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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
42      Herein, we describe LPA as an important mediator of inflammation after spinal cord injury (SCI)
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
47     Interleukin-1 beta (IL-1beta) is a major mediator of inflammation and a growth promoter for many
48                                As a critical mediator of inflammation and apoptosis in various cell t
49 sed by Egr-1, suggesting that Egr-1 is a key mediator of inflammation and apoptosis in vascular cells
50                    The CD40 pathway is a key mediator of inflammation and autoimmunity.
51 lator of CDC42 small G-protein signaling and mediator of inflammation and candidate coregulator of am
52              Moreover, NO is also a critical mediator of inflammation and carcinogenesis.
53           Interleukin (IL)-1 is an important mediator of inflammation and cardiovascular disease.
54 rachidonic acid, a omega-6 PUFA, is a potent mediator of inflammation and cell proliferation.
55                       TNF-alpha is a central mediator of inflammation and critical for host response
56            Nitric oxide (NO) is a ubiquitous mediator of inflammation and immunity, involved in the p
57                Interleukin-1 (IL-1) is a key mediator of inflammation and immunity.
58      The interleukin (IL)-1 pathway is a key mediator of inflammation and innate immune responses.
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
61       These results suggest that fibrin is a mediator of inflammation and may impede the reparative p
62  results indicate that LOX-1 is an important mediator of inflammation and neutrophil dysfunction in s
63                   The TAK1 (MAP3K7) is a key mediator of inflammation and non-canonical TGF-beta sign
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
66  that scavenges isolevuglandins-a downstream mediator of inflammation and oxidative stress.
67 E(2) (PGE(2)) is a prevalent and established mediator of inflammation and pain in numerous tissues an
68                        IL-13 is an important mediator of inflammation and remodeling.
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
72 phospholipase A2alpha (cPLA2alpha)] is a key mediator of inflammation and tumorigenesis.
73  as the immune-suppressive function of lipid mediators of inflammation and alarmins, are just some ex
74 thesis of leukotrienes, potent extracellular mediators of inflammation and allergic disorders.
75  of arachidonic acid to leukotrienes, potent mediators of inflammation and allergy.
76 hesis of eicosanoids and other lipid-derived mediators of inflammation and allergy.
77                     Eicosanoids are powerful mediators of inflammation and are known to drive both th
78    CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous
79                         T cells are critical mediators of inflammation and as such, their migration t
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
85                               Genes encoding mediators of inflammation and host defense, including CD
86                       Cytokines are critical mediators of inflammation and host defenses.
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
90 t of direct interactions between the soluble mediators of inflammation and infectious agents.
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
95         Prostaglandins and NO. are important mediators of inflammation and other physiological and pa
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
103        LPG's inhibitory activity for several mediators of inflammation and the persistence of signifi
104                       Eicosanoids are potent mediators of inflammation and tightly associated with mo
105 ophil cationic protein (ECP), are well-known mediators of inflammation and tissue damage in asthma.
106                    Macrophages are important mediators of inflammation and tissue remodeling.
107 ctivation and mRNA stabilization of numerous mediators of inflammation and tissue repair.
108 ) and prostaglandin E(2) (PGE(2)), important mediators of inflammation and tumor promotion.
109 xygenase-2), which is an important enzymatic mediator of inflammation, and a target of aspirin.
110             Nitric oxide (NO.), an important mediator of inflammation, and beta-catenin, a component
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
113           Prostaglandin E2 (PGE2) is a lipid mediator of inflammation, and its tissue concentration i
114 ONOOCO(2)(-)), a macrophage-derived chemical mediator of inflammation, and the classical one-electron
115                          Monocytes are major mediators of inflammation, and apoptosis provides a mech
116                            Inflammasomes are mediators of inflammation, and constitutively activated
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
120                           Accordingly, these mediators of inflammation are the targets of several ant
121                                Both of these mediators of inflammation are thought to contribute to t
122  to generate arachidonate-derived eicosanoid mediators of inflammation are uncertain.
123 are members of the specialized pro-resolving mediators of inflammation, are produced.
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
126                         We hypothesized that mediators of inflammation associated with atherosclerosi
127   Nitric oxide is believed to be a prominent mediator of inflammation based in part on the correlativ
128        TGF-beta1 is an important suppressive mediator of inflammation, but it can also drive fibrosis
129                COX2 activity is an important mediator of inflammation, but it is not known whether CO
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.
136                Leukotrienes (LTs) are potent mediators of inflammation derived from the 5-lipoxygenas
137  for the first time that ONOO(-) is a potent mediator of inflammation-derived hyperalgesia operating
138                     Specialized proresolving mediators of inflammation drive macrophage efferocytosis
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
141 eased by many cell types and is an important mediator of inflammation during infection.
