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1 ion, history of brain trauma or intracranial vascular malformations).
2 ts a vascular neoplasm, vascular anomaly, or vascular malformation.
3 cular anomaly could be a vascular tumor or a vascular malformation.
4 s were used to examine the cell capacity for vascular malformation.
5 tient 1 was an 8-mo-old girl with voluminous vascular malformation.
6 ut the presumed etiology was an unidentified vascular malformation.
7  p53 plays a direct role in formation of the vascular malformations.
8 d is frequently associated with intracranial vascular malformations.
9 lastoma multiforme and some other tumors and vascular malformations.
10 1), a disease characterised by bleeding from vascular malformations.
11             There were 49 hemangiomas and 38 vascular malformations.
12 re performed in three patients with low-flow vascular malformations.
13 giectasia (HHT1), a disease characterized by vascular malformations.
14 ins were widely patent without thrombosis or vascular malformations.
15 angiomas, consistent with other Sturge-Weber vascular malformations.
16 ECs) acquired mesenchymal markers and caused vascular malformations.
17 ile pericyte differentiation and hemorrhagic vascular malformations.
18 collectively contribute to the prevention of vascular malformations.
19  migration may represent a pathomechanism in vascular malformations.
20 approach for patients with KRAS G12C-related vascular malformations.
21 y or a different mechanism gives rise to the vascular malformations.
22 s in 3D and engineer fine structures such as vascular malformations.
23  predisposing stimuli for the development of vascular malformations.
24    This article focuses on the management of vascular malformations.
25  event in the pathogenesis of HHT-associated vascular malformations.
26        Transplantation of these cells caused vascular malformations.
27 ies into 2 major groups: vascular tumors and vascular malformations.
28 thologies, including brain tumours and brain vascular malformations.
29 ting angiogenic and inflammatory programs in vascular malformations.
30 to our knowledge, have not been described in vascular malformations.
31 nomalies, differentiating high- and low-flow vascular malformations.
32 Tie-2 in blue rubber bleb nevus and sporadic vascular malformations.
33 hways also contribute to atherosclerosis and vascular malformations.
34 d its involvement in two, if not more, human vascular malformations.
35 as (CHs) account for 5% to 12% of all spinal vascular malformations.
36  a potential strategy to treat patients with vascular malformations.
37 tracranial tumors, functional disorders, and vascular malformations.
38 uctive pulmonary disease, cancers, and brain vascular malformations.
39 deficiency or dysfunction is associated with vascular malformations.
40 eds produced CNS-specific hyperproliferative vascular malformations.
41 rment after surgery for epilepsy, tumours or vascular malformations.
42 to oxygen-induced remodeling without causing vascular malformations.
43 yrAkt led to embryonic lethality, edema, and vascular malformations.
44 oplasms, surgeries nearby sinuses and orbit, vascular malformations, acute sinusitis, systemic abnorm
45 s a neurocutaneous disorder characterized by vascular malformations affecting skin, eyes and leptomen
46                                              Vascular malformations, affecting 1% to 1.5% of the popu
47 S can be used to distinguish hemangioma from vascular malformation and detect arterial flow.
48 n and extracellular matrix, correlating with vascular malformation and increased basement membrane th
49 rain vascular innervation, contribute to the vascular malformation and its consequences.
50  levels reached 82.4%, accompanied by severe vascular malformation and steatosis in the liver.
51 ORC1 signaling in endothelial cells promotes vascular malformation and suggest that mTORC1 inhibitors
52 cidate the molecular pathogenesis of hepatic vascular malformation and the safety of therapeutics inh
53                          Given links between vascular malformations and angiosarcoma with activated R
54 genital portosystemic shunts (CPSS) are rare vascular malformations and can be classified into extrah
55 formations represent the most common form of vascular malformations and can cause recurrent bleeding
56 sruption of this mechanism may contribute to vascular malformations and disease.
57 ciency of HIF-1alpha resulted in cardiac and vascular malformations and embryonic lethality at E10.5.
58 e and prevented vessel maturation leading to vascular malformations and endotheliomas.
