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1 uction pathways, indicating it is not solely proinflammatory.
3 ho are more socially isolated show increased proinflammatory activity in response to an inflammatory
4 that exposure to social stressors increases proinflammatory activity, (2) that individuals who are m
5 ocially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who a
7 vitro, as characterized by secretion of both proinflammatory and anti-inflammatory cytokines from mur
11 We detected TLR2-, TLR4-, and C5aR-mediated proinflammatory and fibrotic responses to bacteria that
12 n conclusion, CD8(+)RORgammat(+) T cells are proinflammatory and functionally impaired and may contri
15 nd other inflammation agonists as well as 14 proinflammatory and nine anti-inflammatory eicosanoids w
16 hese molecules on attachment, migration, and proinflammatory and prodestructive activation of RASFs w
17 rophages) and decreased expression levels of proinflammatory and profibrotic markers that were indepe
18 potential for RORgammat-driven expression of proinflammatory and prohypertensive IL-17F in response t
19 pathways leading to abundance shifts between proinflammatory and proresolving lipid mediators provide
20 hoinositol inhibits the de novo synthesis of proinflammatory and prothrombotic compounds and might th
23 n of mechanistic target of rapamycin (mTOR), proinflammatory, and anti-apoptotic signaling pathways,
24 Fc receptors is required for the control of proinflammatory, anti-inflammatory, and immunomodulatory
25 ting that cdN inhibition of RECON promotes a proinflammatory, antibacterial state that is distinct fr
26 exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial ph
27 on caused by vasoactive peptide thrombin and proinflammatory bacterial wall lipopolysaccharide (LPS).
31 erosclerosis by promoting the maintenance of proinflammatory CD11c(+) macrophages within lesions and
32 BOS is associated with increased cytotoxic/proinflammatory CD8+ T, NKT-like, and NK cells in the sm
35 uppressive function is lost in patients upon proinflammatory challenge; protracted modulation of the
37 proximal colon cancer risk was higher in the proinflammatory-change DII group than in the antiinflamm
41 pproaches to show increased infiltration and proinflammatory (classically activated [M1]) polarizatio
43 -M, also known as IRAK-3, is an inhibitor of proinflammatory cytokine and chemokine expression in int
44 IFNs but were associated with altered local proinflammatory cytokine and chemokine responses and dif
48 nza virus-induced lethality and reduced both proinflammatory cytokine gene expression in the lungs an
49 nonrelevant modifications of the prototypic proinflammatory cytokine IL-1beta during an immune respo
50 ated the canonical NF-kappaB pathway and the proinflammatory cytokine IL-6 in autoantibody production
56 at wild type mice had significantly elevated proinflammatory cytokine levels, reduced ejection fracti
58 r (NF)-kappaB, which induced expression of a proinflammatory cytokine module that, along with the ant
60 ng trauma but displayed decreased stimulated proinflammatory cytokine production and significantly re
61 d survival, attenuated hypothermia, and less proinflammatory cytokine production during septic shock
63 ent mice indicated that Acanthamoeba-induced proinflammatory cytokine production was through MyD88-de
69 , and expansion of blood monocytes with less proinflammatory cytokine response to bacterial stimulati
71 e degrading desmosomal proteins and inducing proinflammatory cytokine secretion through protease-acti
73 In this work, we titered bacteria and/or the proinflammatory cytokine TNFalpha in a set of establishe
74 utes to their extraordinary vulnerability to proinflammatory cytokine toxicity and may therefore repr
75 microglia in the ARC, the expression of the proinflammatory cytokine tumor necrosis factor-alpha in
79 tion of inflammation, including reduction of proinflammatory cytokines (CXCL1, CXCL2, CCL3, CCL4, IL6
80 phate nucleotidohydrolase induced SAMHD1 and proinflammatory cytokines (eg, interleukin 6, interleuki
81 r cytotoxic mediators (perforin/granzyme B), proinflammatory cytokines (IFNgamma/TNFalpha), and expre
83 C-treated hearts show enhanced production of proinflammatory cytokines (interleukin-3, interleukin-6,
86 RA101295 abolished sepsis-induced surges in proinflammatory cytokines and attenuated systemic circul
87 stable proliferation arrest and secretion of proinflammatory cytokines and chemokines, the senescence
89 very to the lung downregulates expression of proinflammatory cytokines and improves allergen-induced
90 Activation of Nlrp3 leads to synthesis of proinflammatory cytokines and influences epithelial inte
91 hese macrophage-like nanoparticles sequester proinflammatory cytokines and inhibit their ability to p
92 of infection, WT mice had higher circulatory proinflammatory cytokines and lower anti-inflammatory cy
94 -cycle arrest combined with the secretion of proinflammatory cytokines and mitochondrial dysfunction.
