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1 utagenesis to identify LVS genes that affect neutrophil activation.
2 P2], a lipid second messenger generated upon neutrophil activation.
3 tinct from those that are involved in normal neutrophil activation.
4 rnea, including corneal fibroblasts, and for neutrophil activation.
5 ther inflammatory conditions associated with neutrophil activation.
6 ement activates tyrosine kinases, leading to neutrophil activation.
7  to examine the role of SHIP in TLR2-induced neutrophil activation.
8 yeloperoxidase from neutrophils, a marker of neutrophil activation.
9 ma-hemorrhagic shock-induced lung injury and neutrophil activation.
10 s the degree of T/HS-induced lung injury and neutrophil activation.
11  and Hsp27 dissociates from the complex upon neutrophil activation.
12 ilable, could prove an accurate biomarker of neutrophil activation.
13 etabolic enzyme trafficking affects maternal neutrophil activation.
14 ating endothelial barrier dysfunction during neutrophil activation.
15 ore IR prevented endothelial dysfunction and neutrophil activation.
16 stained endothelial dysfunction and systemic neutrophil activation.
17 es including receptor-mediated responses and neutrophil activation.
18 e interaction would be sufficient to trigger neutrophil activation.
19 or Stim2 to investigate the role of STIM2 in neutrophil activation.
20 on of capillary endothelium by prevention of neutrophil activation.
21 cts of cytokines such as TNF and by blocking neutrophil activation.
22  both be active participants in ANCA-induced neutrophil activation.
23 owth factor-beta (TGF-beta), which inhibited neutrophil activation.
24  in initiating and perpetuating ANCA-induced neutrophil activation.
25 ent; secretory component showed no effect on neutrophil activation.
26 little is known of their individual roles in neutrophil activation.
27 pears to function as a negative regulator of neutrophil activation.
28 matory actions of macrophages and subsequent neutrophil activation.
29 -CSF, at concentrations sufficient to affect neutrophil activation.
30 nal assays, including analysis of downstream neutrophil activation.
31 d as fluid shear stress sensors that control neutrophil activation.
32 ompetitively inhibits the FPR1-induced human neutrophil activation.
33 alize at the cell surface without triggering neutrophil activation.
34 ficiency was shown to contribute to impaired neutrophil activation.
35 hat, unlike M1 or fibrinogen alone, leads to neutrophil activation.
36 trophil binding to erythrocytes and restored neutrophil activation.
37 t kinase isoforms have distinct functions in neutrophil activation.
38  signaling activity can set the timescale of neutrophil activation, adhesion, and diapedesis.
39 a indicate that the pathways leading to lung neutrophil activation after hemorrhage are different fro
40                 Aldehyde generation required neutrophil activation and a free hydroxy-amino acid; it
41  than or equal to 55[corrected]%, indicating neutrophil activation and a reduced phagocytic capacity
42                In its early exudative phase, neutrophil activation and accumulation in the lung lead
43                                     However, neutrophil activation and accumulation into tissues trig
44                 This study suggests that the neutrophil activation and adhesion may vary, depending o
45                   We hypothesized that human neutrophil activation and adhesion vary, depending on th
46 e maladaptive activation of genes that cause neutrophil activation and adhesion, and induction of NO
47 demonstrated by the dose-related increase in neutrophil activation and adhesion.
48 tate in SCD between painful crises involving neutrophil activation and an abnormality of cytokine-reg
49           In this study, the relationship of neutrophil activation and apoptosis as related to releas
50 is work, we construct an integrated model of neutrophil activation and arrest that combines a biomech
51 2 has the ability to specifically potentiate neutrophil activation and chemotaxis in response to a ra
52                          IL-8 involvement in neutrophil activation and chemotaxis may be important in
53 ravascular and extravascular fibrinogenesis, neutrophil activation and clearance, and alveolar fluid
54  impact of streptococcus-secreted factors on neutrophil activation and degranulation.
55 or that, in the absence of SpeB, can trigger neutrophil activation and degranulation.