59  significantly higher for AVM than for other vascular malformations and hemangioma.
60 ents with HHT associated with severe hepatic vascular malformations and high cardiac output, administ
61 AS G12C inhibitor, in reducing the volume of vascular malformations and improving survival in two mou
62             Alk1HEC-KO mice revealed hepatic vascular malformations and increased posthepatic flow, c
63 S patients, include Hashimoto's thyroiditis, vascular malformations and mental retardation.
64 sed on melanoma; other skin diseases such as vascular malformations and psoriasis have also been exam
65                            None of 154 other vascular malformations and tumors harbored an IDH1 R132C
66 gnosis and topographical characterization of vascular malformations and tumors of cervicofacial area
67 stem causing hemorrhage-prone multiple lumen vascular malformations and very severe neurological cons
68 ng seizures for LEAT, 74.0% (328 of 443) for vascular malformation, and 71.5% (2108 of 2948) for hipp
69 atic seizures after presentation, ICH due to vascular malformation, and elevated intracranial pressur
70 sy associated neuroepithelial tumour (LEAT), vascular malformation, and hippocampal sclerosis had the
71 cal issues for patients with hemangiomas and vascular malformations, and (4) the elucidation of seque
72 via the ALK5-SMAD2 signaling induces retinal vascular malformations, and have therapeutic values for
73 morrhagic telangiectasia (HHT), severe liver vascular malformations are associated with mutations in
74                                              Vascular malformations are caused by germline or somatic
75                               Alternatively, vascular malformations are embryologic errors in vasculo
76 ns that underlie the formation of many human vascular malformations are known, the extent to which ab
77                                              Vascular malformations are linked to mutations in RAS p2
78                                              Vascular malformations are non-neoplastic expansions of
79  the cellular and molecular events governing vascular malformations are not yet fully understood.
80                                        Dural vascular malformations are often elusive on all cross-se
81                            In addition, many vascular malformations are related to deregulation of TG
82                                              Vascular malformations are thought to be monogenic disor
83                                   Congenital vascular malformations are tumour-like, non-neoplastic l
84 ism analogous to cancer, in which aggressive vascular malformations arise through the loss of vascula
85                                              Vascular malformations, arterial aneurysms and dissectio
86                  Viewing atherosclerosis and vascular malformations as instances of pathological morp
87 ) may represent a hyperplastic response to a vascular malformation, but the precise etiology remains
88 ascular development and to prevent postnatal vascular malformations, but its molecular effectors are
89                                        Human vascular malformations cause disease as a result of chan
90 ure, which has potential relevance for human vascular malformations caused by EPHB4 mutations.
91 me is a progressive overgrowth disorder with vascular malformations caused by mosaic expression of th
92 ral cavernous malformations (CCMs) are human vascular malformations caused by mutations in three gene
93                  One prevalent form of these vascular malformations, cerebral cavernous malformation,
94 ngiectasia (HHT) is an inherited disorder of vascular malformations characterized by mucocutaneous te
95                                 All targeted vascular malformation compartments were filled with scle
96 om 26 patients in a cohort of mixed types of vascular malformation, comprising 2 fast-flow and 24 slo
97 r, and its deregulation is associated with a vascular malformation consistent with Klippel-Trenaunay
98  primary outcome was change in the volume of vascular malformations detected on magnetic resonance im
99                  Variations in the volume of vascular malformations detected on magnetic resonance im
100 coding SMAD4) or BMPR1A, and the latter is a vascular malformation disorder caused by mutations in EN
101 diologists must identify the MRI features of vascular malformations for better diagnosis and classifi
102            Furthermore, enlarged vessels and vascular malformations form in either the presence or ab
103 or T2-weighted imaging for low-grade tumors, vascular malformations, gliosis after infarction, inflam
104 hin the CPA, including meningiomas, lipomas, vascular malformations, hemangiomas, epidermoid cysts, c
105  potential therapeutic targets against these vascular malformations identified so far, as well as the
106                                         This vascular malformation, if undetected, can lead to seriou
107 genesis may contribute to the development of vascular malformation in IUGR, but in vitro these change
108 us malformations (CCMs) are a common type of vascular malformation in the brain that are a major caus
109 escued flow migration coupling and prevented vascular malformations in Alk1-deficient mice.
