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1 nflammatory proteins (C-reactive protein and interleukin-6).
2 matory markers (tumor necrosis factor-alpha, interleukin-6).
3 versible peaks in plasma levels of renin and interleukin 6.
4 ng extreme elevations of KSHV viral load and interleukin 6.
5 ion of XBP1, and that this activity requires interleukin 6.
6 y weight, and elevated levels of circulating interleukin 6.
7 lar macrophages (AMs) that produce increased interleukin-6.
8 leocapsid antibody nor with proteins such as interleukin-6.
9 bility in newly activated CD8(+) T cells via interleukin-6.
10 ecrosis factor-alpha, interleukin-1beta, and interleukin-6.
11 nhibitors of tumor necrosis factor-alpha and interleukin-6.
14 ferritin (706.9 vs. 334.2 mg/mL; P < 0.01), interleukin-6 (233.9 vs. 174.7 pg/mL; P < 0.05), troponi
18 psis diagnosis and study intervention group, interleukin-6, -8, and -10, tumor necrosis factor-alpha,
19 ve protein, tumor necrosis factor-alpha, and interleukins-6, -8, and -10-which were averaged to form
20 umor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%;
21 2.94 [1.48-5.84]), higher concentrations of interleukin-6 (aHR 1.11 [95%CI 1.02-1.20] per decile inc
22 ssociated among HIV-infected men with higher interleukin 6 and high-sensitivity C-reactive protein an
23 h as augmented microglial numbers, increased interleukin 6 and interleukin 1 receptor antagonist mess
24 al adjustments for circulating levels of IL (interleukin)-6 and high-sensitivity CRP (C-reactive prot
27 aphics, risk factors, and baseline levels of interleukin-6 and high-frequency heart rate variability,
29 Adjusting for NT-proBNPeGFR or inflammation (interleukin-6 and high-sensitive CRP) confirmed results.
30 ion of colchicine attenuated the increase in interleukin-6 and high-sensitivity C-reactive protein co
31 hat females with Down syndrome had increased interleukin-6 and interleukin-8 levels compared to males
33 ity was independently associated with higher interleukin-6 and lower high-frequency heart rate variab
34 revented induction of inflammatory cytokines interleukin-6 and osteopontin, lowered plasma endothelin
35 biomarker model included angiopoietin-2 and interleukin-6 and performed moderately well (area under
38 oduction of tumor necrosis factor alpha, and interleukins 6 and 12 (IL-6 and IL-12p40, respectively)
39 ic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (H
40 droxy-2-nonenal, isoprostane), inflammation (interleukin-6) and iron status (ferritin, hepcidin, tran
41 to 3) associations between circulating IL6 (interleukin-6) and NT-proBNP (N terminal pro B-type natr
42 na and optic nerve, including complement 1q, interleukin 6, and brain-derived neurotrophic factor.
43 n in the expression levels of p21, mTOR/pS6, interleukin 6, and tumor necrosis factor alpha in skin a
44 ulation of genes involved in chemotaxis, IL (interleukin)-6, and NF-kappaB (nuclear factor-kappaB) si
45 e up-regulating tumor necrosis factor alpha, interleukin-6, and C-X-C motif chemokine ligand 1 expres
47 ciated with the reduced expression of c-Jun, interleukin-6, and interleukin-10, which were identified
48 e expression of tumor necrosis factor alpha, interleukin-6, and interleukin-8 in the respiratory trac
49 adhesion molecule, thrombomodulin, endocan, interleukin-6, and interleukin-8 than those without acut
50 thrombomodulin, endocan, C-reactive protein, interleukin-6, and interleukin-8 were different between
51 inflammatory biomarkers (C-reactive protein, interleukin-6, and interleukin-8) were measured from per
53 educed levels of systemic interleukin-1beta, interleukin-6, and monocyte chemoattractant protein-1.
