ライフサイエンスコーパス: inflammatory

1 own to be involved in antimicrobial and anti-inflammatory activities, showed a twofold increase in va

2 c volumes in patients with and without focal inflammatory activity in 161 patients followed over 5 ye

3 e the spatial organization, persistence, and inflammatory activity of gut bacterial populations.

4 managing bacterial spatial organization and inflammatory activity within the gut.

5 inforcing the use of EP2 antagonists as anti-inflammatory agents.

6 Drugs with anti-inflammatory and anti-fibrotic effects are of promise fo

7 e have used Sinomenine (Sino), a potent anti-inflammatory and antioxidant drug conjugated to hydroxyl

8 of venous thromboembolism and the degree of inflammatory and coagulation marker elevation associated

9 cribed role in cancer, our in vivo screen of inflammatory and cytokine pathway genes revealed IL26 to

10 Downstream analysis identified abundant inflammatory and immunologic targets for miR-17 and miR-

11 Our data indicate that anti-inflammatory and immunosuppressive mechanisms are not ne

12 ion that are aberrantly regulated in several inflammatory and infectious diseases.

13 ing to assess key transcriptional changes in inflammatory and lysosomal pathways.

14 ntagonist 1 (TG6-10-1), which displayed anti-inflammatory and neuroprotective actions in rodent model

15 mmatory or reparative phenotypes to modulate inflammatory and reparative responses, respectively.

16 rofilament/neurofilament light chain [NFL]), inflammatory, and antioxidant (enzymes, including heme o

17 ant pharmaceutical compounds, including anti-inflammatory, anti-depressant, anti-bacterial, anti-vira

18 ll features, focusing on compounds with anti-inflammatory, antioxidant or antimicrobial properties.

19 n the airway compartment and neutrophil-rich inflammatory areas of the interstitium, while NET-prone

20 for the most effective and safe treatment of inflammatory arthritis.

21 bilization of mRNA, which is associated with inflammatory autoimmune diseases.

22 ng that GM-CSF is a potential target in many inflammatory/autoimmune conditions.

23 cardiac cell therapy is thus due to an acute inflammatory-based wound-healing response that rejuvenat

24 Based on the anti-inflammatory benefits of the upregulation of the ACE2/An

25 Elevated levels of inflammatory biomarkers are consistently associated with

26 Inflammatory bowel disease (IBD) is a common chronic inf

27 Crohn's disease (CD) is a chronic relapsing inflammatory bowel disease (IBD) that may be marked by d

28 Inflammatory bowel disease (IBD), including Crohn's dise

29 dentified as a novel susceptibility gene for inflammatory bowel disease (IBD).

30 significant risk factor for pCCA followed by inflammatory bowel disease and cirrhosis, whereas other

31 ther immune-mediated diseases, most commonly inflammatory bowel disease and rheumatoid arthritis.

32 hil dysfunction cause serious infections and inflammatory bowel disease in glycogen storage disease t

33 ignificantly correlated with reduction of an inflammatory bowel disease risk gene ATG16L1 and Paneth

34 No deaths or cases of inflammatory bowel disease were reported.

35 on cohort to as high as 78% in patients with inflammatory bowel disease(2).

36 nding its role in various diseases including inflammatory bowel disease, neurologic diseases, cardiov

37 Kingdom) data from the 2015 and 2017 Adelphi Inflammatory Bowel Disease-Specific Programme (IBD-DSP)

38 ms of mucosal dysregulation in patients with inflammatory bowel diseases (IBDs) and differences in in

39 both small-bowel diagnosis and monitoring in inflammatory bowel diseases.

40 cell death response, ultimately supports the inflammatory breakdown of infected cells at later time p

41 rted to act as both antidepressants and anti-inflammatories, but the mechanisms for these effects are

42 e stress, DNA damage, lysosomal dysfunction, inflammatory cascade, apoptosis, genotoxicity, and ultim

43 suggest that blocking the cytokine-mediated inflammatory cell death signaling pathway identified her

44 In stress models, inflammatory cell infiltration was initially lower in kn

45 liber, extent of injury, C4d positivity, and inflammatory cell phenotyping.

46 Contact between inflammatory cells and endothelial cells (ECs) is a cruc

47 a positive feedback loop between peripheral inflammatory cells and networked brain regions involved

48 t with sloughed tracheobronchial tissues and inflammatory cells in a background of dense mucin.

