Phenotype
|
Conditions
|
Figures
|
angiogenesis decreased occurrence, abnormal
|
cancer xenotransplantation, chemical treatment by environment: cisplatin
|
Fig. 6
from Delasoie et al., 2020
|
angiogenesis decreased occurrence, abnormal
|
chemical treatment by environment: sunitinib
|
Fig. 4
from Delasoie et al., 2020
|
angiogenesis disrupted, abnormal
|
chemical treatment: butan-1-ol
|
Fig. 7
from Zeng et al., 2009
|
angiogenesis disrupted, abnormal
|
chemical treatment by environment: eupatilin
|
Fig. 8
from Lee et al., 2020
|
angiogenesis disrupted, abnormal
|
chemical treatment by environment: fucosterol
|
Fig. 8
from Bae et al., 2020
|
angiogenesis disrupted, abnormal
|
chemical treatment by environment: vascular endothelial growth factor receptor antagonist
|
Fig. 1
from Ai et al., 2018
|
angiogenesis disrupted, abnormal
|
chemical treatment by environment: ponatinib
|
Fig. 1
from Ai et al., 2018
|
angiogenesis disrupted, abnormal
|
chemical treatment by environment: glycyrrhetinic acid
|
Fig. 6
from Li et al., 2019
|
angiogenesis disrupted, abnormal
|
chemical treatment: LY294002
|
Fig. 1
from Alvarez et al., 2009
|
angiogenesis disrupted, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Cho et al., 2013
|
angiogenesis increased occurrence, abnormal
|
cancer xenotransplantation
|
Fig. 4
from Zhao et al., 2018
|
angiogenesis increased occurrence, abnormal
|
cancer xenotransplantation
|
Fig. 1
from Yang et al., 2014
|
angiogenesis increased occurrence, abnormal
|
cancer xenotransplantation
|
Fig. 6
from Würth et al., 2017
|
angiogenesis increased occurrence, abnormal
|
cancer xenotransplantation
|
Fig. 1
from Baltrunaite et al., 2017
|
angiogenesis increased occurrence, abnormal
|
cancer xenotransplantation
|
Fig. 3
from Li et al., 2019
|
angiogenesis occurrence, ameliorated
|
chemical treatment by environment: axitinib, cancer xenotransplantation
|
Fig. 1
from Yang et al., 2014
|
angiogenesis occurrence, ameliorated
|
chemical treatment by environment: vatalanib, cancer xenotransplantation
|
Fig. 1
from Yang et al., 2014
|
angiogenesis occurrence, ameliorated
|
chemical treatment by environment: sunitinib, cancer xenotransplantation
|
Fig. 1
from Yang et al., 2014
|
angiogenesis involved in wound healing disrupted, abnormal
|
amputation: caudal fin, chemical treatment: LY294002
|
Fig. 6
from Alvarez et al., 2009
|
angiogenesis involved in wound healing process quality, abnormal
|
amputation: fin, hypoxia, chemical treatment: pharmaceutical, chemical treatment: cobalt dichloride
|
Fig. 6
from Eyries et al., 2008
|
angiogenesis involved in wound healing process quality, normal
|
amputation: fin, chemical treatment: pharmaceutical
|
Fig. 6
from Eyries et al., 2008
|
angiogenic sprout decreased length, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Cho et al., 2013
|
atrioventricular canal cell population proliferation decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. S5
from Banjo et al., 2013
|
atrioventricular canal cell population proliferation decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. S5
from Banjo et al., 2013
|
atrioventricular valve hypoplastic, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 1
from Sarmah et al., 2016
|
atrioventricular valve morphology, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 1
from Sarmah et al., 2016
|
blood circulation decreased occurrence, abnormal
|
physical alteration: intersegmental vessel, chemical treatment by injection: agarose
|
Fig. 1
from Choi et al., 2017
|
blood circulation decreased process quality, abnormal
|
bacterial treatment by injection: Waddlia chondrophila WSU 86-1044
|
Fig. 4
from Fehr et al., 2016
|
blood circulation disrupted, abnormal
|
chemical treatment: herbicide
|
Fig. 5
from Kalén et al., 2009
|
blood island cell death increased process quality, abnormal
|
viral treatment: Sprivirus cyprinus
|
Fig. 2
from Varela et al., 2014
|
blood vasculature broken, abnormal
|
chemical treatment: herbicide
|
Fig. 5
from Kalén et al., 2009
|
blood vessel mcamb expression increased amount, abnormal
|
transection: spinal cord
|
Fig. 4
from Liu et al., 2016
|
blood vessel increased branchiness, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
blood vessel increased branchiness, abnormal
|
chemical treatment: methylglyoxal
|
Fig. 2
from Lodd et al., 2019
|
blood vessel increased branchiness, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
blood vessel increased branchiness, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Jörgens et al., 2015
|
blood vessel malformed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
blood vessel morphology, abnormal
|
chemical treatment: methylglyoxal
|
Fig. 2
from Lodd et al., 2019
|
blood vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3,
Fig. 7
from Chen et al., 2012
|
blood vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
