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1 migration of LSK cells in response to SDF or vascular endothelial growth factor.
2 ta, arginase-1, matrix metalloproteinase and vascular endothelial growth factor.
3 issue inhibitor of metalloproteinases 1, and vascular endothelial growth factor.
6 epithelial phenotype was enhanced following vascular endothelial growth factor A (VEGF-A) exposure.
10 helial cell migration, and tube formation in vascular endothelial growth factor A (VEGF-A) stimulated
11 f two principal effectors of vasculogenesis, vascular endothelial growth factor A (VEGF-A), and plate
14 d new blood vessel sprouts is coordinated by vascular endothelial growth factor A (VEGFA) and Delta-l
15 a-induced factor 1a (Hif1a) and secretion of vascular endothelial growth factor A (Vegfa) by starved
18 dr expression to enable the DH to respond to vascular endothelial growth factor A (VEGFA) ligand from
20 deletion of hypoxia-response element in the vascular endothelial growth factor A (VEGFA) promoter sh
21 h factor AA and BB; placental growth factor; vascular endothelial growth factor A and D; vascular end
22 abundance of the proangiogenic growth factor vascular endothelial growth factor A and promoted the pr
23 ptors present in dermal fibroblasts restores vascular endothelial growth factor A production by these
24 d phosphatidylinositol 3-kinase and inhibits vascular endothelial growth factor A secretion by tumor
25 ally impaired and produce reduced amounts of vascular endothelial growth factor A, resulting in defic
26 rs of proliferation and angiogenesis (Ki-67, vascular endothelial growth factors A/C, vascular endoth
27 us also inhibited Akt and p38 stimulation by vascular endothelial growth factor, a major driver of an
29 action with one of its main natural ligands, vascular endothelial growth factor-A (VEGF-A), contribut
30 n derived neurotrophic growth factor (BDNF), vascular endothelial growth factor-A (VEGF-A), insulin-l
32 (rAAV) (5 x 10(12) viral particles encoding vascular endothelial growth factor-A [VEGF-A] or thymosi
33 Leishmania major increases the expression of vascular endothelial growth factor-A and vascular endoth
37 ar edema does not respond to an initial anti-vascular endothelial growth factor agent, usually after
40 oup to evaluate the effect of switching anti-vascular endothelial growth factor agents for treatment
41 oup to evaluate the effect of switching anti-vascular endothelial growth factor agents for treatment
42 Comparisons of the relative effect of 3 anti-vascular endothelial growth factor agents to treat diabe
44 perfusion injury, amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem c
46 d to four groups: amniotic fluid stem cells, vascular endothelial growth factor-amniotic fluid stem c
48 nib malate, an agent that inhibits both anti-vascular endothelial growth factor and anti-platelet-der
49 Cxcl9 produced by osteoblasts interacts with vascular endothelial growth factor and prevents its bind
50 ctivate receptor-associated tyrosine kinase, vascular endothelial growth factor, and cell cycle pathw
51 luids increased CCA histidine decarboxylase, vascular endothelial growth factor, and MC/EMT/ECM expre
52 iogenesis factors (fibroblast growth factor, vascular endothelial growth factor, and platelet-derived
53 [growth-regulated protein alpha], and VEGF [vascular endothelial growth factor]), and an increase in
54 nvolved in angiogenic pathways such as VEGF (vascular endothelial growth factor), ANG1 (angiopoietin
56 d clinical trial (RCT) evaluating the 3 anti-vascular endothelial growth factor (anti-VEGF) agents af
58 ologists was primarily driven by use of anti-vascular endothelial growth factor (anti-VEGF) injection
60 ipants had been treated previously with anti-vascular endothelial growth factor (anti-VEGF) therapy,
61 7028), retinal OCT imaging (92134), and anti-vascular endothelial growth factor (anti-VEGF) treatment
64 on diabetic macular oedema [DMO] after anti-vascular endothelial growth factor [anti-VEGF] treatment
66 ith the combination of anti-miR-630 and anti-vascular endothelial growth factor antibody in mice resu
70 arin-binding EGF-like growth factor (HBEGF), vascular endothelial growth factor C (VEGFC), betacellul
71 flammation resulted in reduced expression of vascular endothelial growth factor-C and decreased corne
72 gulated the expression of prolymphangiogenic vascular endothelial growth factor-C upon stimulation wi
73 lial cells, isolated HKMECs depended on high vascular endothelial growth factor concentration for sur
74 el permeability and elevated blood levels of vascular endothelial growth factor D and stromal cell-de
