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1 ide (NO) has been recognized as an important mediator of inflammation.
2 ereas bradykinin is a potent vasodilator and mediator of inflammation.
3 mediator of antiviral defenses, it is also a mediator of inflammation.
4 the myelomonocytic lineage and an important mediator of inflammation.
5 e the CTpr level, which is a potential toxic mediator of inflammation.
6 rse physiological actions, particularly as a mediator of inflammation.
7 We concluded that endogenous NO acts as a mediator of inflammation.
8 ive at low doses, induces autophagy and is a mediator of inflammation.
9 cell types such as cardiomyocytes; and as a mediator of inflammation.
10 kinetic factor to an activated and efficient mediator of inflammation.
11 Nuclear factor kappa B (NF-kappaB) is a key mediator of inflammation.
12 40 gene and the genes encoding several other mediators of inflammation.
13 amines and a reduction in canonical cytokine mediators of inflammation.
14 such as periodontitis, with a focus on lipid mediators of inflammation.
15 initiating the biosynthesis of lipid-derived mediators of inflammation.
16 nes with a prominent increase in markers and mediators of inflammation.
17 ed metabolites mapping to pathways for lipid mediators of inflammation.
18 to release peptides in response to trauma or mediators of inflammation.
19 precursor (CTpr) levels are both markers and mediators of inflammation.
20 eukin (IL-1)alpha and IL-1beta are important mediators of inflammation.
21 ing peptides, which are proposed to be major mediators of inflammation.
22 gamma(+/+) cells appear to involve different mediators of inflammation.
23 r enhanced synthesis of paracrine eicosanoid mediators of inflammation.
24 rostaglandins and glucocorticoids are potent mediators of inflammation.
25 on and tissue injury could thus be important mediators of inflammation.
26 is (RA), and can secrete cytokines and other mediators of inflammation.
27 ndins (PGs) and are among the most important mediators of inflammation.
28 rienes (CysLTs) have been defined as central mediators of inflammation.
29 nex multiplex array analysis for established mediators of inflammation.
30 ly active IL-1beta, IL-18, and other soluble mediators of inflammation.
31 ide and hydrogen sulfide are key signals and mediators of inflammation.
32 genase (COX)-derived oxylipins are important mediators of inflammation.
33 lly similar, but functionally distinct lipid mediators of inflammation.
34 osynthesis to the production of proresolving mediators of inflammation.
35 mily of cytokines comprises a set of pivotal mediators of inflammation.
36 act as upstream facilitators and downstream mediators of inflammation.
37 erleukin-1 beta and -18, which are important mediators of inflammation.
38 oxygenase pathways are known to be important mediators of inflammation.
39 h mobility group box 1 are critical cytokine mediators of inflammation.
40 rging evidence that specialized proresolving mediators of inflammation accelerate wound healing by pr
41 nt studies have implicated HMGB1 as an early mediator of inflammation after HS/R and organ ischemia/r
43 Proinflammatory macrophages are important mediators of inflammation after myocardial infarction an
44 ls of expression of messenger RNA (mRNA) for mediators of inflammation, aggrecanases, MMPs, and their
45 noids and platelet-activating factor, potent mediators of inflammation, allergy, apoptosis, and tumor
46 These results suggest that on stimulation by mediators of inflammation, although the basal transcript
49 sed by Egr-1, suggesting that Egr-1 is a key mediator of inflammation and apoptosis in vascular cells
51 lator of CDC42 small G-protein signaling and mediator of inflammation and candidate coregulator of am
59 terleukin-1 beta (IL-1beta) is a pleiotropic mediator of inflammation and is produced in response to
60 Much evidence implicates IL-8 as a major mediator of inflammation and joint destruction in rheuma
62 results indicate that LOX-1 is an important mediator of inflammation and neutrophil dysfunction in s
64 in contrast to the role of HMGB1 as an early mediator of inflammation and organ damage in hepatic I/R
65 flammation of sepsis, HMGB1 acts as an early mediator of inflammation and organ damage in hepatic isc
67 E(2) (PGE(2)) is a prevalent and established mediator of inflammation and pain in numerous tissues an
69 the gene encoding chemokine receptor Ccr2, a mediator of inflammation and several disease processes.
70 hat epithelial-derived MMP-9 is an important mediator of inflammation and tissue damage in colitis.
