ライフサイエンスコーパス: inflammation

1 (-/-) mice by regulating lesion and systemic inflammation.

2 tion manifesting as autoimmunity or allergic inflammation.

3 light on the role of fibroblasts in chronic inflammation.

4 morphometry, islet cellular composition, and inflammation.

5 uent clearance of Brucella and resolution of inflammation.

6 ion between whole-grain (WG) consumption and inflammation.

7 ically tractable target during infection and inflammation.

8 ic autoimmune disorder resulting in synovial inflammation.

9 phages change during protective immunity and inflammation.

10 d factor (SDF)-1 are known to be involved in inflammation.

11 opulation with increased esophageal allergic inflammation.

12 ks contributing to the underlying intestinal inflammation.

13 ating the timely promotion and resolution of inflammation.

14 risk factors, including lifestyle, diet and inflammation.

15 I IFN response and did not ameliorate lethal inflammation.

16 ntigen presenting capacity and T cell-driven inflammation.

17 o be partially secondary to pathogen-induced inflammation.

18 avir reduced viral loads and decreased liver inflammation.

19 nificant decrease in >/=1 marker of systemic inflammation.

20 eous immunopathology in a mouse model of CNS inflammation.

21 improving bacterial clearance while limiting inflammation.

22 e C5aR2 expression in experimental models of inflammation.

23 sis products from keratinocytes promote skin inflammation.

24 f which was strongly associated with genital inflammation.

25 were resistant to leukocyte-mediated neural inflammation.

26 -translational modifications and IL-1-driven inflammation.

27 bute to innate IEL activation during mucosal inflammation.

28 xpressed genes associated with TH1-polarized inflammation.

29 d to regulate adaptive responses in allergic inflammation.

30 t for shifting the immune response away from inflammation.

31 rther leads to systemic oxidative stress and inflammation.

32 bacterial and fungal infections and aberrant inflammation.

33 related to the degree of eosinophilic airway inflammation.

34 morigenesis, and disorders linked to chronic inflammation.

35 tective effects in DN improving perivascular inflammation.

36 model to mimic depression in the context of inflammation.

37 y 92 cluster in ILC2s displayed reduced lung inflammation.

38 e response (gammaH2AX, 53BP1) due to chronic inflammation.

39 on the development of acute allergic airway inflammation.

40 mall-molecule drug design targeting pain and inflammation.

41 nfluence of SD on allergen-induced pulmonary inflammation.

42 to locally modulate cellular function during inflammation.

43 enge phase for neutrophilic and eosinophilic inflammation.

44 entromedial medulla is altered in persistent inflammation.

45 ing a molecular link between coagulation and inflammation.

46 interventions with control of infection and inflammation.

47 ovagal baroreflex sensitivity, and increased inflammation.

48 asma levels in patients with IBD with active inflammation.

49 cle (DNAC), in a mouse model of intrauterine inflammation.

50 the lungs is feasible and reflects pulmonary inflammation.

51 -positive versus infection-negative systemic inflammation.

52 to confer protection against AHR and airway inflammation.

53 strong link between neovascular disease and inflammation.

54 as an early event promoting allergic airway inflammation.

55 l blood monocytes play a role in sarcoidosis inflammation.

56 ith ustekinumab diminished imiquimod-induced inflammation.

57 fection and limit the detrimental effects of inflammation.

58 of these statins on both joint and systemic inflammation.

59 yloid pathology as a regulator of peripheral inflammation.

60 wing reasons - fractures (5 patients, 3.2%), inflammation (2 patients with 3 exchanges, 1.9%).

61 ement representing the most frequent sign of inflammation (90% at diagnosis, 100% at PML-IRIS).

62 Chronic low-grade inflammation, a hallmark of obesity, involves immune cel

63 Aging promotes inflammation, a process contributing to fibrosis and dec

64 Although infection is a known cause of inflammation, a significant proportion of pregnancies ha

65 ammation has been limited.We examine whether inflammation-adjusted ferritin and sTfR concentrations a

66 h concomitant iron deficiency (defined as an inflammation-adjusted ferritin concentration <12 mug/L).

