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1 uced NETosis (citrullinated histone H3, DNA, myeloperoxidase).
2 serum bound dose-dependently to solid-phase myeloperoxidase.
3 cies that are generated by their heme enzyme myeloperoxidase.
4 illations, pancreatic amylase, and pulmonary myeloperoxidase.
5 oxygen metabolites by the NADPH oxidase and myeloperoxidase.
6 panel resulted in various levels of urinary myeloperoxidase.
7 is a selective and irreversible inhibitor of myeloperoxidase.
8 onships of the mammalian peroxidases LPO and myeloperoxidase.
9 and the previously undescribed cancer target myeloperoxidase.
10 cells with endogenous expression of CD20 or myeloperoxidase.
11 was the predominant protein associated with myeloperoxidase.
12 cked lactoferrin but showed normal levels of myeloperoxidase.
13 antitation of the pro-inflammatory biomarker myeloperoxidase.
14 significant for AAT (28.71; P < 0.0001) and myeloperoxidase (62.79; P < 0.0001) over a 3-mo lag and
17 in the initiation of leukocyte trafficking, myeloperoxidase accumulation, and acute reduction in adi
20 n also significantly decreased the increased myeloperoxidase activities and osteoclast and neutrophil
21 ion, neutrophil and osteoclast densities and myeloperoxidase activities were determined in gingival t
24 litic mice significantly reduced the colonic myeloperoxidase activity and alleviated proinflammatory
27 onylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhibited by butylated
28 ity by scoring, joint function by grid test, myeloperoxidase activity by luminescence, vascular leaka
29 roscopic damage scores, bowel thickness, and myeloperoxidase activity compared with untreated animals
30 il numbers, neutrophil CD11b expression, and myeloperoxidase activity compared with wild-type litterm
31 sis factor-alpha and interleukin-1beta), and myeloperoxidase activity followed by Ly6-G positive cell
32 and higher levels of neutrophil elastase and myeloperoxidase activity in apical surface media than in
33 indicate that the ability of EGCG to inhibit myeloperoxidase activity is one of the mechanisms by whi
35 Trypsin activity, cathepsin B activity and myeloperoxidase activity on the first postoperative day
36 Together these results support targeting myeloperoxidase activity to reduce genetic damage leadin
38 production in the tibiotarsal joint, but not myeloperoxidase activity was significantly reduced by Sz
39 ocyte chemokines (KC, MCP-1, and RANTES) and myeloperoxidase activity were also significantly elevate
42 , neutrophils, lung neutrophil accumulation (myeloperoxidase activity), and proinflammatory cytokines
43 related with reduced neutrophil recruitment, myeloperoxidase activity, and air space cytokine concent
44 ransferase, hepatic neutrophil activation by myeloperoxidase activity, and cytokine secretion at spec
45 of colonic inflammation (e.g., weight loss, myeloperoxidase activity, and Ikappabalpha accumulation)
46 Tissue inflammation, evident as increased myeloperoxidase activity, and IL-1alpha, IL-1beta, and I
47 ytic capacity, high peroxide production, low myeloperoxidase activity, and low cytoplasmic granule co
48 serum amylase activity, pathological scores, myeloperoxidase activity, and the expression of inflamma
49 ry hypertension and attenuated the pulmonary myeloperoxidase activity, as well as tissue injury and s
50 ed in aggravated airway neutrophilia, tissue myeloperoxidase activity, cytokine contents, and decreas
51 ng injuries were assessed by bacterial load, myeloperoxidase activity, endothelial permeability (pulm
53 with controls (based on loss of body weight, myeloperoxidase activity, inflammatory cytokine producti