110 inactivation of Klf4 reduces the severity of vascular malformations in Cdc42 mutant mice.
111  beta-catenin transcription activity, reduce vascular malformations in endothelial CCM3-deficient mic
112  are dysregulated during the pathogenesis of vascular malformations in HHT.
113 ) mutation of this domain is associated with vascular malformations in humans.
114 lockers are new potential targets to prevent vascular malformations in patients with hereditary hemor
115  MAP2K1 is sufficient for the development of vascular malformations in the brain, ear, and intestines
116 autosomal dominant disease that manifests as vascular malformations in the brain, lung, liver, gastro
117 he Id1-Id3 double knockout mice also display vascular malformations in the forebrain and an absence o
118 atients; mean age, 32.9 years +/- 14.1) with vascular malformations in the head and neck (n = 64), sp
119 rapping around VEGF-producing fibers, and of vascular malformations in the muscle at high levels, did
120 a scintigraphic image of familial congenital vascular malformations in two sisters.
121 els, defective angiogenic remodeling, severe vascular malformations including arterio-venous malforma
122 nd arteriovenous identities are disrupted in vascular malformations including arteriovenous shunts, t
123  P/LP variants were previously unreported in vascular malformation, including those from HRAS, PIK3CA
124                                              Vascular malformations, including angiodysplasia and Die
125 bral haemorrhage resulting from intracranial vascular malformation, intracranial venous thrombosis, h
126 dothelium-selective Grk2 ablation had marked vascular malformations involving impaired recruitment of
127                                              Vascular malformation is subclassified into fast-flow, i
128 d homeostasis and how mutations give rise to vascular malformations is not well understood.
129 umor cells and also seen in two benign human vascular malformations, juvenile angiofibromas and infan
130 cavernous malformation (CCM) is a disease of vascular malformations known to be caused by mutations i
131 ith pCLAs and 72% of participants with other vascular malformations, leading to a new medical therapy
132 redictor for differentiating hemangioma from vascular malformation (likelihood ratio test = 109.8, P
133 nal period and the observational period (all vascular malformations: mean [SD] difference, -0.001 [0.
134 Alk1-conditional deletion resulted in severe vascular malformations mimicking all pathologic features
135 a, benign peripheral nerve sheath tumor, and vascular malformation (n = 192) were included.
136 a, benign peripheral nerve sheath tumor, and vascular malformation (n = 192) were included.
137 rogenic procedures (n = 14, 16%), congenital vascular malformations (n = 13, 15%), tumor (n = 13, 15%
138 n of both normal retinal anatomy, as well as vascular malformations, nonperfusion, and neovasculariza
139 vent the increase in permeability and retina vascular malformations observed in the absence of Sox17.
140 an exhibiting a systemic vascular phenotype, vascular malformations occur as focal lesions in discret
141                              The majority of vascular malformations occur sporadically; however, inhe
142                     Of the 378 patients with vascular malformation of the lower limbs, 19 patients (5
143 th headache, scalp defects and structural or vascular malformations of the brain.
144  Cerebral Cavernous Malformations (CCMs) are vascular malformations of the central nervous system whi
145 ons (CCMs) are common sporadic and inherited vascular malformations of the central nervous system.
146                                         Most vascular malformations of the head and neck require a mu
147  deafness, facial weakness, hypoventilation, vascular malformations of the internal carotid arteries
148                                              Vascular malformations often exhibit recurrent patterns
149 ipal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early
150  suspicion of neoplasm, bacterial infection, vascular malformation, or thyroid eye disease were exclu
151 ignificantly greater compared with the other vascular malformations (P < .001 in each case).
152                                              Vascular malformations pose a diagnostic and therapeutic
153  ALK1 signaling protects from development of vascular malformations preserving organ-specific endothe
154 other cellular properties in hemangiomas and vascular malformations relevant to vascular development,
155 es provides a state-of-the-art assessment of vascular malformation research at basic, clinical, genet
156 mportant in experimental stroke and cerebral vascular malformation research.
