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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.
39 a indicate that the pathways leading to lung neutrophil activation after hemorrhage are different fro
41 than or equal to 55[corrected]%, indicating neutrophil activation and a reduced phagocytic capacity
46 e maladaptive activation of genes that cause neutrophil activation and adhesion, and induction of NO
48 tate in SCD between painful crises involving neutrophil activation and an abnormality of cytokine-reg
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
53 ravascular and extravascular fibrinogenesis, neutrophil activation and clearance, and alveolar fluid
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
64 findings, inhibition of PGE2 led to enhanced neutrophil activation and host mortality after infection
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.
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
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
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
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
97 and lung microvascular thrombosis, decreased neutrophil activation, and averted histone-induced produ
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
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
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
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
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
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.
133 ely with rising concentrations of markers of neutrophil activation (elastase/alpha 1 antitrypsin) and
136 We discovered that erythrocytes suppressed neutrophil activation ex vivo and in vitro, including re
141 d calcium entry (SOCE) are known to regulate neutrophil activation; however, the precise mechanism of
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
150 shear stress exposure increased PAF-induced neutrophil activation in terms of L-selectin shedding, a
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
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
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
169 Taken together, these findings indicate that neutrophil activation is an important mechanism by which
171 ri factors previously suggested to stimulate neutrophil activation is the H. pylori neutrophil-activa
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
179 Understanding the mechanisms that underlie neutrophil activation, migration, survival and their var
181 fied a mechanistic link between ANCA-induced neutrophil activation, necroptosis, NETs, the AP, and en
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
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
198 n levels, which highlights the importance of neutrophil activation, rather than the presence of neutr
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
206 ) binding to anti-PF4 antibody can stimulate neutrophil activation, similar to previous reports with
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
216 rocesses and also can potentiate LPS-induced neutrophil activation through interactions with its krin
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
227 eaction was followed for 90 minutes, and the neutrophil activation was recorded as the total integrat
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
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
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