ライフサイエンスコーパス: NET

1 NET and ROS release was monitored after the addition of

2 NET and ROS release, as well as the expression of NET-bo

3 NET formation and proteins were analyzed by using confoc

4 NET formation is increased in patients with severe COPD

5 NET formation may be one mechanism contributing to the c

6 NET formation, reactive oxygen species, autophagy activa

7 NET fostered the progression of the indolent NPM1-driven

8 NET patients received somatostatin radiopeptide therapy

9 NET protein complexes (DNA-elastase and histone-elastase

10 NET rs2242446/T-182C may serve as a biomarker to predict

11 NET-induced intravascular coagulation was dependent on a

12 NETs contain the high-mobility group protein B1 (HMGB1),

13 NETs from ANCA-stimulated neutrophils caused endothelial

14 NETs have been reported to directly promote thrombosis i

15 NETs have been shown to activate complement and can be a

16 NETs may serve as a mechanistic link between endothelial

17 NETs promote pathogen clearance but also can lead to thr

18 NETs were critical for the development of sepsis-induced

19 NETs were found to entrap, but not kill, all periodontal

20 rolled patients with advanced grades 1 and 2 NETs with progressive disease or other poor prognostic f

21 nctional, well-differentiated (grade 1 or 2) NETs of lung or gastrointestinal origin.

22 in 54 kidneys, 25 livers, 27 spleens, and 30 NET lesions.

23 Overall, 1,535 NET patients were enrolled and received 3,807 treatment

24 We measured the dose rates from 93 NET patients on leaving the department after undergoing

25 on in the animal model were used to design a NET-related inflammatory gene signature for human myeloi

26 ansferase on (177)Lu-DOTATATE treatment in a NET model.

27 al imaging, and systemic therapy of advanced NETs and discuss results of recent phase 3 studies, syst

28 d to octreotide among patients with advanced NETs.

29 itumor activity among patients with advanced NETs.

30 yndrome during the 3 months before and after NET diagnosis.

31 s involved in MSU crystal-induced aggregated NET formation, but MRS2578 could have additional effects

32 MSU crystal-NET aggregates called aggregated NETs.

33 Survival for all NETs has improved over time, especially for distant-stag

34 The OS rate for all NETs improved from the 2000-2004 period to the 2009-2012

35 ype I IFN-mediated neutrophil activation and NET formation may contribute to inflammatory manifestati

36 rs, eliminates substrate activity at DAT and NET, and decreases abuse liability of the compounds.

37 markers (CD66b and neutrophil elastase) and NET markers (citrullinated histone H3 [H3Cit] and extrac

38 octreotide in large varieties of non-NET and NET.

39 is of reactive oxygen species production and NET formation to decide on required antibiotic and antim

40 iated with reduced leukocyte recruitment and NET formation at the site of thrombosis.

41 f TLR signaling in bacterium-induced ROS and NET release needs to be further elucidated.

42 ordonii, stimulated higher levels of ROS and NET release than others.

43 ingly, TLR inhibitors did not impact ROS and NET release.

44 INTERPRETATION: Neutrophils and NETs form important constituents of cerebral thrombi.

45 Neutrophils and NETs were quantified.

46 The inhibition of neutrophil ROS and NETs by Ent was augmented in Lcn2-deficient neutrophils

47 me, deferoxamine) likewise inhibited ROS and NETs in neutrophils, thus indicating that the chelation

48 dsDNA) to form extracellular fibers known as NETs.

49 ey, thyroid, and lymphoid tissues as well as NETs as reference.

50 N-methyl and N-ethyl 4-MA were substrates at NET, whereas N-propyl and N-butyl 4-MA were not.

51 Mechanistically, we show that attenuated NET formation in Mincle-/- neutrophils correlates with a

52 d of neutrophils, consistent with them being NETs.

53 geneous, but there was a correlation between NET complexes and both microbiota diversity (P = .009) a

54 nship was due to modest correlations between NET complexes and FEV1, symptoms evaluated by using the

55 tor of the purinergic P2Y6 receptor, blocked NET formation triggered by MSU crystals.