54 inistration significantly inhibited gingival myeloperoxidase activity, interleukin (IL)-1beta, tumor
55 nflammatory cytokine concentrations in lung, myeloperoxidase activity, Ly6G immunohistochemistry, and
56 lence of S. pneumoniae, as well as host cell myeloperoxidase activity, proinflammatory cytokine secre
62 n Willebrand factor (VWF), thrombospondin-1, myeloperoxidase, ADAMTS-13, and active VWF (aVWF) were s
63 of environmental enteropathy (calprotectin, myeloperoxidase, alpha1-antitrypsin) and the prevalence
64 ly produced, among various possibilities, by myeloperoxidase, an enzyme implicated in inflammation pr
66 of neutrophil secretory proteins, including myeloperoxidase and elastase, are associated with tissue
68 lts suggest that peroxidase enzymes, such as myeloperoxidase and eosinophil peroxidase, may play a fu
70 tly greater cellular expression of CD11b and myeloperoxidase and higher levels of neutrophil elastase
71 rbonaceous nature of NCS broke down by human myeloperoxidase and horseradish peroxidase enzymes, reve
72 ced neutrophil degranulation with release of myeloperoxidase and hydrogen peroxide (H(2)O(2)) and inc
74 feature of mammalian peroxidases, including myeloperoxidase and lactoperoxidase (LPO) is the existen
75 ents with various forms of crescentic GN for myeloperoxidase and neutrophils, measured serum myeloper
78 IL-6 concentrations as well as cathepsin B, myeloperoxidase and trypsin activities were determined t
79 inflammatory biomarkers C-reactive protein, myeloperoxidase, and adiponectin reduction; EAT attenuat
81 NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these s
84 Neutrophil gelatinase-associated lipocalin, myeloperoxidase, and intracellular ROS levels were highe
86 s, double-stranded DNA, neutrophil elastase, myeloperoxidase, and myeloid-related protein 8/14 were i
87 ereas other NET assays (e.g., cell-free DNA, myeloperoxidase, and myeloperoxidase-DNA complexes) coul
89 e surface mobilization of azurophilic (CD63, myeloperoxidase, and neutrophil elastase) and specific (
90 ents intrinsic neutrophil proteins (eg, MPO [myeloperoxidase] and various proteinases) but can gather
92 ve decreased intracellular and surface-bound myeloperoxidase, are less capable of killing phagocytose
93 throcytes identified increased expression of myeloperoxidase as the likely mechanism accounting for t
96 for 4 weeks lead to significant increases in myeloperoxidase, asymmetrical dimethylarginine, and card
97 results indicate that ceruloplasmin inhibits myeloperoxidase by reducing Compound I and then trapping
98 loperoxidase and neutrophils, measured serum myeloperoxidase concentration in patients with ANCA-asso
99 permeability, increased colonic IL-1beta and myeloperoxidase concentrations, and increased CD11b-posi
100 peroxides within tumor cells by transferring myeloperoxidase-containing granules into tumor cells.
101 asma amylase activity, pancreatic edema, and myeloperoxidase content in pancreas and lungs were quant
103 to quantification of migrated neutrophils by myeloperoxidase correlation, a destructive assay that pr
104 here were significant differences in cardiac myeloperoxidase, cytokines, neutrophil, and macrophage i
106 ferent murine models of myocardial ischemia, myeloperoxidase deficiency profoundly decreased vulnerab
109 vivo investigations linked Cx43 breakdown to myeloperoxidase-dependent activation of matrix metallopr
111 gh-density lipoprotein (HDL) and a target of myeloperoxidase-dependent oxidation in the artery wall.
112 h crescentic GN had extracellular glomerular myeloperoxidase deposition that correlated significantly
115 munofluorescence microscopy, immunoblotting, myeloperoxidase-DNA complex ELISA, and flow cytometry.
