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1 olar hyalinosis, and 32.9% abnormal vascular intimal thickening).
2 h mononuclear cell infiltration and preceded intimal thickening.
3 eficient recipients had increased concentric intimal thickening.
4 al antibody resulted in marked diminution of intimal thickening.
5 on and activity in a model of injury-induced intimal thickening.
6 ter infectious exposure prevents accelerated intimal thickening.
7 beta1 ceased by 4 weeks, the time of maximal intimal thickening.
8 pearance of arterial lesions with concentric intimal thickening.
9 h muscle cells and subsequent development of intimal thickening.
10  levels and activity in relation to flow and intimal thickening.
11 nd lymphatic disruption and resulted in mild intimal thickening.
12 ing in-stent thrombus and obstruction due to intimal thickening.
13 en studied 10 normal coronaries with diffuse intimal thickening.
14 a pigmented (yellow) or nonpigmented (white) intimal thickening.
15 llografts, associated with a 65% increase in intimal thickening.
16 inine could enhance NO generation and reduce intimal thickening.
17 nted human and murine hearts as a concentric intimal thickening.
18 ering arteries susceptible to thrombosis and intimal thickening.
19 uppressed the effect of LTSN cell seeding on intimal thickening.
20 ity, as indicated by the loss of Eph-B4, and intimal thickening.
21 SMC) proliferation and migration and thereby intimal thickening.
22 th, it is not required for the initiation of intimal thickening.
23 on and analyzed for cellular infiltrates and intimal thickening.
24 m traditional SMCs are major contributors to intimal thickening.
25 n the number of adventitial fibroblasts, and intimal thickening.
26 eling T lymphocyte recruitment and preceding intimal thickening.
27 ry arteries allowed quantification of vessel intimal thickening.
28 rotid arteries to induce vascular injury and intimal thickening.
29 th mononuclear cell recruitment and preceded intimal thickening.
30 h mononuclear cell recruitment, and precedes intimal thickening.
31 ial function are associated with progressive intimal thickening.
32 fter stenting and virtually eliminated later intimal thickening.
33 e gene expression, cellular infiltration, or intimal thickening.
34 , leukocytes are recruited as a precursor to intimal thickening.
35 by day 30, and associated with a decrease in intimal thickening.
36 ant recipients with EBD demonstrated greater intimal thickening (0.59 +/- 0.1 vs. 0.32 +/- 0.2 mm; p
37  patterns are observed: (1) shear stabilized intimal thickening, (2) tension induced wall thinning an
38 ram of tissue per hour; P < .01) and reduced intimal thickening 4 weeks later (intima/ media ratio: L
39 : grade I = normal (44 patients); grade II = intimal thickening (52 patients); grade III = atheroma <
40              By day 30, there was concentric intimal thickening, accumulation of alpha-smA+ cells, an
41 ries, in concert with a twofold reduction in intimal thickening after 14 days, compared with arteries
42 mmune response also plays a cardinal role in intimal thickening after acute arterial-wall injury.
43 in the inhibitory effect of T lymphocytes on intimal thickening after arterial injury.
44 the initiation of cellular events leading to intimal thickening after balloon injury in the rat.
45 y artery lesions were classified as adaptive intimal thickening (AIT), pathologic intimal thickening
46          This revealed variable, fluctuating intimal thickening along the length of the vessel.
47 cipients showed severe chronic arteriopathy (intimal thickening, alpha-smooth muscle actin+ cell prol
48  grafted hearts expressed similar amounts of intimal thickening (analysis of variance, P=0.4826).
49                  Furthermore, 30% of diffuse intimal thickening and 22% of medial samples showed cont
50 ly, restenosis after angioplasty, vein graft intimal thickening and atherogenesis.
51 r, and reduced shear predisposes arteries to intimal thickening and atherosclerosis.
52  day 24 posttransplantation and analyzed for intimal thickening and cellular infiltration.
53 d thrombosis and dramatically inhibited both intimal thickening and endogenous bFGF mobilization.
54                                              Intimal thickening and I:M were reduced significantly by
55 vity in SMCs from nonatherosclerotic diffuse intimal thickening and in the overlying endothelial cell
56 tation: early lumen loss primarily caused by intimal thickening and late lumen loss caused by EEM are
57  are the major correlates of coronary artery intimal thickening and luminal stenosis.
58 jury is a critical determinant of consequent intimal thickening and mural thrombus.
59 -microCi stent groups, characterized by both intimal thickening and negative arterial remodeling.
60 emodeling, as suggested by the inhibition of intimal thickening and outward arterial remodeling.
61 ic inflammation is associated with increased intimal thickening and stenosis after arterial allograft
62 rol allografts, which also developed greater intimal thickening and stenosis than hGSTA4-4 transduced
63 itors were shown to decrease coronary artery intimal thickening and stenosis.
64  necrosis and of capillary damage, including intimal thickening and vascular thrombosis.
65 nges in coronary artery structure, including intimal thickening and vessel remodeling, occur early af
66 as indicated by plaque size (plaque area and intimal thickening) and stage of development.
