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1                                              SAA added to POBs inhibited PTH-stimulated cAMP response
2                                              SAA has been detected within atherosclerotic lesions and
3                                              SAA increased IOP by approximately 40% (P < 0.05) in the
4                                              SAA instillation into the lungs elicits robust TLR2-, My
5                                              SAA intake was lower in RTRs compared with controls and
6                                              SAA is a protein precursor of reactive AA amyloidosis, t
7                                              SAA is normally associated with the high-density lipopro
8                                              SAA mRNA expression was positively associated with tissu
9                                              SAA predominately promoted expression of the TH17 polari
10                                              SAA promotes expression of IL-17A in gammadelta T cells
11                                              SAA proteins stimulated the transcription of RANTES (reg
12                                              SAA stimulation led to increased phosphorylation of MAPK
13                                              SAA supplementation, mTORC1 activation, or chemical/gene
14                                              SAA was rapidly incorporated into amyloid, acutely reduc
15                                              SAA, but not CRP, increased proteoglycan sulfate incorpo
16                                              SAA-1 not only induced anti-inflammatory interleukin 10
17                                              SAA-enriched HDL colocalized with cell surface-associate
18                                              SAA-induced cell activation was inhibited by a CD36 pept
19                                              SAA-induced inflammation was markedly reduced by a neutr
20                                              SAA-mediated effects were thermolabile, inhibitable by a
21 We now show that systemic serum amyloid A 1 (SAA-1) controls the plasticity of neutrophil differentia
22                 Elevated levels of IL-1beta, SAA, and IL-17 are present in subjects with severe aller
23                The uptake of Alexa Fluor 488 SAA as well as of other well established CD36 ligands wa
24         Median serum concentrations of IL-6, SAA, ICAM-1, E-selectin, TNFalpha, and MPO and periphera
25    Here, we report long-term follow-up on 67 SAA patients (44 treatment-naive and 23 refractory) trea
26     The atomic ratio Pt:Cu = 1:125 yielded a SAA which exhibited excellent CO tolerance in H2 activat
27         The fibrillation of Serum Amyloid A (SAA) - a major acute phase protein - is believed to play
28                             Serum amyloid A (SAA) 1 and 2 are produced predominantly by the liver and
29 ute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional targets of S100A4 vi
30  of the acute phase protein serum amyloid A (SAA) 1.
31        Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are predictive of card
32 y C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analysed as inflammatory
33 -reactive protein (CRP) and serum amyloid A (SAA) are measures of low-grade chronic inflammation and
34 -associated genes Fizz1 and serum amyloid A (SAA) are significantly up-regulated in M2 macrophages st
35           Here, we identify serum amyloid A (SAA) as a candidate mediator of GC refractory inflammati
36  leads to overproduction of serum amyloid A (SAA) by the liver.
37                       Since serum amyloid A (SAA) concentrations in HDL increase with inflammation, w
38 use AngII increases hepatic serum amyloid A (SAA) expression in an IL-6-dependent manner, we treated
39 The fibrillar deposition of serum amyloid A (SAA) has been linked to the disease amyloid A (AA) amylo
40     The acute phase protein serum amyloid A (SAA) has been well characterized as an indicator of infl
41                             Serum amyloid A (SAA) is a family of acute-phase proteins which are shown
42                             Serum amyloid A (SAA) is a major acute phase protein involved in multiple
43                             Serum amyloid A (SAA) is an acute-phase plasma protein that functions in
44                             Serum amyloid A (SAA) is best known for being the main component of amylo
45     The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory di
46                             Serum amyloid A (SAA) is expressed locally in chronic inflammatory condit
47     The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wh
48                             Serum amyloid A (SAA) is one such marker but its function remains unclear
49 ced histological damage and serum amyloid A (SAA) levels in IL-10(-/-) colitis mice, was efficacious
50                             Serum amyloid A (SAA) promotes neutrophilic inflammation by its interacti
51                             Serum amyloid A (SAA) proteins are strongly induced in the liver by syste
52                             Serum amyloid A (SAA) represents an evolutionarily conserved family of in
53 SP-B), apolipoprotein C-II, serum amyloid A (SAA), and alpha-1-microglobulin/bikunin precursor.
54 g C-reactive protein (CRP), serum amyloid A (SAA), and S100 calcium-binding protein A12 (S100A12).