54 iated with significantly lower plasma sRAGE, interleukin-6, and monocyte chemotactic protein-1 concen
55 for advanced glycation end-products, plasma interleukin-6, and monocyte chemotactic protein-1 were s
57 hil counts; increased C-reactive protein and interleukin-6; and more severe depression than the uninf
58 We used metformin treatment and anti-IL-6 (interleukin-6) antibodies to inhibit the IL-6 pathway.
59 cluding a triad of IP-10, interleukin-10 and interleukin-6, anticipate subsequent clinical progressio
60 D5Rs (DRD5KO mice) to show that carrageenan, interleukin 6, as well as BDNF-induced hyperalgesia and
61 P<0.001) and was superior and incremental to interleukin-6, C-reactive protein, procalcitonin, ferrit
63 ed hippocampal volume, and elevated systemic interleukin-6 characterized a susceptible phenotype that
66 ium, although persistent elevations in serum interleukin-6 concentrations ( P=0.009) and reductions i
67 ated the association between higher maternal interleukin-6 concentrations and lower impulse control.
68 , the primary biomarker end point, change in interleukin-6 concentrations did not differ between grou
71 ular mechanism, we identify OSM, part of the interleukin 6 cytokine family, as a HIF-1alpha target ge
72 nterconnection between the overexpression of interleukin-6 cytokine and the tumor growth, metastasis,
74 ed that in addition to type-I interferon and interleukin-6-dependent inflammatory responses, infectio
77 al, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14
78 forming growth factor beta (TGFbeta) and LIF interleukin-6 family cytokine (LIF) signaling pathways.
80 ination: oncostatin M (OSM), a member of the interleukin-6 family, and downstream mediator tissue inh
82 80) outperformed clinical markers and plasma interleukin-6 for prospectively predicting trauma patien
83 protein-1, tumor necrosis factor alpha, and interleukin-6 from mouse macrophages, while having no ef
85 ion, and reduced plasma levels of cytokines (interleukin 6, granulocyte colony-stimulating factor, in
87 The following measurements were obtained: interleukin 6, high-sensitivity C-reactive protein, solu
88 ct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) ca
89 ological mechanical damage, via induction of interleukin 6 (IL-6) from epithelial cells, tailored eff
90 describe a new mouse strain, in which human interleukin 6 (IL-6) gene encoding the cytokine that is
91 t production of SAA depend on the release of interleukin 6 (IL-6) into the circulation by non-maligna
92 We compared neopterin, CXCL10, CCL2, and interleukin 6 (IL-6) levels in the AHI group to those in
94 rkers including C-reactive protein (CRP) and Interleukin 6 (IL-6) measured in the same individuals.
95 rved that GM-CSF was not regulated by either interleukin 6 (IL-6) or IL-23, which are both potent ind
98 -conditioned supernatant contained increased interleukin 6 (IL-6) that induced E-cadherin loss and N-
99 ding protein (I-FABP), soluble CD14 (sCD14), interleukin 6 (IL-6), and C-reactive protein (CRP) at 6
100 Vascular endothelial growth factor (VEGF), Interleukin 6 (IL-6), and matrix metalloproteinase-2 (MM
101 and independent from the OPN receptor CD44, interleukin 6 (IL-6), and other PMN chemoattractants inc
102 flammatory markers C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (T
103 (tumor necrosis factor alpha (TNFalpha) and interleukin 6 (IL-6), as well as Kelch-like ECH-associat
104 ion of early inflammatory markers, including interleukin 6 (IL-6), IL-1alpha, and tumor necrosis fact
105 and in vivo, including the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surfa
106 5-plex assay measuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), interleuki
107 nducible protein 10, soluble CD163 (sCD163), interleukin 6 (IL-6), interleukin 18, monocyte chemoattr
108 erum levels of the hepatoprotective cytokine interleukin 6 (IL-6), its downstream signal transducer a
109 cytokines and chemokine induction, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-a
113 reactive protein (Hedges's g 0.281, p<0.05), interleukin-6 (IL-6) (0.429, p<0.005), soluble tumour ne
115 pendent on exogenous soluble factors such as interleukin-6 (IL-6) and APRIL, to prevent their cell de
116 ctional associations of inflammatory markers interleukin-6 (IL-6) and C-reactive protein with major d
117 ncreased levels of the inflammatory cytokine interleukin-6 (IL-6) and decreased levels of IL-12, IFN-
119 d significantly increased neonatal levels of interleukin-6 (IL-6) and IL-8 compared with GP controls.
