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1 lar space and those by which drug enters the blood vessel wall.
2 isms that regulate its expression within the blood vessel wall.
3 ne targeted for collagen exposed on diseased blood vessel wall.
4 nding of inflammation and destruction of the blood vessel wall.
5 concave shape, representing a segment of the blood vessel wall.
6 ing metabolic signals to inflammation in the blood vessel wall.
7 blood-borne lipids to initially traverse the blood vessel wall.
8 e collisions during secondary capture on the blood vessel wall.
9 tric properties of the microstructure of the blood vessel wall.
10 the recruitment of inflammatory cells to the blood vessel wall.
11 yte NADPH oxidase produces superoxide in the blood vessel wall.
12 on secondary to loss of the integrity of the blood vessel wall.
13  markedly differential deposition across the blood vessel wall.
14 actors within the complex environment of the blood vessel wall.
15 rafficking of modified lipoproteins into the blood vessel wall.
16 ts to slow down and eventually arrest on the blood vessel wall.
17  eNOS gene increases production of NO in the blood vessel wall.
18 by the development of lipid-laden plaques in blood vessel walls.
19 mesoscale formulation for the NP adhesion to blood vessel walls.
20  is the result of idiopathic inflammation in blood vessel walls.
21 d adhesion and de-adhesion to substrates and blood vessel walls.
22 tenuated for maintaining VSMC homeostasis in blood vessel walls.
23  brain tissue is driven by pulsations of the blood vessel walls.
24 tial number of antiatherogenic effects along blood vessel walls.
25 lyze cellular and molecular abnormalities in blood vessel walls.
26 d molecules involved in leukocyte rolling on blood vessel walls.
27  accumulates within fibrin clots attached to blood vessel walls.
28 o improve delivery of the active compound to blood vessel walls.
29 cular permeability and fibrinoid necrosis of blood vessel walls.
30 vasate through the endothelial lining of the blood vessel wall and enter the underlying tissue.
31     The pathogenic changes that occur in the blood vessel wall and in the blood itself resulting in t
32  of capturing, adhesion, and crawling on the blood vessel wall and require Galphai signaling in neutr
33 -type that senses changes in pressure on the blood vessel wall and the pathway that couples this to c
34                   Endothelial cells line the blood vessel walls and control the trafficking of inflam
35 cible immediate-early gene products found in blood vessel walls and healing cutaneous wounds.
36    The level of SOD3 is particularly high in blood vessel walls and in the lungs.
37 ritical for tumor cell extravasation through blood vessel walls and is mediated by a combination of t
38 lfate chains of proteoglycan, a component of blood vessel walls and the extracellular matrix.
39 ent precocious adhesion of migrating PGCs to blood vessel walls and to connective tissue in the mesen
40 respond to the mechanical environment of the blood vessel wall, and point to cell-cell interactions a
41 dosis, with amyloid deposits in the viscera, blood vessel walls, and connective tissue, is usually fa
42 eptin protein levels in basal keratinocytes, blood vessel walls, and fibroblasts.
43 Cyr61 and Fisp12/mCTGF are present in normal blood vessel walls, and it has been demonstrated that CT
44 s produced by the cellular components of the blood vessel wall are essential, at least for the mainte
45                                         Mean blood vessel wall areas measured in ex vivo coronary art
46                                         Mean blood vessel wall areas measured with CT and US in phant
47 ve interactions between cancer cells and the blood vessel wall as facilitating this process, in a man
48 e is driven primarily by TF derived from the blood vessel wall as opposed to leukocytes.
49 y cells in chorionic plate or umbilical cord blood vessel walls be viewed as a morphologic expression
50 ns showed reactivity to thrombin antibody in blood vessel walls but not in vessels from controls.
51  mediates the attachment of platelets to the blood vessel wall by binding von Willebrand factor (VWF)
52 ls may represent a means of traversal of the blood vessel wall by yeast during disseminated candidias
53 red to facilitate an association of RAS with blood vessel walls by an as-yet-unknown mechanism, ultim
54  We conclude that peristaltic motions of the blood vessel walls can facilitate fluid and solute trans
55                    In an in vitro model of a blood vessel wall consisting of human umbilical vein end
56                               A model of the blood vessel wall, consisting of human umbilical vein en
57                  Brain linear tracks such as blood vessel walls constitute their main invasive routes
58 ting neutrophils and their interactions with blood vessel walls could be a worthwhile therapeutic str
59  refers to the migration of particles toward blood vessel walls during blood flow.
