ライフサイエンスコーパス: inflammation

1 a personalized approach of chronic low-grade inflammation.

2 t, dramatically reduces IL-18 and intestinal inflammation.

3 ation of airway eosinophils, reducing airway inflammation.

4 plays a complex role in lipid metabolism and inflammation.

5 ), in order to discern a specific pattern of inflammation.

6 is would translate to omnipresent persistent inflammation.

7 l strategies to prevent BPD due to antenatal inflammation.

8 al cells (ECs) is a crucial step in vascular inflammation.

9 (ILC2) activation to induce innate allergic inflammation.

10 on, epidermal dysfunction, and T-cell driven inflammation.

11 lammatory diseases by limiting tissue damage/inflammation.

12 f acute T(H)2-cell-dependent allergic airway inflammation.

13 s and how they may behave differently during inflammation.

14 ed to the epidermis in both steady state and inflammation.

15 the pathogenesis of delirium independent of inflammation.

16 rge part because they decrease airway type 2 inflammation.

17 elease, ILC2 cytokine production, and airway inflammation.

18 xpression of biomarkers, EcPV2 infection and inflammation.

19 is imperative to understanding infection and inflammation.

20 al molecules that regulate the resolution of inflammation.

21 cells developed spontaneous peripheral nerve inflammation.

22 2 (Th2) cytokines that promote AHR and lung inflammation.

23 ts exhibited higher levels of senescence and inflammation.

24 amination and modulating peri-implant tissue inflammation.

25 ole for TRAIL receptors in ER-stress-induced inflammation.

26 tive days to evaluate innate airway allergic inflammation.

27 iota are altered and correlate with alveolar inflammation.

28 NO, suggesting increased eosinophilic airway inflammation.

29 for neutrophil adhesion to endothelia during inflammation.

30 procedure we have previously shown produces inflammation.

31 Tfr cells, in the context of allergic airway inflammation.

32 essing brain dysfunction induced by systemic inflammation.

33 t microbial metabolism in the context of gut inflammation.

34 al muscle of mice in response to LPS-induced inflammation.

35 milieu which can hasten oxidative stress and inflammation.

36 in myeloid cell functions during periodontal inflammation.

37 siology, extracellular matrix, clotting, and inflammation.

38 t in diabetic subjects, suggesting continued inflammation.

39 uction, reduction in neutrophil elastase and inflammation.

40 d will thus benefit from therapies targeting inflammation.

41 gene (ISG) pathways and induce psoriasiform inflammation.

42 through Rac1 and thus prevented ACD-induced inflammation.

43 d allergic sensitization and allergic airway inflammation.

44 ociated with oxidative injury and pathogenic inflammation.

45 ve muscle degeneration aggravated by sterile inflammation.

46 ing and SCFA level in response to intestinal inflammation.

47 tion which is reversible upon suppression of inflammation.

48 P < 0.01) compared with mild or nonspecific inflammation.

49 ect the roles of caspase-8 in cell death and inflammation.

50 HIV) and is associated with reduced systemic inflammation.

51 eased IL-33 release and ILC2-mediated airway inflammation.

52 one-dependent manner to limit adipose tissue inflammation.

53 ic or peritoneal disease, likely by inducing inflammation.

54 ial to the host in reducing allergen-induced inflammation.

55 2l2/Nrf2 deficiency restored heme-suppressed inflammation.

56 tinal epithelial barrier and chronic mucosal inflammation.

57 may spread to produce more advanced systemic inflammation.

58 n of nitrosoperoxycarbonate generated during inflammation.

59 induces ZBP1-dependent necroptosis and skin inflammation.

60 selected pathogens and in the regulation of inflammation(1-3).

61 easonably related to the procedure were mild inflammation (13%), IOP spikes (6%), hyphema, corneal ed

62 ients with VRL than in patients with chronic inflammation (65.9% +/- 13.4% and 1.5% +/- 2.6% for IGH

63 Understanding of the role of focal inflammation, a treatable feature, on neuro-axonal injur

64 osinophilia is a hallmark of allergic airway inflammation (AAI).

65 yses should be conducted before applying any inflammation adjustments.

