ライフサイエンスコーパス: MPO

1 MPO contributed only in heparin-treated patients, sugges

2 MPO deficiency caused high body temperature via upregula

3 MPO deficiency was observed in 6/81 MF patients (7.4%),

4 MPO is a glycoprotein (GP) chaperoned by calreticulin (C

5 MPO knockout (MPO(-/-)) mice were protected from HFD-enh

6 MPO levels also significantly correlated with diastolic

7 MPO oxidizes PON1 on tyrosine 71 (Tyr71), a modified res

8 MPO protein and activity measurements and histologic ana

9 MPO was primarily secreted by neutrophils, followed by l

10 MPO, HNE, and citrullinated histone H4 are all associate

11 MPO-EL is catalytically active and mediates angiotoxicit

12 MPO-Gd also helped detect more lesions during subclinica

13 MPO-Gd helps detect earlier (5.2 vs 2.3 days before symp

14 MPO-Gd specifically reveals lesions with inflammatory mo

15 MPO-specific CD4(+) effector T cell proliferation was en

16 ISAs were concordant within 2+/-11 mug l(-1) MPO with similar uncertainty and reproducibility.

17 Serum MMP-8, MMP-9, TIMP-1, MPO, and NE levels in circulation were assessed by enzym

18 MMPs (1, 2, 3, 7, 8, 9, 12), MPO, and tissue inhibitor of matrix metalloproteinase (T

19 f MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MPO, and TIMP-1 using multianalyte bead-based enzyme-lin

20 TnI, CRP, GDF-15, MPO, PlGF, and sFlt-1 levels increased from baseline to

21 infections had been documented in 2/6 (33%) MPO-deficient patients.

22 mutations in the NADPH oxidase complex or a MPO-deficient patient were examined.

23 Lysosomal-accumulated MPO can be both cell-protective, by promoting the degrad

24 MPO in ECs and demonstrate that ECs acquired MPO when contacted by neutrophils directly but not when

25 ades after the first description of acquired MPO deficiency in MPN, we provide the molecular correlat

26 We hypothesized that acquired MPO deficiency in MPN could be associated with the prese

27 exposure indicates that enzymatically active MPO is released.

28 resses Pseudomonas-induced release of active MPO and HNE.

29 tent of endotoxin-induced inflammation in an MPO-dependent manner.

30 idence interval: 1.05 to 1.81; p = 0.02) and MPO (HR: 1.34 per SD; 95% confidence interval: 1.00 to 1

31 There was no relationship between MMP-7 and MPO.

32 Because MMP-8 and MPO are produced by inflammatory cells, particularly neu

33 -9 levels correlated strongly with MMP-8 and MPO levels, and MMP-8 correlated with MPO, but it did no

34 Serum MMP-9 and MPO levels were higher in women with PCOS and gingivitis

35 NE, MMP-8, MMP-9, and MPO levels were elevated in oGVHD tears when compared wi

36 MMP-8, MMP-9, and MPO levels were elevated significantly in SJS and OCP te

37 In controls, NE, MMP-9, and MPO significantly correlated with each other (P < .0001)

38 ted strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic source and provides e

39 were performed between NE, MMP-8, MMP-9, and MPO within study groups.

40 indicators plus BNP, cTnI, ST2, PAPP-A, and MPO (each p</=0.01) [corrected].

41 een PR3-ANCA-associated vasculitis (AAV) and MPO-AAV described in the past have been supplemented dur

42 gular intervals, and tested for PR3-ANCA and MPO-ANCA.

43 Moreover, CD162 and MPO expression increased significantly in intermediate m

44 Likewise, increased CD162 and MPO expression was noted in CD14(++)CD16(-) classical mo

45 uced ROS, NLRP3 inflammasome components, and MPO levels following ICH.

46 hs-CRP and MPO were within normal limits at baseline and decreased

47 new perspectives on the biology of G-CSF and MPO, and on the role of E-selectin receptor/ligand inter

48 tform for electrical detection of h-FABP and MPO in physiological saline.