blood vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Jörgens et al., 2015
|
blood vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
blood vessel endothelial cell tgfb1b expression decreased amount, abnormal
|
chemical treatment: vascular endothelial growth factor receptor antagonist
|
Fig. 4
from Monteiro et al., 2016
|
blood vessel endothelial cell kdrl expression decreased amount, abnormal
|
chemical treatment: vascular endothelial growth factor receptor antagonist
|
Fig. 4
from Monteiro et al., 2016
|
blood vessel endothelial cell tgfb1a expression decreased amount, abnormal
|
chemical treatment: vascular endothelial growth factor receptor antagonist
|
Fig. 4
from Monteiro et al., 2016
|
blood vessel endothelial cell cell-cell junction decreased amount, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from De Smet et al., 2014
|
blood vessel endothelial cell filopodium decreased amount, abnormal
|
chemical treatment by environment: zinc atom
|
Fig. 5
from Xia et al., 2020
|
brain neoplastic, abnormal
|
cancer xenotransplantation, chemical treatment: dexamethasone
|
Fig. 3
from Eden et al., 2015
|
brain central nervous system tumor increased amount, abnormal
|
cancer xenotransplantation
|
Fig. 4
from Pudelko et al., 2018
|
brain central nervous system tumor neoplastic, invasive, abnormal
|
cancer xenotransplantation
|
Fig. 4
from Pudelko et al., 2018
|
brain vasculature disorganized, abnormal
|
chemical treatment by environment: lead diacetate
|
Fig. 5
from Roy et al., 2014
|
brain vasculature morphology, abnormal
|
standard conditions
|
FIGURE 4
from Han et al., 2021
|
branching involved in blood vessel morphogenesis process quality, normal
|
chemical treatment: drug
|
Fig. S2
from Eisa-Beygi et al., 2013
|
branching morphogenesis of an epithelial tube disrupted, abnormal
|
chemical treatment: herbicide
|
Fig. 5
from Kalén et al., 2009
|
cardiac muscle tissue regeneration decreased process quality, abnormal
|
resection: cardiac ventricle, chemical treatment: 4-methylumbelliferone
|
Fig. 3
from Missinato et al., 2015
|
cardiac muscle tissue regeneration increased rate, abnormal
|
chemical treatment by injection: (2E)-2-benzylidene-3-(cyclohexylamino)indan-1-one, resection: cardiac ventricle
|
Fig. 5
from Missinato et al., 2018
|
cardiac muscle tissue regeneration increased rate, abnormal
|
chemical treatment by injection: BCI-215, resection: cardiac ventricle
|
Fig. 5
from Missinato et al., 2018
|
caudal artery morphology, normal
|
standard conditions
|
Fig. 4
from Liu et al., 2008
|
caudal fin morphology, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride
|
Fig. 4
from Alharthy et al., 2017
|
caudal fin morphology, abnormal
|
chemical treatment by environment: benzo[a]pyrene
|
Fig. 4
from Alharthy et al., 2017
|
caudal fin morphology, ameliorated
|
chemical treatment by environment: Fadrozole hydrochloride, chemical treatment by environment: 17beta-estradiol
|
Fig. 4
from Alharthy et al., 2017
|
caudal fin morphology, exacerbated
|
chemical treatment by environment: benzo[a]pyrene, chemical treatment by environment: 17beta-estradiol
|
Fig. 4
from Alharthy et al., 2017
|
caudal fin vasculature blood vessel endothelial cell disorganized, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 2
from Yan et al., 2018
|
caudal fin vasculature blood vessel endothelial cell increased permeability, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 2
from Yan et al., 2018
|
caudal fin vasculature blood vessel endothelial cell morphology, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 2
from Yan et al., 2018
|
caudal fin vasculature blood vessel endothelial cell thickness, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 2
from Yan et al., 2018
|
caudal fin vasculature cholesteryl ester increased amount, abnormal
|
high cholesterol
|
Fig. 5
from Han et al., 2018
|
caudal hematopoietic tissue carcinoma present, abnormal
|
cancer xenotransplantation
|
Fig. 1
from Varanda et al., 2020
|
caudal vein morphology, normal
|
standard conditions
|
Fig. 4
from Liu et al., 2008
|
caudal vein blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
caudal vein blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
caudal vein blood circulation decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
caudal vein lipid amount, ameliorated
|
chemical treatment by diet: cholesterol, chemical treatment by environment: ezetimibe
|
Fig. 1,
Fig. 5
from Yan et al., 2018
|
caudal vein lipid increased amount, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 1,
Fig. 5
from Yan et al., 2018
|
caudal vein plexus decreased area, abnormal
|
chemical treatment: SU6656
|
Figure 6
from Wisniewski et al., 2020
|
caudal vein plexus decreased area, abnormal
|
chemical treatment: PP2
|
Figure 6
from Wisniewski et al., 2020
|