67 y molecules, immune cells may induce myocyte inflammation, adversely regulate myocyte metabolism, and

68 y of ovalbumin-induced acute allergic airway inflammation after adoptive transfer of BMDCs was examin

69 , our results support a model in which acute inflammation after injury initiates important regenerati

70 ction of APC and TC accumulating at sites of inflammation after segmental allergen challenge (SAC).

71 red blood cells (pRBCs) and subsequent lung inflammation after transfusion.

72 is therefore a critical contributor to skin inflammation and a possible therapeutic target in AD and

73 ha, and consequently protects from excessive inflammation and acute shock in vivo.

74 these patients was associated with bronchial inflammation and airway structural changes.

75 The molecular mechanisms underlying vascular inflammation and associated inflammatory vascular diseas

76 zed to investigate the links between chronic inflammation and atherosclerosis development.

77 Accumulating evidence links inflammation and atrial fibrillation (AF).

78 DC homeostasis, is required to modulate lung inflammation and bacterial burden in TB.

79 d that sFRP5 blocks experimental periodontal inflammation and bone loss, suggesting a promising platf

80 ppaB signaling and that miR-19a has roles in inflammation and CAC.

81 the clearance of infection and resolution of inflammation and contributes to mucosal host defense of

82 ole of miR-218-5p in cigarette smoke-induced inflammation and COPD.

83 the culprit of COX-2/PGE2-mediated neuronal inflammation and degeneration remains largely unclear an

84 in experimental optic neuritis, with reduced inflammation and demyelination.

85 Approaching the relationship between inflammation and depression from this evolutionary persp

86 f this transcription factor leads to hepatic inflammation and early signs of fibrosis.

87 on, whereas in the ventricles, it controlled inflammation and endocytosis.

88 ncluding in sphingolipid-mediated apoptosis, inflammation and energy storage/usage.

89 ncreased susceptibility to severe intestinal inflammation and epithelial dysregulation, accompanied b

90 on CRC cell lines, our results suggest that inflammation and ethnicity play a major role in the modu

91 lite subnetworks linked to lipid metabolism, inflammation and glycerophospholipid metabolism that wer

92 pronounced inhibition of HDM-induced airway inflammation and goblet cell hyperplasia.

93 tokines and growth factors are regulators of inflammation and have been implicated in autoimmune and

94 malignancies, being associated with chronic inflammation and hyperinsulinemia.

95 psis-like environment, which included tissue inflammation and hyperproduction of inflammasome-associa

96 ollutants, such as ozone, exacerbates airway inflammation and hyperresponsiveness (AHR).

97 2-AG levels were increased in response to inflammation and hypoxia in Caco-2 cells.

98 Heightened inflammation and immune activation in HIV-1+ infants did

99 cells and primary human promonocytes during inflammation and in splenocytes from mice with sepsis.

100 in the mitochondrial matrix and has roles in inflammation and infection processes, mitochondrial ribo

101 ologic agonists that stimulate resolution of inflammation and infection.

102 In the immature lung, inflammation and injury disrupt the epithelial-mesenchym

103 C2 numbers and activation, as well as airway inflammation and IRF4 and NFAT1 expression.

104 sought to characterize molecularly cutaneous inflammation and its correlation with clinical and barri

105 tifs-4) is a secreted proteinase involved in inflammation and matrix degradation.

106 ctivity of NF-kappaB, a key player in muscle inflammation and myogenesis.

107 tant for early recognition and monitoring of inflammation and neurodegeneration in multiple sclerosis

108 TH2-driven eosinophilic inflammation and neutrophil-associated inflammasome acti

109 ol studies including participants with joint inflammation and no previous definitive gout diagnosis w

110 The Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRI

111 n = 4258) from the Biomarkers Reflecting the Inflammation and Nutritional Determinants of Anemia (BRI

112 tected against UVB-induced oxidative stress, inflammation and papillomagenesis.