55 , C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1 (sICAM-1) and va
56 -reactive protein (hs-CRP), serum amyloid A (SAA), interleukin-6 (IL-6), leukocyte, and neutrophil le
57 Concentrations of HDL-bound serum amyloid A (SAA), lipopolysaccharide binding protein (LBP), apolipop
58 production by adipocytes of serum amyloid A (SAA), monocyte chemoattractant protein (MCP)-1, and hyal
59    SFB cause an increase in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on
60 -reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase response proteins, in th
61 of the acute-phase reactant serum amyloid A (SAA).
62 of the acute-phase protein, serum amyloid A (SAA).
63 ury score (HIS), and plasma serum amyloid A (SAA).
64  and C-reactive protein and serum amyloid A [SAA] levels).
65 C-reactive protein [hsCRP], serum amyloid A [SAA], and IL-6) were determined at 3, 6, 9, 12, and 24 m
66 is factor alpha [TNFalpha], serum amyloid A [SAA], vascular endothelial growth factor, neutrophil cou
67 ], haptoglobin, and serum amyloid protein A [SAA]), inflammatory markers (matrix metalloproteinase 1
68                                            A-SAA in blood correlated with total leukocytes, macrophag
69                                            A-SAA mRNA and protein were increased in the liver.
70   The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reac
71                           Serum amyloid A (A-SAA/Saa3) was shown before to affect osteoblastic metabo
72                                   Finally, A-SAA protein, but not mRNA, was increased in the CNS 24 h
73             We found that both isoforms of A-SAA completely crossed the intact blood-brain barrier, a
74 ammation in our O3 exposure model and that A-SAA could be an important systemic signal of O3 exposure
75                  Our findings suggest that A-SAA is functionally linked to pulmonary inflammation in
76 on and distal systemic acquired acclimation (SAA).
77 tress (termed systemic acquired acclimation [SAA]).
78 ncreased cellular triglyceride accumulation, SAA, and MCP-1 expression; generated reactive oxygen spe
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             To determine its direct actions, SAA was administered into murine lung, leading to induct
83 nosensitive single-unit afferent activities (SAAs) in rats with a bladder outlet obstruction (BOO) an
84                                 In addition, SAA-induced secretion of G-CSF was sensitive to heat and
85 d protein were significantly increased after SAA stimulation.
86 tients with COPD and in vivo using an airway SAA challenge model in BALB/c mice.
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                                     Although SAA is thought to play a key role in plant survival duri
90 inus of SAA, which is highly conserved among SAA sequences in all vertebrates, might play important s
91 s rarely involves the heart, but amyloidotic SAA transgenic mice consistently had minor cardiac amylo
92 lantation (HSCT) in severe aplastic anaemia (SAA) have improved steadily over the past decades, large
93        Targeting the high levels of IL-6 and SAA in catabolic disorders might be a therapeutic approa
94 els of AngII: Hepatic production of IL-6 and SAA increases, and these mediators act synergistically t
95                                Both IL-6 and SAA levels rose significantly in ApoE(-/-) BL/6 mice com
96 CD36 is a receptor mediating SAA binding and SAA-induced pro-inflammatory cytokine secretion predomin
97        Circulating concentrations of CRP and SAA in patients with a range of early to late objective
98 e findings indicate that circulating CRP and SAA levels are highest when the concentration of spiroch
99                                      CRP and SAA levels were significantly elevated in early localize
100         At the end of part 2, median CRP and SAA values were normal (<10 mg per liter for both measur
101                             Elevated CRP and SAA were also associated with reduced disease-free survi
102        Circulating concentrations of CRP and SAA were measured approximately 31 months after diagnosi
103 ch were accompanied by reductions in CRP and SAA, continued over the treatment duration.