120 mation, measured by proinflammatory cytokine interleukin-6 (IL-6) and tumor necroses factor receptor
122 ld application, we establish that endogenous interleukin-6 (IL-6) can be quantified in 2-uL serum sam
123 erclonal communication mechanism mediated by interleukin-6 (IL-6) cytokine secreted from EGFRvIII-pos
125 ilage explants, suppressing pro-inflammatory interleukin-6 (IL-6) expression after interleukin-1 beta
130 xpression in myeloid cells, which results in interleukin-6 (IL-6) induction and STAT3 activation.
139 ons of FITC-dextran gut translocation, serum interleukin-6 (IL-6) levels, bacteremia, and sepsis mort
142 tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-be
144 -stroma interplay, paracrine factors such as interleukin-6 (IL-6) often facilitate disordered angioge
146 s transiently upregulate PD-1 expression and interleukin-6 (IL-6) production in some individuals duri
147 is in OCCC cells whereby tumor-cell-produced interleukin-6 (IL-6) regulates SPINK1 expression to stim
148 expression of the pro-inflammatory cytokine interleukin-6 (IL-6) relative to BALB/cJ and PDE11A WT m
149 e response, which is enhanced by hypoxia and interleukin-6 (IL-6) signaling, two conditions that also
150 nflammatory effects, including inhibition of interleukin-6 (IL-6) that plays a key role in the develo
151 lating microglia are critically dependent on interleukin-6 (IL-6) trans-signaling via the soluble IL-
152 17 (Th17)-cell differentiation triggered by interleukin-6 (IL-6) via STAT3 activation promotes infla
154 in 1 (CHI3L1), C-reactive protein (CRP), and interleukin-6 (IL-6) were independently validated in sep
156 des were functionalised with an antibody for interleukin-6 (IL-6) which is a protein involved in the
157 The assay was evaluated for quantitation of interleukin-6 (IL-6), a cytokine biomarker in serum.
158 ation analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are l
159 ory cytokines interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (T
160 of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1beta, and interferon-gamma (IF
161 s had less severe illness); and (3) elevated interleukin-6 (IL-6), IL-8, and myeloperoxidase levels i
162 rkers, including interferon beta (IFN-beta), interleukin-6 (IL-6), interleukin-6 receptor alpha (IL-6
164 er levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitment, and a
165 in response to the proinflammatory cytokine interleukin-6 (IL-6), suggesting that MSH3 may be a shut
166 ine plasma levels of 4 inflammatory markers (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a
167 s of depression and inflammatory biomarkers [interleukin-6 (IL-6), Tumor Necrosis Factor-Alpha (TNF-a
168 ercentage of 76.0.% The associated cytokines interleukin-6 (IL-6), tumor necrosis factor-alpha, and I
172 epressed mood and proinflammatory cytokines (interleukin-6 (IL-6); tumor necrosis factor-alpha (TNF))
173 red parasite biomass, systemic inflammation (interleukin 6 [IL-6]), endothelial activation (angiopoie
174 pondin 2; intercellular adhesion molecule 1; interleukin 6 [IL-6]; stromal cell-derived factor 1; tis
175 e regulator of inflammatory cytokines (e.g., interleukin-6 [IL-6] and IL-10), in mycobacterial infect
176 cium binding adaptor molecule-1 [Iba-1]) and interleukin-6 [IL-6]) and astrogliosis/astrocyte damage
177 that endothelial cell-derived factors (e.g., interleukin-6 [IL-6]) promote self-renewal of dental pul