113 rom the FRT while reducing tissue-associated inflammation and pathology.

114 f which was characterized by extreme genital inflammation and persistent bacterial vaginosis (BV); th

115 els has revealed that targeting RAGE impairs inflammation and progression of diabetic vascular compli

116 ND To study the relationship between chronic inflammation and protein quality control, we used a mous

117 to switch their functional phenotypes during inflammation and recovery.

118 litis phenotype accompanied by decreased CNS inflammation and reduced frequency of IL-17- and GM-CSF-

119 matics was not associated with airway tissue inflammation and remodeling, although persistent airflow

120 the association between these biomarkers of inflammation and renal outcomes in DKD.

121 However, inflammation and structural deterioration limit transpla

122 y of GSTO1-1 inhibitors in the modulation of inflammation and suggest their possible application in t

123 ably unaffected by development of intestinal inflammation and there were no differences in previously

124 vel therapeutic targets for attenuating this inflammation and thereby preventing CKD-associated cardi

125 agocytic killing, and resulting in increased inflammation and tissue damage and consequent invasivene

126 during early- or late-onset allergic airway inflammation and to address regulatory mechanisms and cl

127 biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative

128 etiological diseases associated with chronic inflammation and underlie a variety of poorly treatable

129 es, micronutrient deficiencies, malaria, and inflammation) and household-level predictors; we also ex

130 rogression such as germ line predisposition, inflammation, and aging.

131 iposity, insulin sensitivity, adipose tissue inflammation, and arterial stiffness and exerts a benefi

132 lls are critically involved in host defence, inflammation, and autoimmunity.

133 at actively regulate the resolution of acute-inflammation, and correlate measurements with clinical o

134 mber of therapeutic areas, including cancer, inflammation, and dementia.

135 r disease risk by inducing oxidative stress, inflammation, and endothelial dysfunction.

136 including neuronal activity, vascular tone, inflammation, and energy metabolism.

137 in the kidney and renal dysfunction, injury, inflammation, and fibrosis.

138 creased airway and tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE production.

139 calcium handling, apoptosis, heme turnover, inflammation, and oxygen and nutrient sensing have been

140 Bronchial hyperreactivity, airway inflammation, and sensitization were significantly diffe

141 etermine the relationship of liver fibrosis, inflammation, and steatosis with the magnetic resonance

142 ntricacies to highlight the contributions of inflammation, angiogenesis, and the ECM to both "healthy

143 Although both persistent itch and inflammation are commonly associated with allergic conta

144 results demonstrate that persistent itch and inflammation are mediated by distinct cellular and molec

145 eated MSC yielded a substantial reduction in inflammation as demonstrated by the decrease in the expr

146 Increasing evidence points to inflammation as one of the key players in diabetes-media

147 local IL-1- and neutrophil-dependent tissue inflammation as shown in the K/BxN serum transfer arthri

148 ol binding protein) in settings of prevalent inflammation as well as the prevention of and control st

149 rocesses related to fatty liver and cellular inflammation associated with atherosclerosis and CAD in

150 ted therapeutic target to limit the damaging inflammation associated with overt production of proinfl

151 Using inflammation-associated neurogenesis models and a transg

152 human immune system for multiple markers of inflammation at a scale that was not previously possible

153 rtance of neuro-immune crosstalk in allergic inflammation at mucosal surfaces.

154 rscored by the devastating toll of excessive inflammation at the cornea - blindness.