49 Deploying FABP and MPO specific scFvs as receptor molecules onto our high-s

50 label-free screening of heart type-FABP and MPO.

51 h after injury reduces the NO, LPO, GFAP and MPO level at injury site by increasing the expression of

52 Notably, PR3, p24(PR3/MBN), and MPO were synthesized in cultured neutrophils from patien

53 uced tissue injury and implicate PMN-MPs and MPO as important regulators of cellular function.

54 patient with MF, a JAK2-V617F mutation, and MPO deficiency, carried 2 previously reported MPO mutati

55 Early increases in TnI and MPO levels offer additive information about the risk of

56 in vivo, HE was injected into wild-type and MPO-deficient (Mpo(-/-)) mice with established peritonit

57 Anti-MPO antibody transfer resulted in nephritic urine by dip

58 agonist of human C5aR/CD88, ameliorated anti-MPO-induced NCGN in mice expressing human C5aR/CD88.

59 of specially engineered anti-h-FABP and anti-MPO single-chain fragment variables (scFv) were immobili

60 In an antimyeloperoxidase (anti-MPO) antibody-mediated disease model, mice transplanted

61 MPO409-428 as a therapeutic attenuated anti-MPO GN.

62 ated by autoimmunity to MPO (autoimmune anti-MPO GN), we assessed the capacity for nasal tolerance in

63 erized mice to animals with established anti-MPO autoimmunity attenuated the subsequent development o

64 In mice with established anti-MPO autoimmunity, nasal insufflation of MPO409-428 as a

65 We induced anti-MPO GN by immunizing mice with MPO and a low dose of ant

66 ve transfer of antibodies to mouse MPO (anti-MPO) induces a mouse model of ANCA NCGN that closely mim

67 of disease attenuated injury in murine anti-MPO GN.

68 ction is based on the immobilization of anti-MPO antibodies onto magnetic beads (MBs).

69 Studies in experimental models of anti-MPO GN suggest that, after ANCA-induced neutrophil local

70 rtance of C5aR/CD88 in the mediation of anti-MPO-induced NCGN and report that C6 is not required.

71 We used passive anti-MPO antibody transfer for NCGN induction in wild-type mi

72 In vitro, challenge with anti-MPO antibody strongly enhanced caspase-1 activity and IL

73 reased in serum, but not in urine, with anti-MPO antibody treatment and was completely abolished with

74 CI, 18.7% to 43.1%) when compared with anti-MPO-positive cases.

75 nuclei, including the medial preoptic area (MPO) and the suprachiasmatic nucleus (SCN) shell after g

76 , IL-6 downward arrow, HMGB1 downward arrow, MPO downward arrow, CD68 downward arrow, IL-4 upward arr

77 oteins other than apoA-I and apoA-II such as MPO and PON1 have important effects on HDL function.

78 pecialized MPO glycovariant, referred to as "MPO-E-selectin ligand" (MPO-EL), is expressed on circula

79 vestigate the utility of 2-Cl-E(+) to assess MPO activity in vivo, HE was injected into wild-type and

80 The enzymatic activity of PMN-MP-associated MPO was enhanced compared with soluble protein, leading

81 0] vs 1.02 [95% CI: 0.89, 1.14]; P = .03) at MPO-Gd MR imaging.

82 more significant role for endothelial-bound MPO than for circulating MPO or elastase with respect to

83 cell clones exacerbated disease mediated by MPO-specific CD4(+) cells in Rag1(-/-) mice.

84 We hypothesized that apoA-I oxidation by MPO levels similar to those present in the artery walls

85 xidation of either apoA1 or HDL particles by MPO impairs their cholesterol acceptor function.

86 er, we identified a pathogenic CD8(+) T cell MPO epitope (MPO431-439) and found that cotransfer of MP

87 sculitis and the nephritogenic murine T cell MPO epitope emphasizes the clinical relevance of this st

88 ed to hypochlorous acid (HOCl), chloramines, MPO/H2O2/chloride, and activated human neutrophils.