66 indings demonstrate that chronic endothelial inflammation adversely impacts niche activity and HSC fu

67 No patient showed recurrence of inflammation after cessation of brimonidine.

68 EP mediated increase in allergen-induced Th2 inflammation and AHR in a mouse model of severe steroid

69 We measured airway inflammation and AHR in wild-type, RAGE(-/-) , TLR4(-/-)

70 ata indicate that omalizumab can induce skin inflammation and anaphylaxis by engaging FcgammaRs, and

71 he tumor microenvironment and cancer-related inflammation and angiogenesis.

72 over, we observed increased small intestinal inflammation and apoptosis after hepatic IR in intestina

73 e, affording a distinct way to control joint inflammation and arthritis.

74 CB2R agonists due to their ability to reduce inflammation and cell proliferation.

75 ory diseases, which cause low-grade systemic inflammation and contribute to several common chronic di

76 hanisms by which Rab27 contributes to airway inflammation and cytokine release remain ambiguous.

77 eron genes) play a critical role in vascular inflammation and destruction.

78 absence of basophils, resulting in increased inflammation and diminished lung function.

79 roptosis is a cell death pathway involved in inflammation and disease.

80 ubin, and iron, is an important regulator of inflammation and epithelial responses in the prostate.

81 e that FGF23 is also linked to iron economy, inflammation and erythropoiesis.

82 e was enrichment of proteins associated with inflammation and extracellular matrix as well as senesce

83 he hypothesis that Acomys has reduced spinal inflammation and fibrosis following SCI.

84 critical role of CXCR6 in the development of inflammation and fibrosis of the kidney in salt-sensitiv

85 upported our hypothesis by showing increased inflammation and fibrosis related gene expression (Serpi

86 tend into the hepatic parenchyma and promote inflammation and fibrosis.

87 h histological evidence of more severe graft inflammation and fibrosis.

88 expression in the DC compartment alleviates inflammation and goblet cell metaplasia.

89 ew light on GM-CSF biology in sterile tissue inflammation and identify several potential therapeutic

90 ed and blood was collected for biomarkers of inflammation and immune activation.

91 opment of NKTCL by showing the importance of inflammation and immune regulation through the IL18-IL18

92 R) are respectively associated with systemic inflammation and immune suppression and have been associ

93 hreatening cardiopulmonary disorder in which inflammation and immunity have emerged as critical early

94 ole in alveolar macrophage homeostasis, lung inflammation and immunological disease.

95 WT) mice evidenced by more severe intestinal inflammation and impaired bacterial clearance.

96 -induced colitis due to prolonged intestinal inflammation and impaired tissue repair.

97 proposed mechanisms contributing to chronic inflammation and increased morbidity and mortality durin

98 ese data support a critical role of SIRT1 in inflammation and insulin resistance in hyperinsulinemia.

99 fat diets and contribute to a state of local inflammation and insulin resistance.

100 or the treatment of diseases such as chronic inflammation and ischemia-reperfusion injury.

101 (18)FDG-PET/CT can visualize both inflammation and malignancy and offers a whole-body asse

102 issues from pL2.Lgr5.p65fl/fl mice had lower inflammation and metaplasia scores than pL2.Lgr5.N2IC mi

103 ps showed favorable root development without inflammation and newly mineralized tissue deposited in t

104 We examined the association between inflammation and NP levels in humans.

105 ted vasculitis characterized by neutrophilic inflammation and nuclear debris in post capillary venule

106 , 22,695 WRA) from the Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRI

107 iators downstream of CCL17 in the control of inflammation and pain.

108 clude a reduction in adipose tissue-mediated inflammation and pro-inflammatory cytokine production, a

109 its absence, AP activation leads to chronic inflammation and promotes hepatic carcinogenesis.

110 In addition to decreasing systemic inflammation and providing glycemic control without incr

111 ZBP1 activation triggers inflammation and pyroptosis, necroptosis, and apoptosis

112 he development of periodontitis and vascular inflammation and remarkably blocked the increased lipid

113 rus 2 (SARS-CoV-2) that results in excessive inflammation and respiratory disease, with cytokine stor

114 in blood, thereby helping to reduce systemic inflammation and reverse insulin resistance.

