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1 rough microbubble potentiated enhancement of microvascular permeability.
2 , showing the impact of CXCR7 on stabilizing microvascular permeability.
3  lung myeloperoxidase activity and pulmonary microvascular permeability.
4 han those stored in EC, indicating decreased microvascular permeability.
5 s is preceded and/or accompanied by enhanced microvascular permeability.
6  did not alter pancreatic edema or pulmonary microvascular permeability.
7  more potent than histamine as an inducer of microvascular permeability.
8 for intrinsic Cat-S/PAR2 in ischemia-induced microvascular permeability.
9 ated arachidonic acid metabolism and altered microvascular permeability.
10  atherosclerotic endothelium is dependent on microvascular permeability.
11 OS)-derived NO is a key factor in regulating microvascular permeability.
12  vessels was associated with increased tumor microvascular permeability.
13 pression of proinflammatory transcripts, and microvascular permeability.
14 rated optical intensity (IOI) as an index of microvascular permeability.
15 adhesions in the physiological regulation of microvascular permeability.
16 ance of endothelial junctional integrity and microvascular permeability.
17 paracellular pathway, resulting in increased microvascular permeability.
18 mouse LECs is a key determinant of increased microvascular permeability.
19 efemoral lymph fistulas in order to estimate microvascular permeability.
20 endothelial cell proliferation and increased microvascular permeability.
21 teraction in the physiological regulation of microvascular permeability.
22 ularity, cutaneous vascular architecture, or microvascular permeability.
23 confirmed small increases in muscle and skin microvascular permeability after ANP.
24 rowth factor (VEGF), is a potent enhancer of microvascular permeability and a selective endothelial c
25 to high tidal volume VILI, with increases in microvascular permeability and bronchoalveolar lavage le
26 AM-1 blockade prevented the increase in lung microvascular permeability and edema formation at all ti
27 tion and prevented the increase in pulmonary microvascular permeability and edema formation in mice a
28 uli, and has profound influences on systemic microvascular permeability and haemodynamics.
29  enhanced inflammation, along with increased microvascular permeability and hemorrhage.
30 t assessed in a murine model of LPS-mediated microvascular permeability and inflammation with marked
31 oefficient (Kf,c), a sensitive index of lung microvascular permeability and injury, was made at basel
32 c endothelial cells is pivotal in regulating microvascular permeability and leukocyte recruitment.
33  modulating inflammatory signals, regulating microvascular permeability and neutrophil recruitment, a
34 tion of the IgE/antigen-mediated increase in microvascular permeability and of bleomycin-induced pulm
35 emission tomography and K(trans) (reflecting microvascular permeability and perfusion) by magnetic re
36 gy can become severe, resulting in extensive microvascular permeability and plasma leakage into tissu
37 orous inflammatory response characterized by microvascular permeability and polymorphonuclear neutrop
38 result of marked increases in both pulmonary microvascular permeability and pressure.
39 saccharide and thrombin increased mouse lung microvascular permeability and resulted in a delayed act
40                            BD also increased microvascular permeability and the expression and activi
41 with reduced parenchymal myeloperoxidase and microvascular permeability, and altered airspace and ser
42 siological processes including inflammation, microvascular permeability, and endothelial mechanotrans
43 increased angiogenesis, microvessel density, microvascular permeability, and growth of malignant tumo
44 tly determined also to promote inflammation, microvascular permeability, and mucus secretion.
45  Data showed that lung edema formation, lung microvascular permeability, and neutrophil infiltration
46 Subsequently, pulmonary vascular resistance, microvascular permeability, and thromboxane were measure
47                    Angiogenesis and enhanced microvascular permeability are hallmarks of a large numb
48  we also examined whether these increases in microvascular permeability are NO-dependent.
49 phonuclear leukocyte; PMN) sequestration and microvascular permeability are not well understood.
50                    Thus, our study points to microvascular permeability as an important driver of inj
51             The LPS-induced increase in lung microvascular permeability as measured by Evans blue ext
52                                              Microvascular permeability, as estimated with the endoth
53   The hallmark of severe dengue is increased microvascular permeability, but alterations in the micro
54  NEP has important roles in regulating basal microvascular permeability by degrading SP and BK, and m
55 ulates endothelial cell growth and increases microvascular permeability by interacting with two endot
56 essed histologically and by determining lung microvascular permeability by measuring accumulated 125I
57 nd neutrophil sequestration, and a decreased microvascular permeability by more than twofold.
58 ly visualize tissue oxygen concentration and microvascular permeability by using a hyperpolarized (1)
59 mice showed reduced neutrophil migration and microvascular permeability changes.
60                                 Quantitative microvascular permeability characteristics estimated fro
61 used canine lung, we identified increases in microvascular permeability coefficients in response to t
62 05) lower respiratory compliance and greater microvascular permeability compared with sham animals.
63 flammatory cytokine concentrations, and lung microvascular permeability compared with transfusion of
64 C) concentrations in the airspaces, and lung microvascular permeability compared with transfusion of
65 l growth factor (VEGF) chronically increases microvascular permeability, compliance and vessel diamet
66 /0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preloa
67           We further show that the increased microvascular permeability depends on neuronal activity
68  mural cells of microvessels, which regulate microvascular permeability, development, and maturation
69 (VEGF) is the principal agent that increases microvascular permeability during physiological and path
70 nd apparently also by declining the enhanced microvascular permeability during the late phase of endo
71 Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) sh
72 helial growth factor (VEGF) greatly enhances microvascular permeability; however, the molecular mecha
73  plays a dual regulatory role in controlling microvascular permeability: (i) as a structural protein
74 ecular mechanisms leading to increased brain microvascular permeability in AD are not fully understoo
75 ole in the changes in systemic and pulmonary microvascular permeability in combined smoke inhalation/
76  establish eNOS as an important regulator of microvascular permeability in inflammation.