75 recommendations for sirolimus treatment and vascular endothelial growth factor D testing and recomme
76 pivotal pathophysiological role of impaired vascular endothelial growth factor-dependent vascular re
78 owth factor, platelet-derived growth factor, vascular endothelial growth factor), endothelin and inhi
80 of the BRB with increased vascular leakage, vascular endothelial growth factor expression, and infil
82 sed HA levels and mesenchymal cells, but not vascular endothelial growth factor in Hyal2(-/-) embryon
83 ceptor tyrosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including trastuzuma
84 evelopment and angiogenesis, but its role in vascular endothelial growth factor-induced endothelial c
85 tamate transporter on astrocytes through the vascular endothelial growth factor inducing favorable ch
88 ed patient experiences specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF
89 have been raised that intravitreal dosing of vascular endothelial growth factor inhibitors in DME cou
94 transforming growth factors beta1 and beta2, vascular endothelial growth factor, interleukin-1beta, m
95 l levels along with inappropriate attenuated vascular endothelial growth factor levels may imply an a
96 E-[c(RGDfK)](2) PET/CT correlated with serum vascular endothelial growth factor levels, whereas basel
97 treatment was associated with decreased free vascular endothelial growth factor (not bound to bevaciz
98 es including intravitreal injections of anti-vascular endothelial growth factor or verteporfin photod
100 tumor necrosis factor-alpha (TNF-alpha), and vascular endothelial growth factor peaked on day 6 (P </
102 blood supply might upregulate production of vascular endothelial growth factor, providing the stimul
104 ib are oral multikinase inhibitors targeting vascular endothelial growth factor receptor (VEGFR) and
105 tions from vascular tumors were stained with vascular endothelial growth factor receptor (VEGFR), vas
106 of vascular endothelial growth factor-A and vascular endothelial growth factor receptor (VEGFR)-2 an
107 l approaches, we show that the expression of vascular endothelial growth factor receptor 1 (VEGFR1) b
108 ssion of CXCR7 expression and recruitment of vascular endothelial growth factor receptor 1 (VEGFR1)-e
109 th factor receptor 2 antibody) or icrucumab (vascular endothelial growth factor receptor 1 antibody)
110 nolase, placental growth factor, and soluble vascular endothelial growth factor receptor 1 levels wer
111 niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (
112 vascular endothelial growth factor A and D; vascular endothelial growth factor receptor 1, 2, and 3;
114 as a new class of potent and selective human vascular endothelial growth factor receptor 2 (VEGFR2) t
115 ptide, based on an amyloidogenic fragment of vascular endothelial growth factor receptor 2 (VEGFR2),
116 ultrasonography (US) by using clinical-grade vascular endothelial growth factor receptor 2 (VEGFR2)-t
117 r docetaxel in combination with ramucirumab (vascular endothelial growth factor receptor 2 antibody)
118 nsity, endothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2 signaling,
119 4, alpha-smooth muscle actin, CD31, phospho-vascular endothelial growth factor receptor 2, and p42/4
120 Cabozantinib is an oral potent inhibitor of vascular endothelial growth factor receptor 2, MET, and
121 by an endothelial nitric oxide synthase/Akt/vascular endothelial growth factor receptor 2/oxidative
122 ngiogenesis by monoclonal antibodies against vascular endothelial growth factor receptor 3 (VEGFR-3)
124 let/endothelial cell adhesion molecule 1 and vascular endothelial growth factor receptor 3 (VEGFR3).
125 tic markers (prospero homeobox protein 1 and vascular endothelial growth factor receptor 3) as well a
126 single dose each of plastic microspheres and vascular endothelial growth factor receptor antagonist i
127 (obese ZSF1) with the combined treatment of vascular endothelial growth factor receptor blocker SU54
128 cular endothelial growth factor signaling by vascular endothelial growth factor receptor inhibition m
129 endothelial growth factor receptor (VEGFR), vascular endothelial growth factor receptor type 1 (VEGF
130 study, the possible localization and role of vascular endothelial growth factor receptor type 2 (VEGF
131 lial growth factor receptor type 1 (VEGFR1), vascular endothelial growth factor receptor type 2 (VEGF
132 growth factor receptor type 2 (VEGFR2), and vascular endothelial growth factor receptor type 3 (VEGF
135 rs for the receptor tyrosine kinases MET and Vascular Endothelial Growth factor Receptor-2 (VEGFR-2).
136 4 and subsets coexpressing CD133, CXCR4, and vascular endothelial growth factor receptor-2 epitopes.