115 , exogenous administration of PGE(2) reduced inflammation and reversed the exacerbated fibrotic profi

116 d house dust mite-driven eosinophilic airway inflammation and significantly reduced Th2 cytokine prod

117 bonyl electrophiles represent a link between inflammation and somatic genomic alterations and are thu

118 High-fat diet (HFD)-induced inflammation and steatosis of adipose tissue and liver a

119 gene regulation during cell fate decisions, inflammation and stem cell heterogeneity.

120 the inhibitory effect of NMP on endothelial inflammation and subsequent monocyte adhesion is KLF2 de

121 shows increased concentrations of markers of inflammation and tissue damage compared with healthy con

122 adaptive immune responses or the balance of inflammation and tissue repair in the resolution of infe

123 oint for the induction and the resolution of inflammation and to NAAA itself as a target for anti-inf

124 species (ROS) is vitally involved in tissue inflammation and tumorigenesis, here we employed a genom

125 ADAMTS5 accumulated in areas of inflammation, and ADAMTS5(+) cells were seen in the tubu

126 nd including anticancer, antimicrobial, anti-inflammation, and anti-diabetic activities, as well as a

127 ificantly attenuated renal tubular necrosis, inflammation, and apoptosis when compared to P2X4 wild-t

128 n most of the nodes, including angiogenesis, inflammation, and cancer-associated fibroblast (CAF) act

129 orfin inhibited KC activation, reduced liver inflammation, and decreased serum ALT/AST levels.

130 eloped liver disease with hepatic steatosis, inflammation, and degeneration.

131 plasma biomarkers related to tubular injury, inflammation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1

132 terized by crystal deposits, tubular injury, inflammation, and fibrosis.

133 deprivation and inhibited by overnutrition, inflammation, and hypersecretion of certain anabolic hor

134 DBA on glomerular cell proliferation, renal inflammation, and immune cells.

135 ostaglandin E2 (PGE2) is a lipid mediator of inflammation, and its tissue concentration is elevated i

136 and improved cardiac dysfunction, myocardial inflammation, and oxidative stress, underlining the impo

137 nction, controls multiple genes critical for inflammation, and prevents atherosclerosis.

138 scular dysfunction, thrombosis, dysregulated inflammation, and respiratory complications.

139 K5, is an emerging drug target in cancer and inflammation, and small-molecule ERK5 kinase inhibitors

140 Cell death, inflammation, and tuft cell markers were downregulated i

141 induced Th cell-associated Th2-, FOXP3/IL2-, inflammation- and finally type1 IFN-signalling subnetwor

142 s, such as bone fracture, osteonecrosis, and inflammation are characterized by excessive osteocyte de

143 and molecular processes including low-grade inflammation are major players in the pathogenesis of ca

144 ration, device infection, and cardiovascular inflammation are successfully gaining clinical acceptanc

145 acterial infections and reducing LPS-induced inflammation are unclear.

146 n of T. suis-infected pigs exhibited general inflammation around day 21 after inoculation with infect

147 it sinuses and effectively reduced sinonasal inflammation as characterized by micro-computed tomograp

148 dentified peripheral lesions and intraocular inflammation as distinct clinical phenotypes of MFC and

149 ed on a patient-reported scale) and systemic inflammation (as shown by an elevated C-reactive protein

150 binant Asp t 36 was able to stimulate airway inflammation, as demonstrated by an influx of eosinophil

151 profile, including ameliorated fibrosis and inflammation, as well as improved lipid and glucose meta

152 r adenosine concentration and dampen chronic inflammation associated with human immunodeficiency viru

153 mine the role of dicarbonyl electrophiles in inflammation-associated carcinogenesis.

154 y were obtained from AMs exposed to allergic inflammation-associated cytokines.

155 whole SN triglycerides were correlated with inflammation-attenuating glycoprotein non-metastatic mel

156 ury model through a unique mechanism of anti-inflammation-based fibrotic scar reduction.

157 xpressing hPXR by a significant reduction in inflammation biomarkers.

158 with DAA attenuated the liver stiffness and inflammation but did not improve VD levels.

159 is necessary and sufficient to regulate lung inflammation but it has no direct antiviral activity aga

160 brake on airway EC responses during allergic inflammation, but is impaired in asthma.

