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1 s (CA) are common vascular anomalies causing brain hemorrhage.
2 al vascular morphogenesis and do not exhibit brain hemorrhage.
3 iven 60 minutes after occlusion but provoked brain hemorrhage.
4 tal discharge and none developed symptomatic brain hemorrhage.
5  not induce reperfusion and induced striking brain hemorrhage.
6 l artery stroke, without thrombocytopenia or brain hemorrhage.
7 th subsequent cerebral edema and devastating brain hemorrhage.
8 ith respiratory failure and intraparenchymal brain hemorrhage.
9 al signs of CM, associated with perivascular brain hemorrhage.
10 based study of the late sequelae of neonatal brain hemorrhage.
11  brain-dead male human recipient following a brain hemorrhage.
12 e observe hindbrain ventricular swelling and brain hemorrhage.
13 at 75 vol% reduces ischemic brain damage and brain hemorrhages.
14 tion of tissue plasminogen activator-induced brain hemorrhages.
15  survived the infection and had little or no brain hemorrhaging.
16 n addition, we tested whether HAE-4 provoked brain hemorrhages, a component of amyloid-related imagin
17 roprotective activities, blocks tPA-mediated brain hemorrhage after transient brain ischemia and embo
18 cificities between 8% (two of 25 images) for brain hemorrhage and 52% (13 of 25 images) for pneumotho
19 ascular and immune cells that contributes to brain hemorrhage and catalog opportunities for targeting
20 min exposure, a model of secondary injury in brain hemorrhage and ferroptosis, activated ERK1/2 in mo
21                     CAA is a common cause of brain hemorrhage and is found in most patients with AD.
22 nts with life-threatening conditions such as brain hemorrhage and ischemic stroke.
23 fusion-induced vascular injury and secondary brain hemorrhage and offers a unique opportunity to eval
24 chemic stroke and 100% (25 of 25 images) for brain hemorrhage and specificities between 8% (two of 25
25 s, 145 had prior infarct, 8 had hypertensive brain hemorrhage, and 164 admissions for PSR were identi
26 a-induced fl02k mutant showed heart failure, brain hemorrhage, and diminished cardiac and vessel lume
27 cularly in patients who are at high risk for brain hemorrhage, and thus provide a new approach for th
28  lens led to neuronal and lens degeneration, brain hemorrhages, and neonatal death.
29 nifestations, including embryonic lethality; brain hemorrhage; and vasculogenic, craniofacial, and ne
30 botic ischemic stroke but is associated with brain hemorrhage; antiplatelet therapy has limited effic
31 ubstantial progress in the identification of brain hemorrhage areas.
32 lth, diabetes mellitus, history of stroke or brain hemorrhage, cognitive function, and self-reported
33 ective endocarditis, with suspected subdural brain hemorrhage, disseminated intravascular coagulopath
34 rate to severe ischemic stroke (HR 1.63) and brain hemorrhage (HR 1.73) were significantly associated
35 rium Borrelia turicatae rapidly succumb to a brain hemorrhage if they are unable to clear peak bacter
36  of 1 or 2 copies of the Thbd gene decreases brain hemorrhage in Pdcd10 (ECKO) mice.
37 myloid angiopathy (CAA) is a common cause of brain hemorrhage in the elderly.
38 ant is deposited in arterial walls and cause brain hemorrhage in young adults.
39 P kinase kinase (MEK) inhibitor U0126 blocks brain hemorrhage-induced death.
40                                              Brain hemorrhage is a serious complication of tissue pla
41                                              Brain hemorrhage is a severe complication of both neopla
42 ge and perinatal death, but the mechanism of brain hemorrhage is unknown.
43     Exogenous NO provided protection against brain hemorrhages (mean, 1.4 vs 24.5 hemorrhagic foci pe
44 neonates with cranial ultrasound evidence of brain hemorrhage, MITS of the brain showed intraventricu
45   The primary end point was ischemic stroke, brain hemorrhage, or death from vascular causes other th
46 x metalloproteinases, inflammation, and high brain hemorrhage rates.
47 ated Tn antigen in these cells and developed brain hemorrhage that was uniformly fatal by embryonic d
48 erebral artery, tPA administration increased brain hemorrhage transformation, infarct volume, and ede
49                                              Brain hemorrhage was more prevalent in patients who expe
50                                              Brain hemorrhage was unlikely to be simply a form of scu
51 stigate the role of tPA and microglia during brain hemorrhage, we induced experimentally ICH by intra
52       Moderate to severe ischemic stroke and brain hemorrhage were found to have a significant negati
53 ical dysfunction and reproducibly results in brain hemorrhages whose appearance is highly reminiscent
54                                     Rates of brain hemorrhage within 24 hours and mortality at 90 day