104 of the acute-phase reactants ESR, hsCRP, and SAA were lower at the higher doses; the difference was s
105     Markers of inflammation (ESR, hsCRP, and SAA) showed statistically significant reductions (P < 0.
106 hermore, coordinate expression of S100A4 and SAA in tumor samples from colorectal carcinoma patients
107  transplantation for severe aplastic anemia (SAA) has improved, with survival rates now approximately
108          Survival in severe aplastic anemia (SAA) has markedly improved in the past 4 decades because
109                      Severe aplastic anemia (SAA) is a life-threatening bone marrow failure disorder
110             Acquired severe aplastic anemia (SAA) is a rare hematologic disease associated with signi
111 irst-line therapy of severe aplastic anemia (SAA) with high-dose cyclophosphamide causes toxicity and
112 ing hematopoiesis in severe aplastic anemia (SAA).
113 in HSCT for acquired severe aplastic anemia (SAA).
114           Although splenic artery aneurysms (SAAs) are common, their giant forms (more than 10 cm in
115 fects were thermolabile, inhibitable by anti-SAA antibody, and also neutralized by association with h
116 proved small-angle scattering approximation (SAA) to radiative transfer for sub-diffusive light refle
117 ieu (IL-6) and acute phase reactants such as SAA may reflect alterations in the Th1/Th2 balance.
118             "Surface-associated astrocytes" (SAAs) in posterior piriform cortex (PPC) are unique by v
119 hese data suggest that during atherogenesis, SAA can amplify the involvement of smooth muscle cells i
120                                      Because SAA-1-producing melanomas promoted differentiation of IL
121                     The relationship between SAA and neutrophils was investigated in lung sections fr
122 alizing antibody to IL-17A was used to block SAA responses in vivo, and a cell-sorting strategy was u
123  During acute exacerbation, peripheral blood SAA levels increased dramatically and were disproportion
124 e SAAs of Adelta-fibers were attenuated, but SAAs of both Adelta- and C-fibers were intermittently en
125        Cellular sources of IL-17A induced by SAA include CD4(+) T cells, gammadelta T cells, and an E
126                       CONCLUSION Circulating SAA and CRP may be important prognostic markers for long
127                             Most circulating SAA is protected from proteolysis and misfolding by bind
128 d into amyloid, acutely reducing circulating SAA concentrations by up to 90%.
129  deposition is determined by the circulating SAA concentration.
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 ion and NFkappaB translocation and decreased SAA and MCP-1 expression and monocyte chemotaxis.
134                Immunohistochemistry detected SAA was in close proximity to airway epithelium, and in
135 e the high sequence identity among different SAA isoforms, not all SAA proteins are pathogenic.
136       This study reports that HS dissociates SAA from HDLs isolated from inflamed mouse plasma.
137 n of Jmjd3 H3K27 demethylase activity during SAA treatment or blockade of granulocyte-macrophage colo
138 oth muscle cells were stimulated with either SAA or CRP (1 to 100 mg/L) and proteoglycans were then i
139                             Results Elevated SAA and CRP were associated with reduced overall surviva
140 flammation, we investigated whether elevated SAA is a causal factor in HDL dysfunction.
141 which secreted IL-22 that induced epithelial SAA production in a Stat3-dependent manner.
142     Mice that received adenovirus expressing SAA had increased TGF-beta concentrations in plasma and
143                                 Extrahepatic SAA was detected locally in COPD bronchoalveolar lavage
144                        Diet was assessed for SAA content and various risk factors were measured.
145                                  The HRs for SAA and CRP tertiles suggested a threshold effect on sur
146 29 microg/ml LDL versus 90 microg/ml LDL for SAA versus control proteoglycans; P < 0.005).
147  show that TLR2 is a functional receptor for SAA.
148 use of an alemtuzumab-based HSCT regimen for SAA results in durable engraftment with a low incidence
149   These results suggest a potential role for SAA in inflammatory diseases through activation of TLR2.
150 nor (MSD) HSCT remains the gold standard for SAA patients younger than 40-50 years, with HLA-matched
151  outcomes of PBPC and BM transplantation for SAA.
