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1                          We also present the vasogenic and cytotoxic bases for HACE and explore venou
2 ctural MRI changes, compatible with cortical vasogenic and cytotoxic edema, partial contrast enhancem
3 ctivation may thus play an important role in vasogenic brain edema in ALF.
4                  In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkabl
5 r movement is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or
6  vivo evidence for enhanced ECS diffusion in vasogenic brain edema, yet greatly slowed diffusion in c
7 -regulation as a novel therapeutic option in vasogenic brain edema.
8  vascular permeability to serum albumin, and vasogenic cerebellar edema (p < 0.01).
9 g (MRI) features suggestive of cytotoxic and vasogenic cerebral edema followed by microhemorrhages in
10  ketoacidosis in children is associated with vasogenic cerebral edema, possibly due to the release of
11 n cerebral blood flow and the development of vasogenic cerebral edema.
12 in animals with focal injury associated with vasogenic edema (cryogenic injury).
13 g was used to show that C57BL/6 mice develop vasogenic edema 4 to 5 weeks after infection with T. gon
14  MMP-9 contributes to the early formation of vasogenic edema after transient FCI.
15 y injury process reflects an extreme form of vasogenic edema and blood-brain barrier breakdown.
16 ropriate proinflammatory response leading to vasogenic edema and cerebral microhemorrhage.
17 rates a 1.6-cm right parietal mass with mild vasogenic edema and four additional brain metastases mea
18  the extracellular water differences between vasogenic edema and infiltrative tissue and training a c
19  (BBB) is associated with the development of vasogenic edema and intracranial hypertension in a numbe
20 ed inflammation (CAA-ri) is characterized by vasogenic edema and multiple cortical/subcortical microb
21 d other chronic retinal diseases, results in vasogenic edema and neural tissue damage, causing vision
22 tein and enzyme activity could contribute to vasogenic edema and the pathogenesis of neuronal dysfunc
23 creased vascular permeability contributes to vasogenic edema and tissue damage, with consequent adver
24  the lesions are likely caused by reversible vasogenic edema and transient breakdown of the blood-bra
25 These observations support the proposal that vasogenic edema due to cerebrovascular autoregulatory dy
26                   Proteinase-3 might mediate vasogenic edema during diabetic ketoacidosis, and select
27         This establishes that Pb(2+)-induced vasogenic edema formation develops via a Flk-1-dependent
28                                              Vasogenic edema had a minimal effect on MT ratio, and ra
29 e rapid growth of solid brain metastases and vasogenic edema in patients with advanced cancer, leadin
30 s can all result in the clinical syndrome of vasogenic edema in the central nervous system leading to
31 performed in the emergency department showed vasogenic edema in the right temporal parietal region, w
32 focus 5 mm or less in diameter surrounded by vasogenic edema that extended less than 7 mm in radius b
33 he metabolic enzyme TYMS; and association of vasogenic edema with the oncogene FOXP1 and PIK3IP1, whi
34 d hematoma and edema volumes, T2 relaxation (vasogenic edema), apparent diffusion coefficient (ADC, c
35 en in the brain and bone, decreased cerebral vasogenic edema, and improved survival, despite increasi
36 with intracranial evidence of hydrocephalus, vasogenic edema, central venous thrombosis, and/or mass
37 se glibenclamide benefitted hematoma volume, vasogenic edema, cytotoxic edema, and BBB integrity afte
38  imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients afte
39 nt with this hypothesis, showing no signs of vasogenic edema, even in ApoE4 carriers.
40 th, pseudocyst-like or multiloculated shape, vasogenic edema, mass effect, and size greater than 3cm.
41 versely, high ADC values, indicative of mild vasogenic edema, were observed in both patients with SNC
42 lleled that of known resistance to spread of vasogenic edema, which suggested that anisotropy may be
43 or 'paravasculitis' plays a critical role in vasogenic edema.
44 Abnormalities ranged from cytotoxic edema to vasogenic edema.
45 ously inhibiting angiogenesis and minimizing vasogenic edema.
46 tion of (131)I-mu81C6 mAb through regions of vasogenic edema.
47 presumed tumor-infiltrated edema from purely vasogenic edema.
48 reased blood-brain barrier permeability, and vasogenic edema.
49 ng lesion surrounded by a variable amount of vasogenic edema.
50 longer treatment windows may be possible for vasogenic edema.
51 ry responses, in order to lower the risk for vasogenic edemas in the clinic.
52 nt, yet distinct stage between cytotoxic and vasogenic edemas.
53                    In a brain tumor model of vasogenic (leaky capillary) edema, FITC-dextran diffusio
54 rroborate the important role of MMP-9 in the vasogenic mechanism of brain edema in ALF.
55                                  The role of vasogenic mechanisms of brain edema has not been explore
56 o suggests that the predominant mechanism is vasogenic (movement of fluid and protein out of the vasc
57 pposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired remova
58                High lysine alone resulted in vasogenic oedema and blood-brain barrier breakdown withi
59 clude MRI signal abnormalities suggestive of vasogenic oedema and sulcal effusions (ARIA-E) and micro
60       However, the increased cellularity and vasogenic oedema associated with inflammation cannot be
61 lves inflammation-associated cellularity and vasogenic oedema in addition to accounting for partial v
62  with an increase in striatal water content, vasogenic oedema in the perihaematomal region presented
63 with multimodal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial act
64 and radiographically might show few areas of vasogenic oedema or even normal brain imaging in some ra
65 ngs include bilateral regions of subcortical vasogenic oedema that resolve within days or weeks.
66 ses: formation of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrh
67 e cellularity in the absence and presence of vasogenic oedema.
68  risk of other cerebral consequences such as vasogenic oedema.
69 erfusion and glucose uptake, and supervening vasogenic oedema; and (3) a chronic stage of striatal at
70 nd dexamethasone in an experimental model of vasogenic peritumoral brain edema.
71 ize the differences between infiltrative and vasogenic peritumoral regions, paving the way for its us
72 ays an important role in the pathogenesis of vasogenic retinal edema.
73  nucleotidase (5'N) is a major source of the vasogenic substance adenosine in most tissues.
74 lood vessels, further confirming that Wolf's vasogenic theory may not be true.
75  and glioblastomas, the former consisting of vasogenic versus the latter containing infiltrative edem