caudal vein plexus decreased width, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Wakayama et al., 2015
|
caudal vein plexus decreased width, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Wakayama et al., 2015
|
caudal vein plexus dilated, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus ephb4a expression increased amount, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus efnb2a expression increased amount, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus efnb2a expression increased distribution, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus ephb4a expression increased distribution, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus malformed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Wakayama et al., 2015
|
caudal vein plexus efnb2a expression mislocalised, abnormal
|
chemical treatment by environment: DMH1
|
Fig. 6
from Esser et al., 2018
|
caudal vein plexus morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 7
from Huang et al., 2008
|
caudal vein plexus morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from De Smet et al., 2014
|
caudal vein plexus morphology, normal
|
chemical treatment: semaxanib
|
Fig. 9
from Ben Shoham et al., 2012
|
caudal vein plexus structure, abnormal
|
chemical treatment: PP2
|
Figure 6
from Wisniewski et al., 2020
|
caudal vein plexus structure, abnormal
|
chemical treatment: SU6656
|
Figure 6
from Wisniewski et al., 2020
|
caudal vein plexus blood vessel development process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from De Smet et al., 2014
|
caudal vein plexus capillary decreased amount, abnormal
|
chemical treatment by environment: zinc atom
|
Fig. 5
from Xia et al., 2020
|
caudal vein plexus sprouting angiogenesis process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Wakayama et al., 2015
|
central artery absent, abnormal
|
chemical treatment by environment: lead diacetate
|
Fig. 5
from Roy et al., 2014
|
central artery decreased length, abnormal
|
chemical treatment by environment: lead diacetate
|
Fig. 6
from Roy et al., 2014
|
ceratobranchial 5 replacement tooth dissociated from pharyngeal arch 7 blood vessel, abnormal
|
chemical treatment: semaxanib
|
Fig. 4
from Crucke et al., 2015
|
ceratobranchial 5 replacement tooth odontogenesis rate, normal
|
chemical treatment: semaxanib
|
Fig. 2
from Crucke et al., 2015
|
ceratobranchial 5 replacement tooth odontogenesis variability of rate, abnormal
|
chemical treatment: semaxanib
|
Fig. 3
from Crucke et al., 2015
|
ceratohyal cartilage chondroblast disorganized, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Ning et al., 2013
|
ceratohyal cartilage chondrocyte differentiation process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Ning et al., 2013
|
chondrocyte Ab2-cspg4 labeling decreased amount, abnormal
|
chemical treatment by environment: SB 505124
|
Fig. 6
from Flanagan-Steet et al., 2018
|
cranial blood vessel has normal numbers of parts of type primordial hindbrain channel, normal
|
control
|
Fig. 2
from Cohen et al., 2020
|
dorsal aorta broken, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 3
from Li et al., 2016
|
dorsal aorta decreased width, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 2
from Li et al., 2016
|
dorsal aorta morphology, abnormal
|
chemical treatment by environment: fucoidan
|
Figure 8
from Bae et al., 2020
|
dorsal aorta morphology, abnormal
|
chemical treatment by environment: eupatilin
|
Fig. 8
from Lee et al., 2020
|
dorsal aorta morphology, normal
|
standard conditions
|
Fig. 4
from Liu et al., 2008
|
dorsal aorta blood vessel endothelial cell decreased length, abnormal
|
chemical treatment: blebbistatin
|
Fig. 8
from Hultin et al., 2014
|
dorsal aorta blood vessel lumenization decreased process quality, abnormal
|
chemical treatment: blebbistatin
|
Fig. 8
from Hultin et al., 2014
|
dorsal aorta endothelial cell morphogenesis decreased process quality, abnormal
|
chemical treatment: blebbistatin
|
Fig. 8
from Hultin et al., 2014
|
dorsal aorta lipid amount, ameliorated
|
chemical treatment by diet: cholesterol, chemical treatment by environment: ezetimibe
|
Fig. 1,
Fig. 5
from Yan et al., 2018
|
dorsal aorta lipid increased amount, abnormal
|
chemical treatment by diet: cholesterol
|
Fig. 1,
Fig. 5
from Yan et al., 2018
|
dorsal aorta morphogenesis decreased process quality, abnormal
|
chemical treatment: blebbistatin
|
Fig. 8
from Hultin et al., 2014
|
dorsal longitudinal anastomotic vessel aplastic, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Lee et al., 2014
|
dorsal longitudinal anastomotic vessel aplastic, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Lee et al., 2014
|
dorsal longitudinal anastomotic vessel aplastic, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Lee et al., 2014
|
dorsal longitudinal anastomotic vessel constricted, abnormal
|