56 ion of phagocytosis nearly completely blocks NET release to both biofilm and planktonic organisms.

57 Moreover, bacterial entrapment by NETs was visualized microscopically, and bacterial killi

58 vised method for thin lung tissue classified NETs with sensitivity/specificity 0.86/0.90.

59 After adjusting for multiple comparisons, NET variant rs2242446 (T-182C) was significantly associa

60 s), but the underlying mechanism controlling NET formation remains unclear.

61 cked characteristic formation of MSU crystal-NET aggregates called aggregated NETs.

62 All 4-MA analogs inhibited uptake at DAT, NET, and SERT, but lengthening the amine substituent fro

63 chain length of 4-MA on interactions at DAT, NET, and SERT.

64 opamine, norepinephrine, and serotonin (DAT, NET, and SERT, respectively).

65 Defective NET formation has thus far been only observed in patient

66 blocking neutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopatholog

67 However, in poorly differentiated NETs, (18)F-FDG PET/CT plays a significant clinical role

68 %) of 28 patients with poorly differentiated NETs, the management decision was based on only the (18)

69 The diminished NET response to C. glabrata biofilms likely contributes

70 this threshold, leading to autophagy-driven NET release, whereas the synchronous inflammatory enviro

71 in an in vivo model of infection, a dynamic NET-platelet-thrombin axis that promotes intravascular c

72 urally dissimilar radioligands was enhanced; NET binding of only one radioligand was enhanced; SERT r

73 ologic inhibition of RIPK1 or (ii) enzymatic NET degradation.

74 r spleens, and +6% (range, -11% to +16%) for NET lesions.

75 etation of (68)Ga-DOTATATE PET/CT images for NET staging is consistent among observers with low and h

76 . albicans and GBS use a related pathway for NET induction, whereas ionophores require an alternative

77 ted deglutathionylation that is required for NET formation on the other.

78 s and mitochondrial DNA release required for NET formation.

79 xygen species production but is required for NET production in primary murine neutrophils.

80 cular model of infection supports a role for NET release in vivo.

81 Restrictive advice is unnecessary for NET patients being discharged from the department.

82 Suggested treatment algorithms for NETs of ileal or jejunal origin and of pancreatic origin

83 We propose a role for NETs in cardiac fibrosis and conclude that PAD4 regulate

84 measured levels of dsDNA, as a surrogate for NETs in 103 consecutive pediatric allogeneic transplant

85 ose cell-cycle proteins and pathways to form NETs.

86 ore neutrophil extracellular trap formation (NETs) in WT compared to pcsk9 (-/-) mice.

87 DEK is detected in spontaneously forming NETs from JIA patient synovial neutrophils, and DEK-targ

88 no direct measurements of the dose rate from NET patients exiting the nuclear medicine department aft

89 18)F-FDG PET/CT had no clinical impact on G1 NETs and a moderate impact on G2 NETs.

90 mpact on G1 NETs and a moderate impact on G2 NETs.

91 or intermediate-grade gastroenteropancreatic NETs took part in this prospective study.

92 for the detection of gastroenteropancreatic NETs.

93 were noted in distant-stage gastrointestinal NETs (HR, 0.71; 95% CI, 0.62-0.81) and distant-stage pan

94 specially for distant-stage gastrointestinal NETs and pancreatic NETs in particular, reflecting impro

95 ps, including distant-stage gastrointestinal NETs and pancreatic NETs.

96 e and course of PHD were analyzed in 274 GEP NET patients from a group of 367 patients with somatosta

97 T/CT (LC and MM), (68)Ga-DOTATOC PET/CT (GEP NET), and (68)Ga-labeled prostate-specific membrane anti

98 were found for the development of PHD in GEP NET patients.

99 urements of LNs in patients with LC, MM, GEP NET, and PCA correlated with(18)F-FDG uptake, (68)Ga-DOT

100 40 patients; MM: 224 LNs of 33 patients; GEP NET: 217 LNs of 35 patients; and PCA: 254 LNs of 40 pati

101 tors for PHD could be identified for the GEP NET patients, not even bone metastasis or estimated BM d

102 oenteropancreatic neuroendocrine tumors (GEP NETs), and prostate cancer (PCA), lymph node (LN) stagin

103 oenteropancreatic neuroendocrine tumors (GEP NETs).