56 s associated with systemic polymorphonuclear neutrophil activation and degranulation.
57  TLR2 mediates O. volvulus/Wolbachia-induced neutrophil activation and development of corneal haze.
58 receptors may act synergistically to amplify neutrophil activation and emigration in the inflamed vas
59 ired fibrinogen function are associated with neutrophil activation and enhanced reactive oxygen speci
60 rolling to firm adhesion is a key element of neutrophil activation and essential to the inflammatory
61 uggest that TF/FVIIa/PAR2 signaling mediates neutrophil activation and fetal death in APS and that st
62        These data suggest possible roles for neutrophil activation and for fibronectin in mediating s
63 y state granulopoiesis, as well as in mature neutrophil activation and function.
64 findings, inhibition of PGE2 led to enhanced neutrophil activation and host mortality after infection
65        Given roles for FcRs in ANCA-mediated neutrophil activation and IgA antibodies in mucosal immu
66 s a negative regulatory role in TLR2-induced neutrophil activation and in the development of related
67 -supplemented CHAB was sufficient to prevent neutrophil activation and intramacrophage killing and su
68 ts Cl, Br, or I) are metabolites mediated by neutrophil activation and its accompanying respiratory b
69 te that a main role of exogenous hVPLA(2) in neutrophil activation and LTB(4) biosynthesis is to acti
70 onstrate that LTB(4) plays a central role in neutrophil activation and migration to formyl peptides.
71      We first describe the discrete steps of neutrophil activation and migration to the site of infec
72 ntial for vagus nerve-mediated regulation of neutrophil activation and migration.
73 ion of proinflammatory genes associated with neutrophil activation and molecular pathways important t
74 w PSDP structural mimetic that blocked human neutrophil activation and mouse lung PI3K activity and i
75                          Type I IFN-mediated neutrophil activation and NET formation may contribute t
76 2-/- mice treated with aPL exhibited reduced neutrophil activation and normal pregnancies, which indi
77 sed neutrophil recruitment, while increasing neutrophil activation and p38 activity at the site of in
78 r pathological venous thrombosis and present neutrophil activation and PAD4 as potential drug targets
79              One hallmark of inflammation is neutrophil activation and production of reactive oxygen
80    Analysis of signaling molecules mediating neutrophil activation and recruitment indicates reductio
81 he adhesion protein P-selectin would prevent neutrophil activation and reduce myocardial reperfusion
82 nks stress-induced inflammatory attacks with neutrophil activation and release of IL-1beta-bearing ne
83 estigate the relationships between H. pylori neutrophil activation and reported variations in HpNAP e
84    The effect was due to their regulation of neutrophil activation and sequestration.
85 n was inhibited by EDTA, which suggests that neutrophil activation and sheddase cleavage occurred.
86 trates that stimulation of FPRL-1 results in neutrophil activation and suggests that the receptor fun
87  evidence of platelet-neutrophil aggregates, neutrophil activation and surface MPO, and plasma MPO el
88 polymers act as a decoy mechanism to prevent neutrophil activation and that this represents an import
89   However, no relationship was found between neutrophil activation and the expression of HpNAP or dif
90 igens in FS implies a direct contribution of neutrophil activation and the production of NET-associat
91 e human-specific variant of resistin affects neutrophil activation and the severity of LPS-induced ac
92 epi LXA4), plays a critical role in limiting neutrophil activation and tissue inflammation, thus prom
93  The neutrophil uptake of NPs does not alter neutrophil activation and transmigration.
94       Here we analyzed how TF contributes to neutrophil activation and trophoblast injury in this mod
95                      The association between neutrophil activation and vacuolating cytotoxin activity
96                 Blocking FcalphaRI inhibited neutrophil activation and, as such, may represent an add
97 and lung microvascular thrombosis, decreased neutrophil activation, and averted histone-induced produ
98 es, production of proinflammatory mediators, neutrophil activation, and bacterial clearance.
