ライフサイエンスコーパス: vasogenic

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 ketoacidosis in children is associated with vasogenic cerebral edema, possibly due to the release of

10 n cerebral blood flow and the development of vasogenic cerebral edema.

11 in animals with focal injury associated with vasogenic edema (cryogenic injury).

12 MMP-9 contributes to the early formation of vasogenic edema after transient FCI.

13 ropriate proinflammatory response leading to vasogenic edema and cerebral microhemorrhage.

14 rates a 1.6-cm right parietal mass with mild vasogenic edema and four additional brain metastases mea

15 (BBB) is associated with the development of vasogenic edema and intracranial hypertension in a numbe

16 ed inflammation (CAA-ri) is characterized by vasogenic edema and multiple cortical/subcortical microb

17 d other chronic retinal diseases, results in vasogenic edema and neural tissue damage, causing vision

18 tein and enzyme activity could contribute to vasogenic edema and the pathogenesis of neuronal dysfunc

19 the lesions are likely caused by reversible vasogenic edema and transient breakdown of the blood-bra

20 These observations support the proposal that vasogenic edema due to cerebrovascular autoregulatory dy

21 Proteinase-3 might mediate vasogenic edema during diabetic ketoacidosis, and select

22 This establishes that Pb(2+)-induced vasogenic edema formation develops via a Flk-1-dependent

23 Vasogenic edema had a minimal effect on MT ratio, and ra

24 e rapid growth of solid brain metastases and vasogenic edema in patients with advanced cancer, leadin

25 s can all result in the clinical syndrome of vasogenic edema in the central nervous system leading to

26 performed in the emergency department showed vasogenic edema in the right temporal parietal region, w

27 focus 5 mm or less in diameter surrounded by vasogenic edema that extended less than 7 mm in radius b

28 he metabolic enzyme TYMS; and association of vasogenic edema with the oncogene FOXP1 and PIK3IP1, whi

29 en in the brain and bone, decreased cerebral vasogenic edema, and improved survival, despite increasi

30 with intracranial evidence of hydrocephalus, vasogenic edema, central venous thrombosis, and/or mass

31 imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients afte

32 nt with this hypothesis, showing no signs of vasogenic edema, even in ApoE4 carriers.

33 lleled that of known resistance to spread of vasogenic edema, which suggested that anisotropy may be

34 or 'paravasculitis' plays a critical role in vasogenic edema.

35 tion of (131)I-mu81C6 mAb through regions of vasogenic edema.

36 presumed tumor-infiltrated edema from purely vasogenic edema.

37 reased blood-brain barrier permeability, and vasogenic edema.

38 ng lesion surrounded by a variable amount of vasogenic edema.

39 In a brain tumor model of vasogenic (leaky capillary) edema, FITC-dextran diffusio

40 rroborate the important role of MMP-9 in the vasogenic mechanism of brain edema in ALF.

41 The role of vasogenic mechanisms of brain edema has not been explore

42 o suggests that the predominant mechanism is vasogenic (movement of fluid and protein out of the vasc

43 pposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired remova

44 High lysine alone resulted in vasogenic oedema and blood-brain barrier breakdown withi

45 clude MRI signal abnormalities suggestive of vasogenic oedema and sulcal effusions (ARIA-E) and micro

46 However, the increased cellularity and vasogenic oedema associated with inflammation cannot be

47 lves inflammation-associated cellularity and vasogenic oedema in addition to accounting for partial v

48 with an increase in striatal water content, vasogenic oedema in the perihaematomal region presented

49 with multimodal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial act

50 and radiographically might show few areas of vasogenic oedema or even normal brain imaging in some ra

51 ngs include bilateral regions of subcortical vasogenic oedema that resolve within days or weeks.

52 ses: formation of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrh

53 e cellularity in the absence and presence of vasogenic oedema.

54 erfusion and glucose uptake, and supervening vasogenic oedema; and (3) a chronic stage of striatal at

55 nd dexamethasone in an experimental model of vasogenic peritumoral brain edema.

56 ays an important role in the pathogenesis of vasogenic retinal edema.

57 nucleotidase (5'N) is a major source of the vasogenic substance adenosine in most tissues.

58 lood vessels, further confirming that Wolf's vasogenic theory may not be true.