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1 and angiopoietin signalling (NO-Tie-mediated arteriogenesis).
2 odeling of pre-existing collateral arteries (arteriogenesis).
3 ontribute to native collateral formation and arteriogenesis.
4 ndicate VEGF and VEGFR-1 are determinants of arteriogenesis.
5 epicardial beta-catenin pathway in coronary arteriogenesis.
6 in endothelial regeneration and compensatory arteriogenesis.
7 ntial for embryonic vascular development and arteriogenesis.
8 collateral arterial formation and branching arteriogenesis.
9 not sufficient, condition for nerve-induced arteriogenesis.
10 ndothelial-monocyte interactions involved in arteriogenesis.
11 ortance of vasculogenesis, angiogenesis, and arteriogenesis.
12 s that both resolve inflammation and promote arteriogenesis.
13 understood, much remains to be learned about arteriogenesis.
14 as associated with impaired angiogenesis and arteriogenesis.
15 by VEGF withdrawal in the face of unimpeded arteriogenesis.
16 shaping physiological and ischemia-triggered arteriogenesis.
17 d adult angiogenesis, lymphangiogenesis, and arteriogenesis.
18 ndothelial growth factor A (VEGF) to enhance arteriogenesis.
19 actor A (VEGF-A) expression and induction of arteriogenesis.
20 d its role in regulation of angiogenesis and arteriogenesis.
21 hat myoglobin overexpression does not affect arteriogenesis.
22 genesis but impaired developmental and adult arteriogenesis.
23 ative contributions of various cell types to arteriogenesis.
24 erturbs nerve-vessel alignment and abolishes arteriogenesis.
25 signaling pathway can effectively stimulate arteriogenesis.
26 the GK model includes both angiogenesis and arteriogenesis.
29 of ADMA on angioadaptation (angiogenesis and arteriogenesis) after hindlimb ischemia, as assessed by
30 quely demonstrate that functional collateral arteriogenesis alone is not necessarily sufficient for a
33 play differential roles in ischemia-mediated arteriogenesis and angiogenesis, partly because of their
35 dothelial ERK signaling is critical for both arteriogenesis and arterial-venous patterning and that R
36 ese results can serve as a genomic model for arteriogenesis and as a database for developing new ther
41 S knockout mice [eNOS (-/-)] have defects in arteriogenesis and functional blood flow reserve after m
43 th intrarenal angiogenesis and peri-stenosis arteriogenesis and increased the expression of angiogeni
46 ive synthetic phenotype during physiological arteriogenesis and pathological conditions such as ather
47 essing vessels, transport vessels undergoing arteriogenesis and peritumor vessels influenced by tumor
48 are central to both developmental and adult arteriogenesis and provide a model for future studies of
49 tification of regional changes in CT-defined arteriogenesis and quantification of 201Tl perfusion.
50 n increase in the biomarkers of angiogenesis/arteriogenesis and reduction in the markers of thrombosi
51 g permits serial, regional quantification of arteriogenesis and resting tissue perfusion after limb i
52 tify the endocardium as a site of endogenous arteriogenesis and source of endothelial cells to promot
57 in ischemic muscle to enhance angiogenesis, arteriogenesis, and perfusion recovery in experimental P
59 type ischemic muscle decreased angiogenesis, arteriogenesis, and perfusion, whereas transfer of wild-
60 -93-25(-/-) PAD mice increased angiogenesis, arteriogenesis, and the extent of perfusion, which corre
61 macrophage at the center of ischemia-induced arteriogenesis, and they establish a novel role for Myos
62 ying the mechanisms underlying angiogenesis, arteriogenesis, and vascular disorders, such as HHT and
65 in preserving blood flow, thereby promoting arteriogenesis, angiogenesis, and mural cell recruitment
66 mpaired limb perfusion recovery with reduced arteriogenesis, angiogenesis, and recruitment of inflamm
68 ium and bone marrow plays a critical role in arteriogenesis/angiogenesis in vivo and suggests that Bm
70 rge into large conduit arteries in ischemia (arteriogenesis) are major determinants of the severity o
71 n additional phenotype of defective coronary arteriogenesis associated with RXRalpha deficiency and i
72 percholesterolemia results in delayed native arteriogenesis because of reduced early monocyte/macroph
74 diabetes-related impairment of angiogenesis, arteriogenesis, blood flow, and functional recovery in a
77 size and promoted vascular proliferation and arteriogenesis, but did not surpass single therapies wit
78 that nerve-derived VEGF may be important for arteriogenesis, but its role in vivo remains unclear.