99  increased neutrophil recruitment, decreased neutrophil activation, and decreased p38 activity at the
100 poor outcome are degree of oxidative stress, neutrophil activation, and infiltration of tissues, espe
101 hout affecting Mac-1 mobilization or general neutrophil activation, and inhibit cleavage of L-selecti
102 downregulation of PECAM-1 indicates an early neutrophil activation, and its inhibition may represent
103 risk factors, biomarkers of inflammation and neutrophil activation, and the presence of magnetic reso
104 f ADAM17 is highly inducible and occurs upon neutrophil activation as well as apoptosis.
105 roparticles/neutrophil count, a surrogate of neutrophil activation associated with septic shock-induc
106 supramolecular network that was required for neutrophil activation but was distinct from a fibrin clo
107 marrow chimeric mice and in vitro studies of neutrophil activation by anti-MPO IgG indicated that sev
108 pand on the possible roles of complement and neutrophil activation by dialysis membranes, which may p
109 ukocyte surface chondroitin sulfates promote neutrophil activation by enhancing immune-complex bindin
110                                              Neutrophil activation by FN, but not other extracellular
111                    These studies demonstrate neutrophil activation by influenza virus and highlight t
112  depending on other stimuli, HS can suppress neutrophil activation by intercepting multiple receptor
113 r integrity, enterohepatic recirculation and neutrophil activation by luminal contents including bact
114  integrity, enterohepatic recirculation, and neutrophil activation by luminal contents, including bac
115 I3K) and PI3K-associated signaling events in neutrophil activation by MBP.
116                                 We evaluated neutrophil activation by measuring degranulation marker
117 fects of LPS required the presence of serum, neutrophil activation by MTB 19-kDa lipoprotein occurred
118  analysis, alanine aminotransferase, hepatic neutrophil activation by myeloperoxidase activity, and c
119 e that fluid shear stress exposure increases neutrophil activation by PAF, and, taken together with p
120 examined the intracellular signals following neutrophil activation by soluble E-selectin.
121 ns that mediate these functions, we examined neutrophil activation by the basement membrane protein,
122 eutrophil attractant IL-8, while PEPI blocks neutrophil activation by tumor necrosis factor, preventi
123 hrombosis, and specifically examined whether neutrophil activation can affect fibrinogen modification
124                                    Excessive neutrophil activation causes posttraumatic complications
125                               In this study, neutrophil activation conditions generating high-affinit
126                                Inappropriate neutrophil activation contributes to the pathogenesis of
127 zonensis or its lipophosphoglycan can induce neutrophil activation, degranulation, and LTB4 productio
128 l tumor cells, there is growing evidence for neutrophil activation driving tumor progression and meta
129      Acute CO poisoning causes intravascular neutrophil activation due to interactions with platelets
130 gocytic activation, and provides a marker of neutrophil activation during infection and inflammation.
131 ajor protein targets of calcium signaling in neutrophil activation during inflammatory disease.
132                    An increase in markers of neutrophil activation (e.g., serum elastase) accompanies
133 ely with rising concentrations of markers of neutrophil activation (elastase/alpha 1 antitrypsin) and
134               Further supporting the role in neutrophil activation, EMR2 expression on circulating ne
135                                           On neutrophil activation, EMR2 is rapidly translocated to m
136   We discovered that erythrocytes suppressed neutrophil activation ex vivo and in vitro, including re
137 monocyte production of interleukins (IL) and neutrophil activation factors.
138                                              Neutrophil activation follows a 2-step process in which
139                                  Conversely, neutrophil activation for generation of Mac-1/CR3/uPAR c
140 f uPA to participate directly in LPS-induced neutrophil activation has not been examined.
141 d calcium entry (SOCE) are known to regulate neutrophil activation; however, the precise mechanism of
142  inflammatory monocytes can directly inhibit neutrophil activation in a PGE2-dependent manner.
143        Finally, LGALS3BP was able to inhibit neutrophil activation in a sialic acid- and Siglec-depen
144 ion between TF and PAR2, reduced aPL-induced neutrophil activation in aPL-treated mice.