155 nduces intestinal pathology, as indicated by inflammation, barrier dysfunction, and visceral hypersen

156 will be a valuable resource to the field of inflammation biology and will be an important asset in f

157 m to sites of tissue infection is central to inflammation, but also promotes chronic inflammatory dis

158 mediate several functions in the context of inflammation, but little is known about the potential fu

159 ovascularization is strongly associated with inflammation, but the source of inflammatory signals and

160 P2X7 deficiency resolved plaque inflammation by inhibition of lesional inflammasome acti

161 marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (

162 Intrauterine and systemic infection and inflammation cause 30-40% of spontaneous preterm labor (

163 polymorphonuclear neutrophils (PMNs) during inflammation critically depends on the beta2 integrins l

164 Depending on the approach used to adjust for inflammation (CRP plus AGP), the estimated prevalence of

165 Depending on the approach used to adjust for inflammation (CRP+AGP), the estimated prevalence of VAD

166 ctors that are associated with resolution of inflammation, Dectin-1, CD206 (mannose receptor), and IL

167 ion to systemic inflammation, local arterial inflammation, driven by monocyte-derived macrophages, pr

168 Here we delineated an inflammation-driven inhibitory mechanism of beige adipog

169 eshold that could more easily be breached by inflammation during critical periods of brain developmen

170 All four had marked systemic inflammation, fever and fluctuating radiologic findings.

171 We demonstrate that hepatic inflammation, fibrosis stage, fibrosis progression rate,

172 diceal diameter, presence of periappendiceal inflammation, fluid, appendicoliths, and white blood cel

173 nimal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacological blocka

174 Low-grade, chronic inflammation has been associated with many diseases of a

175 , but its use worldwide and in settings with inflammation has been limited.We examine whether inflamm

176 function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs.

177 monocytes, which are rapidly mobilized upon inflammation in a CC-chemokine receptor 2-dependent mann

178 human ILC2s through ICOSL to control airway inflammation in a humanized ILC2 mouse model.

179 ome has been shown to play a pivotal role in inflammation in a mouse kidney disease model.

180 by limiting the extent of endotoxin-induced inflammation in an MPO-dependent manner.

181 ion of the lower airways, the actual site of inflammation in asthma, which is hardly accessible in po

182 creasing evidence suggests a crucial role of inflammation in cytokine-mediated beta-cell dysfunction

183 of activation of multiple pathways of type 2 inflammation in early life are at greatest risk for asth

184 The study of inflammation in fear- and anxiety-based disorders has ga

185 iciency, inhibits IBMIR and cytokine-induced inflammation in islets.

186 f asthma, produces spontaneous type 2 airway inflammation in juvenile beta-epithelial Na(+) channel (

187 ty to silver nanoparticle-induced acute lung inflammation in mice.

188 Increasing evidence suggests a role for inflammation in neuropsychiatric conditions, including a

189 to be an inevitable consequence of long-term inflammation in patients who did not respond to anti-inf

190 thway might be induced to resolve intestinal inflammation in patients with colitis.

191 fication due to carbohydrate fermentation or inflammation in response to accumulated plaque select fo

192 glial exosomal miR-124-3p inhibited neuronal inflammation in scratch-injured neurons.

193 tumorigenesis significantly correlated with inflammation in SPF-housed Apc(Min/+) ;Il10(-/-) , but n

194 ently, the presence of epithelial injury and inflammation in the airways of athletes was demonstrated

195 t type 2 cytokine responses and eosinophilic inflammation in the airways remained unaffected.

196 sm that coordinates neuronal homeostasis and inflammation in the CNS.

197 ells migrate to the circulation and initiate inflammation in the HEL-expressing recipient eyes.

198 decreased chemokine expression, and reduced inflammation in the lungs compared with transfers into R

199 As the inflammation in the lungs of the sanroque mice could hav

200 Allergic asthma is a chronic Th2 inflammation in the lungs that constricts the airways an

201 est that urban PM2.5 may exacerbate allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-si

202 lant recipients enrolled in the Malnutrition-Inflammation in Transplant-Hungary study.

