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1  not BBB dysfunction, underlie developmental cerebral hemorrhage.
2 pholino-induced suppression of foxc1 induced cerebral hemorrhage.
3 mproves functional outcome without producing cerebral hemorrhage.
4  surgical procedure and 1 death secondary to cerebral hemorrhage.
5  and thrombocytopenia that resulted in fatal cerebral hemorrhage.
6 e that can result in meningoencephalitis and cerebral hemorrhage.
7  or from migrating neurons did not result in cerebral hemorrhage.
8 eases in this protein can profoundly enhance cerebral hemorrhage.
9 ease (AD) and may contribute to dementia and cerebral hemorrhage.
10  glial cells leads to embryonic and neonatal cerebral hemorrhage.
11 d time, a ruptured miliary aneurysm within a cerebral hemorrhage.
12 A leads to loss of vessel wall integrity and cerebral hemorrhage.
13 ing ischemic volume without increasing intra-cerebral hemorrhage.
14 d irregular blood vessels that often lead to cerebral hemorrhage.
15 ype is lethal at embryonic day 10 because of cerebral hemorrhage.
16 sed in the donors as primary brain tumors or cerebral hemorrhage.
17 f the brain causing headaches, seizures, and cerebral hemorrhage.
18 , blood-brain-barrier hyperpermeability, and cerebral hemorrhage.
19 eases the risk for gastrointestinal (GI) and cerebral hemorrhages.
20 on neural progenitors also caused widespread cerebral hemorrhaging.
21 irin; OR, 1.04; 95% CI, 0.82-1.33; P = .72), cerebral hemorrhage (0.6% aspirin vs 0.4% no aspirin; OR
22                     Ripk3 deficiency reduces cerebral hemorrhage and delays the onset of neural damag
23 er, the patient suddenly developed a massive cerebral hemorrhage and died before full therapy could t
24 olic stroke models, MMP inhibitors decreased cerebral hemorrhage and injury after treatment with tPA.
25 ult rapidly activates necroptosis to promote cerebral hemorrhage and neuroinflammation.
26 s a significant risk, potentially leading to cerebral hemorrhage and severe complications.
27 ple CNS and non-CNS abnormalities, including cerebral hemorrhages and altered cortical development.
28 s include diffuse cerebral ischemia, stroke, cerebral hemorrhage, and brain death.
29 trial flutter, indirect hyperbilirubinaemia, cerebral hemorrhage, and mental status change (in two [1
30 ogical outcome after traumatic brain injury, cerebral hemorrhage, and other neuropathological disorde
31 apparent and silent, cerebral microinfarcts, cerebral hemorrhage, and reduced cerebral blood flow.
32 protection against cerebral malaria, reduced cerebral hemorrhages, and increased survival.
33  cortical lamination defects, as well as the cerebral hemorrhages, and restored a normal vascular pat
34 d Care After Acute Stroke Due to Spontaneous Cerebral Hemorrhage Associated With Antiplatelet Therapy
35 poE genotypes of 36 patients presenting with cerebral hemorrhage associated with histologically confi
36 al, 1.8 to 3.4), but the rate of subdural or cerebral hemorrhage associated with vacuum extraction di
37 ecause of adverse inflammatory reactions and cerebral hemorrhaging associated with the treatments.
38 e second Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH-II) trial.
39 AbetaE22Q variant usually present with lobar cerebral hemorrhages before 50 years of age.
40   Except for diffuse alveolar hemorrhage and cerebral hemorrhage, bleeding is infrequently recorded a
41 ervous system glia and neurons also leads to cerebral hemorrhage, but additionally to severe neurolog
42 st history of cancer who have a nontraumatic cerebral hemorrhage cause concern because this hemorrhag
43  Scale (NIHSS) score, but not as a result of cerebral hemorrhage, compared with baseline.
44 the development of portable and non-invasive cerebral hemorrhage detection systems.
45 ntenna specifically for microwave imaging in cerebral hemorrhage detection.
46 n of apoE epsilon 2 may be a risk factor for cerebral hemorrhage due to CAA, apoE epsilon 4 is a risk
47 ce lacking the alphav or beta8 genes develop cerebral hemorrhage due to defective interactions betwee
48 rior segment dysgenesis occurs together with cerebral hemorrhages, genetic analysis of COL4A1 should
49                                              Cerebral hemorrhages had occurred in 4 individuals, in 3
50                                            A cerebral hemorrhage has been reported in one patient wit
51      Consistent with AVM pathology, we found cerebral hemorrhage, hypoxia and necrosis, and neurologi
52 y recurrent stroke (ischemic stroke or intra-cerebral hemorrhage [ICH]) and ICH during follow-up.