chemical treatment by environment: diacetylmonoxime
|
Fig. 7
from Nakajima et al., 2017
|
dorsal longitudinal anastomotic vessel disassembled, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 2
from De Smet et al., 2014
|
dorsal longitudinal anastomotic vessel hypoplastic, abnormal
|
chemical treatment: antagonist
|
Fig. 1
from Chen et al., 2017
|
dorsal longitudinal anastomotic vessel malformed, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
dorsal longitudinal anastomotic vessel morphology, abnormal
|
chemical treatment by environment: diacetylmonoxime
|
Fig. 7
from Nakajima et al., 2017
|
dorsal longitudinal anastomotic vessel morphology, abnormal
|
chemical treatment by environment: fucoidan
|
Figure 8
from Bae et al., 2020
|
dorsal longitudinal anastomotic vessel morphology, abnormal
|
chemical treatment by environment: eupatilin
|
Fig. 8
from Lee et al., 2020
|
dorsal longitudinal anastomotic vessel split, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
dorsal longitudinal anastomotic vessel truncated, abnormal
|
chemical treatment by environment: semaxanib
|
Fig. 3
from Carretero-Ortega et al., 2019
|
dorsal longitudinal anastomotic vessel blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
dorsal longitudinal anastomotic vessel blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
dorsal longitudinal anastomotic vessel endothelial cell detached from dorsal longitudinal anastomotic vessel endothelial cell, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 2
from De Smet et al., 2014
|
dorsal longitudinal anastomotic vessel sprouting angiogenesis decreased occurrence, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
embryonic pectoral fin morphogenesis process quality, abnormal
|
chemical treatment: thalidomide
|
Fig. S18
from Ito et al., 2010
|
endocardial cushion aplastic, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Banjo et al., 2013
|
endocardium cell decreased amount, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 5
from Sarmah et al., 2017
|
endothelial cell tjp1a expression increased amount, abnormal
|
chemical treatment by gavage: bexarotene, chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
endothelial cell tjp1a expression increased amount, abnormal
|
chemical treatment by gavage: isotretinoin, chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
endothelial cell tjp1b expression increased amount, abnormal
|
chemical treatment by gavage: bexarotene, chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
endothelial cell cell-cell junction ab1-tjp1 labeling spatial pattern, abnormal
|
chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
endothelial cell cell-cell junction ab1-tjp1 labeling spatial pattern, ameliorated
|
chemical treatment by gavage: bexarotene, chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
endothelial cell cell-cell junction ab1-tjp1 labeling spatial pattern, ameliorated
|
chemical treatment by gavage: isotretinoin, chemical treatment by injection: doxorubicin
|
Fig. 6
from Ma et al., 2020
|
epithelial cell protruding, abnormal
|
bacterial treatment by injection: Escherichia coli
|
Fig. 2
from Barber et al., 2016
|
eye decreased size, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride, chemical treatment by environment: 17beta-estradiol
|
Fig. 3
from Alharthy et al., 2017
|
eye decreased size, abnormal
|
chemical treatment by environment: 17beta-estradiol
|
Fig. 3
from Alharthy et al., 2017
|
eye decreased size, abnormal
|
chemical treatment by environment: benzo[a]pyrene, chemical treatment by environment: 17beta-estradiol
|
Fig. 3
from Alharthy et al., 2017
|
eye decreased size, abnormal
|
chemical treatment by environment: benzo[a]pyrene
|
Fig. 3
from Alharthy et al., 2017
|
eye decreased size, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride
|
Fig. 3
from Alharthy et al., 2017
|
eye carcinoma decreased size, ameliorated
|
cancer xenotransplantation, chemical treatment by environment: quininib
|
Figure 10
from Slater et al., 2020
|
eye carcinoma decreased size, ameliorated
|
chemical treatment by environment: montelukast, cancer xenotransplantation
|
Figure 10
from Slater et al., 2020
|
eye carcinoma present, abnormal
|
cancer xenotransplantation
|
Figure 10
from Slater et al., 2020
|
fin regeneration disrupted, abnormal
|
chemical treatment by injection: heparin, amputation: caudal fin
|
Fig. 7
from Farwell et al., 2017
|
gut angiogenesis decreased occurrence, abnormal
|
chemical treatment by injection: docosahexaenoic acid
|
Fig. 4
from Wang et al., 2016
|
gut blood vasculature decreased branchiness, abnormal
|
chemical treatment by injection: docosahexaenoic acid
|
Fig. 4
from Wang et al., 2016
|
hatching decreased occurrence, abnormal
|
chemical treatment by environment: benzo[a]pyrene, chemical treatment by environment: 17beta-estradiol
|
Fig. 2