95 duced sepsis, decreases the plasma levels of proinflammatory cytokines and organ injury markers in a
96 f atherosclerotic plaques, the production of proinflammatory cytokines and reactive oxygen species, t
97 glucocorticoid biosynthesis is suppressed by proinflammatory cytokines and that glucocorticoid defici
98 mulated insulin secretion in the presence of proinflammatory cytokines and triggered gene expression
99 tion, and leukocyte migration plus genes for proinflammatory cytokines and various toll-like receptor
100 mmation, accompanied by a massive release of proinflammatory cytokines at the maternal-fetal interfac
101 ens at various nonmucosal sites by eliciting proinflammatory cytokines by human macrophages, monocyte
102 these glycolipids induced the production of proinflammatory cytokines by macrophages, thereby sugges
105 ungs and their relationship with circulating proinflammatory cytokines during ischemia-reperfusion in
108 o, these dendrimers reduced the secretion of proinflammatory cytokines from mice and human monocyte-d
111 R4 activation to limit the production of the proinflammatory cytokines IL-6 and IL-12p40 while enhanc
112 The mRNA and protein expression levels of proinflammatory cytokines IL6, IL8 and CCL5 were determi
114 ased survival rates and heightened levels of proinflammatory cytokines in both peritoneal lavage and
115 he reduced capacity of leukocytes to release proinflammatory cytokines in response to ex vivo stimula
117 d mononuclear cells (MMCs) and the levels of proinflammatory cytokines in the blood and the brains of
118 , and quantitative RT-PCR (qRT-PCR), and the proinflammatory cytokines interleukin 1beta, interferon
119 dent subjects compared with controls for the proinflammatory cytokines interleukin-6 and interleukin-
121 iologics are currently available that target proinflammatory cytokines produced by T lymphocytes, but
122 cer cells in vitro induced the expression of proinflammatory cytokines such as CXCL5 by activating St
123 h covR-deficient S. agalactiae produced less proinflammatory cytokines than those infected with wild-
124 nalysis of human macrophages showed that the proinflammatory cytokines TNF and type I interferons ind
125 atory protein cyclooxygenase (COX)-2 and the proinflammatory cytokines TNF-alpha, IL-6, and IL-12.
126 ults together suggest that NRTIs up-regulate proinflammatory cytokines via a Wnt5a signaling-dependen
127 s significant inhibition in the synthesis of proinflammatory cytokines with a concordant blockade of
129 (less cardiac infiltrates and suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis,
130 binding to TLR2 induced robust expression of proinflammatory cytokines, and end products of lipid oxi
131 traumatic insult), become activated, produce proinflammatory cytokines, and recruit monocytes and den
132 inflammatory cells with local production of proinflammatory cytokines, and subsequent epithelial dis
133 on of TNF-alpha and IL-1beta, widely studied proinflammatory cytokines, did not induce persistent dis
134 phages results in the coordinated release of proinflammatory cytokines, followed by regulatory mediat
136 , P2X7R activation induces the production of proinflammatory cytokines, including IL-1beta and IL-18,
137 the dysregulation of osteoclast activity by proinflammatory cytokines, including TNF, interferes wit
138 tivation characterized by elevated levels of proinflammatory cytokines, including type I interferons
139 with pH1N1/NSs-6mut induced lower levels of proinflammatory cytokines, likely due to a general inhib
140 ges (pH1N1/NSs-6mut) induced lower levels of proinflammatory cytokines, resulting in viral attenuatio
141 gnificantly higher expression and release of proinflammatory cytokines, such as chemokine (C-C motif)
142 +) monocytes, as well as increased levels of proinflammatory cytokines, such as TNF-alpha and IL-17.