203 e role in suppressing neovascularization and inflammation in vivo Comparing AGN 211377 with a close s

204 ior (6 weeks) normal histology, in 3.4% with inflammation, in 13.8% with IFTA, and in 24.5% with IFTA

205 OCA-salt rats with serelaxin decreased renal inflammation, including the expression of TGF-beta, NFka

206 Psychological stressors and inappropriate inflammation increase the risk and severity of mood diso

207 Enhancing TLR2-mediated inflammation increased fibrosis in vivo Furthermore, sol

208 Inflammation increased pulmonary expression of CXCR7, an

209 rker was significantly down-regulated during inflammation induced by acute contact hypersensitivity (

210 lated protein changes caused by a well-known inflammation inducer and a familial AD mutation.

211 s, immunosenescence, and a low-grade chronic inflammation (inflammaging).

212 50), we measured parasite biomass, systemic inflammation (interleukin 6 [IL-6]), endothelial activat

213 Inflammation is a host defense process against infection

214 mice, providing evidence that virus-induced inflammation is a major component of disease in the deve

215 Inflammation is one of the major risk factors for cancer

216 Robust lung inflammation is one of the prominent features in the pat

217 Intestinal inflammation is the central pathological feature of coli

218 Allergic airway inflammation is triggered by allergen exposure through s

219 diated effects as shown by a reduced cardiac inflammation (less cardiac infiltrates and suppression o

220 In addition to systemic inflammation, local arterial inflammation, driven by mon

221 o the most recent applications in cancer and inflammation management, including therapeutics, imaging

222 Levels of 13 inflammation markers.

223 susceptibility to injury after preterm birth.Inflammation mediated by microglia plays a key role in b

224 In this study, we have investigated how inflammation-mediated CD11d upregulation contributes to

225 understand cell-type-specific regulation of inflammation mediators and shedding new light on the rol

226 o analyze the formation of the most relevant inflammation mediators including proteins and lipids in

227 is a chronic airway disease characterized by inflammation, mucus hypersecretion and abnormal airway s

228 Levels of airway inflammation, mucus, fibrosis, and airway smooth muscle

229 mune attack on the CNS that leads to chronic inflammation, neuroaxonal degeneration and remyelination

230 ositivity, P < .005), and less lung allergic inflammation (number of lung eosinophils, P < .005).

231 Thus, microglia and low-grade inflammation of myelinated tracts emerged as the trigger

232 (WBC) were significantly correlated with the inflammation of the appendix.

233 se SF concentrations increase in response to inflammation or infection.

234 urotransmitter balance, increases in chronic inflammation, or exacerbated hypothalamic-pituitary-adre

235 ROS plays an important role in a variety of inflammation, our data demonstrate that IL-27 is a poten

236 ity, insulin secretion, steatosis, metabolic inflammation, pancreatic islet morphometry, islet cellul

237 The inflammation pattern at diagnosis was similar to the pat

238 However, until primed by inflammation, peripheral DOR is analgesically incompeten

239 ONALE: Sympathetic nervous system control of inflammation plays a central role in hypertension.

240 dings suggest that an overexuberant systemic inflammation plays a primary role in ACLF progression.

241 Inflammation plays a significant role in the development

242 eral biological processes such as autophagy, inflammation, proliferation and differentiation of stem

243 During inflammation, proteins and lipids act in a concerted fas

244 marrow activity (r=0.47; p<0.0001), arterial inflammation (r=0.49; p<0.0001), and risk of cardiovascu

245 ata further suggest that lower is better for inflammation reduction with canakinumab.

246 Significant interest has emerged in how inflammation regulates HSC fate and how it affects the l

247 Likewise, colonic inflammation related to prolonged exposure to morphine w

248 onsistently observed decreased expression of inflammation-related genes NLRP3 and IL-1beta in Nrf2-de

249 n number and changes in expression levels of inflammation-related genes, monitored by both flow cytom

250 iR-142 family, miR-142-5p and miR-142-3p, as inflammation-related miRNAs with potential roles in woun

251 he mechanisms responsible for producing this inflammation remain unclear.

252 ular events that initiate and propagate such inflammation remain unclear.

253 mechanisms that connect excess GC to tissue inflammation remain unknown.