152 ed in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of poly
153                                 Furthermore, SAA can be found in association with apoB-containing lip
154                                 Furthermore, SAA drives production of IL-1alpha, IL-1beta, IL-6, IL-2
155                                 Furthermore, SAA levels in ESRD-HDL inversely correlated with its ant
156                                 Furthermore, SAA up-regulated biglycan via the induction of endogenou
157                                 Furthermore, SAA-differentiated macrophages stimulated with lipopolys
158 year-old male patient with symptomatic giant SAA (13 cm) was urgently admitted to our hospital for th
159 an be an efficient method to treat the giant SAA.
160 se of this method of treatment of true giant SAA.
161 neously binds to two apolipoproteins of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.
162 injected with an adenovirus expressing human SAA-1, a null virus, or saline.
163 ion of a disease-associated isoform of human SAA - human SAA1.1 (hSAA1.1) - using techniques ranging
164            Here we show that mouse and human SAAs are retinol binding proteins.
165                              Mouse and human SAAs bound retinol with nanomolar affinity, were associa
166      Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate
167                    Our results thus identify SAAs as a family of microbe-inducible retinol binding pr
168 TSP4, TIMP-2, SEPR, MRC-2, Antithrombin III, SAA, CRP, NPS-PLA2, LEAP-1, and LBP.
169 rapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that
170 anti-CD52 mAb alemtuzumab might be active in SAA because of its lymphocytotoxic properties.
171    Although cyclophosphamide has activity in SAA, its toxicity is not justified when far less dangero
172 We conclude that alemtuzumab is effective in SAA, but best results are obtained in the relapsed and r
173  that HDL from HD+ patients were enriched in SAA but had lower levels of sialylation across glycoprot
174        HDL from HD patients were enriched in SAA, LBP, ApoC-III, di-sialylated ApoC-III (ApoC-III2) a
175 nd apex of the hexamer, that are involved in SAA association with heparin.
176 nderstanding of the role HSCT has to play in SAA with particular emphasis on alternative donor source
177                                Diets rich in SAA stimulated expression of enzymes and transporters in
178 ource for unrelated donor transplantation in SAA.
179 ocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(50) 43 nM).
180 age, tumor stage, race, and body mass index (SAA P trend < .0001; CRP P trend = .002).
181 s of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.
182                      Of particular interest, SAAs lack the domain organization observed in neocortex
183                               Interestingly, SAA activated smooth muscle cell IL-1beta mRNA expressio
184 wer Th17 and Treg proportions and intestinal SAA expression than in controls, suggesting key roles in
185                                Intriguingly, SAA reverses T(reg) anergy via its interaction with mono
186                                   High level SAA expression induced amyloidosis in all mice after a s
187 imals receiving a high-protein diet with low SAA content, the kidney excreted alkaline urine, with lo
188 higher number of microcontractions and lower SAAs of Adelta-fibers compared with those of the Sham gr
189 ladder filling, the bladder mechanosensitive SAAs of Adelta-fibers were attenuated, but SAAs of both
190 s indicate that CD36 is a receptor mediating SAA binding and SAA-induced pro-inflammatory cytokine se
191  functions as a novel SAA receptor mediating SAA proinflammatory activity.
192                             Prolonged modest SAA overexpression occasionally produced amyloidosis aft
193                                    Moreover, SAA activated the inhibitor of NF-kappaB kinase (IKK) in
194 -free survival was 58% in 44 treatment-naive SAA patients.
195 ucture of SAA1.1, suggesting that the native SAA is nonpathogenic.
196  slowly regressed with restoration of normal SAA production after doxycycline withdrawal.
197                       Levels of CRP, but not SAA, were also found to be significantly increased in pa
198 s B scavenger receptor, functions as a novel SAA receptor mediating SAA proinflammatory activity.