89 r endothelial-bound MPO than for circulating MPO or elastase with respect to blood pressure regulatio

90 se of the deleterious effects of circulating MPO, there is a great interest in the development of new

91 of the CNS MPO scoring algorithm, termed CNS MPO.v2.

92 indings led to a modified version of the CNS MPO scoring algorithm, termed CNS MPO.v2.

93 Conclusion MPO is a suitable imaging biomarker for identifying and

94 Conclusion MPO-Gd showed elevated MPO activity in NAFLD mouse model

95 n of whole blood with levosimendan decreased MPO release after PMN-stimulation (8.2 +/- 1.4-fold incr

96 However, lysosomal-delivered MPO also disrupts lysosomal acidification in RPE cells,

97 xtracellular space, with lysosomal-delivered MPO exhibiting a half-life of 10 h.

98 A-induced neutrophil localization, deposited MPO within glomeruli is recognized by autoreactive T cel

99 xperiments confirmed that neutrophil-derived MPO contributes importantly to protection from endotoxem

100 rt a novel bioluminescence assay, designated MPO activity on a polymer surface (MAPS), for measuring

101 myeloperoxidase (MPO) activity, could detect MPO activity in nonalcoholic steatohepatitis (NASH) mous

102 tive MPO assays and flow cytometry to detect MPO in ECs and demonstrate that ECs acquired MPO when co

103 nce emission over luminol alone in detecting MPO activity in lung tissues after lipopolysaccharide ch

104 inexpensive and rapid assay for determining MPO activity in plasma samples from patients with CVD or

105 unprocessed proMPO versus the mature dimeric MPO and the functional role of the propeptide.

106 and CF isolates of P. aeruginosa induce DNA, MPO, and HNE release from human neutrophils.

107 Our data describe in vitro details of DNA, MPO, and HNE release from neutrophils activated by P. ae

108 y of the detection strategy reported, a dual MPO mass and activity assay has been finally applied to

109 Conclusion MPO-Gd showed elevated MPO activity in NAFLD mouse models and human liver biops

110 stant to confounding effects from endogenous MPO inhibitors.

111 lted in neutrophil infiltration and enhanced MPO expression and activity in epididymal white adipose

112 dation or physiological levels of enzymatic (MPO) oxidation and incubated at 37 degrees C and pH 6.0

113 zyme-linked immunosorbent assays (ELISA) for MPO concentration are costly and time-intensive.

114 a useful selective and sensitive marker for MPO activity in addition to 3-Cl-Tyr.

115 Clinical evidence suggests a causal role for MPO in various autoimmune and inflammatory disorders inc

116 These results show a pathogenic role for MPO-specific CD8(+) T cells, provide evidence that CD8(+

117 era [PV], 94 ET, and 81 MF) was screened for MPO deficiency.

118 ow partition ratios and high selectivity for MPO over thyroid peroxidase and cytochrome P450 isoforms

119 ing chemotherapy treatment, elicited further MPO-dependent increase in TOP2A and especially TOP2B-DNA

120 vival rate and decreased the levels of H2O2, MPO, NO, TNFalpha, IL-6 and IL-10 in compressed muscle.

121 Histologically, MPO-AAV and PR3-AAV are similar but show qualitative dif

122 of SPIN bound to a recombinant form of human MPO at 2.4-A resolution.

123 strong homology between the pathogenic human MPO B cell epitope recognized by ANCA in patients with a

124 yeloid-derived suppressor cells (MDSC), (ii) MPO-regulated release, and (iii) blockade of MDSC immuno

125 vitro that in the absence of CALR, immature MPO protein precursors are degraded in the proteasome.

126 imaged with gadopentetate dimeglumine and in MPO knockout NASH mice with MPO-Gd, which proves specifi

127 enhance the regulatory role of mast cells in MPO-AAV.

128 nd IL-6 (P = .0001) that mirrored changes in MPO activity.

129 s supporting a posttranscriptional defect in MPO production.

