ライフサイエンスコーパス: acute inflammation

1 ic inflammation) and 70% during endotoxemia (acute inflammation).

2 ury, and suppress the detrimental effects of acute inflammation.

3 ls, suggesting a role in innate immunity and acute inflammation.

4 t of severe acute pancreatitis as a model of acute inflammation.

5 r steatohepatitis, and also in patients with acute inflammation.

6 in-1 neddylation is central to resolution of acute inflammation.

7 emory T cells is necessary for resolution of acute inflammation.

8 by epithelial disorganization, fibrosis and acute inflammation.

9 inistered directly into lungs, IL-25 induces acute inflammation.

10 cytes of noninflamed skin but induced during acute inflammation.

11 keratinocyte nuclei and rapidly lost during acute inflammation.

12 on the homeostasis at the site of injury or acute inflammation.

13 rchestrate resolution in diverse settings of acute inflammation.

14 t stereoselectively stimulates resolution of acute inflammation.

15 life-threatening platelet depletions during acute inflammation.

16 tory cytokine, inhibits vascular response in acute inflammation.

17 thereby facilitating PMN trafficking during acute inflammation.

18 gonist mAb suppressed CD4(+) T cell-mediated acute inflammation.

19 des, gammadeltaT cells promote resolution of acute inflammation.

20 t is detrimental for survival in LPS-induced acute inflammation.

21 nfectious agents to facilitate recovery from acute inflammation.

22 of tissues from the damaging consequences of acute inflammation.

23 ivity of IL-6 during the different stages of acute inflammation.

24 ion of C3 by hepatocytes is increased during acute inflammation.

25 cal to limit unintended tissue injury during acute inflammation.

26 pressive adenosine, are therefore pivotal in acute inflammation.

27 iogenic response that fits the time scale of acute inflammation.

28 ular risk factors in obesity but exacerbates acute inflammation.

29 ved in LFA-1-mediated PMN trafficking during acute inflammation.

30 by catecholamines and glucocorticoids during acute inflammation.

31 vented the arrival of leukocytes at sites of acute inflammation.

32 function-associated antigen 1 (LFA-1) during acute inflammation.

33 hils that have undergone karyorrhexis during acute inflammation.

34 n evaluation of microvasculature function in acute inflammation.

35 neutrophil recruitment in several models of acute inflammation.

36 is, foci of hepatocellular degeneration, and acute inflammation.

37 t can be systemically induced in response to acute inflammation.

38 ms to induce Tregs and enhance resolution of acute inflammation.

39 to protect mice from liver damage induced by acute inflammation.

40 esponses and viral replication, but increase acute inflammation.

41 Improvements or worsening may be possible in acute inflammation.

42 raction may be involved in the resolution of acute inflammation.

43 metabolism with the early and late stages of acute inflammation.

44 ominant innate immune cell type activated in acute inflammation.

45 animal models of inflammatory arthritis and acute inflammation.

46 he reduction in serum zinc (hypozincemia) of acute inflammation.

47 TSP-1 production in the target organ during acute inflammation.

48 n result from either inadequate or excessive acute inflammation.

49 cts without known coronary artery disease or acute inflammation.

50 ination, which is provided in the context of acute inflammation.

51 or high capacity clearance of neutrophils in acute inflammation.

52 well known cytokine involved in systemic and acute inflammation.

53 eir influence on endothelial function during acute inflammation.

54 amage, senescence, p53, p16, and chronic and acute inflammation.

55 on and suppressing that of cells that typify acute inflammation.

56 er without triggering fibrosis, necrosis, or acute inflammation.

57 deling, than under baseline conditions or in acute inflammation.

58 on, but it often comes with the price tag of acute inflammation.

59 ponses that may exacerbate mucosal injury in acute inflammation.

60 e adhesion during lipopolysaccharide-induced acute inflammation.

61 may exert their effects by the modulation of acute inflammation.

62 suggest that each plays a role in resolving acute inflammation.

63 hronic pre-existing lesions without signs of acute inflammation.

64 phases restore homeostasis following initial acute inflammation.

65 to RVM under basal conditions, as well as in acute inflammation.

66 paradox is that ovulation is known to induce acute inflammation.

67 at they release during thrombus formation or acute inflammation.

68 tle is known about these interactions during acute inflammation.

69 rafficking of Ly6c(hi) monocytes to sites of acute inflammation.

70 hronic inflammation, with little evidence of acute inflammation.

71 e to maintaining platelet homeostasis during acute inflammation.

72 system for the modulation of IL-27-dependent acute inflammation.

73 recruited to the bloodstream in response to acute inflammation.