from Alharthy et al., 2017
|
hatching decreased occurrence, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride
|
Fig. 2
from Alharthy et al., 2017
|
hatching decreased occurrence, abnormal
|
chemical treatment by environment: benzo[a]pyrene
|
Fig. 2
from Alharthy et al., 2017
|
hatching decreased occurrence, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride, chemical treatment by environment: 17beta-estradiol
|
Fig. 2
from Alharthy et al., 2017
|
heart straight, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 1
from Sarmah et al., 2016
|
heart contraction arrested, abnormal
|
chemical treatment by environment: diacetylmonoxime
|
Fig. 7
from Nakajima et al., 2017
|
heart contraction increased rate, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 1
from Sarmah et al., 2016
|
heart valve development disrupted, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Banjo et al., 2013
|
hyaloid vessel branchiness, abnormal
|
chemical treatment: LY294002
|
Fig. 5
from Alvarez et al., 2009
|
hyaloid vessel decreased branchiness, abnormal
|
chemical treatment: SH-11037
|
Fig. 2
from Sulaiman et al., 2016
|
hyaloid vessel irregular spatial pattern, abnormal
|
chemical treatment: LY294002
|
Fig. 1 ,
Fig. 4
from Alvarez et al., 2009
|
hyaloid vessel irregular spatial pattern, abnormal
|
chemical treatment: EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
|
Fig. 4
from Alvarez et al., 2009
|
hyaloid vessel angiogenesis decreased occurrence, abnormal
|
chemical treatment by environment: sunitinib
|
Fig. 4
from Ward et al., 2019
|
hyaloid vessel angiogenesis decreased occurrence, abnormal
|
chemical treatment: SH-11037
|
Fig. 2
from Sulaiman et al., 2016
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
hyaloid vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sasore et al., 2014
|
intersegmental artery absent, abnormal
|
angiogenesis inhibitor: anti-angiogenic agent
|
Fig. 4
from Venkateswaran et al., 2014
|
intersegmental artery decreased width, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 2
from Li et al., 2016
|
intersegmental artery morphology, abnormal
|
chemical treatment by environment: ethanol
|
Fig. 3
from Li et al., 2016
|
intersegmental vein absent, abnormal
|
angiogenesis inhibitor: anti-angiogenic agent
|
Fig. 4
from Venkateswaran et al., 2014
|
intersegmental vessel aplastic, abnormal
|
chemical treatment: vascular endothelial growth factor receptor antagonist
|
Fig. 4
from Monteiro et al., 2016
|
intersegmental vessel aplastic, abnormal
|
chemical treatment: wortmannin
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel aplastic, abnormal
|
chemical treatment: U0126
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel brochidodromous, abnormal
|
chemical treatment: wortmannin
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel brochidodromous, abnormal
|
chemical treatment: U0126
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel collapsed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 2
from De Smet et al., 2014
|
intersegmental vessel decreased functionality, abnormal
|
chemical treatment: herbicide
|
Fig. 5
from Kalén et al., 2009
|
intersegmental vessel decreased length, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
intersegmental vessel decreased length, abnormal
|
chemical treatment by environment: ponatinib
|
Fig. 1
from Ai et al., 2018
|
intersegmental vessel decreased length, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Cho et al., 2013
|
intersegmental vessel decreased size, abnormal
|
chemical treatment by environment: ponatinib
|
Fig. 1
from Ai et al., 2018
|
intersegmental vessel disassembled, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 2
from De Smet et al., 2014
|
intersegmental vessel disorganized, abnormal
|
chemical treatment: wortmannin
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel disorganized, abnormal
|
chemical treatment: U0126
|
Fig. S8
from Liu et al., 2008
|
intersegmental vessel disorganized, abnormal
|
chemical treatment: DAPT
|
Fig. 4
from Jensen et al., 2012
|
intersegmental vessel has extra parts of type vascular sprouts, abnormal
|
chemical treatment: DAPT
|
Fig. 4
from Jensen et al., 2012
|
intersegmental vessel has extra parts of type blood vessel, abnormal
|
chemical treatment: DAPT
|
Fig. 4
from Jensen et al., 2012
|
intersegmental vessel hypoplastic, abnormal
|
chemical treatment: antagonist
|
Fig. 1
from Chen et al., 2017
|
intersegmental vessel hypoplastic, abnormal
|
chemical treatment by environment: glycyrrhetinic acid
|
Fig. 6
from Li et al., 2019
|
intersegmental vessel immature, abnormal
|
chemical treatment by environment: semaxanib
|
Fig. S10
from Fu et al., 2017
|
intersegmental vessel immature, abnormal
|
chemical treatment: semaxanib
|
Fig. 1
from Crucke et al., 2015
|
intersegmental vessel increased branchiness, abnormal