161 nveil the role of a novel lncRNA in vascular inflammation by cis-regulating MAP3K4 via a p38 MAPK pat

162 PDD005 treatment also reduced neuro-inflammation by decreasing interleukin-1beta expression,

163 TANs can be part of tumour-promoting inflammation by driving angiogenesis, extracellular matr

164 keleton remodeling, response to stimuli, and inflammation can impact resistance to tumorigenesis in D

165 ain-enhancer of activated B cells)-dependent inflammation, caspase-dependent apoptosis, or necroptosi

166 ocesses, as well as innate immunity, chronic inflammation, cell cycle, circadian rhythm, and olfactor

167 estrogen promotes involution by exacerbating inflammation, cell death and adipocytes repopulation.

168 ized by markers of type-2 immune activation, inflammation, cellular infiltration, tissue repair enzym

169 lling acute-stage poliomyelitis (gray matter inflammation), chronic axonal degeneration, and inflamma

170 Inflammation, clinical score, and weight loss were also

171 -DCA-Anaero showed attenuation of intestinal inflammation compared to Cj-P1.

172 gh-sensitivity C-reactive protein (hsCRP), z-inflammation composite score [ICS, combining elevated hs

173 ant advancements in our understanding of how inflammation contributes to the pathogenesis and progres

174 xygen/glucose deprivation (OGD) that reflect inflammation, depolarization and ischemia respectively,

175 ession biomarkers associate with macroscopic inflammation detectable via MRI.

176 e forefront of the pathophysiology of airway inflammation, different approaches to diagnose and targe

177 H. pylori-induced carcinogenesis by causing inflammation, DNA damage, and activation of beta-catenin

178 ss of ATG16L1 from IECs increases markers of inflammation, DNA damage, and cell proliferation and inc

179 host IL-6 response in the regulation of lung inflammation during AA and the control of S. pneumoniae

180 loring the molecular mechanisms that prevent inflammation during caloric restriction may yield promis

181 ant role both in the presence of periodontal inflammation during pregnancy and subsequent PLBW.

182 they are potentially obscured by the chronic inflammation elicited by muscle damage in humans.

183 SARS-CoV-2 may modulate macrophage-mediated inflammation events by altering the balance between angi

184 associated with smooth muscle cells (SMCs), inflammation, extracellular matrix remodeling, and mitog

185 ediators of physiological processes, such as inflammation, fever, allergy, and pain, their roles in C

186 mechanism that ensures robust termination of inflammation for tissue repair and restoration of normal

187 was associated with indices of microvascular inflammation (glomerulitis, peritubular capillary infilt

188 Inflammation has a pivotal role in the pathogenesis of C

189 In this context, adipose tissue and liver inflammation have been particularly well studied; howeve

190 Saroglitazar improved steatosis, lobular inflammation, hepatocellular ballooning and fibrosis sta

191 We hypothesized that unique obesity-inflammation HFpEF phenotypes exist and are associated w

192 Inadequate plaque control, peri-implant inflammation, history of previous implant failures, and

193 e correlates with the early stages of muscle inflammation identified by histological analysis on musc

194 examined, including markers of atopy, type 2 inflammation, immune cell populations, and cytokines.

195 phenotypically recapitulates the persistent inflammation, immunosuppression, and catabolism syndrome

196 B(2) -R activation markedly improved hepatic inflammation, impaired microcirculation, and fibrosis.

197 FN-lambda in immune dysregulation and tissue inflammation in a model of TLR7-induced lupus.

198 s nerve at the tragus (LLTS) reduces cardiac inflammation in a rat model of heart failure with preser

199 ssion that involve stem/progenitor cells and inflammation in a tissue-specific manner.

200 hibits neutrophil recruitment in response to inflammation in a zebrafish model.

201 to effectively reduce airway obstruction and inflammation in allergic asthma.

202 onfirm that hyperglycemia leads to a chronic inflammation in and around the implanted collagen membra

203 Despite mounting evidence implicating inflammation in cardiovascular diseases, attempts at cli

204 st an important role by NK cells in inducing inflammation in CL, thereby contributing to disease immu

205 Treg function may be useful in treating skin inflammation in DOCK8 deficiency.

206 rmine the immunologic rules that govern skin inflammation in early life.