74 on provides a mechanism to limit and resolve acute inflammation.

75 -3 in promoting leukocyte recruitment during acute inflammation.

76 system might be targeted therapeutically in acute inflammation.

77 noic acid, have tissue protective effects in acute inflammation.

78 n systemic endothelial barrier properties in acute inflammation.

79 ammatory processes controlling resolution of acute inflammation.

80 mice, as well as in an in vivo LPS model of acute inflammation.

81 ned insulin deficiency and endotoxin-induced acute inflammation.

82 During acute inflammation, 3 neutrophil subsets are found in th

83 Interestingly, immune cells associated with acute inflammation aberrantly infiltrated into reproduct

84 IKKbeta(EE)(IEC) mice succumb to destructive acute inflammation accompanied by enterocyte apoptosis,

85 rcuit that is operative in the resolution of acute inflammation activated by the proresolving mediato

86 In noninfectious models of acute inflammation, activation of A2B adenosine receptor

87 nflammation is a normal process in our body; acute inflammation acts to suppress infections and suppo

88 on is associated with tumorigenesis, but how acute inflammation affects the tumor microenvironment is

89 ng MPhis form distinct subpopulations during acute inflammation after challenge with LPS or influenza

90 gether, our results support a model in which acute inflammation after injury initiates important rege

91 in murine myocardial infarction, a model of acute inflammation after ischemic injury.

92 uide future cartilage studies related to the acute inflammation after joint trauma.

93 ivation and poly:IC signatures, representing acute inflammation and a complex mix of potential diseas

94 anisms by which the anaphylatoxin C5a limits acute inflammation and antagonizes the IL-17A/IL-23 axis

95 endotoxin (lipopolysaccharide; LPS)-induced acute inflammation and associated whole-animal damage/dy

96 es and is effective in preclinical models of acute inflammation and autoimmunity.

97 esterified oxylipin levels decreased during acute inflammation and before recovering.

98 with innate immune responses, which occur in acute inflammation and chronic inflammatory conditions s

99 Mice with carrageenan-induced acute inflammation and collagen-induced arthritis (CIA)

100 in Cx32 are protected against liver damage, acute inflammation and death caused by liver-toxic drugs

101 may represent a useful human model to study acute inflammation and determine beneficial systemic eff

102 e, we apply this technique to the context of acute inflammation and discover both infiltrating and ti

103 e initiation, progression, and resolution of acute inflammation and display specific, epithelial-dire

104 The shift to late acute inflammation and elevated fatty acid oxidation req

105 Both acute inflammation and fibrotic cohort of rats demonstra

106 Phagocytes orchestrate acute inflammation and host defense.

107 timulated upregulation of pathways linked to acute inflammation and immune cell migration, and activa

108 reater numbers in the blood of patients with acute inflammation and infectious diseases.

109 Acute inflammation and its resolution are essential proc

110 g/Pla in key events during the resolution of acute inflammation and its underlying mechanisms.

111 tolysis of ruminant leukocytes, resulting in acute inflammation and lung tissue damage.

112 pically administered lewisite induced potent acute inflammation and microvesication in the skin of Pt

113 nce for age-dependent resolution pathways in acute inflammation and novel means to activate resolutio

114 t immunoresolvent, stimulating resolution of acute inflammation and organ protection.

115 ll point to a relationship between excessive acute inflammation and p47(phox) deficiency in macrophag

116 We conclude that acute inflammation and peripheral nociceptor sensitizati

117 Using a mouse model of LPS-induced acute inflammation and plasma samples from sepsis patien

118 maresin sulfido-conjugates actively resolve acute inflammation and promote tissue regeneration.

119 ings expand our knowledge of Mo/MPhi flux in acute inflammation and provide the groundwork for novel

120 therapeutic option in the future to suppress acute inflammation and simultaneously promote recovery f

121 t the loss of ALX/FPR2 results in unresolved acute inflammation and SMG dysfunction (xerostomia) in r

122 tive players that counter-regulate excessive acute inflammation and stimulate molecular and cellular

123 del by using combined insulin deficiency and acute inflammation and tested which intracellular mediat

124 tion of immune complexes is a major event in acute inflammation and that GF mice have a distinct Ig r

125 nanoparticles provide a platform that limits acute inflammation and tissue destruction, at a favorabl

126 igration, cannabinoids contribute to resolve acute inflammation and to reestablish homeostasis.

127 Moreover, PGDHi attenuated both acute inflammation and weight loss, and decreased mortal

128 rticipate transiently in tissue repair after acute inflammation, and assume an aberrant stimulatory r

129 esenchymal stem cells on lung fluid balance, acute inflammation, and bacterial clearance.