130 The role of genetics in MPO-ANCA NCGN severity was investigated using 13 inbred

131 Although several steps in MPO biosynthesis and processing have been elucidated, ma

132 confirmed a critical role for apoA1 Trp72 in MPO-mediated inhibition of the ATP-binding cassette tran

133 ctants (MIP-2, KC), neutrophil infiltration (MPO activity), lipid peroxidation (4-HNE), and nitric ox

134 siniabactin and ferrichrome) fail to inhibit MPO activity.

135 ouble mutant (DeltaaroB/DeltafepA), inhibits MPO activity and exhibits enhanced survival in inflamed

136 vidence that levosimendan treatment inhibits MPO release by PMNs in decompensated heart failure patie

137 ctional findings provide novel insights into MPO biosynthesis and processing.

138 sm-based inhibitor and inhibits irreversibly MPO at nanomolar concentration.

139 MPO knockout (MPO(-/-)) mice were protected from HFD-enhanced body wei

140 nd cell-mediated autoimmunity to full-length MPO and the development of GN.

141 TSG-6-treated animals had significantly less MPO (P = 0.027) at 24 hours and IL-1beta (P = 0.027) at

142 ant, referred to as "MPO-E-selectin ligand" (MPO-EL), is expressed on circulating G-CSF-mobilized leu

143 aracterized by increased CD3(+) lymphocytes, MPO(+) cells and elevated TNF-alpha and IL-17 mRNA level

144 ECT/CT imaging of MPO activity showed marked MPO-sensor retention at 6 hours (P = .003) that continue

145 -hexosaminidase A and the azurophilic marker MPO in human neutrophils using immunocytochemistry.

146 vage to the heavy and light chains of mature MPO protomers, and (iii) three covalent bonds between he

147 y on a polymer surface (MAPS), for measuring MPO activity in human plasma samples using the biolumine

148 In patients with increased DNA methylation, MPO and PRTN3 expression correlated with DNA methylation

149 nce of ischemic lesions associated with mild MPO-mediated enhancement in the thoracolumbar spine at 2

150 way, passive transfer of antibodies to mouse MPO (anti-MPO) induces a mouse model of ANCA NCGN that c

151 PMN-MP/MPO-dependent inhibition of IEC wound healing was due to

152 ce markers (CD106, CD162 and myeloperoxidase MPO) was analyzed.

153 Myeloperoxidase (MPO) is a circulating cardiovascular disease (CVD) bioma

154 Myeloperoxidase (MPO) is a heme peroxidase that catalyzes the production

155 Myeloperoxidase (MPO) is a well defined autoantigen in ANCA-associated va

156 Myeloperoxidase (MPO) is released during polymorphonuclear neutrophil (PM

157 Myeloperoxidase (MPO) is synthesized by neutrophil and monocyte precursor

158 inhibitor of MMP (TIMP)-1, myeloperoxidase (MPO), and neutrophil elastase (NE) in patients with hype

159 rentiation factor (GDF)-15, myeloperoxidase (MPO), placental growth factor (PlGF), soluble fms-like t

160 metalloproteinase (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibit

161 he pathogenesis of acquired myeloperoxidase (MPO) deficiency, a rare phenomenon observed in patients

162 Proteinase 3 (PR3) and myeloperoxidase (MPO) are two major autoantigens in patients with vasculi

163 alloproteinases (MMPs), and myeloperoxidase (MPO) in tear washes of patients with ocular graft-vs-hos

164 s lactoperoxidase (LPO) and myeloperoxidase (MPO), nicotinamide adenine dinucleotide phosphate (NADPH

165 1beta, IL-6, TNF-alpha, and myeloperoxidase (MPO).

166 eutrophil elastase (NE) and myeloperoxidase (MPO).

167 active protein (hs-CRP) and myeloperoxidase (MPO).

168 vatives would abrogate anti-myeloperoxidase (MPO) antibody-induced NCGN in a mouse model.

169 on ANCA target antigens are myeloperoxidase (MPO) and proteinase 3.

170 other peroxidases, such as myeloperoxidase (MPO) and eosinophil peroxidase (EPO).

