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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
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
29 ute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional targets of S100A4 vi
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
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
45 The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory di
47 The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wh
49 ced histological damage and serum amyloid A (SAA) levels in IL-10(-/-) colitis mice, was efficacious
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
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
70 The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reac
74 ammation in our O3 exposure model and that A-SAA could be an important systemic signal of O3 exposure
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
83 nosensitive single-unit afferent activities (SAAs) in rats with a bladder outlet obstruction (BOO) an
88 e we demonstrate that the single-atom alloy (SAA) strategy applied to Pt reduces the binding strength
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
94 els of AngII: Hepatic production of IL-6 and SAA increases, and these mediators act synergistically t
96 CD36 is a receptor mediating SAA binding and SAA-induced pro-inflammatory cytokine secretion predomin
98 e findings indicate that circulating CRP and SAA levels are highest when the concentration of spiroch
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
111 irst-line therapy of severe aplastic anemia (SAA) with high-dose cyclophosphamide causes toxicity and
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.
119 hese data suggest that during atherogenesis, SAA can amplify the involvement of smooth muscle cells i
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
131 peared-because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 responses to the sunflower oil
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
142 Mice that received adenovirus expressing SAA had increased TGF-beta concentrations in plasma and
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
152 ed in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of poly
158 year-old male patient with symptomatic giant SAA (13 cm) was urgently admitted to our hospital for th
161 neously binds to two apolipoproteins of HDL, SAA and ApoA-I, and thereby induce SAA dissociation.
163 ion of a disease-associated isoform of human SAA - human SAA1.1 (hSAA1.1) - using techniques ranging
166 Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate
169 rapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that
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
176 nderstanding of the role HSCT has to play in SAA with particular emphasis on alternative donor source
184 wer Th17 and Treg proportions and intestinal SAA expression than in controls, suggesting key roles in
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
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
203 A chronically high plasma concentration of SAA results in the aggregation of amyloid into cross-bet
206 iting transcription eliminated the effect of SAA on sPLA(2) mRNA suggested that the increase was tran
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
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
222 l stability and resistance to proteolysis of SAA oligomers at pH 3.5-4.5 help them escape lysosomal d
227 es suggest a novel anti-inflammatory role of SAA in the induction of a micro-environment that support
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
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
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
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
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
253 At 37 degrees C and inflammation-related SAA concentrations, SAA1.1 exhibits an oligomer-rich fib
260 onse relationship (highest v lowest tertile: SAA HR = 3.15; 95% CI, 1.73 to 5.65; CRP HR = 2.27; 95%
264 Here we provide unexpected evidences that SAA induces the proliferation of the tolerogenic subset
268 In conclusion, our findings suggest that SAA can promote a distinct CD11c(high)CD11b(high) macrop
271 We have also shown for the first time that SAA stimulate their own transcription as well as that of
278 , which appears to partially result from the SAA component of HDL binding to cell-surface proteoglyca
281 e was performed under flow conditions on the SAA NPs supported on alumina without activity loss in th
286 ith cardiovascular disease, but whether this SAA contributes causally to atherosclerosis development
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
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
295 ns with the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA2 (secreted phosph
297 rpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis an
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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