145      We have previously reported a defect in neutrophil activation in children with polyarticular juv
146 ween acute respiratory distress syndrome and neutrophil activation in experimental pancreatitis in ra
147 ignaling through PAR2, inhibited aPL-induced neutrophil activation in mice that expressed human TF.
148 e than a decade ago it was demonstrated that neutrophil activation in plasma results in the time-depe
149                                Mechanisms of neutrophil activation in response to chemoattractants re
150  shear stress exposure increased PAF-induced neutrophil activation in terms of L-selectin shedding, a
151                Together, these events induce neutrophil activation in the lungs, causing endothelial
152 was shown to increase, rather than decrease, neutrophil activation in the presence of platelet activa
153  in the microvasculature was shown to reduce neutrophil activation in the presence of the chemoattrac
154 d myeloperoxidase activity (one indicator of neutrophil activation in the recruited cells).
155 ular signaling pathways that are involved in neutrophil activation in the setting of ALI.
156                  TAFIa abrogated C5a-induced neutrophil activation in vitro.
157 itiated phenotypic changes characteristic of neutrophil activation, including down-regulation of CD62
158  found that a variety of stimuli involved in neutrophil activation, including fMet-Leu-Phe (fMLP), pl
159 ral position in regulating endotoxin-induced neutrophil activation, including that involved in ALI.
160 rrelate with fluid shear stress exposure, as neutrophil activation increased in a shear stress magnit
161  OspA induce surface markers associated with neutrophil activation: increased CD10 and CD11b expressi
162   Recently, spinorphin was reported to block neutrophil activation induced by the chemotactic N-formy
163  inhibited the recruitment of T lymphocytes, neutrophil activation/infiltration, and repressed the ex
164 -induced matrix degradation, originated from neutrophil activation, initiated the formation of an amp
165                                              Neutrophil activation (intracellular oxidative burst act
166 tis (SAH) patients and their contribution to neutrophil activation, intracellular stress, and alterat
167      Limitation of unnecessary intravascular neutrophil activation is also important to prevent serio
168                                     However, neutrophil activation is also linked to autoimmune disea
169 Taken together, these findings indicate that neutrophil activation is an important mechanism by which
170                The appropriate regulation of neutrophil activation is critical for maintaining host d
171 ri factors previously suggested to stimulate neutrophil activation is the H. pylori neutrophil-activa
172                   Thus, mechanically induced neutrophil activation is understood as the competition b
173                                         Upon neutrophil activation, L-selectin is rapidly and efficie
174 ecidual neutrophils expressed high levels of neutrophil activation markers and the angiogenesis-relat
175  included altered B-cell pathways, increased neutrophil activation markers, and increased reactive ox
176 n impaired host defenses, while simultaneous neutrophil activation may aggravate inflammation.
177                                     Although neutrophil activation may be beneficial at early stages
178                                              Neutrophil activation may play an important role in the
179   Understanding the mechanisms that underlie neutrophil activation, migration, survival and their var
180                                       During neutrophil activation, NE translocates to the nucleus to
181 fied a mechanistic link between ANCA-induced neutrophil activation, necroptosis, NETs, the AP, and en
182                                         Upon neutrophil activation, NSP4 was released into the supern
183                  These data indicate that in neutrophils activation of MEKK in addition to Raf may un
184 epletion of DCs did not require infiltrating neutrophils, activation of nuclear factor-kappaB, or sig
185 In this study, we investigated the effect of neutrophil activation on endothelial monolayer integrity
186 ferences between the 2 major Akt isoforms in neutrophil activation on the basis of studies in which w
187 gen species production, suggesting decreased neutrophil activation or increased neutrophil exhaustion
188 ed cytokine and chemokine genes required for neutrophil activation or recruitment, growth factor rece
189 ate TREM-1 signaling to evaluate its role in neutrophil activation, pathogen clearance, proinflammato
190                     This identifies a second neutrophil-activation pathway that is as important as ac
191 gnificantly correlated with peripheral blood neutrophil activation patterns (r = 0.75, p = 0.001 for
192 se results suggest that early alterations in neutrophil activation patterns, particularly involving t
193 ammatory diseases characterized by excessive neutrophil activation, PIPPs can serve as structural tem
194 ring episodes of vascular occlusion in which neutrophil activation plays a major role.