104 -differentiated gastroenteropancreatic (GEP) NETs took part in the study.

105 te, neutrophil-dependent glomerulonephritis, NETs are generated in the glomerular capillaries, where

106 Nude mice xenografted with the human NET cell line GOT1 were treated with semiefficient doses

107 minase-4-deficient mice (which have impaired NET production), resulted in significantly lower quantit

108 s found in granulocytes, leading to impaired NET formation.

109 nhibition of NADPH-oxidase partially impairs NET production.

110 killing of biofilm parallels the decrease in NET production.

111 4)Cu-DOTATATE with that of (68)Ga-DOTATOC in NET patients.

112 Enrichment in NET structures was found in the bone marrow of patients

113 Genes involved in NET formation in the animal model were used to design a

114 l function upstream to pyrin, is involved in NET release and regulation of IL-1beta, and might consti

115 68)Ga-DOTATOC in the detection of lesions in NET patients.

116 the risk of developing diabetes mellitus in NET patients, whereas diabetes mellitus does not appear

117 n locating the site of an unknown primary in NET patients who present with metastatic NET, but no kno

118 neumoniae, indicating its regulatory role in NET formation.

119 teropancreatic sites, and 0.84 per 100000 in NETs with an unknown primary site.

120 DNA in NETs colocalizes well with human histone H3 and with the

121 laborative interaction between histone H4 in NETs, platelets, and the release of inorganic polyphosph

122 g the existence of temporal heterogeneity in NETs production, perhaps having implications in the type

123 and (68)Ga somatostatin-receptor ligands in NETs has been expanding.

124 Most contained myeloperoxidase, as seen in NETs in other tissues, whereas intraglomerular NETs did

125 he detailed mechanism of MSU crystal-induced NET formation remains unknown.

126 (SK&F96365) also reduced MSU crystal-induced NET release.

127 gen species is required for particle-induced NET release by neutrophils.

128 DNA from patients with CPB > 100 min induced NETs release by neutrophils from healthy donors which wa

129 hibitors of molecules crucial to PMA-induced NETs including protein kinase C, calcium, reactive oxyge

130 or individual histone proteins, human intact NETs do not directly initiate or amplify coagulation in

131 In contrast, neither intact NETs, reconstituted chromatin, individual nucleosome par

132 characterized, the mechanism by which intact NETs promote thrombosis is largely unknown.

133 n vivo imaging revealed that intraglomerular NETs were present only transiently, suggesting that NETs

134 Ts in other tissues, whereas intraglomerular NETs did not contain significant levels of the histone H

135 n vivo multiphoton microscopy to investigate NET formation in the acutely inflamed glomerulus.

136 imaging agent to assess patients with known NET and frequently leads to a change in management.

137 ed, non-functional, gastrointestinal or lung NETs, with no relevant differences noted between the eve

138 emission are resistant to autophagy-mediated NET release, which can be overcome through REDD1 inducti

139 requirement of autophagy in Mincle-mediated NET formation was further supported by exogenous treatme

140 We found that Mincle mediates NET formation in response to several activation stimuli

141 as a regulator of autophagy, which mediates NET formation without affecting ROS generation.

142 naling and neutrophil migration in mediating NET formation induced by MSU crystals.

143 unknown primary in patients with metastatic NET (4 papers, yield was 44%); impact on subsequent NET

144 Forty patients with metastatic NET and unknown primary site underwent (68)Ga-DOTATOC PE

145 in NET patients who present with metastatic NET, but no known primary tumor.

146 unknown primary in patients with metastatic NET.

147 well-differentiated inoperable or metastatic NETs and disease progression after first-line treatment.

148 Ten patients with metastatic NETs underwent a 45-min dynamic PET examination followed

149 ompared with intensified treatment of midgut NETs with long-acting and repeatable octreotide, PRRT re

150 -induced neutrophil activation, necroptosis, NETs, the AP, and endothelial damage.