130 g at the organismic level in homeostasis, in acute inflammation, and during the generation and regula

131 ve suggested a link among dental procedures, acute inflammation, and endothelial dysfunction.

132 n immunoresolvent that governs resolution of acute inflammation, and its local metabolism in the cont

133 liferation in cancer, cytokine production in acute inflammation, and so forth.

134 ors that actively regulate the resolution of acute-inflammation, and correlate measurements with clin

135 The magnitude and duration of acute inflammation are controlled by active resolution p

136 ous mechanisms that act in the resolution of acute inflammation are essential for host defense and th

137 us mechanisms that orchestrate resolution of acute inflammation are essential in host defense and the

138 These early cellular events in acute inflammation are pivotal to timely resolution by m

139 nfections contribute to active resolution of acute inflammation are unknown.

140 mice were better protected from LPS-induced acute inflammation as exemplified by their superior clin

141 s control both the duration and magnitude of acute inflammation as well as the return of the site to

142 mena are linked, the mechanisms facilitating acute inflammation-associated cytopenias are unknown.

143 al-1 in regulatory programs operating during acute inflammation, autoimmune diseases, allergic inflam

144 el leakiness is an early, transient event in acute inflammation but can also persist as vessels under

145 y correlated with Banff scores indicative of acute inflammation but not with scores indicative of fib

146 phils have long been known to participate in acute inflammation, but a role in chronic inflammatory a

147 We find that exercise enhances resolution of acute inflammation by augmenting resolvin D1 (RvD1) leve

148 Resolvins protect the host against acute inflammation by blocking the migration of polymorp

149 a3 only appears in plasma after induction of acute inflammation by some but not all inflammatory stim

150 lular uptake, significantly attenuated early/acute inflammation by suppressing pro-inflammatory cytok

151 ia is the major insult of stroke and induces acute inflammation by triggering excessive production of

152 Acute inflammation can also be shifted to a chronic infl

153 Unregulated acute inflammation can lead to collateral tissue injury

154 Although acute inflammation can result in defective LVs, TLO LVs

155 ere significantly higher for fibrotic versus acute inflammation cohort of rats at 0% (3.4 +/- 1.1 vs

156 caspase-1 protein and cell death in areas of acute inflammation, compared with active UC patients wit

157 morphonuclear neutrophils (PMNs) to sites of acute inflammation critically depends on beta2 integrins

158 An acute inflammation Crohn disease model was produced by t

159 rence tomography (OCT) were used to quantify acute inflammation, demyelination, conduction block, and

160 suggest that the host's health status during acute inflammation depends in a nonlinear fashion on the

161 ptor 4 is not required for the initiation of acute inflammation during cholestasis.

162 antigens in the steady state and regulating acute inflammation during infection.

163 ay plays a role in the S100 alarmin-mediated acute inflammation during VVC using the experimental mou

164 e deficient in IL-1 signaling have extensive acute inflammation following C. albicans water-soluble c

165 r-1alpha in type 2 cell is a major driver of acute inflammation following lung contusion.

166 Acute inflammation follows defined phases of induction,

167 After acute inflammation from 10 weeks of UVB irradiation subs

168 ors generated during the resolution phase of acute inflammation from the omega-3 polyunsaturated fatt

169 as regulatory cells throughout the course of acute inflammation, from its initiation to resolution.

170 of >/= 2 culture media positive for growth, acute inflammation (>/= 5 neutrophils/high-power field)

171 two weeks after injury, a time during which acute inflammation has largely subsided and lesions have

172 (CS) surveys indicate that individuals with acute inflammation have higher plasma ferritin (pF), and

173 echanisms that bring about the resolution of acute inflammation have uncovered a new genus of pro-res

174 and expression increased during chronic and acute inflammation; high levels were detected in colon t

175 activity is associated with a moderation of acute inflammation, higher antioxidant defences and adip

176 Acute inflammation impairs reverse cholesterol transport

177 n vivo, and their secretion products blocked acute inflammation in a model of peritonitis.

178 In this study, we investigated resolution of acute inflammation in aging and the roles of SPMs.

179 timulated epinephrine enhances resolution of acute inflammation in an alpha1-AR-dependent manner.

180 Following BLM injury, acute inflammation in CKO mice was similar to controls b

181 The demonstration of impaired acute inflammation in Crohn's disease provides a novel m

182 use lipopolysaccharide inhalation to induce acute inflammation in healthy volunteers and examine the

183 nan from Saccharomyces cerevisiae induced an acute inflammation in inbred mouse strains resembling hu

184 both H(2)O(2) and caspase 8 activity during acute inflammation in living mice.