67  on the two time scales of thrombosis and of intimal thickening, and by using local protein release t
68 led only mild perivascular fibrosis, minimal intimal thickening, and preserved myocardial architectur
69 s during infiltration of inflammatory cells, intimal thickening, angiogenesis and plaque rupture whic
70       Single balloon injury produced limited intimal thickening at 3 weeks (intimal area, 0.40+/-0.05
71        Vasculopathy was graded for degree of intimal thickening based on the involvement of vascular
72                                              Intimal thickening became evident at 14 days.
73 evealed patent ductus arteriosus with normal intimal thickening but dilated cardiac chambers.
74 ate that adventitial angiogenesis stimulates intimal thickening but does not initiate it.
75 as in both recipient groups developed florid intimal thickening by 4 to 10 weeks, with marked lipid d
76 duction with an iNOS inhibitor increased the intimal thickening by 57.2%, indicating that NO suppress
77 ere histologically stained and evaluated for intimal thickening by deriving a neointimal index (NI) u
78  year, 4 with consecutive biopsies developed intimal thickening by intravascular ultrasound.
79 ing of the lumen primarily due to concentric intimal thickening caused by proliferation of alpha-smoo
80 ts undergoing chronic rejection was arterial intimal thickening comprising smooth muscle cell prolife
81 in graft failure is the result of medial and intimal thickening consequent upon medial vascular smoot
82 ether angiographically silent early coronary intimal thickening could predict long-term morbidity and
83 ophy, arteriolar hyaline thickening, fibrous intimal thickening (CV), and fraction of sclerotized glo
84 s infiltrate the donor heart before vascular intimal thickening develops, but the specific mediators
85 , whereas arteriolar hyalinosis and vascular intimal thickening did not.
86 r smooth muscle cells (VSMCs) contributes to intimal thickening during atherosclerosis and restenosis
87 sitive than coronary angiography and detects intimal thickening (early CAV) in the coronary arteries
88 s were classified as lesions with pathologic intimal thickening, fibrous-cap atheromas with cores in
89  Finally, a method was devised to quantitate intimal thickening from a sampling of three tissue cross
90 reduced abdominal aorta lipid deposition and intimal thickening from aortic arch throughout the abdom
91                                          The intimal thickening generated significant luminal narrowi
92 ever, separation of normal aorta and minimal intimal thickening (grades I and II) from more complex a
93                        CAV was defined as an intimal thickening &gt;/= 0.5 mm in the follow-up with rega
94 lticenter study suggests that progression of intimal thickening &gt;/=0.5 mm in the first year after tra
95 nd specificity of 81% and 75% to detect CAV (intimal thickening &gt;0.5 mm), whereas the PPV and NPV wer
96 P< or =0.0239) decrease in coronary arterial intimal thickening (GVD) of approximately 43%.
97                  In a rabbit model, arterial intimal thickening has been induced by direct intravascu
98 of the coronary segments with progression of intimal thickening have compensatory dilation of the ves
99 ing inflammatory cells on the development of intimal thickening in a heterotopic mouse transplant mod
100 T lymphocyte and macrophage recruitment, and intimal thickening in a murine model of CAV.
101  L-749,329, was evaluated as an inhibitor of intimal thickening in a porcine balloon/stent model of c
102 luated for their ability to inhibit vascular intimal thickening in a porcine coronary artery model of
103 ith mononuclear cell recruitment and precede intimal thickening in cardiac allograft vasculopathy (CA
104 , an inhibitor of NO synthesis, enhanced the intimal thickening in injured vessels in adult rats but
105 uishable from values obtained by analysis of intimal thickening in multiple sections covering the ent
106                                              Intimal thickening in PPH was most prominent in small pu
107 ntranasal C pneumoniae infection accelerates intimal thickening in rabbits given a modestly cholester
108 that this defect contributes to the enhanced intimal thickening in response to injury in old animals.
109    Vitamin supplementation failed to prevent intimal thickening in the carotid or iliac arteries.
110                                              Intimal thickening in the coronary arteries of murine ca
111                     Dietary arginine reduced intimal thickening in the injured vessels of hypercholes
112 id artery, Ang II is not a major mediator of intimal thickening in the pig coronary artery.
113  found that Met-RANTES significantly reduced intimal thickening in this model of chronic rejection an
114 reduced CD4(+) T lymphocyte infiltration and intimal thickening in this model.