199     A pronounced reduction (up to 60-75%) of SAA-induced pro-inflammatory cytokine secretion was obse
200 eoglycans in the ECM restored the ability of SAA-containing HDL to inhibit palmitate-induced inflamma
201 ergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize m
202                           The association of SAA with high density lipoprotein abrogated the SAA-indu
203   A chronically high plasma concentration of SAA results in the aggregation of amyloid into cross-bet
204                               This effect of SAA is dependent on Toll-like receptor 2 (TLR2).
205                                The effect of SAA on gene expression of cultured human TM cells was te
206 iting transcription eliminated the effect of SAA on sPLA(2) mRNA suggested that the increase was tran
207 ing that the induction is a direct effect of SAA.
208 r 25 mmol/l (high) glucose for evaluation of SAA, MCP-1, and HA regulation in vitro.
209 xycycline-inducible transgenic expression of SAA in mice, we show that AA amyloid deposition can occu
210 njected S100A4 protein induced expression of SAA proteins and cytokines in an organ-specific manner.
211 s in the oligomerization and fibrillation of SAA, we truncated the proline-rich final 13 residues of
212 omerization, misfolding, and fibrillation of SAA.
213                  The biological functions of SAA in inflammation have not been fully defined, althoug
214                 Conversely, incorporation of SAA into HDL preparations reduced antiinflammatory prope
215 ceptors and lead to allosteric inhibition of SAA-initiated epithelial responses (pA(2) 13 nM).
216                                    Levels of SAA, sTNF-R1, and sTNF-R2 were measured with enzyme-link
217                       However, management of SAA patients remains challenging, both acutely in addres
218 ients with COPD and a chronic mouse model of SAA exposure.
219  understand the amyloid formation pathway of SAA, we characterized the oligomerization, misfolding, a
220 arison between the biophysical properties of SAA isoforms with distinct pathogenicities, and the resu
221 ent structural and biophysical properties of SAA.
222 l stability and resistance to proteolysis of SAA oligomers at pH 3.5-4.5 help them escape lysosomal d
223                       Selective reduction of SAA-induced gene expression was observed in tlr2-/- mous
224 lipoprotein involves only the apex region of SAA and can be inhibited by heparin.
225                               Reinduction of SAA overproduction revealed that, following amyloid regr
226                   In this study, the role of SAA in regulating macrophage differentiation was investi
227 es suggest a novel anti-inflammatory role of SAA in the induction of a micro-environment that support
228                     To determine the role of SAA on aortic smooth muscle cell gene expression, a prel
229 imental evidence supporting a causal role of SAA with atherosclerosis.
230 ature suggesting that localized synthesis of SAA within the vasculature, or adipose tissue, may play
231 leavage or removal of the C-terminal tail of SAA resulted in formation of various-sized structural ag
232 reas the importance of the amino terminus of SAA for fibril formation has been well documented, the i
233 results suggest that the carboxy terminus of SAA, which is highly conserved among SAA sequences in al
234 in crucial steps for successful treatment of SAA.
235  that the spatially distributed character of SAAs in PPC reflects and supports the spatially distribu
236 unique and functionally relevant features of SAAs in PPC of the rat were identified by light and elec
237 er, blocking IL-1 receptors had no effect on SAA-mediated activation of sPLA(2) expression.
238 ther apolipoproteins that bind to CD36, only SAA induced a 10-50-fold increase of interleukin-8 secre
239 tion of these uremia-specific proteins, only SAA mimicked ESRD-HDL by promoting inflammatory cytokine
240       Transient gut colonization with SFB or SAA administration alone transiently increased the H3K27
241 matory conditions associated with persistent SAA expression.
242 re any differences in colon length or plasma SAA.
243 s separable events, each sensitive to plasma SAA concentration.
244 d that, in addition to descending processes, SAAs give rise to an extensive matrix of "superficial pr
245 p them escape lysosomal degradation, promote SAA accumulation in lysosomes, and ultimately damage cel
246 ta (MIP-1beta), and serum amyloid A protein (SAA) during acute SIVmac251 infection, but not during SI
247 e protein (CRP) and serum amyloid A protein (SAA).
248                            Serum AA protein (SAA), an acute phase plasma protein, is deposited extrac
249 etween ROS and abscisic acid regulates rapid SAA to heat stress in plants.