143 ading to cell type-specific amplification of proinflammatory cytokines, such as TNF-alpha, IL-1beta,
144 Kal directly activated monocytes to produce proinflammatory cytokines, up-regulated their C5aR and F
145 in Ld-infected cells curtails production of proinflammatory cytokines, which are otherwise detriment
146 itantly, S. aureus elicits the production of proinflammatory cytokines, which could ultimately pertur
157 ases 1 (TIMP-1), downregulated expression of proinflammatory cytokines/chemokines, and significantly
161 novicida infection due to overproduction of proinflammatory effectors including prostaglandin E2.
162 and phthalates may have immunomodulatory and proinflammatory effects and thereby adversely affect res
164 nhibits both myometrial contractions and the proinflammatory effects of OT without the biased agonist
167 s, membrane release of AA, and generation of proinflammatory eicosanoids and may account for increase
169 e models of WNV infection demonstrate that a proinflammatory environment is induced within the centra
170 ough ROS production is typically viewed as a proinflammatory event, our observations identify the imp
171 T cell accumulation, and high levels of the proinflammatory factors IFN-gamma, TNF-alpha, and induci
172 eport on a novel mechanism that promotes the proinflammatory function of PGE2 We showed previously th
175 inhibition of NEDDylation by MLN4924 blocked proinflammatory gene expression and NF-kappaB activation
176 n may represent a novel approach to modulate proinflammatory gene expression and open new therapeutic
177 c plaque formation, characterized by reduced proinflammatory gene expression and plaque macrophage co
178 meres were concordant with proosteoblast and proinflammatory gene network alterations in human NOTCH1
179 at HCMV induces the upregulation of multiple proinflammatory gene ontologies, with the interferon-ass
180 d with oxLDL, whereas the induction of other proinflammatory genes by TLR4 (LPS), TLR3 (polyriboinosi
185 sponses in the lung, including activation of proinflammatory IL-17-producing gammadelta T cells, with
188 as to determine the changes in expression of proinflammatory innate and T-cell-derived cytokines duri
189 ulated expression levels were found for most proinflammatory innate cytokines, including tumor necros
190 note was an increase in the abundance of the proinflammatory leukotriene B4 (LTB4) and a correspondin
192 okines that correlated with severity, 13 are proinflammatory, likely contributing to many of the symp
194 e signature within the pancreas, and reduced proinflammatory M1 macrophage responses were observed.
196 ing heterogeneous phenotypes, from classical proinflammatory M1 to alternative anti-inflammatory M2 m
197 ting the expression of genes associated with proinflammatory (M1) macrophage activation and was prote
198 f macrophages from anti-inflammatory (M2) to proinflammatory (M1) subtype after incubation with MfP.
202 mediated by inflammatory monocytes (IM) and proinflammatory macrophages (M1), followed by polarizati
204 te recruitment (T lymphocytes and classic M1 proinflammatory macrophages) and decreased expression le
206 atment with 2-AG suppresses TNFalpha-induced proinflammatory markers and improves IR and glucose upta
207 ssociated with reduced NF-kappaB activation, proinflammatory markers, endoplasmic reticulum stress, a
209 on resolving) and granulocyte-M-CSF (GM-CSF; proinflammatory) may contribute to the inconsistency of
210 s on intestinal MCs indicated an increase in proinflammatory MC function in advanced stages of the di
212 functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and it alters the integrity an
213 aride model of inflammation, RVX-297 reduced proinflammatory mediators assessed in splenic gene expre
214 bly was associated with reduced secretion of proinflammatory mediators from microglia cells, ultimate
215 popolysaccharide (LPS) significantly induced proinflammatory mediators in a dose-dependent manner.
