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.

180 In acute inflammation, SAA plasma levels increase ~1,000 fold, suggesting that

181 wer Th17 and Treg proportions and intestinal SAA expression than in controls, suggesting key roles in

182 In this review, we begin by introducing SAAs and describe how model systems and nanoparticle cat

183 n, as determined with a fluorescent-labelled SAA antibody and correlative light electron microscopy (

184 High level SAA expression induced amyloidosis in all mice after a s

185 imals receiving a high-protein diet with low SAA content, the kidney excreted alkaline urine, with lo

186 higher number of microcontractions and lower SAAs of Adelta-fibers compared with those of the Sham gr

187 ntly, we reported that inflammatory markers (SAA and chitotriosidase) and oxidative stress markers (p

188 ladder filling, the bladder mechanosensitive SAAs of Adelta-fibers were attenuated, but SAAs of both

189 stemic signaling pathways that could mediate SAA, very little information is known about the extent o

190 In infected mice, SAA proteins circulate in association with the vitamin A

191 Prolonged modest SAA overexpression occasionally produced amyloidosis aft

192 Moreover, SAA sequestered free fatty acids and lysophospholipids t

193 In the bloodstream of infected mice, most SAA is complexed with high-density lipoprotein (HDL).

194 ucture of SAA1.1, suggesting that the native SAA is nonpathogenic.

195 slowly regressed with restoration of normal SAA production after doxycycline withdrawal.

196 Levels of CRP, but not SAA, were also found to be significantly increased in pa

197 eoglycans in the ECM restored the ability of SAA-containing HDL to inhibit palmitate-induced inflamma

198 ergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize m

199 A chronically high plasma concentration of SAA results in the aggregation of amyloid into cross-bet

200 ery of these multiple and complex effects of SAA on coagulation invite further mechanistic analyses.

201 xycycline-inducible transgenic expression of SAA in mice, we show that AA amyloid deposition can occu

202 njected S100A4 protein induced expression of SAA proteins and cytokines in an organ-specific manner.

203 s in the oligomerization and fibrillation of SAA, we truncated the proline-rich final 13 residues of

204 omerization, misfolding, and fibrillation of SAA.

205 ol was associated with the small fraction of SAA proteins that circulate without binding to HDL, thus

206 Our studies suggest that the impact of SAA on inflammasome stimulation is mediated in part by t

207 Conversely, incorporation of SAA into HDL preparations reduced antiinflammatory prope

208 ceptors and lead to allosteric inhibition of SAA-initiated epithelial responses (pA(2) 13 nM).

209 The level of SAA protein appeared to be positively associated with th

210 Levels of SAA, sTNF-R1, and sTNF-R2 were measured with enzyme-link

211 However, management of SAA patients remains challenging, both acutely in addres

212 ients with COPD and a chronic mouse model of SAA exposure.

213 Overexpression of SAA by hepatocytes also occurs in patients with pancreat

214 understand the amyloid formation pathway of SAA, we characterized the oligomerization, misfolding, a

215 owing clot formation in PPP, the presence of SAA increased amyloid formation of fibrin(ogen) as deter

216 hepatocytes and the subsequent production of SAA depend on the release of interleukin 6 (IL-6) into t

217 arison between the biophysical properties of SAA isoforms with distinct pathogenicities, and the resu

218 ent structural and biophysical properties of SAA.

219 l stability and resistance to proteolysis of SAA oligomers at pH 3.5-4.5 help them escape lysosomal d

220 lipoprotein involves only the apex region of SAA and can be inhibited by heparin.

221 Reinduction of SAA overproduction revealed that, following amyloid regr

222 HLA-DPB1 alleles revealed increased risk of SAA associated with Val76-encoding alleles DPB1(*)03:01,

223 ain HLA-DPB1 alleles might influence risk of SAA through mechanisms involving DP peptide binding spec

224 To study the role of SAA in coagulation and thrombosis, in vitro experiments

225 ducts constitutes a vital primordial role of SAA in innate immunity; this role remains to be tested i

226 In this study, the role of SAA in regulating macrophage differentiation was investi

227 imental evidence supporting a causal role of SAA with atherosclerosis.

228 leavage or removal of the C-terminal tail of SAA resulted in formation of various-sized structural ag

229 reas the importance of the amino terminus of SAA for fibril formation has been well documented, the i

230 results suggest that the carboxy terminus of SAA, which is highly conserved among SAA sequences in al

231 in crucial steps for successful treatment of SAA.

232 Due to the unique geometry of SAAs, the location of the transition state and the bindi

233 In accordance with the known role of SAAs in regulating Th17 cell effector function, epitheli

234 tion of these uremia-specific proteins, only SAA mimicked ESRD-HDL by promoting inflammatory cytokine

235 Knocking down HNF4alpha or SAA enzymes in HNF4alpha-positive epithelial liver cance

236 Transient gut colonization with SFB or SAA administration alone transiently increased the H3K27

237 matory conditions associated with persistent SAA expression.

238 re any differences in colon length or plasma SAA.

239 s separable events, each sensitive to plasma SAA concentration.