60 Surprisingly, these structures penetrate the blood vessel wall exclusively at sites of vascular remod
61 iven to the physiological phenomenon whereby blood vessel walls exhibit rhythmic oscillations in diam
62 tes the initial adhesion of platelets to the blood vessel wall following injury.
63                               In the damaged blood vessel wall, for example in atherosclerotic lesion
64 f vascular smooth muscle cells (SMCs) in the blood vessel wall from a differentiated to a proliferati
65 ediates superoxide release from VSMCs in the blood vessel wall in response to angiotensin II or PDGF-
66  follicles, and fibrotic thickening of small blood vessel walls in the lung and kidney.
67 cells (HSPCs) emerge and develop adjacent to blood vessel walls in the yolk sac, aorta-gonad-mesoneph
68 cle cells present in the medial layer of the blood vessels wall in the fully differentiated state (dV
69 could liberate antiangiogenic fragments from blood vessels' walls, including endorepellin.
70 nd a mixed inflammatory cell infiltration of blood vessel walls indicative of a necrotizing vasculiti
71  critical role in vascular thrombosis at the blood-vessel wall interface under flow conditions.
72              Recruitment of monocytes to the blood vessel wall is an early event in atherogenesis.
73 mal adherence of red blood cells (RBC to the blood vessel wall is believed to contribute to the vascu
74                             Integrity of the blood vessel wall is essential for vascular homeostasis
75  Sickle red blood cell (RBC) adhesion to the blood vessel wall is hypothesized to be the initiating e
76                                          The blood vessel wall is largely composed of three cell type
77           The TFA data obtained in umbilical blood vessel wall lipids were related to the neurologic
78 ection double inversion-recovery (DIR) black-blood vessel wall magnetic resonance (MR) imaging was de
79 hase-sensitive dual inversion recovery black-blood vessel wall magnetic resonance imaging (TRAPD) was
80                Thus, TSP-1 expression in the blood vessel wall may increase, providing a molecular li
81 lution of ~10 mum, enabling visualization of blood vessel wall microstructure in vivo at an unprecede
82   We identify a new type of stem cell in the blood vessel wall, named multipotent vascular stem cells
83                            CT numbers within blood vessel wall of CT cross sections classified as lip
84                           Mean CT numbers in blood vessel wall of ex vivo coronary arteries identifie
85 (alpha4beta1gamma1), was expressed mainly in blood vessel walls of GBMs and histologically normal tis
86 (alpha4beta2gamma1), was expressed mainly in blood vessel walls of low-grade tumors and normal brain.
87 rombi that can deliver growth factors to the blood vessel wall or be incorporated into developing vas
88 lood-brain barrier, with ~90% contacting the blood vessel wall or its extracellular matrix.
89 pothesis that estrogen receptors (ER) in the blood vessel wall play a role in the modulation of the r
90 keletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage
91 cytes, and their influence on disease of the blood vessel wall, remain to be determined.
92                     An in vitro model of the blood vessel wall revealed that an increased number of h
93 ested, including Hb extravasation across the blood vessel wall, scavenging of endothelial nitric oxid
94 , we utilized a three-dimensional model of a blood vessel wall that endogenously supports DC developm
95 e in acute hypoxia occurs via actions on the blood vessel walls: there was no evidence that adenosine
96 oducts engage their receptor in cells of the blood vessel wall, thereby activating mechanisms linked
97 le (SS) red blood cell (RBC) adhesion to the blood vessel wall, thereby contributing to vaso-occlusiv
98 ntiating into mature adipocytes, stabilizing blood vessel walls through endothelial cell function, an
99  alter the pattern of gene expression in the blood vessel wall to enhance potential effects of PAI-1
100             We used an in vitro model of the blood vessel wall to test the premise that the vascular
101 seen in Alzheimer's disease and Abeta in the blood vessel walls was characteristic of cerebral amyloi
102  factors involved in lipid metabolism in the blood vessel wall, we have cloned unique molecular isofo
103                                CT numbers of blood vessel wall were determined in ex vivo coronary ar
104                    Platelets adherent to the blood vessel wall were observed in few areas in the hear
105 e concentrated and stayed as clusters near a blood vessel wall when tumors were exposed to a magnetic
106 s the motive force for such transport within blood vessel walls, which is in the opposite direction t
107                                   To mimic a blood vessel wall with IL-8 expressed on the luminal sur
108 rmal lung in nine of 10 specimens, and up to blood vessel walls without evidence of vessel (>4 mm) th

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