|
chemical treatment by injection: oxidised phospholipid
|
Fig. 6
from Hitzel et al., 2018
|
intersegmental vessel increased mass density, abnormal
|
chemical treatment: DAPT
|
Fig. 4
from Jensen et al., 2012
|
intersegmental vessel malformed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Lee et al., 2014
|
intersegmental vessel malformed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Lee et al., 2014
|
intersegmental vessel malformed, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Lee et al., 2014
|
intersegmental vessel morphology, abnormal
|
chemical treatment by environment: fucoidan
|
Figure 8
from Bae et al., 2020
|
intersegmental vessel morphology, abnormal
|
radiation
|
Fig. 5,
Fig. 6,
Fig. 7
from Dong et al., 2008
|
intersegmental vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
intersegmental vessel morphology, abnormal
|
chemical treatment: methylglyoxal
|
Fig. 2
from Lodd et al., 2019
|
intersegmental vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Jörgens et al., 2015
|
intersegmental vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
intersegmental vessel morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3,
Fig. 7
from Chen et al., 2012
|
intersegmental vessel morphology, abnormal
|
chemical treatment by injection: oxidised phospholipid
|
Fig. 6
from Hitzel et al., 2018
|
intersegmental vessel morphology, abnormal
|
chemical treatment: butan-1-ol
|
Fig. 7
from Zeng et al., 2009
|
intersegmental vessel morphology, normal
|
standard conditions
|
Fig. 4
from Liu et al., 2008
|
intersegmental vessel non-functional, abnormal
|
chemical treatment by environment: glycyrrhetinic acid
|
Fig. 6
from Li et al., 2019
|
intersegmental vessel normal length, normal
|
chemical treatment by environment: NAD
|
Fig. 2
from Bailey et al., 2019
|
intersegmental vessel shortened, abnormal
|
constant light
|
Fig. 1
from Jensen et al., 2012
|
intersegmental vessel structure, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1
from Jörgens et al., 2015
|
intersegmental vessel structure, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
intersegmental vessel structure, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 1,
Fig. 5,
Fig. 6
from Jörgens et al., 2015
|
intersegmental vessel truncated, abnormal
|
chemical treatment by environment: semaxanib
|
Fig. 3
from Carretero-Ortega et al., 2019
|
intersegmental vessel angiogenesis disrupted, abnormal
|
chemical treatment by environment: cabozantinib
|
Fig. 1
from Wu et al., 2020
|
intersegmental vessel angiogenesis disrupted, abnormal
|
chemical treatment by environment: regorafenib
|
Fig. 1
from Wu et al., 2020
|
intersegmental vessel blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
intersegmental vessel blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
intersegmental vessel blood circulation absent, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 6
from Pruvot et al., 2014
|
intersegmental vessel blood vessel endothelial cell spade-shaped, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
intersegmental vessel carcinoma neoplastic, metastatic, abnormal
|
cancer xenotransplantation
|
Fig. 3
from Ganaie et al., 2018
|
intersegmental vessel cell junction morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sauteur et al., 2014
|
intersegmental vessel cell junction morphology, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sauteur et al., 2014
|
intersegmental vessel endothelial cell decreased adhesivity, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from De Smet et al., 2014
|
intersegmental vessel endothelial cell detached from intersegmental vessel endothelial cell, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 2
from De Smet et al., 2014
|
intersegmental vessel sprouting angiogenesis decreased occurrence, abnormal
|
chemical treatment by environment: SKF-96365 hydrochloride
|
Fig. 7
from Savage et al., 2019
|
intersegmental vessel sprouting angiogenesis decreased occurrence, abnormal
|
chemical treatment: antagonist
|
Fig. 1
from Chen et al., 2017
|
intersegmental vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from Sasore et al., 2014
|
intersegmental vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from Sasore et al., 2014
|
intersegmental vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from Sasore et al., 2014
|
intersegmental vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from Sasore et al., 2014
|
intersegmental vessel sprouting angiogenesis decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 3
from Sasore et al., 2014
|
intersegmental vessel unidimensional cell growth process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 5
from Sauteur et al., 2014
|
intestine vasculature branchiness, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Oehlers et al., 2011
|