115                 In 2 weeks, the formation of intimal thickening in tk-expressing grafts was significa
116 o the coronary circulation, LITA grafts show intimal thickening, increased intima/media ratio, and ma
117 ities were present in all children including intimal thickening (intima/lumen cross-sectional area ra
118 recipients, angiography was normal; however, intimal thickening (intima/media cross-sectional area ra
119                                The degree of intimal thickening is correlated with abnormalities in c
120                                              Intimal thickening is driven by damage to the endotheliu
121              Vascular remodeling rather than intimal thickening is the most important determinant of
122                                              Intimal thickening is usually attributed to the migratio
123 PSV is less than 125 cm/sec and no plaque or intimal thickening is visible; (ii) <50% stenosis when I
124 CA PSV is less than 125 cm/sec and plaque or intimal thickening is visible; (iii) 50%-69% stenosis wh
125 4% vs. 32.7 +/- 9.7%, p = 0.01) at day 7 and intimal thickening (maximal intimal area 0.61 +/- 0.09 v
126                              The severity of intimal thickening measured as the percentage of luminal
127 ially drive the various vascular phenotypes (intimal thickening, media hypertrophy, adventitial thick
128                            However, dramatic intimal thickening (neointimal area 2.1+/-0.3) and media
129               These results suggest that the intimal thickening observed in transplant atherosclerosi
130  stents give equally profound suppression of intimal thickening, obviating the need for precise size
131 l ultrasound study revealed that most of the intimal thickening occurred during the first year after
132                                              Intimal thickening of allograft arteries progressed to l
133        Luminal occlusion as a consequence of intimal thickening of graft coronary arteries developed
134 e, changes in right ventricular pressure and intimal thickening of pulmonary small artery are a littl
135         Fourteen days after transplantation, intimal thickening of the allografts in each of the thre
136 Cs together with fibrosis provoke concentric intimal thickening of the coronary arteries, which is th
137               The average scores of arterial intimal thickening on day 45 after transplantation were
138 ger than 400 micrometer showed a significant intimal thickening only in CTED.
139 (plaque erosion), most often on pathological intimal thickening or fibroatheromas.
140 d iron were found in lesions with pathologic intimal thickening or fibrous-cap atheromas with cores i
141  transplantation in the group with pigmented intimal thickening (p < 0.05).
142 ntly smaller than control vessels because of intimal thickening (P=0.003).
143                    LITA showed a significant intimal thickening (P=0.05) and a nonsignificant medial
144 daptive intimal thickening (AIT), pathologic intimal thickening (PIT), or intimal xanthoma (IXA).
145    Lesions were classified into pathological intimal thickening (PIT), VH-IVUS-derived thin-capped fi
146 we propose and study a mathematical model of intimal thickening, posed as a free boundary problem.
147 ted with increased aortic external diameter, intimal thickening, preserved vascular smooth muscle cel
148 re significantly correlated with severity of intimal thickening (R = 0.54, P < 0.0001).
149 ealed intact global architecture and minimal intimal thickening, respectively.
150 is disease which is characterized by diffuse intimal thickening resulting from smooth muscle cell mig
151  of normal medial samples and 31% of diffuse intimal thickening samples also were skewed toward one X
152 he two angioscopic groups revealed increased intimal thickening, serum cholesterol, low density lipop
153 lates most strongly with venous and small IV intimal thickening, similar to the pattern observed in P
154 ute rejection as an independent predictor of intimal thickening suggests that mechanisms beyond those
155 tion ensues within 4 weeks, characterized by intimal thickening, T-cell infiltrates, and vascular cel
156                      Vascular injury induced intimal thickening that was largely composed of vascular
157 29 mice into the CD40L(-/-) mice reduced the intimal thickening to the level comparable to the thicke
158  various vascular changes ranging from focal intimal thickening to total vascular lumen blockade due
159 we show that outward vascular remodeling and intimal thickening, two manifestations of arterioscleros
160      The coronary arteries were analyzed for intimal thickening using a neointimal index (NI) derived
161                                Consequently, intimal thickening was diminished, thrombotic occlusion
162                                              Intimal thickening was enhanced 3.4-fold in Csrp2(-/-) c
163  CD40 ligand knockout (CD40L(-/-)) mice, the intimal thickening was increased 3-fold compared with th
164 on of allograft myointimal proliferation and intimal thickening was induced directly by IGF-I.
165                                              Intimal thickening was observed after 1 week only in CCA
166                                              Intimal thickening was quantitated morphometrically.
167                                              Intimal thickening was quantitated morphometrically.
168 helium in preventing vascular thrombosis and intimal thickening, we designed a series of experiments
169 nificant clinical predictors of nonpigmented intimal thickening were advanced donor age and lower mea
170 tery intimal thickness and the prevalence of intimal thickening were lower in the patients receiving
171  bFGF mobilization, medial repopulation, and intimal thickening were measured.
172                                The scores of intimal thickening were significantly reduced to 0.97+/-
173 ver, the control allografts developed marked intimal thickening, whereas Ad3rsFas-transduced allograf
174 rafts (without MSCs) resulted in significant intimal thickening, whereas cellular grafts (with MSCs)
175 c rejection characterized by circumferential intimal thickening with partial disruption of the elasti
176  typically characterized by diffuse coronary intimal thickening with pathological vessel remodeling,
177  CCR1-deficient recipients, it increased GAD intimal thickening with SMLC proliferation in only the w
178 cimens comprised an undiseased portion (thin intimal thickening with the underlying media) and a dise
179 s harvested at day 30 showed circumferential intimal thickening, with accumulation of alpha-smA+ cell

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