49 in function, the specific role of immune and inflammatory cells in neurodegenerative diseases remain

50 IVCM shows that inflammatory cells invade only the stroma during an acut

51 edema, infiltration of lung and pancreas by inflammatory cells, and plasma amylase activity compared

52 ar smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/macrophages, cellular

53 hat JAK3 inhibition enhances infiltration of inflammatory cells, reduces expression of Wnt3a and Dvl3

54 Atherosclerotic lesions exhibited inflammatory cells.

55 Inflammatory challenge led to robust eGFP-L10a upregulat

56 cost of enhancing mortality to a subsequent inflammatory challenge.

57 root canal system, while FM group presented inflammatory changes with the continuation of root devel

58 hypercalprotectinemia and hyperzincemia with inflammatory complications accompanied by cytopenia.

59 uations and is used clinically to assess the inflammatory component of the disease, particularly the

60 Psoriasis is a chronic inflammatory condition that is associated with increased

61 tory bowel disease (IBD) is a common chronic inflammatory condition, and the United States has the hi

62 Inflammatory conditions as they occur during periodontal

63 ssion of CD163 was analyzed under normal and inflammatory conditions in mice.

64 ed by several orders of magnitude in various inflammatory conditions including aging and obesity.

65 a manner representative of thrombotic or pro-inflammatory conditions such as arterial thrombosis.

66 In inflammatory conditions, costimulation of human brain en

67 s unknown how robust this dichotomy is under inflammatory conditions, when additionally monocyte-deri

68 ifferent PI3K isoforms under homeostatic and inflammatory conditions.

69 and macrophage content, plaque size, and pro-inflammatory cytokine expression.

70 at maternal immune activation (MIA) elevates inflammatory cytokine levels in the maternal and fetal c

71 jection of the hybrid system locally reduces inflammatory cytokine levels.

72 Intriguingly, GM-CSF signaling amplifies inflammatory cytokine production in recruited monocytes

73 -PE and IFN-gamma on AML blasts generated an inflammatory cytokine profile and activated NK cells.

74 ges induce an interleukin-1 (IL-1)-dependent inflammatory cytokine response by recruited monocytes an

75 Functional enrichment analysis revealed pro-inflammatory cytokine signaling pathways as dysregulated

76 TAT proteins can regulate both pro- and anti-inflammatory cytokine signaling.

77 M-CSF), a myelopoietic growth factor and pro-inflammatory cytokine, plays a critical role in alveolar

78 Tregs suppress effector T cell-mediated and inflammatory cytokine-induced CEnC death, and to elucida

79 Inflammatory cytokine/chemokine concentrations were dete

80 XAA in MCC cells reactivates their antitumor inflammatory cytokine/chemokine production.

81 The anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and

82 PG-CAT greatly reduced the concentration of inflammatory cytokines and chemokines, including IL-1, T

83 Elevated local production of inflammatory cytokines and MMPs, together with apparent

84 on in the injured brain areas by suppressing inflammatory cytokines expression whereas free Sino trea

85 ts of perioperative intravenous n-3 PUFAs on inflammatory cytokines in colon cancer surgery.

86 Inflammatory cytokines induce the expression of IFITM3 i

87 Elevated inflammatory cytokines such as IL-1beta and IL-18 and co

88 agocytosis and does not induce expression of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

89 activity, including increased levels of pro-inflammatory cytokines(3,4) that may be produced by a su

90 s in vivo and reduced systemic levels of pro-inflammatory cytokines.

91 mortality due to sustained production of pro-inflammatory cytokines.

92 contributes to exacerbation of postischemic inflammatory damage of the myocardium and corresponding

93 The association between chronic inflammatory demyelinating polyneuropathy (CIDP) and dia

94 Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)

95 lammation), chronic axonal degeneration, and inflammatory demyelination due to loss of protective ant

96 A highly inflammatory diet is associated with metabolic syndrome,

97 iHS/DRESS) is a potentially fatal multiorgan inflammatory disease associated with herpesvirus reactiv

98 Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint destruction

99 riments and evaluated susceptibility to oral inflammatory disease in mice harboring distinct microbio

100 (EA) is a relatively rare, benign and local inflammatory disease involving the epiploic appendices.

101 s suggests an LNP which delivers mRNA to one inflammatory disease may not deliver mRNA to another.