137 od mononuclear cells expressing CD34, CD133, vascular endothelial growth factor receptor-2, and chemo
138 angiogenesis and lymphangiogenesis involving vascular endothelial growth factor-receptor tyrosine kin
139 plex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth factor receptors (VEGFRs) th
140 of tyrosine kinase activity associated with vascular endothelial growth factor receptors 1, 2, and 3
141 67, vascular endothelial growth factors A/C, vascular endothelial growth factor receptors 2/3, angiop
142 years, tyrosine kinase inhibitors targeting vascular endothelial growth factor receptors and RET (re
143 s an inhibitor of kinases, including MET and vascular endothelial growth factor receptors, and has sh
144 othelial growth factor-A (VEGF-A) acts via 2 vascular endothelial growth factor receptors, VEGFR-1 an
146 pg/mL, P<0.001) and significantly decreased vascular endothelial growth factor/sFlt1 ratio (P=0.012)
147 ial tissue and SF, as they may interact with vascular endothelial growth factor signaling and exRNA.
148 iogenic TSP1 fragment, suppresses heightened vascular endothelial growth factor signaling and preserv
149 ribose) polymerase inhibition and/or reduced vascular endothelial growth factor signaling by vascular
150 se abrogating hypoxia inducible factor (HIF)/vascular endothelial growth factor signaling, are initia
152 ral approaches, including the use of soluble vascular endothelial growth factor (sVEGF)-VEGF165, have
153 Our data provide rationale for combining vascular endothelial growth factor-targeting therapy wit
154 tic macular edema (DME) after months of anti-vascular endothelial growth factor therapy and its effec
155 Current treatment options, including anti-vascular endothelial growth factor therapy and laser ret
157 nforms the debate regarding the role of anti-vascular endothelial growth factor therapy in patients w
159 opathy complexes are less responsive to anti-vascular endothelial growth factor therapy with no prosp
160 he amount of visual loss sustained with anti-vascular endothelial growth factor therapy, and have the
163 lthier lifestyles and implementation of anti-vascular endothelial growth factor treatment are the mos
165 umab treatment, suggesting that earlier anti-vascular endothelial growth factor treatment of center-i
166 nvAMD are primarily aimed at optimizing anti-vascular endothelial growth factor treatments that have
168 Delivery of the growth factors bFGF and vascular endothelial growth factor using a mineral coate
169 g/mL, Group II: 0.11 (0.11) ng/mL, P = .01); vascular endothelial growth factor (VEGF) (Group I: 157.
170 t, administered in combination with the anti-vascular endothelial growth factor (VEGF) agent ranibizu
172 provide additional outcomes comparing 3 anti-vascular endothelial growth factor (VEGF) agents for DME
173 ce on the ocular safety and efficacy of anti-vascular endothelial growth factor (VEGF) agents for the
175 anibizumab are the most frequently used anti-vascular endothelial growth factor (VEGF) agents injecte
177 thesis and investigate concentrations of: 1) vascular endothelial growth factor (VEGF) and 2) platele
178 d fibroblasts by enhancing the activities of vascular endothelial growth factor (VEGF) and fibroblast
180 e I trial evaluated epigenetic modulation of vascular endothelial growth factor (VEGF) and hypoxia-in
181 ng to pFUS-treated CLI muscle expressed more vascular endothelial growth factor (VEGF) and interleuki
182 differentiation of chondrocytes by promoting vascular endothelial growth factor (VEGF) and matrix met
183 ral tyrosine kinase inhibitor active against vascular endothelial growth factor (VEGF) and platelet-d
184 ity biosensor that can simultaneously detect vascular endothelial growth factor (VEGF) and prostate-s
185 ies, we show that TTF-1 positively regulates vascular endothelial growth factor (VEGF) and that the V
189 ons of AKB-9778 combined with suppression of vascular endothelial growth factor (VEGF) causes a signi
191 gate signalling in liver buds, and show that vascular endothelial growth factor (VEGF) crosstalk pote
192 generation (nAMD) treated with a single anti-vascular endothelial growth factor (VEGF) drug monothera
193 r the treatment of ischemic diseases.Soluble vascular endothelial growth factor (VEGF) enhances vascu
194 ures, tumor microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) fr
195 BDNF-IV and BDNF-I transcripts and increased vascular endothelial growth factor (VEGF) expression.
197 By basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF) gene therapy v
199 ich is paralleled by increased expression of vascular endothelial growth factor (VEGF) in macrophages
201 hat affects some, but not all, recipients of vascular endothelial growth factor (VEGF) inhibitors giv
202 before and after intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors.