254 understand whether maintenance of lung TH17 inflammation requires environmental agents in addition t

255 Furthermore, the concept of dysregulated inflammation resolution in atherosclerosis has been know

256 at encapsulated (R)-roscovitine can speed up inflammation resolution in vivo more efficiently than th

257 Inflammation resolution is an active process that functi

258 During inflammation resolution, neutrophils undergo apoptosis b

259 ic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thi

260 d, aggregated proteins in neurons can induce inflammation, resulting in multiple forms of brain toxic

261 In the lipopolysaccharide model of inflammation, RVX-297 reduced proinflammatory mediators

262 ion loss, mild anterior chamber and vitreous inflammation, sectoral retinal hemorrhages in areas of i

263 ay be a significant contributor to excessive inflammation seen in Irgm1-deficient mice in different c

264 of liver fat, lipogenic indices, markers of inflammation, serum levels of fibroblast growth factor 2

265 labeling assay was performed, and intestinal inflammation severity was evaluated histologically.

266 antiviral programmed cell death pathways on inflammation, shows that caspase-8 activation may go han

267 ConA induced inflammation, sinusoidal congestion, and extensive midzo

268 ficiency, PLCG2, and a negative regulator of inflammation, SLAMF8.

269 atient population includes adults with joint inflammation suspected to be gout.

270 ocholate), lobular (glycocholate) and portal inflammation (taurolithocholate), and hepatocyte balloon

271 Because Mrgprs mediate some aspects of inflammation that had been considered mediated by neurok

272 as potent regulators of BBB permeability and inflammation that influence leukocyte transport across t

273 haled pathogens, thus favoring infection and inflammation that may eventually lead to tissue remodeli

274 peri-vascular, peri-bronchial, and allergic inflammation that was unresponsive to inhaled corticoste

275 early phase after fracture reduced systemic inflammation, the recruitment of immune cells, and bone

276 vely hypoxic, particularly during periods of inflammation, these findings may have important implicat

277 Systemic inflammation through persistent monocyte activation and

278 deregulated necroptosis results in systemic inflammation, tissue fibrosis, and autoimmunity.

279 rtant to examine how AgNPs affect microglial inflammation to fully assess AgNP neurotoxicity.

280 mal from other etiologies including chemical inflammation (turpentine) and cancer (breast carcinoma).

281 In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or

282 iated with glucose homeostasis variables and inflammation variables (all P < 0.01).

283 of microglia in neonates exposed to in utero inflammation via an endogenous cerebral cholinergic anti

284 expression, mucus hypersecretion, and airway inflammation was assessed by using in vivo models of IL-

285 Inflammation was associated with low levels of SIV RNA i

286 Ocular surface inflammation was common during the acute phase in both S

287 estingly, although the DEP-enhanced allergic inflammation was marginally reduced in ILC2-deficient mi

288 phylactic or therapeutic fashion, autoimmune inflammation was markedly attenuated in vivo.

289 o Il1b detection in the brain, when systemic inflammation was minimal.

290 Inflammation was not directly correlated with distance t

291 myloid protein is detected before markers of inflammation, we argue that old, age-associated, aggrega

292 Using a mouse model of allergic airway inflammation, we found that adoptive transfer of IMs iso

293 n matrix and during resolution of peritoneal inflammation, whereas migration of CD11b(-/-) M1 macroph

294 ve allograft fibrosis include graft quality, inflammation (whether "nonspecific" or related to a spec

295 iency in mice caused increased basal colonic inflammation, which led to a less-diverse microbiome and

296 innate protection, POP2 reduces detrimental inflammation while preserving and enhancing protective i

297 hat can lead to central nervous system (CNS) inflammation with long-term behavioral and cognitive alt

298 , SERCA2a 971-990, induces widespread atrial inflammation without affecting noncardiac tissues; the c

299 t proportion of pregnancies have evidence of inflammation without any detectable infection.

300 y, 1F11 showed efficacy in several models of inflammation yet was less potent at inhibiting chemotaxi