79 Myeloid cells are important contributors to arteriogenesis, but their key molecular triggers and cel
81 r (VEGF) expression gene on angiogenesis and arteriogenesis by using cardiovascular magnetic resonanc
82 mice were correlated with ischemia-initiated arteriogenesis, capillary formation, and vessel maturati
83 3-25(-/-)) showed decreased angiogenesis and arteriogenesis correlating with increased M1-like macrop
84 during vasculogenesis and ischemia-mediated arteriogenesis could be temporally assessed by noninvasi
85 strategies that target both angiogenesis and arteriogenesis could yield the most efficacious treatmen
86 flow recovery after femoral artery ligation (arteriogenesis) dependent on the attenuation of leukocyt
87 he first evidence that VEGF is necessary for arteriogenesis from a primitive capillary plexus in vivo
88 miR-17 approximately 92 to ischemia-induced arteriogenesis has not been investigated in an in vivo m
89 eft DM and arise only after-and dependent on-arteriogenesis, implicating arteries as drivers of gut l
91 Synectin modulates developmental and adult arteriogenesis in an endothelial cell-autonomous fashion
95 ovide evidence for an inductive function for arteriogenesis in heart development distinct from its ro
96 ice displayed improved vascular survival and arteriogenesis in ischemic hind limbs, leading to the ac
97 ted arterial growth in adult mice, restoring arteriogenesis in mice lacking synectin and in atheroscl
98 paired angiogenesis in the setting of normal arteriogenesis in response to femoral artery ligation, a
99 d bone marrow-derived cells is essential for arteriogenesis in response to hindlimb ischemia in mice.
101 physiologically significant angiogenesis or arteriogenesis in the chronically ischemic porcine heart
103 roles for NRP1 in postnatal angiogenesis and arteriogenesis in the heart and retina, pathological neo
104 results yield further evidence for a role of arteriogenesis in the induction of impulse-conducting Pu
110 ently, ischemia-initiated collateral growth (arteriogenesis) in the upper limb and capillary formatio
114 rmation of arterial vasculature, here termed arteriogenesis, is a central process in embryonic vascul
115 a novel candidate that negatively regulates arteriogenesis, meriting additional studies to unravel t
117 IGN AND Angiogenesis (capillary density) and arteriogenesis (number of collaterals and intratree anos
119 showing that endocardial flowers develop by arteriogenesis of Cx40(-) cells and by outgrowth of pre-
123 h factor-B (VEGF-B), which promotes coronary arteriogenesis, physiological cardiac hypertrophy, and i
128 ow us to uncouple nerve-vessel alignment and arteriogenesis, revealing that nerve-derived Cxcl12 stim
129 te the functional and clinical importance of arteriogenesis, the biology of the process is poorly und
130 Though alterations in shear stress stimulate arteriogenesis, the migration of monocytes into the peri
132 py on circulating biomarkers of angiogenesis/arteriogenesis, thrombosis, inflammation, and leukocyte
134 age polarization to promote angiogenesis and arteriogenesis to revascularize ischemic muscle in exper
135 to determine whether nicotine could enhance arteriogenesis, to compare the magnitude of this effect
136 e relative contributions of angiogenesis and arteriogenesis toward the overall reperfusion response a
137 plays an essential role in angiogenesis and arteriogenesis, two processes critical to restoration of
140 us VEGF in ischemia-induced angiogenesis and arteriogenesis was measured by capillary density and mic
141 he specific role of beta-catenin in coronary arteriogenesis, we have generated conditional beta-caten
144 myogenic marker expression, blood flow, and arteriogenesis when transplanted into the ischemic hindl
146 mined the impairment to be defective induced arteriogenesis, whereas developmental vasculogenesis was
147 be useful in studies of stroke and cerebral arteriogenesis, which require the accurate assessment of
148 nsory nerves or Schwann cells prevent proper arteriogenesis, while those that disorganize the nerves
149 BMC injection had a substantial effect on arteriogenesis, with normalization of total arterial are
150 or (PlGF) stimulated robust angiogenesis and arteriogenesis without significant side effects, whereas
151 inates macrophage-mediated inflammation with arteriogenesis, wound healing, and blood flow control.
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