207 acterize changes in glutamine metabolism and inflammation in human glioma samples and explore the use

208 e mechanisms driving influenza virus-induced inflammation in humans.

209 tor activation and suppressing C3aR-mediated inflammation in mammalian physiology and disease.

210 l migration, TNF-alpha secretion, and tissue inflammation in mice (female BALB/c strain) with an LPS-

211 work has described induction of intrauterine inflammation in mice with a single injection of lipopoly

212 t role of YAP in KCs for regulation of liver inflammation in NASH.

213 tinal microbiome, and circulating markers of inflammation in patients with quiescent IBD.

214 have shown the presence of increased type 2 inflammation in patients with severe asthma and those wi

215 erapies to enhance fibrinolysis and decrease inflammation in PE and DVT patients, respectively, and o

216 gut integrity, microbial translocation, and inflammation in PHIV is poorly understood.

217 targeting IL-17 for the treatment of chronic inflammation in preclinical models and in patients affli

218 cohort, supporting the concept of a role for inflammation in PRKN/PINK1-linked Parkinson's disease.

219 rsus axial and peripheral osteoproliferative inflammation in SpA.

220 DSC in preventing the catabolic responses of inflammation in stimulated chondrocytes.

221 as a potential therapy for attenuating early inflammation in TBI.

222 Inflammation in the central nervous system (CNS) has bee

223 key chemokine controlling liver fibrosis and inflammation in the context of YAP/TAZ.

224 ase (PERK) protects oligodendrocytes against inflammation in the experimental autoimmune encephalomye

225 Single dose of D-Sino attenuated inflammation in the injured brain areas by suppressing i

226 resistance, but induced fibrogenic genes and inflammation in the liver.

227 been implicated as an essential regulator of inflammation in the oral cavity.

228 emic administration of BK1.3 potently blocks inflammation in vivo Identification and characterization

229 tions and imiquimod-triggered psoriatic skin inflammation, indicating that E-cadherin on LC does not

230 Cpn 60.1, named IRL201104, on allergic lung inflammation induced by ovalbumin (OVA) in mice and by h

231 ffect of the COX pathway on innate pulmonary inflammation induced by protease-containing fungal aller

232 rogression in HFD-fed mice by inducing liver inflammation, injury, and p38 activation.

233 Given that inflammation is considered an important driver of postop

234 e-dependent signaling.SIGNIFICANCE STATEMENT Inflammation is critical for the emergence of hypertensi

235 Whether the associated mucosal inflammation is important or redundant for effective ind

236 The recruitment of leukocytes, a hallmark of inflammation, is regulated by chemokines, which activate

237 f IL-1beta in controlling local and systemic inflammation, its overall regulation is still not fully

238 vaccine did not induce immune activation or inflammation known to be associated with increased susce

239 shed, molecular understanding of how chronic inflammation leads to the development of colon cancer is

240 tanding of basic mechanisms and the roles of inflammation, macrovascular and microvascular dysfunctio

241 atory mediators, and the mechanisms by which inflammation may inhibit immunity.

242 l immunosuppressive strategy to control skin inflammation mediated by the IL-23/IL-1beta/IL-17 axis.

243 stic analysis of TSLP-mediated type 2 airway inflammation METHODS: To dissect the mechanisms of TSLP-

244 birth cohort, we measured biomarkers of gut inflammation (myeloperoxidase, neopterin), permeability

245 Other frequent pathophysiologies were inflammation (n = 104, 35.6%) related to sepsis, respira

246 f cerebrospinal fluid microRNAs that control inflammation, neuronal injury, autophagy and vesicular t

247 at EP acts as an adjuvant by enhancing local inflammation, notably via granulocytes, monocytes/macrop

248 ory responses that contribute to the chronic inflammation observed in cancer, obesity, and other cond

249 r obesity conditions and thereby counteracts inflammation of peripheral insulin-sensitive tissues and

250 PD apparently fuels the inflammation of T2D and associates with poor glycemic co

251 (IBD) is a chronic disorder characterized by inflammation of the gastrointestinal (GI) tract, and it

252 ozygous mutant mice develop lethal postnatal inflammation of the salivary glands and mediastinum.