71 complement C5a system, which is an important mediator of inflammation and tissue regeneration, is act
73 as the immune-suppressive function of lipid mediators of inflammation and alarmins, are just some ex
78 CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous
80 pro-HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also
81 ransfusion requirements, and levels of serum mediators of inflammation and cardiac troponin I were si
82 These elevated gene products are molecular mediators of inflammation and collagen degradation in ac
83 dent atrial fibrillation was associated with mediators of inflammation and fibrosis (MMP2 [matrix met
84 ern recognition receptors that are essential mediators of inflammation and host defense in the gastro
87 e derived from arachidonic acid and serve as mediators of inflammation and immediate hypersensitivity
88 A (dsRNA)-activated genes, including several mediators of inflammation and immune cell recruitment.
89 Statins have diverse effects on the cellular mediators of inflammation and immunity that may be parti
91 thelial cells were cultured and assessed for mediators of inflammation and injury, such as ICAM-1, AP
92 airways quantitatively with respect to known mediators of inflammation and intercellular communicatio
93 synovial intimal lining of the joint are key mediators of inflammation and joint destruction in rheum
94 scle (SkM) atrophy and dysfunction, decrease mediators of inflammation and normalize metabolic pertur
96 expression with indices of disease severity, mediators of inflammation and outcome indicates a key ro
97 the synthesis of leukotrienes LTB4 and LTC4, mediators of inflammation and pain, were found in the UT
98 that this was, in part, due to the effect of mediators of inflammation and predicted that greater cha
99 ood pressure (BP), heart rate, cortisol, and mediators of inflammation and reductions in heart rate v
100 NOS; NOS-2) and cyclooxygenase-2 (COX-2) are mediators of inflammation and regulators of epithelial c
101 sis of eicosanoids and other bioactive lipid mediators of inflammation and resolution underlying dise
102 , these cytokines are also recognized as key mediators of inflammation and the pathobiology of divers
105 ophil cationic protein (ECP), are well-known mediators of inflammation and tissue damage in asthma.
111 e, CO blocked expression of Egr-1, a central mediator of inflammation, and decreased tissue damage; i
112 rosis factor alpha (TNF-alpha) is a critical mediator of inflammation, and its production is tightly
114 ONOOCO(2)(-)), a macrophage-derived chemical mediator of inflammation, and the classical one-electron
117 Expression is modulated by serum factors, mediators of inflammation, and kinase activators and inh
118 ritic inflammation and inhibited the defined mediators of inflammation, angiogenesis, cell survival,
119 sis factor alpha (TNF-alpha) is an important mediator of inflammation, apoptosis, and the development
124 Here, we examine the association of upstream mediators of inflammation as ascertained by fatty-acid d
125 exists between vascular cellular hypoxia and mediators of inflammation associated with aortic aneurys
127 Nitric oxide is believed to be a prominent mediator of inflammation based in part on the correlativ
130 ensitivity is differentially associated with mediators of inflammation by studying 2 chronic inflamma
131 onstitutive decay of instable mRNAs encoding mediators of inflammation by various experimental approa
132 ults of these studies indicate that a common mediator of inflammation can lead to the induction of SS
133 ntation abolished the expression of mRNA for mediators of inflammation (cyclooxygenase 2, 5-lipoxygen
134 Resolvin E1 (RvE1) is a potent proresolving mediator of inflammation derived from omega-3 eicosapent
135 ienes (cys-LTs) are a family of potent lipid mediators of inflammation derived from arachidonic acid.
137 for the first time that ONOO(-) is a potent mediator of inflammation-derived hyperalgesia operating
139 though TNF-alpha is believed to be a central mediator of inflammation-driven atherosclerosis, genetic
140 response to inflammatory cytokines and novel mediators of inflammation-driven degradation in tissue-e
143 highly conserved and regulated, pleiotropic mediators of inflammation, essential to respond adequate
146 tivating factor (PAF), a potent phospholipid mediator of inflammation, for its ability to activate CR
147 Leukotriene B(4) (LTB(4)) is a potent lipid mediator of inflammation formed by the 5-lipoxygenase (5
150 se), the expression of which is regulated by mediators of inflammation, had a strong, positive associ
151 ucible nitric-oxide synthase (iNOS), a major mediator of inflammation, has been implicated in beta-ce
152 Inducible nitric-oxide synthase (iNOS), a mediator of inflammation, has been implicated in many hu
153 ur data support the hypothesis that cellular mediators of inflammation have a role in atherogenesis a
155 or necrosis factor (TNF) alpha is a critical mediator of inflammation; however, TNFalpha is rarely re
157 estigated why the production of IL-23, a key mediator of inflammation in autoimmunity, is blocked whe
158 rP was induced in glia by TNF-alpha, a known mediator of inflammation in brain and of PTHrP induction
159 valuated whether prostacyclin is a necessary mediator of inflammation in graded bacteremia or is suff
161 otubule dysfunction has been implicated as a mediator of inflammation in multiple diseases such as di
162 Thus, TNF-alpha appears to be an important mediator of inflammation in patients with poor viral con
163 by antibody to cyclophilin A (CyPA), a known mediator of inflammation in peripheral tissues, and by c
164 Tumor necrosis factor (TNF) is a powerful mediator of inflammation in rheumatoid arthritis (RA).
165 ypothesis that osteopontin may be a critical mediator of inflammation in specific disease and injury
167 TING signalling pathway has emerged as a key mediator of inflammation in the settings of infection, c
169 ogenesis of bacterial meningitis as a potent mediator of inflammation in the subarachnoid space.