102 Takayasu arteritis is a rare inflammatory disease of large arteries.

103 tes in the sinonasal cavity, with non-type 2 inflammatory disease on one end, type 2 inflammatory, eo

104 latelet activation in thrombosis and thrombo-inflammatory disease settings.

105 ic esophagitis (EoE) is an allergen-mediated inflammatory disease with no approved treatment in the U

106 is known, ulcerative colitis (UC), a chronic inflammatory disease, is closely related to immune dysfu

107 effector functions and role in infection and inflammatory disease.

108 Chronic inflammatory diseases including human immunodeficiency v

109 ondyloarthritis (SpA) represents a family of inflammatory diseases of the spine and peripheral joints

110 2), which are associated with severe chronic inflammatory diseases that span several organ systems(3-

111 eased levels of putative markers for several inflammatory diseases, which were reduced by the benzimi

112 otential to trigger or exacerbate intestinal inflammatory diseases.

113 exudative retinal detachment (ERD) in ocular inflammatory diseases.

114 r therapeutic potential for the treatment of inflammatory diseases.

115 rapeutically target the chemokine network in inflammatory diseases.

116 n of PMN-associated tissue damage in chronic inflammatory diseases.

117 Atopic dermatitis (AD) is a complex inflammatory disorder with multiple interactions between

118 lso designated as acne inversa) is a chronic inflammatory disorder, which affects the intertriginous

119 idence of 7.4% after a median of 19 months), inflammatory disorders (VTE risk is 4.7% in patients wit

120 Administration-approved in a few autoimmune/inflammatory disorders and are being evaluated in many o

121 of chronic diseases including metabolic and inflammatory disorders and tumorigenesis.

122 such as degenerative diseases, metabolic and inflammatory disorders, and cancer.

123 naling has been implicated in autoimmune and inflammatory disorders.

124 to infection foci, and 3) production of anti-inflammatory effectors IL-10 and thioredoxin 1.

125 AdipoRon also exerted anti-inflammatory effects by reducing microglial and astrocyt

126 ents implicated a humoral factor in the anti-inflammatory effects generated by endothelial PHD2/HIF-1

127 The anti-inflammatory effects of vagus nerve stimulation are well

128 Furthermore, this mild inflammatory environment promotes oligodendrocyte progen

129 LI3 levels with a miR-744-5p antagomir in an inflammatory environment resulted in reduced levels of I

130 uced MC degranulation even in the absence of inflammatory environment.

131 pe 2 inflammatory disease on one end, type 2 inflammatory, eosinophil-heavy disease on the other and

132 Asthma exacerbations are inflammatory events that rarely result in full hospitali

133 In this scenario, pro-inflammatory factors are intensely released into the blo

134 Further analysis of an inflammatory gene cluster revealed that genes associated

135 B signaling completely reversed elevated pro-inflammatory gene expression in macrophages.

136 These novel inhibitors suppress inflammatory gene expression induced by EP2 receptor act

137 ound to membrane-associated TNF and dampened inflammatory gene expression through reverse signaling.

138 IDL and ethyl linoleate/oleate downregulated inflammatory gene expression, but IDL more effectively u

139 f inflammation, which broadly attenuates pro-inflammatory gene programs in macrophages.

140 ide LP17 resulted in decreased levels of pro-inflammatory genes for the moderate and severe isolates.

141 nib, a selective FLT3 inhibitor, upregulates inflammatory genes in DTPs and thereby confers susceptib

142 ons in CHIP, lead to increased expression of inflammatory genes in innate immune cells, potentially e

143 nergy utilization and the expression of anti-inflammatory genes.

144 s and thereby confers susceptibility to anti-inflammatory glucocorticoids (GCs).

145 A differential diagnosis between inflammatory, idiopathic, and myopic CNV may be challeng

146 ction for IL-33, Tph1, and ICOS in promoting inflammatory ILC2 responses and type 2 immunity at mucos

147 en described: steady-state natural ILC2s and inflammatory ILC2s, which are elicited following helmint

148 from other, noninfectious causes of systemic inflammatory illness.

149 opment of therapeutic agents to modulate pro-inflammatory immune reactions.

150 Balanced regulation of cell death and inflammatory immune responses is essential to promote pr

151 bsence of IFD, can result in deleterious pro-inflammatory immune responses.