intestine vasculature structure, normal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Oehlers et al., 2011
|
lateral zone of dorsal telencephalon blood cell dilated, abnormal
|
chemical treatment by environment: pentetrazol
|
Fig. 2
from Duy et al., 2017
|
lateral zone of dorsal telencephalon leukocyte increased amount, abnormal
|
chemical treatment by environment: pentetrazol
|
Fig. 2
from Duy et al., 2017
|
liver vasculature dilated, abnormal
|
chemical treatment: ethanol
|
Fig. S2
from Howarth et al., 2013
|
lymphangiogenesis disrupted, abnormal
|
chemical treatment: indometacin
|
Figure 1
from Iwasaki et al., 2019
|
lymphangiogenesis disrupted, ameliorated
|
chemical treatment: indometacin, chemical treatment: sulprostone
|
Figure 1
from Iwasaki et al., 2019
|
lymphangiogenic sprout absent, abnormal
|
chemical treatment by environment: SL-327
|
Fig. 4
from Shin et al., 2016
|
lymphangiogenic sprout Ab10-prox1 labeling absent, abnormal
|
chemical treatment by environment: SL-327
|
Fig. 4
from Shin et al., 2016
|
MAPK cascade disrupted, abnormal
|
chemical treatment: 2-(2-amino-3-methoxyphenyl)chromen-4-one
|
Fig. 4
from Le Guen et al., 2014
|
mid cerebral vein morphology, abnormal
|
chemical treatment by environment: lead diacetate
|
Fig. 5
from Roy et al., 2014
|
motor neuron axon guidance process quality, normal
|
chemical treatment: butan-1-ol
|
Fig. 7
from Zeng et al., 2009
|
ocular blood vessel decreased amount, abnormal
|
chemical treatment: EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
|
Fig. 4
from Alvarez et al., 2009
|
ocular blood vessel decreased amount, abnormal
|
chemical treatment: LY294002
|
Fig. 1 ,
Fig. 4 ,
Fig. 5
from Alvarez et al., 2009
|
ocular blood vessel diameter, ameliorated
|
chemical treatment by environment: PK-11195, chemical treatment by environment: 4-hydroxynon-2-enal
|
Fig. 9
from Lou et al., 2020
|
ocular blood vessel immature, abnormal
|
chemical treatment by environment: Maxacalcitol
|
Fig. 4
from Merrigan et al., 2020
|
ocular blood vessel increased diameter, abnormal
|
chemical treatment by environment: 4-hydroxynon-2-enal
|
Fig. 9
from Lou et al., 2020
|
ocular blood vessel increased thickness, abnormal
|
chemical treatment: glucose
|
Fig. 1
from Alvarez et al., 2010
|
ocular blood vessel adherens junction increased width, abnormal
|
chemical treatment: D-mannitol
|
Fig. 2
from Alvarez et al., 2010
|
ocular blood vessel adherens junction increased width, abnormal
|
chemical treatment: glucose
|
Fig. 2
from Alvarez et al., 2010
|
ocular blood vessel basement membrane increased thickness, abnormal
|
chemical treatment: glucose
|
Fig. 2
from Alvarez et al., 2010
|
ocular blood vessel bicellular tight junction increased width, abnormal
|
chemical treatment: glucose
|
Fig. 2
from Alvarez et al., 2010
|
ocular blood vessel bicellular tight junction increased width, abnormal
|
chemical treatment: D-mannitol
|
Fig. 2
from Alvarez et al., 2010
|
ocular blood vessel sprouting angiogenesis increased occurrence, abnormal
|
chemical treatment by environment: 4-hydroxynon-2-enal
|
Fig. 9
from Lou et al., 2020
|
ocular blood vessel sprouting angiogenesis occurrence, ameliorated
|
chemical treatment by environment: PK-11195, chemical treatment by environment: 4-hydroxynon-2-enal
|
Fig. 9
from Lou et al., 2020
|
optic artery vascular endothelium increased thickness, abnormal
|
high cholesterol, high glucose
|
Fig. 2
from Wang et al., 2013
|
optic artery vascular endothelium thickness, ameliorated
|
high cholesterol, high glucose, chemical treatment: metformin
|
Fig. 2
from Wang et al., 2013
|
optic artery vascular endothelium thickness, ameliorated
|
high cholesterol, high glucose, chemical treatment: pioglitazone
|
Fig. 2
from Wang et al., 2013
|
optokinetic behavior occurrence, normal
|
chemical treatment: LY294002
|
Fig. 8
from Alvarez et al., 2009
|
optomotor response decreased occurrence, abnormal
|
chemical treatment by environment: sunitinib
|
Fig. 4
from Ward et al., 2019
|
palatoquadrate cartilage chondroblast disorganized, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Ning et al., 2013
|
palatoquadrate cartilage chondrocyte differentiation process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Ning et al., 2013
|
parachordal vessel absent, abnormal
|
chemical treatment by environment: SL-327
|
Fig. 4
from Shin et al., 2016
|
parachordal vessel vasculature development decreased occurrence, abnormal
|
chemical treatment by environment: SL-327
|
Fig. 4
from Shin et al., 2016
|
pectoral fin morphology, abnormal
|
chemical treatment by environment: benzo[a]pyrene
|
Fig. 4
from Alharthy et al., 2017
|
pectoral fin morphology, exacerbated
|
chemical treatment by environment: benzo[a]pyrene, chemical treatment by environment: 17beta-estradiol
|
Fig. 4
from Alharthy et al., 2017
|
pectoral fin blood vessel aplastic, abnormal
|
chemical treatment: thalidomide