171 are extensively oxidized by myeloperoxidase (MPO).

172 primary granule components, myeloperoxidase (MPO) and human neutrophil elastase (HNE), are inflammato

173 d brain edema and decreased myeloperoxidase (MPO) levels at 24 hours, and improved neurological funct

174 ice has been used to detect myeloperoxidase (MPO), a cardiovascular biomarker.

175 ulmonary appearance, edema, myeloperoxidase (MPO) activity, and histopathology.

176 The heme enzyme myeloperoxidase (MPO) participates in innate immune defense mechanism thr

177 ain component of the enzyme myeloperoxidase (MPO), a well-known lysosomal peroxidase.

178 maging probe for the enzyme myeloperoxidase (MPO), might be a more sensitive contrast agent for the d

179 oxygen species, the enzymes myeloperoxidase (MPO) and neutrophil elastase.

180 imaging agent specific for myeloperoxidase (MPO) activity, could detect MPO activity in nonalcoholic

181 Oxidants derived from myeloperoxidase (MPO) contribute to inflammatory diseases.

182 on of the autoantigen genes myeloperoxidase (MPO) and proteinase 3 (PRTN3) in leukocytes of patients

183 creased the levels of H2O2, myeloperoxidase (MPO) and nitric oxide (NO) in serum and compressed muscl

184 ly binds and inhibits human myeloperoxidase (MPO), a major player in the oxidative defense of neutrop

185 s were immunised with human myeloperoxidase (MPO).

186 human neutrophils including myeloperoxidase (MPO), azurocidin, and neutrophil elastase.

187 Likely, myeloperoxidase (MPO) secreted by activated macrophages in atheroscleroti

188 in, the inflammatory marker myeloperoxidase (MPO), and the cytokine receptor for nuclear factor kappa

189 ions in experimental murine myeloperoxidase (MPO)-ANCA-associated vasculitis (AAV) show mast cells de

190 Neutrophil myeloperoxidase (MPO) catalyzes the H2O2-dependent oxidation of chloride

191 zing enzyme of neutrophils, myeloperoxidase (MPO), can effectively open the corked NCNCs through GNP

192 decreasing the activity of myeloperoxidase (MPO) and the expression of pro-inflammatory mediators.

193 munosensor for detection of myeloperoxidase (MPO) in human plasma is reported.

194 and also reduced levels of myeloperoxidase (MPO) in the gastric mucosa.

195 i, is a potent inhibitor of myeloperoxidase (MPO), a bactericidal enzyme of the host.

196 Activation of myeloperoxidase (MPO), a heme protein primarily expressed in granules of

197 kade or genetic deletion of myeloperoxidase (MPO), a key neutrophil enzyme, significantly increased m

198 nosorbent assay analysis of myeloperoxidase (MPO), tumor necrosis factor (TNF)-alpha, interleukin (IL

199 proteinase 3 (PR3)-ANCA or myeloperoxidase (MPO)-ANCA, were included in our study, followed at regul

200 ainst proteinase 3 (PR3) or myeloperoxidase (MPO).

201 (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal

202 Specifically, myeloperoxidase (MPO), which is abundantly expressed in PMN azurophilic g

203 ging technologies targeting myeloperoxidase (MPO) can reveal early inflammation associated with spina

204 ue was used to quantify the myeloperoxidase (MPO) activity and tumor necrosis factor (TNF)-alpha and

205 pensable constituent of the myeloperoxidase (MPO)-H2 O2 -halide system that produces the potent micro

206 ally, Scl-1 interferes with myeloperoxidase (MPO) release, a prerequisite for NET production, thereby

207 t options for patients with myeloperoxidase (MPO)-ANCA-associated GN are needed.

208 inding proteins (FABP) and myeloperoxidases (MPO) are associated with many chronic conditions in huma

209 Here we analyze the role of ROS, NE, MPO and PAD4 in the netosis stimulated by Leishmania ama

210 fflation of the immunodominant nephritogenic MPO peptide (MPO409-428) to attenuate this disease.