157 dilated and fragile blood vessels similar to vascular malformations seen in HHT patients.
158 temic thrombolysis in a patient with a known vascular malformation should be individualized.
159 agnosed disorders related to the presence of vascular malformations should undergo periodic follow-up
160           Mouse model of Pik3caH1047R-driven vascular malformations showed that proliferation was ind
161  and displayed reduced sprouting, leading to vascular malformations similar to those seen in humans w
162 rmed, and genomic DNA was extracted from the vascular malformation specimen and normal skin.
163 the cerebral vasculature, such as congenital vascular malformations, stroke and tumors, compromise ne
164                                The 3 primary vascular malformation subclassifications are lymphatic,
165 ibromatosis (NF1), nor is it associated with vascular malformations, such as in the recently reported
166           The genetic basis for a variety of vascular malformation syndromes have been described, wit
167               Genes responsible for familial vascular malformation syndromes have increasingly been s
168 ity pathways are good candidates for causing vascular malformation syndromes.
169 cyte protein of 76 kDa (SLP76) resulted in a vascular malformation that directed blood flow through m
170    Here, we focus on two of the most studied vascular malformations that are induced by deregulation
171              Cavernous angiomas are cerebral vascular malformations that are usually congenital.
172 pathological angiogenesis is angiodysplasia, vascular malformations that cause severe gastrointestina
173 ons (CCMs) are common inherited and sporadic vascular malformations that cause strokes and seizures i
174                                              Vascular malformations that occur inside bone tissue are
175 llary beds, and the formation of hemorrhagic vascular malformations that remain adherent to the menin
176                            Congenital cardio-vascular malformations, the most frequent birth defect,
177 in turn perpetuates reduced osteogenesis and vascular malformation through direct SSC-endothelial cro
178 s an autosomal dominant disorder that causes vascular malformations throughout the body.
179 ed to endothelial proliferative lesions from vascular malformations to vascular tumors in adult mice.
180 placental anomalies including thrombosis and vascular malformations, together with growth restriction
181 ve therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, p
182 and miR-155 knock-out in mice causes retinal vascular malformations typical of faulty maturation, mim
183 irming that mucocutaneous and internal organ vascular malformations undergo the same molecular mechan
184 meruloid microvascular proliferations (GMP), vascular malformations (VM), feeding arteries (FA), and
185 usative for autosomal-recessive intraosseous vascular malformation (VMOS) in five different families.
186                                              Vascular malformations (VMs) are rare disorders of vascu
187 HHT) is a Mendelian disease characterized by vascular malformations (VMs) including visceral arteriov
188 festations include skin and bony overgrowth, vascular malformations (VMs), cysts and benign tumors.
189 of PIK3CA are associated with development of vascular malformations (VMs).
190              Staged surgical excision of the vascular malformation was performed, and genomic DNA was
191 an adaptor protein whose mutation results in vascular malformations, we have found that it is involve
192  (<1 year), venous or orthopedic surgery, or vascular malformations were clinically stratified for CV
193  clinically based on stereotypical cutaneous vascular malformations were included.
194        In static and whole-body examinations vascular malformations were visualised in the area of th
195 rteriovenous malformations (AVMs) are common vascular malformations, which may result in hemorrhagic
196 data from the Scottish Audit of Intracranial Vascular Malformations, which prospectively identified i
197 children aged 6 to 18 years with a slow-flow vascular malformation who were recruited between Septemb
198 tinterventional perfusion changes within the vascular malformation with calculation of changes in con
199 nd without complications by filling targeted vascular malformations with sclerosing agent.
200 ial Notch1 from birth led to similar hepatic vascular malformations within 2 weeks.
201 ous malformations (AVMs) are the most common vascular malformations worldwide and the leading cause o
202 tion of hemangiomas (48 of 49) compared with vascular malformations (zero of 38) consisted of a solid

 
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