152 rdial infarction, whereas high HDL oxidative-inflammatory index values (OR(1SD), 1.53; 95% CI, 1.01-2

153 These results demonstrate that inflammatory-induced activation of Ccr2 signaling in myo

154 to determine the extent of connective tissue inflammatory infiltrate (CTII) using the following marke

155 yocardial (18)F-FOL uptake colocalizing with inflammatory lesions (SUV(mean), 2.1 +/- 1.1), whereas u

156 showed many FR-beta-positive macrophages in inflammatory lesions.

157 ic stress manifest within monocytes in acute inflammatory lesions.

158 nced by the increased glycolytic activity of inflammatory lesions.

159 Drug induced liver injury (DILI) is a necro-inflammatory liver disease caused by several drugs commo

160 We investigated the signal from the inflammatory liver for this pathogenic process in the he

161 Oral inflammatory load (OIL) was assessed in a salivary rinse

162 Allergic asthma is a chronic inflammatory lung disease associated with increased cyto

163 ages can phagocytose tumor cells, while anti-inflammatory M2 macrophages such as tumor-associated mac

164 ther a proinflammatory (M1) state or an anti-inflammatory (M2) state.

165 ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaqu

166 In fact, pro- and anti-inflammatory macrophages differ in the expression of ser

167 ort-acting beta-agonists (SABAs), while anti-inflammatory maintenance with inhaled corticosteroids (I

168 Individual and/or inflammatory marker patterns were associated with neuroi

169 aging data of 18kDa translocator protein (an inflammatory marker) in MWA patients (n = 11) who experi

170 Conversely, mRNA levels of pro-inflammatory markers (IL-6, IL-1beta, COX-2 and TNF-alph

171 ss this question, we investigated neural and inflammatory markers from mice deficient for ELOVL2 (Elo

172 rate suggested benefit, and those with lower inflammatory markers had better outcomes.

173 ensity lipoprotein uptake, and expression of inflammatory markers in monocytes and plasma.

174 a recovery of SG function and a decrease in inflammatory markers in the mice.

175 itudinal analyses to determine whether these inflammatory markers predict future CVD events, and are

176 Relations between PZC and inflammatory markers were inconsistent, suggesting that

177 Tumor inflammatory markers were quantified using electrochemil

178 e responses and a concomitant rise in plasma inflammatory markers.

179 sses that are at least partly independent of inflammatory mechanisms can develop early in people with

180 nvestigated the ability of soy PG to inhibit inflammatory mediator expression in response to activato

181 sf2/GM-CSF as a primary complement-dependent inflammatory mediator.

182 cytes/macrophages inhibited the secretion of inflammatory mediators IL-1beta and MCP-1.

183 erved, and modulated key bone remodeling and inflammatory mediators in rats with ligature-induced per

184 hocytes and higher levels of a wide array of inflammatory mediators in their MEE compared to that of

185 r, the NF-kappaB-dependent production of pro-inflammatory mediators is not affected by C/EBPgamma.

186 ealed IL26 to be one of the most significant inflammatory mediators of mammary engraftment and lung m

187 of inflammaging, the cellular source of the inflammatory mediators, and the mechanisms by which infl

188 inked to a decrease in the production of pro-inflammatory mediators, such as TNF-alpha and IL-6.

189 polarizations, particularly upon exposure to inflammatory mediators.

190 tion and to NAAA itself as a target for anti-inflammatory medicines.

191 Furthermore, numerous infectious, inflammatory, metabolic and genetic diseases, as well as

192 m GLA and result in proinflammatory and anti-inflammatory metabolites, respectively.

193 ogical mechanisms of platelet recruitment to inflammatory micro-environments remain incompletely unde

194 egeneration (n = 115, 39.4%), and immune and inflammatory modulation (n = 79, 27.1%).

195 the fact that it acts as a hemolytic and pro-inflammatory molecule.

196 nes(3,4) that may be produced by a subset of inflammatory monocytes(5,6), lymphopenia(7,8) and T cell

197 esis, increased infiltration of neutrophils, inflammatory monocytes, and T cells, and increased activ

198 ammatory neutrophils and the infiltration of inflammatory monocytes.

199 ntly by testing C2C activity in the formalin inflammatory mouse pain model.

200 s the expression of TNF-alpha to regulate an inflammatory network in ovarian cancer.