178 anscription or secretion of proinflammatory (interleukin-6 [IL-6], granulocyte-macrophage colony-stim
179 nd production of six inflammatory molecules (interleukin-6 [IL-6], tumor necrosis factor alpha [TNFal
180 plasma levels of four inflammatory markers (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-a
183 marker genes interleukin 1beta (IL1beta) and interleukin 6 (IL6) along with the M2 markers arginase-1
184 mote pro-inflammatory response by increasing interleukin 6 (IL6) expression and impede reparative res
185 fection, expressing proinflammatory cytokine interleukin 6 (IL6) mRNA, which was subsequently also ob
187 IVs who were breastfed, levels of sCD163 and interleukin 6 (IL6) were higher than levels in PHIV who
188 hogenicity genes (thrombospondin 1-(THBS 1), interleukin 6 (IL6), and arginine decarboxylase 2 (ADC2)
189 re; Egfr(f/f) mice had reduced expression of interleukin 6 (IL6), and epithelial STAT3 activation was
190 5 II), human epididymis protein 4 (HE4), and interleukin 6 (IL6), with limits of detection (LOD) as l
191 cy of tumor necrosis factor alpha-producing, interleukin 6 (IL6)-producing, and IL17-producing cells
194 lls (CA-MSC) produce not only high levels of interleukin-6 (IL6) but also the related cytokine leukem
197 cts of high-sensitive C-reactive protein and interleukin-6 (IL6) measured in blood were related to ob
203 ity and has been successfully used to detect interleukin-6 in blood samples collected from patients s
204 trial, blocking the activity of the cytokine interleukin-6 in vivo prevented systemic inflammation an
206 PCR deficiency attenuated the elaboration of interleukin-6, infiltration of macrophages, and neoangio
209 B, alpha-II-spectrin breakdown product 150, interleukin 6, interleukin 1 receptor antagonist, and c-
210 inflammatory biomarkers (C-reactive protein, interleukin 6, interleukin 10, tumor necrosis factor alp
211 ed SAMHD1 and proinflammatory cytokines (eg, interleukin 6, interleukin 1beta, and tumor necrosis fac
212 of proinflammatory cytokines (interleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophag
213 phenotype, reflected by the up-regulation of interleukin-6, interleukin-1beta, bone sialoprotein, ost
214 al injury (angiopoietin-2) and inflammation (interleukin-6, interleukin-8, and interleukin-33 and sol
215 nes (e.g., interleukin-1beta, interleukin-2, interleukin-6, interleukin-8, and monocyte chemoattracta
216 ceptor expressed on myeloid cells [sTREM-1], interleukin-6, interleukin-8, chitinase-3-like protein-1
217 a 24-hour period, including interleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.00
220 ls of interleukin-1beta, interleukin-1alpha, interleukin-6, interleukin-8, interleukin-10, interleuki
221 higher expression of nuclear factor kappa B, interleukin-6, interleukin-8, transforming growth factor
222 er N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligan
226 Here, we assessed inflammation by indexing interleukin-6 level in blood and measured psychomotor sp
230 ice and found that aging led to elevated IL (interleukin)-6 levels and mitochondrial dysfunction, ass
231 alysis, the association of sodium levels and interleukin-6 levels (which has been linked to nonosmoti
237 n markers were suggestive of cytokine storm (interleukin-6 median, 135 pg/mL) and macrophage activati
238 secretion of tumor necrosis factor alpha and interleukin-6 mediated through TLR2 and TLR4 signaling.