185 flammatory proteins by macrophages and block acute inflammation in mice.

186 a enterica serovar Typhimurium benefits from acute inflammation in part by using host-derived nitrate

187 These data demonstrate that acute inflammation in response to a bacterial agent in t

188 gain insights into age-dependent changes in acute inflammation in response to bacterial endotoxin (L

189 Acute inflammation in response to both exogenous and end

190 and DSS treatment despite the lack of early acute inflammation in response to chemically induced inj

191 Although acute inflammation in response to myocardial cell death

192 vivo, and in vitro approach to the study of acute inflammation in shock states, and suggest hypothes

193 Clinical relapses reflect acute inflammation in the central nervous system (CNS),

194 Acute inflammation in the lung is essential to health.

195 ular and cellular effectors of resolution of acute inflammation in the lung.

196 tributing to efficient virus replication and acute inflammation in the lungs of pigs infected with th

197 (2.0 mg) of TA was as effective in reducing acute inflammation in the ocular posterior segment as hi

198 arrier and maintain barrier integrity during acute inflammation in vitro.

199 We demonstrate slings in a model of acute inflammation in vivo and on P-selectin in vitro, w

200 r, the ability of oral vitamin D to modulate acute inflammation in vivo has not been established in h

201 during dextran sulfate sodium (DSS)-induced acute inflammation in vivo, and administration of the No

202 te cellular infiltration in association with acute inflammation in vivo.

203 2-IIA), a bactericidal enzyme induced during acute inflammation, in innate immunity against GBS.

204 dy we explored the role of IRF5 in models of acute inflammation, including antigen-induced inflammato

205 Although many reproductive events induce acute inflammation, increased LOY was associated with lo

206 four different conditions: i) baseline, ii) acute inflammation induced by bradykinin, iii) sustained

207 confirm this conclusion in another model of acute inflammation induced by noninfectious stimuli.

208 Moreover, oxidative stress from the acute inflammation induced DNA damage and strand breaks

209 function confers increased susceptibility to acute inflammation-induced cognitive deficits.

210 causes compromised tissue repair by shifting acute inflammation into a more chronic profibrotic state

211 Acute inflammation is a host-protective response that is

212 Acute inflammation is a key feature of innate immunity t

213 The resolution of acute inflammation is a process that allows for inflamed

214 Resolution of acute inflammation is an active event accompanied by bio

215 Resolution of acute inflammation is an active process governed by spec

216 Resolution of acute inflammation is an active process orchestrated by

217 Resolution of acute inflammation is an active process that involves th

218 literature demonstrating that resolution of acute inflammation is an active process.

219 The early initiation phase of acute inflammation is anabolic and primarily requires gl

220 The leukocyte response in acute inflammation is characterized by an initial recrui

221 Whereas the resolution of acute inflammation is characterized by restoration to a

222 s processes that govern normal resolution of acute inflammation is critical for determining why steri

223 Whereas acute inflammation is critical for host defence, chronic

224 Neutrophil adhesion in acute inflammation is initiated by activation of alphaLb

225 A classical hallmark of acute inflammation is neutrophil infiltration of tissues

226 Acute inflammation is neutrophilic (75% of ocular CD45 +

227 < 0.01) in neutrophil influx at a time when acute inflammation is normally waning.

228 Accordingly, acute inflammation is self-limiting and is normally atte

229 Acute inflammation is traditionally characterized by pol

230 Because its level in plasma increases during acute inflammation, it may also play previously unsuspec

231 CNTs and long asbestos was characterized by acute inflammation, leading to progressive fibrosis on t

232 stimulating factor 3 (CSF3), released during acute inflammation, mediates potent STAT3-dependent neut

233 opy of a tumor necrosis factor-alpha-induced acute inflammation model in both murine arterial and ven

234 Acute inflammation model studies with transgenic and kno

235 -inflammatory effects were further tested in acute inflammation models in mice.

236 uated by exogenous and endogenous mediators, acute inflammation must be resolved for tissue repair to

237 Causes of use included acute inflammation (n=6), chronic rhinosinusitis (n=2),

238 During acute inflammation, neutrophil recruitment into extravas

239 Neither acute inflammation nor mineralized tissue was noted in a

240 Acute inflammation normally resolves in an actively orch

241 s (MMPs) contribute to tissue remodeling and acute inflammation not only by degrading extracellular m

242 During the resolution phase of acute inflammation, novel mediators, including lipoxins

243 l study, the change of signs and symptoms of acute inflammation of the ocular surface and adnexa was

244 Acute inflammation of the pancreas was produced by injec

245 nogenesis, but the mechanism responsible for acute inflammation of the skin is not well understood.