201 o many P2X7-dependent pathologies, including inflammatory, neurological, and immune diseases.

202 ICANS is an inflammatory neurotoxicity typically occurring after CRS

203 resulted in a remarkable decrease in cardiac inflammatory neutrophils and the infiltration of inflamm

204 Whereas IgA2 acts pro-inflammatory on neutrophils and macrophages, IgA1 does n

205 ve low-pressure regimen does not up-regulate inflammatory or immune responses.

206 tion of the terminals in simulated models of inflammatory or neuropathic hyperexcitability led to a c

207 or cardiac repair as they can adopt both pro-inflammatory or reparative phenotypes to modulate inflam

208 patient populations with chronic infectious, inflammatory, or metabolic diseases.

209 both CCL17-dependent and unique CCL17-driven inflammatory pain and arthritis models, the latter permi

210 ein 1-associated myeloid-related proteinemia inflammatory (PAMI) syndrome is a novel genetic disorder

211 were isolated 24 hours later, and fibrogenic/inflammatory parameters were analyzed.

212 -driven immunogenicity can be uncoupled from inflammatory pathogenicity.

213 ating that GM-CSF constitutes a nonredundant inflammatory pathway in the GI tract.

214 of asymptomatic hyperuricaemia in these pro-inflammatory pathways.

215 miR-31-associated EGLN3/NF-kappaB-controlled inflammatory pathways.

216 d thus inspire the development of novel anti-inflammatory peptides that therapeutically target the ch

217 ts define a therapeutic window targeting the inflammatory phase for optimal effects of S100A9 blockad

218 w the patient's immune system toward an anti-inflammatory phenotype and therefore could provide unant

219 osignals a functional shift in iMo toward an inflammatory phenotype associated with CAD progression i

220 f a single allele of Cebpb prevented the pro-inflammatory phenotype.

221 m microbiome is associated with clinical and inflammatory phenotypes in COPD.

222 acetylation, in CF mice restores growth and inflammatory phenotypes to wild type (WT) profiles.

223 cells is upregulated and is associated with inflammatory polarization of macrophages and fibroblasts

224 mong patients with polyps, the prevalence of inflammatory polyps was higher in the IBD group (55%) co

225 This inflammatory process can be partially reversed by immuno

226 ted immune dysregulation is a T(H)1-mediated inflammatory process driven by the IFN-gamma pathway.

227 nary cultures, fermented-AP counteracted the inflammatory processes and the effects of oxidative stre

228 neuroinflammation to better characterise the inflammatory processes underlying various diseases and t

229 nts but disrupted it in HVs independently of inflammatory processes.

230 sis also suggested differential IL-6-related inflammatory programs in WT versus IRF3-KO mice.

231 member of the IL-1 superfamily and has anti-inflammatory properties similar to those of IL-37 but th

232 hyperexcitability and neuron loss, have anti-inflammatory properties, and are well tolerated by the b

233 collectively) were associated with increased inflammatory proteins and more severe depression but dif

234 The increased inflammatory, prothrombotic, and procoagulant responses

235 t cause loss of gasdermin D function convert inflammatory pyroptotic cell death into immunologically

236 ferent antigens that trigger distinct immune-inflammatory reactions.

237 n-coding RNAs which are reported to regulate inflammatory response and cell proliferation.

238 anscriptional dysregulation indicative of an inflammatory response and cellular function deficits.

239 -treated myocardium and a suppression of the inflammatory response and mitogen-activated protein kina

240 etal muscle radiodensity (SMD), the systemic inflammatory response as measured by the modified Glasgo

241 sed to MIA can be temporarily rescued by the inflammatory response elicited by the administration of

242 The systemic inflammatory response syndrome (SIRS) frequently occurs

243 surgery, and variceal bleeding; R: systemic inflammatory response syndrome (SIRS), spontaneous bacte

244 iral detection and had more intense systemic inflammatory response than those carrying non-PnIST or n

245 o, it was able to attenuate an overly robust inflammatory response that is detrimental to the host du

246 onstrated its capacity to generate a similar inflammatory response to a wild-type rabbit strain and,

247 ung macrophages are important in mounting an inflammatory response to injury, but they are also invol

248 ays an essential role in dampening the early inflammatory response to LPS by regulating macrophage fu

249 emokine gene promoters, facilitating a rapid inflammatory response to microbial pathogens.