53  myocardial infarction, ischemic stroke, and cerebral hemorrhage, identified from the patient registr
54 d in the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II) randomized clinical tr
55  (3.6%), seizures in 83 patients (1.8%), and cerebral hemorrhage in 80 patients (1.8%).
56 wall may contribute to loss of integrity and cerebral hemorrhage in CAA.
57 stroke, cerebral micro-bleeds which predicts cerebral hemorrhage in hypertensive patients, as well as
58 nital vascular lesions that often present as cerebral hemorrhage in young adults.
59 s in the primary and secondary prevention of cerebral hemorrhage include the treatment of hypertensio
60 condition exist and include cerebral anoxia, cerebral hemorrhage, infection, and genetic syndromes.
61  prevent hemorrhage and that the location of cerebral hemorrhage is dependent on when thrombocytopeni
62 l knockout technology to address whether the cerebral hemorrhage is due to primary defects in vascula
63 o MRI of stroke-positive rat brains detected cerebral hemorrhages, microhemorrhages, and ischemia wit
64 tory mediators released from the blood after cerebral hemorrhage might cause secondary brain injury a
65 s (n = 2), silent cerebral infarcts (n = 3), cerebral hemorrhage (n = 2), and reversible posterior le
66 d a significantly higher rate of subdural or cerebral hemorrhage (odds ratio, 2.7; 95 percent confide
67 ls of European ancestry from the Genetics of Cerebral Hemorrhage on Anticoagulation study, and replic
68 th strikingly different clinical phenotypes: cerebral hemorrhage or dementia.
69 mes with flagrant clinical effects caused by cerebral hemorrhages or seizure disorders, keeps clinici
70  (OR, 1.57; 95% CI, 1.38-1.79), nontraumatic cerebral hemorrhage (OR, 1.54; 95% CI, 1.24-1.91), peric
71     Advanced-stage clinical symptoms include cerebral hemorrhage, renal failure and the HELLP (hemoly
72  that primarily occur in adulthood and cause cerebral hemorrhage, stroke, and seizures.
73  and the differential clinical phenotypes of cerebral hemorrhage/stroke in some patients and dementia
74 rmation of cerebral capillaries resulting in cerebral hemorrhage, strokes, and seizures.
75 y of CVD and without elevated risk for GI or cerebral hemorrhages that would contraindicate aspirin u
76 ac (two cancers, one traumatic accident, one cerebral hemorrhage, two bronchopneumonia, one peritonit
77 tion and altered vasoreactivity that follows cerebral hemorrhage via stimulation of ETA receptor.
78 ot performed and the pathogenesis or type of cerebral hemorrhage was undefined.
79 a and congestive heart failure and one fatal cerebral hemorrhage were reported.
80                                              Cerebral hemorrhages were infrequent in both groups.
81  with either acute traumatic brain injury or cerebral hemorrhage who were intubated within 6 hrs of a
82 ongophilic amyloid angiopathy, or hereditary cerebral hemorrhage with amyloid.
83 tients with the Icelandic form of hereditary cerebral hemorrhage with amyloidosis (HCHWA-I).
84 of parenchymal amyloid, mimicking hereditary cerebral hemorrhage with amyloidosis Dutch type (HCHWA-D
85  is also the principal feature of hereditary cerebral hemorrhage with amyloidosis Dutch type, a famil
86 s including Alzheimer disease and hereditary cerebral hemorrhage with amyloidosis Dutch-type (HCHWA-D
87 eature of Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis Dutch-type, can lea
88 tain related disorders, including hereditary cerebral hemorrhage with amyloidosis of the Dutch type (
89                                In hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-
90 e and related disorders including hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D
91 amino acid substitution linked to hereditary cerebral hemorrhage with amyloidosis-Dutch type, [Gln-22
92                             Two subjects had cerebral hemorrhages with transient symptoms.
93 death suggest that the rapid accumulation of cerebral hemorrhages, with accompanying fluid egress, ma
94            Half of the mutant mice died with cerebral hemorrhage within a day of birth, and approxima