123 ent of animals with APC abrogated release of myeloperoxidase from neutrophils, a marker of neutrophil
127 3 to hypochlorous acid (HOCl), produced by a myeloperoxidase-H2O2-Cl(-) system, and determined its re
131 utrophils strongly correlated with BAL fluid myeloperoxidase, IL-8, IL-1alpha, IL-6, granulocyte colo
132 of the mouse ileum after allo-HCT by in vivo myeloperoxidase imaging and found that infiltration leve
134 ory biomarkers matrix metallopeptidase-9 and myeloperoxidase in plasma and sputum; ANC lower than 1.5
136 e recipient was connected to lower levels of myeloperoxidase in the intestinal tract of mice developi
137 for a causal rather than bystander role for myeloperoxidase in the progression of cerebrovascular di
139 potently inhibit the proinflammatory enzyme myeloperoxidase in vitro in a dose-dependent manner over
140 n analysis of ischaemic stroke subtypes, the myeloperoxidase increasing genetic risk score was strong
142 -deficient (CD11b(-/-)) mice and intravenous myeloperoxidase infusion revealed that neutrophil infilt
143 loplasmin was a potent inhibitor of purified myeloperoxidase, inhibiting production of hypochlorous a
144 hese factors have led to the hypothesis that myeloperoxidase inhibition could protect hematopoietic c
149 his response was blocked by the irreversible myeloperoxidase inhibitor 4-amino-benzoic acid hydrazide
150 ect of myeloperoxidase inhibition, using the myeloperoxidase inhibitor AZM198, to understand its pote
151 by the recent development of novel specific myeloperoxidase inhibitors for use in inflammatory disea
155 uded complement component 3; angiopoietin 2; myeloperoxidase; lactoperoxidase; major histocompatibili
157 of neutrophil elastase activity, as well as myeloperoxidase levels compared to children without bact
159 und that RvD5 did not reduce lung neutrophil myeloperoxidase levels in PLD2(-/-) mice compared to WT
160 (3) elevated interleukin-6 (IL-6), IL-8, and myeloperoxidase levels in the airway are indicative of s
161 g that common genetic variants that increase myeloperoxidase levels increase risk of primary intracer
162 We hypothesized that genetic determinants of myeloperoxidase levels influence the development of vasc
163 A genetic risk score reflecting elevated myeloperoxidase levels was constructed from 15 common si
164 Genetic determinants of elevated circulating myeloperoxidase levels were associated with both primary
166 tion, histopathology, malondialdehyde (MDA), myeloperoxidase levels, and antioxidant enzyme expressio
167 alveolar space, decreased total protein and myeloperoxidase levels, and lower cytokine levels in the
171 isocyanate derived from urea dissociation or myeloperoxidase-mediated catabolism of thiocyanate to fr
172 im was to determine the relationship between myeloperoxidase-mediated oxidative damage to apolipoprot
175 The gingival tissue was used to quantify the myeloperoxidase (MPO) activity and tumor necrosis factor
176 al bleeding index (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL)
177 examining their pulmonary appearance, edema, myeloperoxidase (MPO) activity, and histopathology.
178 ic resonance (MR) imaging agent specific for myeloperoxidase (MPO) activity, could detect MPO activit
179 ally mediating inflammatory response through myeloperoxidase (MPO) and biologically promoting metasta
180 peroxidasin from other peroxidases, such as myeloperoxidase (MPO) and eosinophil peroxidase (EPO).
184 , advanced protein oxidation product (APOP), myeloperoxidase (MPO) and nitric oxide (NO), while deple
185 fic DNA methylation of the autoantigen genes myeloperoxidase (MPO) and proteinase 3 (PRTN3) in leukoc
187 olitis in mice by decreasing the activity of myeloperoxidase (MPO) and the expression of pro-inflamma
188 es and their derivatives would abrogate anti-myeloperoxidase (MPO) antibody-induced NCGN in a mouse m
192 ive molecular imaging technologies targeting myeloperoxidase (MPO) can reveal early inflammation asso
198 ion of hydrogen peroxide and the presence of myeloperoxidase (MPO) derived from inflammatory cells, w
202 (NE), matrix metalloproteinases (MMPs), and myeloperoxidase (MPO) in tear washes of patients with oc
210 ls and Methods Female wild-type (n = 23) and myeloperoxidase (MPO) knock-out (n = 5) mice were infect
211 knockdown reduced brain edema and decreased myeloperoxidase (MPO) levels at 24 hours, and improved n
212 ngi, including the action of enzymes such as myeloperoxidase (MPO) or NADPH oxidase, and the release
214 oxidants including hypochlorous acid, human myeloperoxidase (MPO) plays a critical role in innate im
218 eleased by E. coli, is a potent inhibitor of myeloperoxidase (MPO), a bactericidal enzyme of the host
221 ponse to cytarabine (AraC) and overexpressed myeloperoxidase (MPO), a heme protein that converts hydr
224 n that specifically binds and inhibits human myeloperoxidase (MPO), a major player in the oxidative d
225 m of the heavy chain component of the enzyme myeloperoxidase (MPO), a well-known lysosomal peroxidase
226 ivation of neutrophil markers, Calprotectin, Myeloperoxidase (MPO), and IL-8 are significantly increa
227 -8, MMP-9, tissue inhibitor of MMP (TIMP)-1, myeloperoxidase (MPO), and neutrophil elastase (NE) in p
228 leptin and resistin, the inflammatory marker myeloperoxidase (MPO), and the cytokine receptor for nuc
229 ilic granules of human neutrophils including myeloperoxidase (MPO), azurocidin, and neutrophil elasta
230 A potent oxidizing enzyme of neutrophils, myeloperoxidase (MPO), can effectively open the corked N
231 resonance (MR) imaging probe for the enzyme myeloperoxidase (MPO), might be a more sensitive contras
232 terized gut inflammation and permeability by myeloperoxidase (MPO), neopterin (NEO), and alpha-1-anti
233 and serum matrix metalloproteinase (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP
234 peroxidase enzymes lactoperoxidase (LPO) and myeloperoxidase (MPO), nicotinamide adenine dinucleotide
235 NP), growth differentiation factor (GDF)-15, myeloperoxidase (MPO), placental growth factor (PlGF), s
236 nzyme-linked immunosorbent assay analysis of myeloperoxidase (MPO), tumor necrosis factor (TNF)-alpha
238 sitive for either proteinase 3 (PR3)-ANCA or myeloperoxidase (MPO)-ANCA, were included in our study,
239 ss toxic treatment options for patients with myeloperoxidase (MPO)-ANCA-associated GN are needed.