174 ic DNA (cytoDNA) species are emerging as key mediators of inflammation in diverse physiological and p
175 arachidonyl-phosphatidyl choline (PAPC), are mediators of inflammation in endothelial cells (ECs) and
178 demonstrates the differential expression of mediators of inflammation in the esophageal mucosa of pa
179 te immune complement component C5a, a potent mediator of inflammation, in the pathogenesis of DKD in
180 anscription factor that is activated by many mediators of inflammation including IL-1, IL-6, and bact
181 ern diet, are precursors for a number of key mediators of inflammation including the 2-series of pros
182 ve target for inhibiting Ca(2+) responses to mediators of inflammation, including C5a, UDP, PAF, and
183 tion of SCW-induced arthritis and changes in mediators of inflammation, including T cell subsets, pro
184 peralgesia and interacts with many different mediators of inflammation, including the MAPK signaling
185 oleamine 2,3-dioxygenase (IDO), is a pivotal mediator of inflammation-induced depression, its mechani
188 the optimal 10 mg/kg dose downregulated key mediators of inflammation-induced lymphangiogenesis, cor
189 mis, are the sites for the expression of two mediators of inflammation, inducible nitric oxide syntha
190 at prostaglandin E(2) (PGE(2)), a well-known mediator of inflammation, inhibits mucosal T(regs) in a
194 r necrosis factor-alpha (TNF-alpha), a major mediator of inflammation, is chronically produced in the
195 tivity of the NLRP3 inflammasome, a critical mediator of inflammation, is controlled by accessory pro
197 e synthesis of prostanoids, which are potent mediators of inflammation, is dramatically increased.
200 ammation and cancer, and it is believed that mediators of inflammation may be responsible for this ph
202 n vivo may represent previously unrecognized mediators of inflammation-mediated protein modification
203 and c) changes in the inflammatory cells and mediators of inflammation of the respiratory secretions
204 essed the effect of myeloperoxidase (MPO), a mediator of inflammation, on nitrosation observed during
205 the production of prostaglandins, important mediators of inflammation, pain, cardiovascular disease,
207 s recent developments in the role of soluble mediators of inflammation, particularly arachidonic acid
210 )-irradiated keratinocytes secrete the lipid mediator of inflammation, platelet-activating factor (PA
211 ucible nitric-oxide synthase (iNOS), a major mediator of inflammation, plays an important role in obe
213 ust is compartmentalized, involving specific mediators of inflammation released by macrophages, neutr
215 These findings establish CSPGs as critical mediators of inflammation resolution failure after SCI i
218 and APCs, are major producers of the central mediator of inflammation, soluble TNF-alpha (sTNF).
222 nd its expression is markedly upregulated by mediators of inflammation such as tumor necrosis factor
223 AS1 is a transcription factor that activates mediators of inflammation, such as tumor necrosis factor
224 chronic hyperglycemia seems to be a stronger mediator of inflammation than cigarette smoking in patie
228 factor (PAF) is a phosphoglycerylether lipid mediator of inflammation that is implicated in infection
229 These findings identify TGR5 as a negative mediator of inflammation that may serve as an attractive
230 GMP-AMP synthase (cGAS) has emerged as a key mediator of inflammation that underlies cardiovascular d
231 lso possess a repertoire of potent preformed mediators of inflammation that are released on activatio
232 s suggest that the production of pleiotropic mediators of inflammation that influence cartilage homeo
233 elet-activating factor (PAF) is an important mediator of inflammation, the action of which in endothe
234 s an initial step in the production of lipid mediators of inflammation: the Ca2+-dependent translocat
236 ism is key to the control of essential early mediators of inflammation, TNF, CXCL1, and CXCL2, as wel
237 ed for the renal induction of genes encoding mediators of inflammation (vcam-1, s100A9, and Il-1b) an
238 y throughout the lung, caused by blood-borne mediators of inflammation, voluminous aspiration, or inh
240 ation of hepatic stellate cells, but hepatic mediators of inflammation were not significantly differe
242 latelet-activating factor (PAF), both potent mediators of inflammation, were used as triggers for gen
243 uce the aggregation of HMGB1 protein, a late mediator of inflammation, which subsequently stimulates
244 products of arachidonic acid metabolism are mediators of inflammation with an important role in the