250 toll-like receptor-4 (TLR4) markedly reduced SAA and MCP-1 expression in response to palmitate but no
251 in treatment-naive, relapsed, and refractory SAA in 3 separate research protocols at the National Ins
252                     Patients with refractory SAA fared less well after high-dose cyclophosphamide the
253     At 37 degrees C and inflammation-related SAA concentrations, SAA1.1 exhibits an oligomer-rich fib
254                  In the acute-phase response SAA is synthesized by the liver and transported primaril
255 ults from a solid-phase binding assay showed SAA interaction with the ectodomain of TLR2.
256 ssociations were of borderline significance (SAA P trend = .04; CRP P trend = .07).
257                     However, unbound soluble SAA is intrinsically disordered and is either rapidly de
258  connections have a role in spatial-temporal SAA induction.
259  component of both immediate and longer term SAA signaling responses.
260 onse relationship (highest v lowest tertile: SAA HR = 3.15; 95% CI, 1.73 to 5.65; CRP HR = 2.27; 95%
261           In this study, we demonstrate that SAA is a potent endogenous stimulator of granulocyte col
262                  We further demonstrate that SAA is stress specific and that a temporal-spatial inter
263                           Demonstrating that SAA increased expression of sPLA(2) heteronuclear RNA an
264    Here we provide unexpected evidences that SAA induces the proliferation of the tolerogenic subset
265 fined, although recent reports indicate that SAA induces proinflammatory cytokine expression.
266                         Here, we report that SAA in plants requires at least two different signals: a
267                         These data show that SAA proteins are effectors for the metastasis-promoting
268     In conclusion, our findings suggest that SAA can promote a distinct CD11c(high)CD11b(high) macrop
269 se in serum amyloid A (SAA), suggesting that SAA might mediate SFB's effects on BMDCs.
270 usly forms fibrils in vitro, suggesting that SAA proteins are inherently amyloidogenic.
271   We have also shown for the first time that SAA stimulate their own transcription as well as that of
272                             We conclude that SAAs provide a potential substrate for bidirectional sig
273                                          The SAA mRNA levels were increased in glaucoma TM tissues by
274                                          The SAA-IL-17A axis represents an important innate defense n
275                                          The SAA-induced increase in sPLA(2) was validated by real ti
276                                          The SAA-rich diet increased diuresis paralleled by downregul
277  with high density lipoprotein abrogated the SAA-induced increase in sPLA(2) expression.
278 , which appears to partially result from the SAA component of HDL binding to cell-surface proteoglyca
279                                 However, the SAA fragments potently synergized with CCL3 to induce mo
280             Furthermore, dissociation of the SAA hexamer appears insufficient to initiate amyloidogen
281 e was performed under flow conditions on the SAA NPs supported on alumina without activity loss in th
282                             We have used the SAA isoform, SAA2.2, from the CE/J mouse strain, as a mo
283                                          The SAAs of Adelta- or C-fibers from the L6 dorsal roots wer
284              In the BOO group at day 10, the SAAs of both Adelta- and C-fibers at the "ascending" pha
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                                        Thus, SAA alters vascular proteoglycans in a pro-atherogenic m
288 nd three MAPKs all appeared to contribute to SAA-induced cytokine release.
289 n of the microbiota and systemic exposure to SAA can influence myelopoiesis and susceptibility to ame
290      HeLa cells expressing TLR2 responded to SAA with potent activation of NF-kappaB, which was enhan
291  in sPLA(2) expression were not secondary to SAA-induced IL-1 receptor activation.
292 of the basic signaling mechanisms underlying SAA in plants and reveal that signaling events and trans
293 proximity to airway epithelium, and in vitro SAA triggered release of IL-8 and other proinflammatory
294                                     In vivo, SAA administration induced the development of a CD11c(hi
295 ns with the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA2 (secreted phosph
296 med most mice for explosive amyloidosis when SAA production subsequently increased.
297 rpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis an
298                         To determine whether SAA stimulated proteoglycan synthesis in vivo, ApoE(-/-)
299  lung macrophages (CD68(+)) colocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(
300      Differentiation of human monocytes with SAA stimulated the proinflammatory monokines IL-6 and IL

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