151 Fifty-nine NET patients were scanned with both (64)Cu-DOTATATE and

152 -Tyr(3)-octreotide in large varieties of non-NET and NET.

153 (SERT), dopamine (DAT), and norepinephrine (NET) are targets of multiple psychoactive agents, and th

154 modulators decreased ROS production but not NET production in response to the bacteria.

155 nagement occurred in 44% (range, 16%-71%) of NET patients after SSTR PET/CT.

156 lar perfusion in response to the blockade of NET-induced coagulation, which correlated with reduced m

157 However, the dynamics of NET formation in the glomerulus and their functional con

158 nd ROS release, as well as the expression of NET-bound antimicrobial proteins, elastase, myeloperoxid

159 e COPD assessment test, and higher levels of NET complexes in patients with frequent exacerbations (P

160 does not appear to increase the mortality of NET patients undergoing receptor-targeted radiopeptide t

161 Here, we present an overview of NET as a target for theranostics; review its current rol

162 vivo and experimentally after stimulation of NET formation.

163 ymptoms and biomarker findings suggestive of NET, but with negative conventional imaging (3 papers, y

164 ical relevance, mechanistic understanding of NET formation is poor.

165 Of the 64971 cases of NETs, 34233 (52.7%) were women.

166 Various components of NETs have also been implicated as activators of coagulat

167 sensitive imaging technique for detection of NETs.

168 Dissolution of NETs via DNase I did not alter anti-glomerular basement

169 ing mechanisms, suggesting that extrusion of NETs is important in host defence.

170 H3Cit, a hallmark of NETs, was observed in almost all thrombi.

171 ation of (68)Ga-OPS202 for PET/CT imaging of NETs is therefore warranted.

172 th (18)F-MFBG allows for same-day imaging of NETs.

173 Investigation of NETs under flow conditions in vitro supported this conce

174 his pathway to be targeted for modulation of NETs while preserving ROS production, an important innat

175 ormation is yet available on the presence of NETs in cerebral occlusions.

176 utrophils confirmed the specific presence of NETs.

177 The incidence and prevalence of NETs are steadily rising, possibly owing to detection of

178 mated 20-year limited-duration prevalence of NETs in the United States on January 1, 2014, was 171321

179 4 and 6 (CDK4/6) as essential regulators of NETs and show that the response is inhibited by the cell

180 further established the in vivo relevance of NETs and the requirement of RIPK1/3/MLKL-dependent necro

181 Removal of NETs via DNase infusion, or in peptidylarginine deiminas

182 revolutionized the diagnosis and staging of NETs and the evaluation of treatment outcomes.

183 Targeting of NETs with DNase 1 might have prothrombolytic potential i

184 al role of immunotherapy in the treatment of NETs.

185 in clot formation within (and downstream of) NETs in vivo.

186 zation, leading to higher IL-1beta levels on NETs.

187 e either actin and tubulin polymerization or NET formation on activation.

188 aged mice and investigated the role of PAD4/NETs in age-related organ fibrosis.

189 t-stage gastrointestinal NETs and pancreatic NETs in particular, reflecting improvement in therapies.

190 t-stage gastrointestinal NETs and pancreatic NETs.

191 CI, 0.62-0.81) and distant-stage pancreatic NETs (HR, 0.56; 95% CI, 0.44-0.70).

192 ubgroup analysis of patients with pancreatic NETs.

193 human neutrophils were stimulated to produce NETs in platelet-free plasma (PFP) or in buffer using ph

194 solated from patients spontaneously produced NETs and displayed indicators of oxidative and mitochond

195 Although the effects of purified NET components including DNA, histone proteins, and neut

196 We quantitated NET levels in gout synovial fluid supernatants and detec

197 eutrophils, and DEK-targeted aptamers reduce NET formation.

198 egative bacteria E. coli, results in reduced NET production in FlnA-depleted neutrophils.

199 The reference NET cases, incubated with a smaller amount of tracer, we

200 Mincle, a C-type lectin receptor, regulates NET formation.

201 glabrata biofilms, neutrophils also release NETs, but significantly fewer than in response to plankt

202 Neutrophil stimulation resulted in robust NET release.

203 s of the norepinephrine transporter (SLC6A2, NET) and serotonin transporter (SLC6A4, SERT) genes and

204 resence of neutrophils and more specifically NETs in ischemic stroke thrombi.