195                                              Neutrophil activation plays an important role in the inf
196                                           On neutrophil activation, polyisoprenyl diphosphate phospha
197 e investigated the role of B. cepacia LPS in neutrophil activation processes.
198 n levels, which highlights the importance of neutrophil activation, rather than the presence of neutr
199                                              Neutrophil activation releases granule proteins together
200            However, significant reduction in neutrophil activation remained compared to that of PBS a
201  presence of surface bound factor H enhanced neutrophil activation resulting in a two- to fivefold in
202  the vinyl ether bond of plasmalogens during neutrophil activation resulting in the production of alp
203  is secreted from mononuclear cells, causing neutrophil activation, resulting in the secretion of bac
204 ts (P < 0.01) which strongly correlated with neutrophil activation, rolling ligand P-selectin glycopr
205                        Genes associated with neutrophil activation, ROS production, intracellular ant
206 ) binding to anti-PF4 antibody can stimulate neutrophil activation, similar to previous reports with
207                                              Neutrophil activation studies suggest that Pactolus does
208 lar diseases, this can result in exacerbated neutrophil activation, subsequent vascular injury and ob
209 ole of shear forces on earlier indicators of neutrophil activation, such as L-selectin shedding and a
210 degranulation, and Alternaria did not induce neutrophil activation, suggesting specificity for fungal
211 tor usage, and differential peripheral blood neutrophil activation that could contribute to HCMV diss
212 otential for rapid release of IFN-gamma upon neutrophil activation, the first step during responses t
213 e repairing the vascular damage inflicted by neutrophil activation, thereby maintaining vascular inte
214 atients, vary in level over time, and induce neutrophil activation through engagement with Fc recepto
215 olipids (lyso-PLs) may also signal for human neutrophil activation through G2A.
216 rocesses and also can potentiate LPS-induced neutrophil activation through interactions with its krin
217                                  Conversely, neutrophil activation through TLR4, as well as through a
218                                              Neutrophil activation to release granules containing pro
219 R2), and stimulation of this receptor led to neutrophil activation, trophoblast injury, and fetal dea
220 ce posttraumatic complications by preventing neutrophil activation via chemotactic factors released d
221 uggest that physiological shear forces alter neutrophil activation via FPR by reducing L-selectin she
222                                              Neutrophil activation via PAF was found to correlate wit
223                                              Neutrophil activation was assessed by measurement of sec
224                                              Neutrophil activation was assessed by measuring down-reg
225 egulation of inflammatory mediators of human neutrophil activation was investigated.
226                                              Neutrophil activation was observed at 30 min after reper
227 eaction was followed for 90 minutes, and the neutrophil activation was recorded as the total integrat
228  IgA and IgG ANCA together, IgG ANCA induced neutrophil activation was reduced (P = 0.0001).
229                                              Neutrophil activation was reduced by curcumin treatment
230   In this study, the effects of CD50 mAbs on neutrophil activation were examined.
231           Genes associated with platelet and neutrophil activation were expressed at higher levels in
232 LPS has been shown to be a major mediator of neutrophil activation which is accompanied by an early d
233 us, the secreted glycoprotein inhibits early neutrophil activation, which likely affects the host res
234          We also present a state diagram for neutrophil activation, which relates beta(2)-integrin de
235 different from ADAM17 stimulation upon overt neutrophil activation, which requires MAPK p38 or ERK, b
236 nate substances in blood products, result in neutrophil activation, which, in a susceptible patient,
237  to our knowledge, fully stochastic model of neutrophil activation, which, though simplified, can rec
238 ne the microvascular endothelial response to neutrophil activation with a focus on myosin light chain
239 -stage and midstage disease, and evidence of neutrophil activation with advanced disease.
240 n of both IL-12 and CCL2 was increased after neutrophil activation with IFN-gamma.

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