ライフサイエンスコーパス: acute inflammation

1 e to maintaining platelet homeostasis during acute inflammation.

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

3 nfectious agents to facilitate recovery from acute inflammation.

4 of tissues from the damaging consequences of acute inflammation.

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

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

7 cal to limit unintended tissue injury during acute inflammation.

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

9 ular risk factors in obesity but exacerbates acute inflammation.

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

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

12 by catecholamines and glucocorticoids during acute inflammation.

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

14 hils that have undergone karyorrhexis during acute inflammation.

15 recruited to the bloodstream in response to acute inflammation.

16 n evaluation of microvasculature function in acute inflammation.

17 neutrophil recruitment in several models of acute inflammation.

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

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

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

21 esponses and viral replication, but increase acute inflammation.

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

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

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

25 ominant innate immune cell type activated in acute inflammation.

26 animal models of inflammatory arthritis and acute inflammation.

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

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

29 n result from either inadequate or excessive acute inflammation.

30 cts without known coronary artery disease or acute inflammation.

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

32 -3 in promoting leukocyte recruitment during acute inflammation.

33 or high capacity clearance of neutrophils in acute inflammation.

34 well known cytokine involved in systemic and acute inflammation.

35 eir influence on endothelial function during acute inflammation.

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

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

38 system might be targeted therapeutically in acute inflammation.

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

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

41 e adhesion during lipopolysaccharide-induced acute inflammation.

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

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

44 dogenous pro-resolving agonists in resolving acute inflammation.

45 ors that actively regulate the resolution of acute inflammation.

46 itment of macrophages and neutrophils during acute inflammation.

47 primary chlamydial infection is the onset of acute inflammation.

48 nctional PSGL-1 up-regulation in PBLs during acute inflammation.

49 lecular events that govern the resolution of acute inflammation.

50 ng of functional PSGL-1 up-regulation during acute inflammation.

51 via functional Cftr during anti-CD3-mediated acute inflammation.

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

53 ical response of the pulmonary system during acute inflammation.

54 us and lead to excessive organ damage during acute inflammation.

55 esponse to microbial infection that promotes acute inflammation.

56 n systemic endothelial barrier properties in acute inflammation.

57 ammatory processes controlling resolution of acute inflammation.

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

59 ned insulin deficiency and endotoxin-induced acute inflammation.

60 tle is known about these interactions during acute inflammation.

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

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

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

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

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

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

67 by epithelial disorganization, fibrosis and acute inflammation.

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

69 cytes of noninflamed skin but induced during acute inflammation.

70 hronic inflammation, with little evidence of acute inflammation.

71 keratinocyte nuclei and rapidly lost during acute inflammation.

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

73 rchestrate resolution in diverse settings of acute inflammation.

74 t stereoselectively stimulates resolution of acute inflammation.

75 life-threatening platelet depletions during acute inflammation.

76 tory cytokine, inhibits vascular response in acute inflammation.

77 thereby facilitating PMN trafficking during acute inflammation.

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

79 des, gammadeltaT cells promote resolution of acute inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Nlrp3 inflammasome activity can diminish the acute inflammation and damage associated with tissue inj

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

95 ested both compounds in two animal models of acute inflammation and demonstrated that both compounds

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

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

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

99 e results suggest that Akt1 is necessary for acute inflammation and exerts its actions primarily via

100 receptor activation under conditions such as acute inflammation and experimental autoimmune encephalo

101 Both acute inflammation and fibrotic cohort of rats demonstra

102 Phagocytes orchestrate acute inflammation and host defense.

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

104 that META060 reduces swelling in a model of acute inflammation and inhibits bone and cartilage destr

105 ) infiltration into tissues is a hallmark of acute inflammation and is crucial for the rapid removal

106 Acute inflammation and its resolution are essential proc

107 llular and molecular mechanisms that control acute inflammation and its resolution are of wide intere

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

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

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

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

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

113 We conclude that acute inflammation and peripheral nociceptor sensitizati

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

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

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

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

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

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

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

121 relative ability of IgG subclasses to cause acute inflammation and the roles of specific effector me

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

123 r active bone marrow edema representative of acute inflammation, and anteroposterior radiographs of t

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

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

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

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

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

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

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

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

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

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

134 Mechanisms controlling resolution of acute inflammation are of wide interest.

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

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

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

138 During acute inflammation, as in sepsis, aerobic metabolism app

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

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

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

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

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

144 a-dependent NF-kappaB activation exacerbates acute inflammation, but attenuates chronic inflammatory

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

146 quantities promote phagocyte removal during acute inflammation by regulating leukocyte infiltration,

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

148 Acute inflammation can also be shifted to a chronic infl

149 Unregulated acute inflammation can lead to collateral tissue injury

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

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

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

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

154 An acute inflammation Crohn disease model was produced by t

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

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

157 Recent results indicate that acute inflammation does not simply passively resolve as

158 can be held in check against "missing self," acute inflammation driven by infection can rapidly break

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

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

161 he mechanisms used by NK cells to facilitate acute inflammation during septic shock.