243 body, is an indispensable constituent of the myeloperoxidase (MPO)-H2 O2 -halide system that produces
255 s were observed between groups of EC and NS (myeloperoxidase [MPO], matrix metalloproteinase-9) as we
256 we measured biomarkers of gut inflammation (myeloperoxidase, neopterin), permeability (alpha-1-antit
257 The release of granule proteases, such as myeloperoxidase, neutrophil elastase, and matrix metallo
258 en the 5th and 95th percentile (0.25) was by myeloperoxidase over a 2-mo lag.Of the 3 fecal biomarker
260 e and lacunar stroke, directly implicate the myeloperoxidase pathway in the pathogenesis of cerebral
261 pport of our experimental findings, baseline myeloperoxidase plasma levels were independently associa
266 by the observation of a decreased number of myeloperoxidase positive neutrophils, and concomitantly
268 ge range, 4-76 years) was mainly composed of myeloperoxidase-positive immature myelomonocytic cells w
269 del of ischemia, the post-ischemic influx of myeloperoxidase-positive neutrophils and CD14(+) monocyt
272 species (IC50 in the range 22.4-40.6muM) and myeloperoxidase release (IC50 in the range 22.2-32.2muM)
275 lecule) were associated with PLT, while MPO (myeloperoxidase) showed significant association with MPV
277 ciated with high plasma levels of sTIM-3 and myeloperoxidase, suggesting activated and potentially ex
279 against RNA, neutrophil cytoplasmic Ags, and myeloperoxidase than do TMPD-injected wild-type BALB/c m
280 tates to hydrogen peroxide, which is used by myeloperoxidase to generate other oxidants, including th
281 ed back the dramatic reduction in neutrophil myeloperoxidase to the myeloid progenitors showing down-
282 Compound I, the Fe(V) redox intermediate of myeloperoxidase, to Compound II, which has Fe(IV) in its
283 e inflammatory biomarkers (interferon-gamma, myeloperoxidase, tumor necrosis factor, interleukin 6, s
284 it induced significantly elevated levels of myeloperoxidase, tumor necrosis factor, monocyte chemoat
289 mic inflammation during atherogenesis, human myeloperoxidase was incubated with glycine, H2O2, malond
292 Here, by quantifying extracellular DNA or myeloperoxidase, we demonstrate that APC binds human leu
293 hods: Colonic concentrations of IL-1beta and myeloperoxidase were determined by ELISA, and colonic in
294 atment; and (3) levels of sCD25, sTIM-3, and myeloperoxidase were inversely correlated with degree of
295 (zonula occludens 1), and neutrophil influx (myeloperoxidase) were assessed using immunohistochemistr
296 Gly domain-containing linker protein 2, and myeloperoxidase) were differentially regulated in monocy
297 that related to intestinal function-AAT and myeloperoxidase-were associated with small but highly st
298 active protein, interleukin-receptor 1A, and myeloperoxidase, whereas MR-pro-ADM levels correlated wi
299 thione peroxidase, serum catalase, and colon myeloperoxidase while decreasing total fecal short-chain
300 ular inflammation, but prior studies linking myeloperoxidase with stroke risk have been inconclusive.