250 The inflammatory response to severe acute respiratory syndro

251 s-on-a-chip and display a more dynamic, less inflammatory response to TNFalpha, that resembles more t

252 s were mainly associated with cell adhesion, inflammatory response, and extracellular exosome.

253 To help ameliorate the inflammatory response, corticosteroids are used as an ad

254 aracterized by high viral load, uncontrolled inflammatory response, dysregulated adaptive immunity, c

255 Gene networks dysregulated in PMD included inflammatory response, early/late E2-response, and chole

256 ight therefore be expected to induce a local inflammatory response.

257 essential role of this pathway in macrophage inflammatory response.

258 pyelonephritis, which are associated with an inflammatory response.

259 droxymethylated regions were associated with inflammatory response/disease, organismal injury, and re

260 estration in organs and consequent excessive inflammatory responses and endothelial damage.

261 d transcriptome profiling identified several inflammatory responses and immune response signaling pat

262 n-3 (omega-3) PUFAs modulate inflammatory responses and may help to prevent a proinfl

263 s their inhibition attenuated scratching and inflammatory responses in mouse atopic dermatitis models

264 Cibinetide ameliorated the local inflammatory responses in the liver and improved glycemi

265 oV-2 and develop bronchopneumonia and strong inflammatory responses in the lungs with neutrophil infi

266 Pulmonary inflammatory responses lie under circadian control; howe

267 virus replication and in suppressing the pro-inflammatory responses of human pathogenic viruses, incl

268 ory bowel diseases (IBDs) and differences in inflammatory responses of patients with ulcerative colit

269 pressive histone methylation dynamics during inflammatory responses remain enigmatic.

270 ss or mitochondrial stress, can also promote inflammatory responses that contribute to the chronic in

271 ate inflammasomes but then subvert resulting inflammatory responses to avoid elimination.

272 gether with interventions to abrogate stress-inflammatory responses, should be evaluated in conjuncti

273 A major cause of damage is local inflammatory responses, which may spread to produce more

274 signaling changes; (iv) Oxidative stress and inflammatory responses.

275 activate this pathway and trigger extensive inflammatory responses.

276 se of epidermal differentiation and enhanced inflammatory responses.

277 component of therapeutic strategies for many inflammatory rheumatic diseases.

278 Next to the recently discovered pro-inflammatory role of cytosolic LPS, our data reveal a di

279 nal transduction that impacts cell death and inflammatory signaling downstream of various innate immu

280 Proteases, inflammatory signaling molecules, as well as proteins in

281 n that activate sets of genes in response to inflammatory signals.

282 Psoriasis is a frequent, inflammatory skin disease characterized by keratinocyte

283 Psoriasis is an inflammatory skin disease that is associated with multip

284 on of the AHR/CYP1A1 axis may play a role in inflammatory skin disease.

285 c risk factor for AD and is related to a pro-inflammatory state.

286 s a disease spectrum encompassing a range of inflammatory states in the sinonasal cavity, with non-ty

287 sentative data characterizing the immune and inflammatory status in coronavirus disease 2019 patients

288 te exchange, and biomarkers of oxidative and inflammatory stress were also measured.

289 t can develop a life-threatening multisystem inflammatory syndrome (MIS-C)(3-5).

290 adoxical TB-associated immune reconstitution inflammatory syndrome (TB-IRIS) when they commence antir

291 tation of tuberculosis immune reconstitution inflammatory syndrome (TB-IRIS).

292 month into the epidemic, a novel multisystem inflammatory syndrome in children (MIS-C) emerged.

293 novel pediatric disorder termed multisystem inflammatory syndrome in children (MIS-C) emerged.

294 A multisystem inflammatory syndrome in children (MIS-C) is associated

295 lure, including antidiabetic therapies, anti-inflammatory therapies, and novel immunometabolic agents

296 We also tested whether inflammatory tissue conditions synergize with dicarbonyl

297 the expression of MAFG and MAT2alpha and pro-inflammatory transcriptional modules, contributing to CN

298 ll lung cancer (NSCLC), accumulation of anti-inflammatory tumor-associated macrophages (TAM) is assoc

299 gene signatures, elevated expression of pro-inflammatory tumorigenic cytokines, such as IL-17A and I

300 heterocellular aggregate formation drive the inflammatory vaso-occlusive processes associated with si