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

163 ven a subinhibitory dose of levofloxacin had acute inflammation, edema, and masses of bacteria, while

164 In contrast, markers of acute inflammation, except for interleukin-6, and disord

165 In acute inflammation, extracellular ATP activates P2X(7) i

166 ible for blocking regeneration, we prevented acute inflammation following amputation by antisense rep

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

168 Acute inflammation follows defined phases of induction,

169 d IL-1beta consistent with a broader role in acute inflammation for ALOX15.

170 After acute inflammation from 10 weeks of UVB irradiation subs

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

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

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

174 f prostatic CA and calculi and suggests that acute inflammation has a role in their biogenesis--an in

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

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

177 isolated from experimental murine models of acute inflammation identified during the natural spontan

178 Acute inflammation impairs reverse cholesterol transport

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

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

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

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

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

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

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

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

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

188 Acute inflammation in response to both exogenous and end

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

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

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

192 mice, which also displayed a higher level of acute inflammation in the endocervix, oviduct, and mesos

193 Acute inflammation in the lung is essential to health.

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

195 (2.0 mg) of TA was as effective in reducing acute inflammation in the ocular posterior segment as hi

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

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

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

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

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

201 2-IIA), a bactericidal enzyme induced during acute inflammation, in innate immunity against GBS.

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

203 and limits regenerative capacity through an acute inflammation-independent mechanism.

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

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

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

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

208 onstrate, for the first time in humans, that acute inflammation induces systemic IR following modulat

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

210 Acute inflammation is a host-protective response that is

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

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

213 Resolution of acute inflammation is an active process essential for ap

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

215 The resolution of acute inflammation is an active process mediated by spec

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

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

218 ody of evidence indicates 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 < 0.01) in neutrophil influx at a time when acute inflammation is normally waning.

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

228 Acute inflammation is traditionally characterized by pol

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

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

231 Acute inflammation model studies with transgenic and kno

232 emigration of neutrophils in this cutaneous acute inflammation model.

233 d the roles of the isoforms Akt1 and Akt2 in acute inflammation models by using mice deficient in eit

234 ty, and robust efficacy in a murine model of acute inflammation (murine LPS-TNFalpha).

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

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

237 During acute inflammation, neutrophil recruitment into extravas

238 Neither acute inflammation nor mineralized tissue was noted in a

239 Acute inflammation normally resolves in an actively orch

240 Together, these data indicate that acute inflammation not only activates mature myeloid cel

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 a role for YopM in bubonic plague, in which acute inflammation occurs soon after infection.

244 of encephalitis, a syndrome characterized by acute inflammation of the brain.

245 T-cell mediated acute inflammation of the ileum may occur during Crohn's

246 s for protection from development of severe, acute inflammation of the intestine.

247 rapeutic target for diseases associated with acute inflammation of the lungs.

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

249 Acute inflammation of the pancreas was produced by injec

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

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

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

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

254 After acute inflammation or infection, tissue-resident macroph

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

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

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

258 In mice with acute inflammation, oral administration of META060 reduc

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

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

261 nstitutive lymphocyte homing and chronic and acute inflammation processes.

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

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

264 Successful regulation of acute inflammation requires biosynthesis of specialized

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

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

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

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

269 Conversely, acute inflammation seems to have the opposite effect.

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

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

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

273 P-D in a murine bacterial pneumonia model of acute inflammation, suggesting that MPO-derived reactive

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

275 Acute inflammation that arises during Pseudomonas aerugi

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

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

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

279 cally before age 50 and are characterized by acute inflammation, the appearance of autoantibodies, an

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

281 fibroblasts are important in the switch from acute inflammation to adaptive immunity.

282 Our findings indicate that conversion of acute inflammation to chronic inflammation may be due to

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

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

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 In addition, myeloid p38 alpha limited acute inflammation via activation of anti-inflammatory g

288 ive effects: p53 activation and reduction of acute inflammation via Cox-2 enzyme inhibition, increase

289 Increased acute inflammation was associated with significantly inc

290 Acute inflammation was followed in mice with coronary li

291 Acute inflammation was induced in mice and intestines we

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

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

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

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

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

297 are counteracted by IFN alpha, a mediator of acute inflammation, which also restores the ability of t

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

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

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