|
Fig. S18
from Ito et al., 2010
|
pectoral fin bud decreased size, abnormal
|
chemical treatment: thalidomide
|
Fig. S18
from Ito et al., 2010
|
pericardium edematous, abnormal
|
chemical treatment by environment: Fadrozole hydrochloride
|
Fig. 3
from Alharthy et al., 2017
|
pericardium edematous, abnormal
|
chemical treatment by environment: benzo[a]pyrene
|
Fig. 3
from Alharthy et al., 2017
|
pericardium edematous, abnormal
|
chemical treatment: SH-11037
|
Fig. 2
from Sulaiman et al., 2016
|
pericardium edematous, abnormal
|
bacterial treatment by injection: Waddlia chondrophila WSU 86-1044
|
Fig. 4
from Fehr et al., 2016
|
pericardium edematous, ameliorated
|
chemical treatment by environment: Fadrozole hydrochloride, chemical treatment by environment: 17beta-estradiol
|
Fig. 3
from Alharthy et al., 2017
|
pericardium edematous, ameliorated
|
chemical treatment by environment: benzo[a]pyrene, chemical treatment by environment: 17beta-estradiol
|
Fig. 3
from Alharthy et al., 2017
|
phagocytosis process quality, normal
|
fungal treatment by injection: Candida albicans
|
Fig. 2
from Brothers et al., 2011
|
pharyngeal arch EGFP expression decreased amount, abnormal
|
standard conditions
|
Fig. 6
from Chen et al., 2018
|
pharyngeal arch cell population proliferation decreased process quality, abnormal
|
chemical treatment: pharmaceutical
|
Fig. 4
from Ning et al., 2013
|
post-vent region carcinoma neoplastic, metastatic, abnormal
|
cancer xenotransplantation
|
Fig. 3
from Ganaie et al., 2018
|
post-vent region neoplasm increased amount, abnormal
|
cancer xenotransplantation
|
Fig. 1
from Baltrunaite et al., 2017
|
posterior cardinal vein morphology, normal
|
standard conditions
|
Fig. 4
from Liu et al., 2008
|
posterior caudal vein vascular sprouts absent, abnormal
|
chemical treatment by environment: SL-327
|
Fig. 4
from Shin et al., 2016
|
primary motor neuron branched, abnormal
|
chemical treatment: butan-1-ol
|
Fig. 7
from Zeng et al., 2009
|
primordial hindbrain channel angiogenesis normal process quality, normal
|
control
|
Fig. 2
from Cohen et al., 2020
|
regenerating fin lmo2 expression increased amount, abnormal
|
resection: caudal fin
|
Fig. 5
from Meng et al., 2016
|
regenerating fin tek expression increased amount, abnormal
|
resection: caudal fin
|
Fig. 5
from Meng et al., 2016
|
regenerating fin angiogenesis decreased process quality, abnormal
|
amputation: caudal fin, chemical treatment: BGJ-398
|
Fig. 5
from De Smet et al., 2014
|
regenerating fin angiogenic sprout increased amount, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
Fig. 2
from Khatib et al., 2016
|
regenerating fin artery absent, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
text only
from Ma et al., 2017
|
regenerating fin blood vessel disorganized, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
text only
from Ma et al., 2017
|
regenerating fin blood vessel remodeling decreased occurrence, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
Fig. 2
from Khatib et al., 2016
|
regenerating fin blood vessel remodeling disrupted, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
text only
from Ma et al., 2017
|
regenerating fin endothelial cell proliferation decreased occurrence, abnormal
|
chemical treatment by injection: heparin, amputation: caudal fin
|
Fig. 7
from Farwell et al., 2017
|
regenerating fin vasculature development disrupted, abnormal
|
chemical treatment by injection: heparin, amputation: caudal fin
|
Fig. 6 ,
Fig. 7
from Farwell et al., 2017
|
regenerating fin vein absent, abnormal
|
chemical treatment by environment: cobalt dichloride, amputation: caudal fin
|
text only
from Ma et al., 2017
|
regenerating tissue jag2b expression decreased amount, abnormal
|
chemical treatment by environment: GI254023X, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue jag2b expression decreased amount, abnormal
|
chemical treatment by environment: environmental contaminant, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue dll4 expression decreased amount, abnormal
|
chemical treatment by environment: GI254023X, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue dll4 expression decreased amount, abnormal
|
chemical treatment by environment: environmental contaminant, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue hey2 expression decreased amount, abnormal
|
chemical treatment by environment: GI254023X, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue hey2 expression decreased amount, abnormal
|
chemical treatment by environment: environmental contaminant, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue jag1a expression decreased amount, abnormal
|
chemical treatment by environment: GI254023X, amputation: caudal fin
|
Fig. 2
from Baek et al., 2017
|
regenerating tissue jag1a expression decreased amount, abnormal |