205 Sputum NET complexes were associated with the severity of COPD

206 as reduced in patients with increased sputum NET complexes.

207 gardless of the method of quantifying sputum NETs.

208 r results indicate that bacterium-stimulated NET release may arise in part via NADPH oxidase-independ

209 nist) did not inhibit MSU crystal-stimulated NET release.

210 We studied NET production in neutrophils from healthy donors with i

211 papers, yield was 44%); impact on subsequent NET patient management (4 papers, change in management i

212 ost widely used theranostic agents targeting NET is metaiodobenzylguanidine (MIBG), a guanethidine an

213 PET tracers targeting NET appear promising and may be more convenient options

214 In the present study, we found that NET components were released in mouse models of both lip

215 ores require an alternative pathway but that NETs produced by all stimuli are proteolytically active,

216 We observed that NETs provided a scaffold for AP activation that in turn

217 Here we show that NETs are induced by mitogens and accompanied by inductio

218 re present only transiently, suggesting that NETs were susceptible to disruption under the high shear

219 exiting the nuclear medicine department, the NET patients injected with (68)Ga-DOTATOC or (123)I MIBG

220 However, carcinoid syndrome frequency in the NET population has never been rigorously assessed, nor h

221 tophagy inducer tamoxifen, which rescued the NET formation defect in Mincle-/- neutrophils.

222 To further quantify CitH3 in the NETs, we established a CitH3 specific enzyme-linked immu

223 oduction of IL-1beta and its release through NETs.

224 ages via signaling of danger signals through NETs.

225 g of sst2 by sst2 antagonists, comparable to NET radiotargeting with sst2 agonists.

226 on of NETosis inhibited platelet adhesion to NETs.

227 The norepinephrine transporter (NET) is essential for norepinephrine uptake at the synap

228 5 nM) and at the norepinephrine transporter (NET).

229 s production, neutrophil extracellular trap (NET) formation, and neutrophil elastase translocation.

230 h, leading to neutrophil extracellular trap (NET) formation.

231 capacity, and neutrophil extracellular trap (NET) generation (NETosis) were measured from 1 day to up

232 that included neutrophil extracellular trap (NET) structures and that the bacteria mainly persisted i

233 e release of neutrophil extracellular traps (NETs [NETosis]), orchestrated by peptidylarginine deimin

234 by releasing neutrophil extracellular traps (NETs) (NETosis), which were more obvious upon PPTT using

235 t to release neutrophil extracellular traps (NETs) against Acinetobacter.

236 Neutrophil extracellular traps (NETs) are critical for the clearance of large pathogens

237 Neutrophil extracellular traps (NETs) are extracellular defense mechanisms used by neutr

238 Neutrophil extracellular traps (NETs) are found abundantly in the synovial fluid of gout

239 Neutrophil extracellular traps (NETs) constitute antimicrobial function of neutrophils b

240 roduction of neutrophil extracellular traps (NETs) from single neutrophils isolated from peripheral b

241 Neutrophil extracellular traps (NETs) have been documented in glomeruli of patients with

242 Neutrophil extracellular traps (NETs) have been observed in the airway in patients with

243 Neutrophil extracellular traps (NETs) have been shown to promote thrombus formation.

244 e release of neutrophil extracellular traps (NETs) in a size-dependent manner by human neutrophils.

245 es (ROS) and neutrophil extracellular traps (NETs) in mouse and human neutrophils.

246 beta-bearing neutrophil extracellular traps (NETs) in patients with FMF.