239 onspecifically, likely through inhibition of interleukin 6-mediated signaling to B cells and plasma c
240 Elderly had significantly lower levels of interleukin-6, monocyte chemotactic protein-1, monocyte
241 ide significance, including 2 new loci: IL6 (interleukin 6) on 7p15.3 and ALPL (alkaline phosphatase)
244 There was no significant effect on plasma interleukin-6 or D-dimer levels, nor on monocyte/T-cell
246 did not reduce levels of interleukin-1beta, interleukin-6, or C-reactive protein and did not result
247 e did not result in lower interleukin-1beta, interleukin-6, or C-reactive protein levels than placebo
249 erivascular fibrillar collagen and pulmonary interleukin-6 overexpression discriminated rats that dev
250 efensin alpha 5 (P = 0.03) increased whereas interleukin-6 (P = 0.02) and serum LBP (P = 0.009) reduc
251 s demonstrated stimulation of interferon and interleukin-6 pathways in bronchoalveolar lavage samples
252 tic livers of beta2SP(+/-) mice treated with interleukin-6 (pIL6; (IL6) beta2SP(+/-) LSCs) were highl
256 strongly suppress tumor necrosis factor and interleukin-6 production and compromise cell viability.
257 Moreover, thrombin- and histamine-stimulated interleukin-6 production required both TAB1-TAB2 and TAB
259 Furthermore, elevated osteocyte TNF-alpha, interleukin-6, RANKL, OPG, and sclerostin corresponded w
260 r of tumor necrosis factor alpha (TNFalpha), interleukin 6 receptor (IL-6R), and epidermal growth fac
261 uble tumor necrosis factor receptor and anti-interleukin 6 receptor antibody induce long-term (>=1 ye
262 sp358Ala variant (rs2228145; A>C) in the IL (interleukin)-6 receptor ( IL6R) gene has been implicated
263 es to map integratively the epitope of human interleukin-6 receptor (IL-6R) for two adnectins with di
264 on gamma-induced protein 10 (IP-10), soluble interleukin-6 receptor (sIL-6R), sCD14, and sGP130-were
266 feron beta (IFN-beta), interleukin-6 (IL-6), interleukin-6 receptor alpha (IL-6Ralpha), soluble inter
267 lations, the safety and efficacy of the anti-interleukin-6 receptor antibody tocilizumab in patients
268 eukin-6 receptor alpha (IL-6Ralpha), soluble interleukin-6 receptor beta (sIL-6Rbeta, or gp130), IL-8
270 gle variant, as did plasma concentrations of interleukin-6 receptor subunit alpha (also based on a si
271 humanised monoclonal antibody targeting the interleukin-6 receptor, reduced the risk of relapse in p
272 uated glutamate uptake, intramyelinic edema, interleukin-6 release, complement activation, inflammato
273 uced nuclear levels of phosphorylated STAT3, interleukin 6 secretion, foam cell formation, and lipid
274 ect to inhibiting lipopolysaccharide-induced interleukin-6 secretion in human macrophages, but its ab
275 to play a role in regulating CSR through the interleukin-6 signaling pathway and in proper IgA expres
278 ing pressure and the plasma concentration of interleukin-6, soluble receptor for advanced glycation e
279 igher AT1RaAbs correlated significantly with interleukin-6 (Spearman r=0.33, P<0.0001), systolic bloo
280 ological indicator of maternal inflammation (interleukin-6) that has been shown to influence fetal br
281 protein 1, tumor necrosis factor alpha, and interleukin 6) through YAP association with the TEA doma
282 ion of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-alpha and interleuk
283 astrocyte activation, and interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and interleu
284 evels of pro-inflammatory factors, including interleukin-6, tumor necrosis factor-alpha, and matrix m
286 an also directly activate KSHV-encoded viral interleukin-6 (vIL-6) and, thus, contribute to the patho
287 data demonstrate that the KSHV protein viral interleukin-6 (vIL-6) can induce integrin beta3 in an in
292 CE Human herpesvirus 8 (HHV-8)-encoded viral interleukin-6 (vIL-6) was the first viral IL-6 homologue
294 ive aptasensor for quantitative detection of interleukin-6 was developed by using a glassy carbon ele
297 ide-binding protein, C-reactive protein, and interleukin 6 were differentially expressed between coun
300 luble tumor necrosis factor-receptor I], and interleukin-6), YKL-40 (related to liver injury and infl