77  not pancreatic edema or increased pulmonary microvascular permeability in mild, secretagogue-induced
78 bserved that E. coli failed to increase lung microvascular permeability in p47(phox-/-) and gp91(phox
79 ovascular reserve, and for the assessment of microvascular permeability in patients with intracranial
80 that neuronal activity induces modulation of microvascular permeability in the healthy brain and that
81  leads to a major increase in epithelial and microvascular permeability in the lungs.
82 l retention) and the LPS-induced increase in microvascular permeability in these organs.
83 r endothelial growth factor (VEGF) increases microvascular permeability in vivo and has been hypothes
84 ese data suggest that VEGF acutely increases microvascular permeability in vivo through a mechanism t
85 d (4) caveolin-1 inhibits eNOS regulation of microvascular permeability in vivo.
86 le of deltaPKC, which is thought to regulate microvascular permeability, in the development of hypert
87 pendent endothelial cell death and increased microvascular permeability, in turn facilitating extrava
88  of Cx43 completely blocked thrombin-induced microvascular permeability increases.
89 in on myocardial perfusion (MP) and coronary microvascular permeability index (PI) at baseline and du
90                      The increased pulmonary microvascular permeability induced by E. coli is solely
91  lungs, heart, and liver; and c) increase in microvascular permeability induced by LPS in these organ
92 itment of PMNs in lungs and increase in lung microvascular permeability induced by TNF-alpha.
93                                 It increases microvascular permeability, induces endothelial cell mig
94 ions drawn from such studies in the areas of microvascular permeability, inflammation, mechanotransdu
95  molecular basis of focal adhesion-dependent microvascular permeability is currently under investigat
96              Understanding the regulation of microvascular permeability is essential for the identifi
97                                              Microvascular permeability is mediated by (i) the caveol
98 etic macular edema, resulting from increased microvascular permeability, is the most prevalent cause
99  sequestration (approximately 16-fold), lung microvascular permeability K(f,c) (approximately 5.7-fol
100 tional model yielded MR imaging estimates of microvascular permeability (K(PS)) and fractional plasma
101 del was used to quantify the sciatic nerve's microvascular permeability (Ktrans), volume fraction of
102 ies, and because VPF/VEGF promotes increased microvascular permeability leading to activation of the
103 d VPF/VEGF(164) induced an early increase in microvascular permeability, leading within 24 hours to e
104 posure to parasite egress products increases microvascular permeability, likely due to transcriptiona
105 fference between the two study groups in the microvascular permeability of burned tissue.
106 est this hypothesis directly, we studied the microvascular permeability of Cav-1 null mice using a va
107 ation levels, local oxygen concentration and microvascular permeability of OX63 can be simultaneously
108                         An effect on albumin microvascular permeability of the synthetic colloids dex
109 F/VEGF and did not affect other mediators of microvascular permeability or endothelial-cell prolifera
110 l) (EPA+GLA), and antioxidants improves lung microvascular permeability, oxygenation, and cardiopulmo
111 l nitric oxide synthase (eNOS) regulation of microvascular permeability remain unresolved.
112 lycocalyx to one critical vascular function, microvascular permeability, remains unclear.
113 nthase (iNOS) plays a role in the changes in microvascular permeability seen with this injury.
114 enes contract airway smooth muscle, increase microvascular permeability, stimulate mucus secretion, d
115  gene expression and VPF/VEGF enhancement of microvascular permeability, suggesting that these distin
116 al ischemia/reperfusion-mediated increase in microvascular permeability than those treated with CMV o
117                  Dynamic MR imaging revealed microvascular permeability to a high-molecular-weight co
118       However, red blood cell velocities and microvascular permeability to albumin were higher in the
119 ar diameters, red blood cell velocities, and microvascular permeability to albumin.
120 al surface layer in parallel with defects in microvascular permeability to both water and albumin, in
121 helial glycocalyx are critical regulators of microvascular permeability to both water and albumin.
122 th U and the previously described changes in microvascular permeability to K(+) with U, suggest that
123                                    Increased microvascular permeability to plasma proteins and neutro
124 ivo role of RhoGDI-1 in regulating pulmonary microvascular permeability using RhoGDI-1(-/-) mice.
125 ts injected locally with agents that enhance microvascular permeability: vascular permeability factor
126 h, serum alanine aminotransferase, and liver microvascular permeability vs. KIM6+-infected animals (p
127 f the lung was determined by flow cytometry, microvascular permeability was assessed by the extravasa
128    The sepsis-induced increase in peripheral microvascular permeability was associated with significa
129  T2-weighted magnetic resonance imaging, and microvascular permeability was estimated by strain gauge
130 kappaB) in TNF-induced increases in cerebral microvascular permeability was evaluated both in vitro,
131                             No difference in microvascular permeability was found between the 2 group
132 ient (Kf), a sensitive measure of changes in microvascular permeability, was determined.
133 ation of neutrophils and increased pulmonary microvascular permeability, was reduced in NK1R-/- anima
134                         Changes in pulmonary microvascular permeability were significantly suppressed

 
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