142 ents of microorganisms and are critical host mediators of inflammation during infection.
143  highly conserved and regulated, pleiotropic mediators of inflammation, essential to respond adequate
144                                              Mediators of inflammation, fibrosis, and regeneration we
145 iator of lethality in sepsis and as an early mediator of inflammation following injury.
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
148                 Leukotrienes (LTs) are lipid mediators of inflammation formed by enzymatic oxidation
149            The leukotrienes are potent lipid mediators of inflammation formed by the 5-lipoxygenase-c
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
154          Neutrophils and macrophages, as key mediators of inflammation, have defined functionally imp
155 or necrosis factor (TNF) alpha is a critical mediator of inflammation; however, TNFalpha is rarely re
156           Although PAF plays a key role as a mediator of inflammation in acute pancreatitis, the site
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
160 oncanonical inflammasome activation as a key mediator of inflammation in macrophages.
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
166 rt the conclusion that MCP-1 is an important mediator of inflammation in the CNS.
167 TING signalling pathway has emerged as a key mediator of inflammation in the settings of infection, c
168         Originally identified as a potential mediator of inflammation in the skin, we recently report
169 ogenesis of bacterial meningitis as a potent mediator of inflammation in the subarachnoid space.
170                   Therefore, PDE3 is a novel mediator of inflammation in VSMCs.
171  Recent work indicates T cells are important mediators of inflammation in a mouse model of T2D.
172 e cyclooxygenase (COX) enzymes are important mediators of inflammation in arthritis.
173        Expression of CARD8 was correlated to mediators of inflammation in atherosclerotic lesions usi
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
176 staglandin E2 (PGE2) have been implicated as mediators of inflammation in OA.
177                                          The mediators of inflammation in spondyloarthropathies have
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
186                        However, the specific mediators of inflammation-induced injury remain unclear.
187 st invading pathogens but are also important mediators of inflammation-induced injury.
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
191                            As an established mediator of inflammation, interleukin-6 (IL-6) is implic
192                                 An important mediator of inflammation is extracellular adenosine trip
193                      Insight into pathogenic mediators of inflammation is essential for targeted and
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
196                                 COX-2, a key mediator of inflammation, is upregulated in activated mo
197 e synthesis of prostanoids, which are potent mediators of inflammation, is dramatically increased.
198            Although originally identified as mediators of inflammation, it is now apparent that chemo
199  45) for the presence of cytokines and lipid mediators of inflammation (LMIs).
200 ammation and cancer, and it is believed that mediators of inflammation may be responsible for this ph
201                         The reduction in the mediators of inflammation may thus be responsible for th
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,
206                                  Circulating mediators of inflammation participate in the mechanisms
207 s recent developments in the role of soluble mediators of inflammation, particularly arachidonic acid
208                               Information on mediators of inflammation permeated many sessions, havin
209                            Because the lipid mediator of inflammation, platelet-activating factor (PA
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
212           Cellular senescence is a plausible mediator of inflammation-related tissue dysfunction.
213 ust is compartmentalized, involving specific mediators of inflammation released by macrophages, neutr
214  inflammatory trigger as well as a potential mediator of inflammation resolution.
215   These findings establish CSPGs as critical mediators of inflammation resolution failure after SCI i
216                                        Lipid mediators of inflammation resolution, e.g., resolvin D2,
217        Platelet-activating factor (PAF) is a mediator of inflammation shown to orchestrate inflammato
218 and APCs, are major producers of the central mediator of inflammation, soluble TNF-alpha (sTNF).
219         The biliary epithelium is exposed to mediators of inflammation such as bacterial endotoxin or
220 nnate sources of type 2 cytokines and innate mediators of inflammation such as the alarmins.
221                                    Important mediators of inflammation such as the cytokine tumor nec
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
225         Prostaglandin E(2) is a potent lipid mediator of inflammation that effects changes in cell fu
226            The anaphylatoxin C5a is a potent mediator of inflammation that exerts a broad range of ac
227                                    CD95 is a mediator of inflammation that has also been proposed as
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
235                                     They are mediators of inflammation through the production of path
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
239              KLF4 was an epithelial-specific mediator of inflammation; we developed a new mouse model
240 ation of hepatic stellate cells, but hepatic mediators of inflammation were not significantly differe
241                                Levels of key mediators of inflammation were reduced in patient tears
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
245                     Prostaglandins (PGs) are mediators of inflammation with pronociceptive actions wi

 
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