211 utations had reduced MPO protein, but normal MPO messenger RNA (mRNA) levels supporting a posttranscr

212 chronic cellular uptake and accumulation of MPO in lysosomes coincides with N-retinylidene-N-retinyl

213 osure results in progressive accumulation of MPO in lysosomes.

214 d well with the presence and accumulation of MPO-secreting inflammatory cells in the brain (r = 0.93)

215 We conclude that activation of MPO in adipose tissue contributes to the development of

216 n has potential for blocking the activity of MPO and limiting oxidative stress during inflammation.

217 ifferent magnitude for each concentration of MPO tested, two detection strategies have been compared,

218 cellular uptake and lysosomal degradation of MPO mediates elimination of this harmful enzyme, whereas

219 tor-mediated cellular uptake and delivery of MPO to lysosomes of retinal pigmented epithelial (RPE) c

220 eads (MBs) for the simultaneous detection of MPO endogenous peroxidase activity and quantification of

221 ent mice had no effect on the development of MPO autoimmunity or GN.

222 tive disease demonstrated hypomethylation of MPO and PRTN3 and increased expression of the autoantige

223 SPECT/CT imaging of MPO activity showed marked MPO-sensor retention at 6 hou

224 of BALP, leukocyte infiltration; increase of MPO, TNF-alpha, and IL-1beta; immunostaining increase fo

225 en administered before or after induction of MPO autoimmunity in these mice, disodium cromoglycate at

226 esions correlated with early infiltration of MPO-secreting monocytes and neutrophils into the brain (

227 lthiouracils also demonstrated inhibition of MPO activity in lipopolysaccharide-stimulated human whol

228 To gain insight into inhibition of MPO by SPIN, we solved the cocrystal structure of SPIN b

229 Inhibition of MPO may be a potential strategy for prevention and treat

230 racils as potent and selective inhibitors of MPO.

231 ere performed after intravenous injection of MPO sensors (bis-5-hydroxytryptamide-tetraazacyclododeca

232 Lack of MPO also attenuated HFD-induced macrophage infiltration

233 Identifying the mechanism of MPO and HNE release from neutrophils is of high clinical

234 The number of MPO-Gd-enhancing lesions correlated with early infiltrat

235 ammatory diseases leads to redistribution of MPO to the extracellular space, where it can mediate tis

236 tration to the lung tissues and reduction of MPO activity.

237 ice with MPO-Gd, which proves specificity of MPO-Gd.

238 These findings thus define a G-CSF effect on MPO chemical biology that endows unsuspected functional

239 induction of N-linked sialofucosylations on MPO, with concomitant cell surface display of the molecu

240 dependence of the chemiluminescent signal on MPO activity using MPO-deficient mice.

241 elected by this virtual method and tested on MPO in vitro.

242 ted the effects of levosimendan-treatment on MPO in patients with acute decompensation of chronic hea

243 damage, serum amylase levels, and pancreatic MPO concentrations (P<0.05-0.001).

244 GBI, PD, MPO, ABL, and histopathologic examinations demonstrated

245 ch were transgenic for a myeloid peroxidase (MPO)-specific TCR.

246 Plasma MPO levels were significantly decreased after levosimend

247 Robust inhibition of plasma MPO activity was demonstrated with the lead compound 2-(

248 biochemical studies show that G-CSF programs MPO-EL expression on human blood leukocytes and marrow m

249 at S. aureus secretes a unique proteinaceous MPO inhibitor to enhance survival by interfering with MP

250 s with homozygous CALR mutations had reduced MPO protein, but normal MPO messenger RNA (mRNA) levels

251 ATV decreased bone loss, reduced MPO, TNF-alpha, IL-1beta, IL-6, and IL-8, and increased

252 ophils from CD11b gene-deleted mice, reduced MPO transfer.

253 PO deficiency, carried 2 previously reported MPO mutations and showed normal EPX activity.

254 erophore-binding host protein, which rescues MPO from Ent-mediated inhibition.

255 arameters and serum MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio.