203 re used to identify the total number of anti-vascular endothelial growth factor (VEGF) injections adm
209 th platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) is increased d
210 migration of the developing forebrain, while vascular endothelial growth factor (VEGF) is known to in
214 al arterial diseases (PAD) by increasing the vascular endothelial growth factor (VEGF) level in endot
216 rize the first 10 years of intravitreal anti-vascular endothelial growth factor (VEGF) medication use
218 fficiently cleaves, the AP for activation of vascular endothelial growth factor (VEGF) or endonucleas
220 pes through randomised trials, incorporating vascular endothelial growth factor (VEGF) pathway inhibi
223 dentified in 10 articles that addressed anti-vascular endothelial growth factor (VEGF) pharmacotherap
224 nvestigated the influence of this pathway on vascular endothelial growth factor (VEGF) production and
225 ivo, alpha3/alpha5beta1 scaffolds delivering vascular endothelial growth factor (VEGF) promoted non-t
226 of CCN1 as a negative feedback regulator of vascular endothelial growth factor (VEGF) receptor activ
229 e we show that tivozanib, a pan-inhibitor of vascular endothelial growth factor (VEGF) receptors, inh
233 r data further demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for
234 chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in M
235 scriptional pathways activated downstream of vascular endothelial growth factor (VEGF) signaling duri
236 project, the redundancy between endoglin and vascular endothelial growth factor (VEGF) signaling in a
237 ous signaling transducers and isoforms along vascular endothelial growth factor (VEGF) signaling path
239 diated arteriolargenesis requires endogenous vascular endothelial growth factor (VEGF) signalling.
240 In previous studies, we showed that renal vascular endothelial growth factor (VEGF) therapy attenu
243 etter outcomes in RVO eyes treated with anti-vascular endothelial growth factor (VEGF) therapy may pr
245 ntagonizing CXCR4 with POL5551 disrupts anti-vascular endothelial growth factor (VEGF) therapy-induce
247 arenchyme (hepatocytes), which then produces vascular endothelial growth factor (VEGF) to enable the
248 cular degeneration (nAMD) for different anti-vascular endothelial growth factor (VEGF) treatment sche
249 ated macular degeneration (nAMD) during anti-vascular endothelial growth factor (VEGF) treatment.
250 epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) were targeted
251 -phosphate-guanine, is robustly inhibited by vascular endothelial growth factor (VEGF), a previously
252 erformed for hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), and c-Met rec
253 duction of pro-angiogenic factors, CXCL1 and vascular endothelial growth factor (VEGF), and reduced C
254 nhanced soluble signaling factors, including vascular endothelial growth factor (VEGF), and that CAFs
257 elevated pAkt activation and expressions of vascular endothelial growth factor (VEGF), Flk1, and VE-
258 production of pro-angiogenic signals such as vascular endothelial growth factor (VEGF), hypoxia also
259 stromal cell-derived factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF), hypoxia-induc
260 ion, supplementation decreased the levels of vascular endothelial growth factor (VEGF), inducible nit
261 host hepatocyte, but not tumour cell-derived vascular endothelial growth factor (VEGF), is responsibl
262 angiogenesis, including the potent promoter vascular endothelial growth factor (VEGF), is therefore
263 (Avastin(R)), a monoclonal antibody against vascular endothelial growth factor (VEGF), is used clini
264 ucible protein 10, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyte chem
265 s, which migrate in response to gradients of vascular endothelial growth factor (VEGF), stalk cells,
267 vels of endogenous growth factors, including vascular endothelial growth factor (VEGF), that normally
270 HA-enriched matrices increased production of vascular endothelial growth factor (VEGF), while matrice
273 ing EVs or premiR-150 transfection increased vascular endothelial growth factor (VEGF)-A mRNA and sec
276 s of GSH-protein adducts, capillary density, vascular endothelial growth factor (VEGF)-A, and HIF-1al
277 nhanced cell proliferation by regulating the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGF
279 cular cells, von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C expression w
280 where doxycycline-induced overexpression of vascular endothelial growth factor (VEGF)-C was driven b
283 pressed on pancreatic tumor endothelium in a vascular endothelial growth factor (VEGF)-independent ma
284 LSD1 cooperates with CBP and MTA1 to enhance vascular endothelial growth factor (VEGF)-induced tumor
292 esis of periodontal diseases, supported with vascular endothelial growth factor (VEGF-A) and tumor ne
295 cancer cells where it was shown to modulate vascular endothelial growth factor (VEGFR)-2 and epiderm
296 rations of classic vasoactive factors (e.g., vascular endothelial growth factor) were similar in ERM
297 tion elicits a substantial increase of VEGF (vascular endothelial growth factor), which mediates the
298 nant gliomas, inhibition with bevacizumab of vascular endothelial growth factor, which is an importan
299 hosphorylated at tyrosine 731 in response to vascular endothelial growth factor, which likely contrib
300 gnificantly down-regulated the expression of vascular endothelial growth factor while increasing that
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