216 ion, increased expression of profibrotic and proinflammatory mediators, and increased TRPC6, PKC-alph
219 LRP1 gene silencing increases expression of proinflammatory mediators; however, the observed respons
221 bic exercise is feasible and can improve the proinflammatory metabolic milieu in patients with modera
222 nic back pain and is linked to production of proinflammatory molecules by nucleus pulposus (NP) and o
223 challenge, leading to enhanced production of proinflammatory molecules upon other subsequent, and tem
226 ation with increases in IL-23 and IL-17A and proinflammatory monocytosis and neutrophilia that preced
229 ) has been identified as a critical brake on proinflammatory nuclear factor kappa light chain enhance
230 program in tumor-associated macrophages to a proinflammatory one, with a concomitant reduction of the
231 In addition to hypercholesterolemia, the proinflammatory Paigen diet significantly increased VCAM
232 ls promote the asthma phenotype and that the proinflammatory pathway downstream of the beta2AR involv
233 rted for ebolavirus species and suggest that proinflammatory pathways represent an intriguing target
234 ives resident and transplanted MSCs toward a proinflammatory phenotype and restricts their survival a
236 ted that the epithelial barrier to bacterial proinflammatory products is impaired when biofilm lysine
237 ut changing the number of macrophages with a proinflammatory profile (M1 [F4/80(low) Gr1(+) CD11b(med
239 d (monosodium urate [MSU]) crystals induce a proinflammatory profile in isolated human term cytotroph
240 , NFAT5 enhanced functions associated with a proinflammatory profile such as bactericidal capacity an
241 valuated in human tumor xenograft models the proinflammatory properties of an oncolytic adenovirus (O
243 26 expressed in inflammatory lesions confers proinflammatory properties to DNA released by dying cell
244 as detected by the reduced induction of the proinflammatory protein cyclooxygenase (COX)-2 and the p
245 factor kappa B and reduced the expression of proinflammatory proteins (inducible nitric oxide synthas
246 mmation coincident with massive increases in proinflammatory proteins and IFN-alpha in distal airways
247 arginase 1, indicating that it could promote proinflammatory readiness by regulating independent gene
248 ly, prediction analysis showed inhibition of proinflammatory regulators and activation of anti-inflam
249 itotic origin, micronuclei formation and the proinflammatory response following DNA damage are cell-c
250 etermine whether rosuvastatin can reduce the proinflammatory response induced by Aggregatibacter acti
251 ncy in the pig and may serve to regulate the proinflammatory response of endometrium to IL1B2 during
252 /6 mice resist various pathogens through the proinflammatory response of their M1 macrophages (MPs).
253 summary, whereas TonEBP participates in the proinflammatory response to TNF-alpha, therapeutic strat
254 oxisomes blocked the TLR4 ligand LPS-induced proinflammatory response, as detected by the reduced ind
255 s expected, EBOV infection led to a profound proinflammatory response, including strong induction of
257 itate conditions macrophages for exacerbated proinflammatory responses (lower IL-10 and CCL2, higher
259 3, which down-regulates T-helper cell type 1 proinflammatory responses and is associated with chronic
260 required for IL-1beta- or IL-1alpha-mediated proinflammatory responses and the stimulatory effects of
261 al IL18 haplotype associated with heightened proinflammatory responses confers susceptibility to stre
262 clude that T. suis secretes PGE2 to suppress proinflammatory responses in human DCs, thereby modulati
263 icus, both increased in MS patients, induced proinflammatory responses in human peripheral blood mono
264 acellular signaling pathways involved in the proinflammatory responses of macrophages are well charac
266 portant for viral clearance, modify the host proinflammatory responses through effects on the inflamm
267 tein (pH1N1/NSs-6mut) inhibited host IFN and proinflammatory responses to a greater extent than that
270 key immunoregulatory mediator and can dampen proinflammatory responses via activation of histamine re
271 gulatory network leading to the dampening of proinflammatory responses, expansion of type 1 regulator
274 We aimed to provide an understanding of the proinflammatory role of bronchoalveolar lavage fluid (BA
276 We also inhibited the production of the proinflammatory secretome of senescent cells using a JAK
278 mmunity and implicate TLR-mediated NF-kappaB proinflammatory signaling from the late endocytic pathwa
279 responses to atherogenic diet by restraining proinflammatory signaling in endothelial cells and BM-de
283 y drugs (NSAIDs) (Pinteraction = 0.055), the proinflammatory-stable DII group was at increased risk o
286 In mouse models, TRX80 was associated with a proinflammatory status and increased atherosclerosis.
290 and sFRP5 was differentially regulated by a proinflammatory stimulus (lipopolysaccharide [LPS] from
292 -associated kinase (ROCK)2 downregulates the proinflammatory T cell response while increasing the reg
294 2 infusion was associated with reduced donor proinflammatory Th1 and Th17 cells, accumulation of dono
300 tion in myeloid cells restored activation of proinflammatory tumor-associated macrophages (TAM) and i
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