256 ytes and neutrophils, which actively secrete MPO.

257 We used sensitive MPO assays and flow cytometry to detect MPO in ECs and d

258 Significantly higher serum MPO levels were detected in patients with hypertension a

259 (P <0.05); however, the difference in serum MPO levels was not significant between the healthy contr

260 Confocal microscopy showed MPO internalization by ECs with cytoplasmic and nuclear

261 This specialized MPO glycovariant, referred to as "MPO-E-selectin ligand"

262 From a therapeutic standpoint, MPO catalyzes the in vitro degradation of N-retinylidene

263 Lysosomal-targeted MPO exerts both cell-protective and cytotoxic functions.

264 d tomography (CT) (n = 15) studies targeting MPO activity were performed after intravenous injection

265 However, evidence has emerged that MPO-derived oxidants contribute to propagation of inflam

266 1 ) provides good preclinical evidence that MPO-Gd, a gadolinium-based magnetic resonance (MR) imagi

267 ular and Parkinson's diseases, implying that MPO inhibitors may represent a therapeutic treatment opt

268 Here we show that MPO activity can be assessed using hydroethidine (HE), a

269 The MPO inhibitor 4-aminobenzoic acid hydrazide reduced pero

270 neutrophil chemoattractants, as well as the MPO activity in the lungs of septic mice.

271 apoA1 and HDL that have been modified by the MPO-H2O2-Cl(-) system.

272 observed when glycine was injected into the MPO and dorsal subparaventricular zone.

273 g that prevents H2O2 substrate access to the MPO active site.

274 suggest that a molecular hotspot within the MPO molecule contains important CD8(+), CD4(+), and B ce

275 tudy, 20 leptin receptor-deficient and three MPO knockout mice were injected with endotoxin (lipopoly

276 Thus, MPO-mediated oxidation may be implicated in the mechanis

277 l necrotizing GN mediated by autoimmunity to MPO (autoimmune anti-MPO GN), we assessed the capacity f

278 vivo studies showed that nasal tolerance to MPO is mediated by both conventional and induced T regul

279 oxidase activity and quantification of total MPO.

280 Mice underwent MPO-Gd- or DTPA-Gd-enhanced MR imaging on days 6, 8, and

281 Eleven human liver biopsy samples underwent MPO-Gd-enhanced MR imaging ex vivo and subsequent histol

282 versible mechanism, which was dependent upon MPO catalysis, consistent with mechanism-based inactivat

283 hemiluminescent signal on MPO activity using MPO-deficient mice.

284 In vivo MPO activity is commonly assessed by the accumulation of

285 CD4(+) cells mediated glomerular injury when MPO was planted in glomeruli.

286 eases inside the neutrophil phagosome, where MPO is located, compared with outside the neutrophil.

287 mmon in northern parts of the world, whereas MPO-AAV is more common in southern regions of Europe, As

288 However, whether MPO mediates high-fat diet (HFD)-induced obesity and obe

289 Purpose To test whether MPO-Gd, an activatable molecular magnetic resonance (MR)

290 nonrenal disease (36 with PR3-ANCA, 26 with MPO-ANCA).

291 renal involvement (72 with PR3-ANCA, 32 with MPO-ANCA) and 62 patients had nonrenal disease (36 with

292 ich relapse was induced by re-challenge with MPO.

293 -8 and MPO levels, and MMP-8 correlated with MPO, but it did not reach significance in SJS patients.

294 erimental NASH and underwent MR imaging with MPO-Gd.

295 itor to enhance survival by interfering with MPO-mediated killing.

296 induced anti-MPO GN by immunizing mice with MPO and a low dose of anti-glomerular basement membrane

297 meglumine and in MPO knockout NASH mice with MPO-Gd, which proves specificity of MPO-Gd.

298 Five out of 6 patients with MPO deficiency carried a homozygous CALR mutation and we

299 nts with PR3-AAV as opposed to patients with MPO-AAV and/or healthy controls.

300 asculitis occurs more often in patients with MPO-AAV.