253 ophage population that controls overwhelming inflammation on one hand but is also necessary for an ef

254 group by day 2 after challenge, and limited inflammation or detectable viral genome or antigen was n

255 Of these PTBs, >25% are a result of inflammation or infection.

256 fecal microbiota independent of active liver inflammation or injury.

257 ogenous itaconate does not affect PM-induced inflammation or NRF2 activation in macrophages in vitro

258 m and plays a key role in microbial defense, inflammation, organ development, and tissue regeneration

259 allergen and rhinovirus-induced symptoms and inflammation over time is unclear.

260 ine acute lung injury models of neutrophilic inflammation, overexpression of SEMA3F delayed inflammat

261 Inflammation plays a central role in the pathogenesis of

262 Inflammation plays an important role in cardiovascular d

263 tralization and tissue-specific neutrophilic inflammation preserve tissue integrity during infection.

264 f age on the overall changes in the systemic inflammation profiles in subpopulation of TB patients.

265 es have identified multiple types of chronic inflammation ranging from autoimmune disease, which atta

266 tentiation of ovalbumin-induced eosinophilic inflammation; recruitment of platelet-adherent eosinophi

267 are characterized by a strong enrichment in inflammation-related gene signatures, elevated expressio

268 ated regions in glucocorticoid signaling and inflammation-related genes were associated with alcohol

269 flammation, overexpression of SEMA3F delayed inflammation resolution with slower neutrophil migratory

270 g and contraction, and impaired hallmarks of inflammation resolution, including dampening of the T he

271 WT neutrophils into Par4(-/-) mice restored inflammation resolution, reduced cardiac rupture inciden

272 try in brain parenchyma in over 40% of "high inflammation" schizophrenia brains.

273 on based on their relevance to sepsis, acute inflammation, sepsis-related immune suppression, and sep

274 COTS), supported by the International Ocular Inflammation Society, International Uveitis Study Group,

275 A higher inflammation subgroup was defined by elevations in a gro

276 of transcription factors are key drivers of inflammation that activate sets of genes in response to

277 mune disease characterized by attacks of CNS inflammation that are often severe and predominantly aff

278 vivo is characterized by extensive systemic inflammation that can exacerbate infection by potentiall

279 trauma but is also responsible for unchecked inflammation that causes neuronal cell death, systemic s

280 Inflammation that is not resolved in due course becomes

281 e of oxidized lysoPL of stressEVs in sterile inflammation that promotes chronic diseases.

282 h as house dust mite-induced allergic airway inflammation, the lack of IRF4 expression in the DC comp

283 icantly with endophenotype modules governing inflammation, thrombosis, and fibrosis in the human inte

284 gical functions: free IgE initiated allergic inflammation through FcepsilonRI on allergic effector ce

285 butes to cholestasis-mediated cell death and inflammation through mechanisms involving activation of

286 maternal immune activation, or uncontrolled inflammation triggered by viral infections during pregna

287 a-knockout (ko) mice are susceptible to lung inflammation, tumorigenesis and metastasis, which resemb

288 genetic or pharmacological tools ameliorates inflammation, vascular leakage, neurodegeneration, and n

289 ene expression for effectors associated with inflammation, vascularization, and bone formation.

290 rproliferative cell which appears to promote inflammation via elaboration of complement-dependent ana

291 Here, we found that chronic inflammation was a determinant for the competitive advan

292 Therefore, neuronal loss rather than inflammation was critical for AD progression in this mou

293 pidermidis to degrade the barrier and induce inflammation was examined by using human keratinocyte ti

294 d intestinal damage, driven by STAT1-induced inflammation, was also prevented in EW RV-infected mice.

295 s a critical intrinsic negative regulator of inflammation, which broadly attenuates pro-inflammatory

296 very low levels were detected after sterile inflammation with silver nitrate despite levels of Saa1

297 macological neuromodulation to reduce tissue inflammation with the aim of preventing respiratory fail

298 ace special emphasis on redox regulation and inflammation, with a focus on IL-1beta, which is secrete

299 collateral damage from sustained myocardial inflammation within the infarct zone.

300 l states encountered in bacterial infection, inflammation, wounds, cardiovascular defects and cancer.