247 and release neutrophil extracellular traps (NETs) into their surroundings to immobilize and kill inv

248 hesized that neutrophil extracellular traps (NETs) mechanistically link endothelial damage with compl

249 ANCA induces neutrophil extracellular traps (NETs) via receptor-interacting protein kinase (RIPK) 1/3

250 ytes to form neutrophil extracellular traps (NETs) was determined using fluorescence microscopy and p

251 hils release neutrophil extracellular traps (NETs) which ensnare pathogens and have pathogenic functi

252 e release of neutrophil extracellular traps (NETs), associated antimicrobial proteins, and reactive o

253 lity to form neutrophil extracellular traps (NETs), but the underlying mechanism controlling NET form

254 ntly release neutrophil extracellular traps (NETs), complexes of DNA, histones, and proteins capable

255 formation of neutrophil extracellular traps (NETs), known as NETosis.

256 hils to form neutrophil extracellular traps (NETs).

257 the form of neutrophil extracellular traps (NETs).

258 the form of neutrophil extracellular traps (NETs).

259 component of neutrophil extracellular traps (NETs).

260 Neutrophil extracellular traps (NETs; webs of DNA coated in antimicrobial proteins) are

261 he blood from neutrophil extracellular traps(NETs) in response to severe infection, and CitH3 may be

262 hese findings show that C. glabrata triggers NET release.

263 ding the management of neuroendocrine tumor (NET) patients.

264 tients presenting with neuroendocrine tumor (NET) with metastases.

265 tions in patients with neuroendocrine tumor (NET).

266 treatment planning of neuroendocrine tumor (NET).

267 y among patients with neuroendocrine tumors (NETs) - even among those with the same site, stage, and

268 nce and prevalence of neuroendocrine tumors (NETs) are thought to be rising, but updated epidemiologi

269 Neuroendocrine tumors (NETs) can be treated by peptide receptor radionuclide th

270 functional imaging of neuroendocrine tumors (NETs) for the last 2 decades.

271 Treatment options for neuroendocrine tumors (NETs) remain limited.

272 etter tools to target neuroendocrine tumors (NETs) than sst2 agonists.

273 histologically proven neuroendocrine tumors (NETs) underwent both (68)Ga-DOTATATE and (18)F-FDG PET/C

274 ging and treatment of neuroendocrine tumors (NETs) with radiolabeled somatostatin analogs represent a

275 n receptor-expressing neuroendocrine tumors (NETs), and SUV measurements are suggested for treatment

276 astroenteropancreatic neuroendocrine tumors (NETs), but detection rates, especially of liver metastas

277 st decade for imaging neuroendocrine tumors (NETs).

278 anaging patients with neuroendocrine tumors (NETs).

279 etry of (18)F-MFBG in neuroendocrine tumors (NETs).

280 iopeptide therapy for neuroendocrine tumors (NETs).

281 agonists in detecting neuroendocrine tumors (NETs).

282 s in 29 patients with neuroendocrine tumors (NETs; n = 21) or meningioma (n = 8) after the administra

283 In neuroendocrine tumors, NET can be targeted for imaging as well as therapy.

284 Neuroendocrine tumours (NETs) can secrete bioactive amines into the bloodstream,

285 in the treatment of neuroendocrine tumours (NETs) that are relevant for clinicians and clinical rese

286 rointestinal or lung neuroendocrine tumours (NETs).

287 ect treatment for patients with unresectable NETs because some patients can survive decades without t

288 We sought to determine whether NETs are associated with disease severity in patients wi

289 treatment decision making for patients with NET.

290 , 9512 eligible patients were diagnosed with NETs, of whom 1786 (19%) had carcinoid syndrome.

291 med a prospective study of 184 patients with NETs (128 [69.6%] with metastases and 11 patients [6.0%]

292 on the intended management of patients with NETs (50% of changes) and notably demonstrated a high im

293 sis assessed the proportion of patients with NETs and carcinoid syndrome in the USA and associated cl

294 The number of patients with NETs and carcinoid syndrome increased from 50 (11%) of 4

295 as conducted to evaluate 64971 patients with NETs from 1973 to 2012.

296 y of presenting symptoms among patients with NETs might permit more tailored assessment and managemen

297 ighly promising for imaging of patients with NETs, especially children with neuroblastoma.

298 TATATE TV in a large cohort of patients with NETs, in terms of PFS and disease-specific mortality.

299 ed analysis of tumor volume in patients with NETs.

300 peutic advances on survival of patients with NETs.

301 TR PET/CT on the management of patients with NETs.