246 ents are efficacious and safe treatments for acute inflammations of the ocular surface or adnexa, and

247 a prior cohort of fetal membranes shows that acute inflammation only takes place after these first st

248 f the EC adaptive or maladaptive response to acute inflammation or bacterial infection based on compe

249 aintaining homeostasis but also promotion of acute inflammation or immune suppression in chronic infl

250 After acute inflammation or infection, tissue-resident macroph

251 c treatment with repertaxin had no effect on acute inflammation or liver injury.

252 own at air-liquid interface, without causing acute inflammation or toxicity.

253 receive Salmonella typhi vaccine (a model of acute inflammation) or placebo in a double-blind study.

254 meterize a mechanistic mathematical model of acute inflammation originally calibrated for "young" (2-

255 lphaCD11b uptake in the inflamed ears in the acute inflammation phase than the chronic phase, consist

256 many indications associated with TBI, where acute inflammation plays a critical role in disease prog

257 During acute inflammation, prazosin abrogated exercise-enhanced

258 lopment, few studies discuss the patterns of acute inflammation prior to cancer diagnosis.

259 of intermediate monocytes in the setting of acute inflammation prior to treatment in a cohort of 41

260 Acute inflammation recruits neutrophils with a band-shap

261 tive oxygen species (ROS) contributor during acute inflammation, reduces sulfenylation of SIRT6, gluc

262 plore monocyte trafficking in the context of acute inflammation, relying predominantly on data from m

263 Successful regulation of acute inflammation requires biosynthesis of specialized

264 Resolution of neutrophilia characteristic of acute inflammation requires cessation of neutrophil recr

265 identify Mertk as a significant link between acute inflammation resolution and organ function.

266 e surviving seven rats 7 days later to allow acute inflammation resolution.

267 However, in acute inflammation, resolution is known to be orchestrat

268 In vivo quantitative imaging analyses of acute inflammation revealed a 24-hour rhythm in leukocyt

269 In acute inflammation, SAA plasma levels increase ~1,000 fo

270 gs highlight the significant contribution of acute inflammation sensitization prior to an asphyxial i

271 nclusion based on their relevance to sepsis, acute inflammation, sepsis-related immune suppression, a

272 s indicate that CO accelerates resolution of acute inflammation, shortens resolution intervals, enhan

273 In response to acute inflammation, SL-MkPs become activated, resulting

274 were detectable in the recipient lung after acute inflammation subsided.

275 n promotes the recruitment of neutrophils in acute inflammation, supporting an important role for pla

276 Acute inflammation that arises during Pseudomonas aerugi

277 Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten ba

278 iting immune system cells that will initiate acute inflammation that leads to tissue destruction.

279 racamerally injected into rabbit eyes caused acute inflammation that quickly resolved.

280 These results reveal how IFN-I mediates acute inflammation through macrophage necroptosis.

281 r pores in eukaryotic membranes and promotes acute inflammation, tissue damage, and bacteremia.

282 at pDC have to be turned down during ongoing acute inflammation to not initiate autoimmunity.

283 The contribution of acute inflammation to sensory nerve regeneration was inv

284 psis, from the host-pathogen interaction, to acute inflammation, to immune suppression.

285 or necrosis factor (TNF), a key regulator of acute inflammation, to lentiviral pathogenesis, rhesus m

286 Acute inflammation triggers the innate immune response o

287 Acute inflammation was evoked in a human model of experi

288 Acute inflammation was followed in mice with coronary li

289 Acute inflammation was induced in mice and intestines we

290 polymorphonuclear neutrophils (PMNs) during acute inflammation was investigated.

291 Using a human dermal model of acute inflammation, we found that, although inflammatory

292 Furthermore, in a mouse model of acute inflammation, we have shown that the most potent 2

293 s system in mediating tissue adaption during acute inflammation, we hypothesized that Neo1 enhances h

294 tially appreciated as important mediators of acute inflammation, we now know that this complex system

295 ormed in optimal conditions, such as lack of acute inflammation, we urge caution in applying this tec

296 n this behavior for the molecular imaging of acute inflammation, which is characterized by elevated l

297 traperitoneally, cholesterol crystals induce acute inflammation, which is impaired in mice deficient

298 lmitis caused by Bacillus cereus develops as acute inflammation with infiltrating neutrophils, and vi

299 from patients with Crohn's disease accompany acute inflammation; with treatment, these change to rese

300 onverting the chronic inflammation milieu to acute inflammation within tumors.