240 d that, in addition to descending processes, SAAs give rise to an extensive matrix of "superficial pr

241 p them escape lysosomal degradation, promote SAA accumulation in lysosomes, and ultimately damage cel

242 ta (MIP-1beta), and serum amyloid A protein (SAA) during acute SIVmac251 infection, but not during SI

243 Serum AA protein (SAA), an acute phase plasma protein, is deposited extrac

244 flow cytometry, and serum amyloid proteins (SAA) were analyzed by quantitative real-time polymerase

245 etween ROS and abscisic acid regulates rapid SAA to heat stress in plants.

246 in treatment-naive, relapsed, and refractory SAA in 3 separate research protocols at the National Ins

247 At 37 degrees C and inflammation-related SAA concentrations, SAA1.1 exhibits an oligomer-rich fib

248 In the acute-phase response SAA is synthesized by the liver and transported primaril

249 ling with systemic transcriptomic responses, SAA, and plant acclimation to HL stress.

250 lluminate a structural basis for the retinol-SAA interaction.

251 Previous studies have shown SAAs are elevated following stroke and cerebral ischemia

252 However, unbound soluble SAA is intrinsically disordered and is either rapidly de

253 tion or blockade of components of IL-6-STAT3-SAA signalling prevents the establishment of a pro-metas

254 connections have a role in spatial-temporal SAA induction.

255 component of both immediate and longer term SAA signaling responses.

256 Our studies demonstrate that SAA increases the cytokine interleukin-1beta (IL-1beta),

257 We further demonstrate that SAA is stress specific and that a temporal-spatial inter

258 ischemia, and our studies demonstrated that SAA-deficient mice reduce inflammation and infarct volum

259 Here we provide unexpected evidences that SAA induces the proliferation of the tolerogenic subset

260 The data presented here indicate that SAA can affect coagulation by inducing amyloid formation

261 Here, we report that SAA in plants requires at least two different signals: a

262 These data show that SAA proteins are effectors for the metastasis-promoting

263 In conclusion, our findings suggest that SAA can promote a distinct CD11c(high)CD11b(high) macrop

264 from thromboelastography (TEG) suggest that SAA causes atypical coagulation with a fibrin(ogen)-medi

265 se in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on BMDCs.

266 usly forms fibrils in vitro, suggesting that SAA proteins are inherently amyloidogenic.

267 We have also shown for the first time that SAA stimulate their own transcription as well as that of

268 We conclude that SAAs provide a potential substrate for bidirectional sig

269 Here, we show that SAAs additionally direct a pathogenic pro-inflammatory T

270 itamin A derivative retinol, suggesting that SAAs transport retinol during infection.

271 The SAA-IL-17A axis represents an important innate defense n

272 The SAA-rich diet increased diuresis paralleled by downregul

273 and systemic acclimation in Arabidopsis, the SAA response to HL stress of myb30 mutants and wild-type

274 , which appears to partially result from the SAA component of HDL binding to cell-surface proteoglyca

275 However, the SAA fragments potently synergized with CCL3 to induce mo

276 Furthermore, dissociation of the SAA hexamer appears insufficient to initiate amyloidogen

277 e was performed under flow conditions on the SAA NPs supported on alumina without activity loss in th

278 Taken together, the SAA-TLR axis plays an important role in the chronicity o

279 We have used the SAA isoform, SAA2.2, from the CE/J mouse strain, as a mo

280 The SAAs of Adelta- or C-fibers from the L6 dorsal roots wer

281 In the BOO group at day 10, the SAAs of both Adelta- and C-fibers at the "ascending" pha

282 t T cell signaling pathways modulated by the SAAs may be attractive targets for anti-inflammatory the

283 Therefore, SAA solubilized lipid bilayers to generate substrates fo

284 le deficiency substantially diminished these SAA-mediated proinflammatory responses.

285 Unlike intact SAA1alpha, these SAA fragments failed to directly chemoattract neutrophil

286 ith cardiovascular disease, but whether this SAA contributes causally to atherosclerosis development

287 temic inflammatory response mediated through SAA that contributes to the pathological outcomes.SIGNIF

288 n of the microbiota and systemic exposure to SAA can influence myelopoiesis and susceptibility to ame

289 of the basic signaling mechanisms underlying SAA in plants and reveal that signaling events and trans

290 h structural underpinnings for understanding SAA interactions with its key functional ligands, its ev

291 proximity to airway epithelium, and in vitro SAA triggered release of IL-8 and other proinflammatory

292 In vivo, SAA administration induced the development of a CD11c(hi

293 ns with the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA2 (secreted phosph

294 med most mice for explosive amyloidosis when SAA production subsequently increased.

295 In the present study, we tested whether SAA is involved in the pathogenesis of periapical lesion

296 possibly class I (HLA-B) are associated with SAA.

297 lung macrophages (CD68(+)) colocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(

298 e-wide association study of individuals with SAA genetically matched to healthy controls in discovery

299 Differentiation of human monocytes with SAA stimulated the proinflammatory monokines IL-6 and IL

300 induction of IL-1beta by inhibiting ROS with SAA treatment.