ライフサイエンスコーパス: microhemorrhage

1 ird, anti-ROS therapy attenuates CAA-related microhemorrhage.

2 -induced vessel dysfunction, and CAA-related microhemorrhage.

3 rance of pre-existing plaque without causing microhemorrhage.

4 onse leading to vasogenic edema and cerebral microhemorrhage.

5 oid but increase VAbeta and the incidence of microhemorrhage.

6 luding brain T cell infiltration or cerebral microhemorrhage.

7 taining, and occasionally presented signs of microhemorrhage.

8 ith certain anti-Abeta antibodies can induce microhemorrhage.

9 age, and there was little to no evidence of microhemorrhage.

10 sociated with reductions in microgliosis and microhemorrhages.

11 sease model without inducing microgliosis or microhemorrhages.

12 as CNS T cell or macrophage infiltration or microhemorrhages.

13 ion of the blood-brain barrier, and cerebral microhemorrhages.

14 ility maps (mean +/- standard deviation, 9.8 microhemorrhages +/- 12.8 vs 13.7 microhemorrhages +/- 1

15 ation, 9.8 microhemorrhages +/- 12.8 vs 13.7 microhemorrhages +/- 16.6; P = .019).

16 ity mapping-derived quantitative measures of microhemorrhages all decreased over time, suggesting tha

17 ity mapping-derived quantitative measures of microhemorrhages also decreased over time: -0.85 mm(3) p

18 association between the presence of vascular microhemorrhage and branched dilated microvessels in the

19 al and symmetric cerebral lesions, including microhemorrhages and hyperintensities on fluid-attenuate

20 The number of microhemorrhages and quantitative susceptibility mapping

21 nd 4) the presence of lactate with necrosis, microhemorrhages, and edema (r = 0.996, P < 0.0001 in th

22 ve rat brains detected cerebral hemorrhages, microhemorrhages, and ischemia with middle cerebral arte

23 hemorrhagic infarctions, neuronal ischemia, microhemorrhages, and microvascular alterations suggests

24 microangiopathies, including microaneurysms, microhemorrhages, and nerve layer infarcts known as cott

25 sis for the association of ischemic lesions, microhemorrhages, and strokes in humans.

26 sive cell mediated inflammation and cerebral microhemorrhages are two forms of toxicity which can occ

27 brain were present, including microinfarcts, microhemorrhages, bland angiopathy, thrombotic angiopath

28 T2-weighted hyperintense areas and microhemorrhages did not collocate by visual inspection.

29 cerebellar edema formation without affecting microhemorrhage formation or blood-brain barrier permeab

30 An identical pattern of microhemorrhages has previously been described in mounta

31 te cerebral amyloid angiopathy (CAA)-related microhemorrhage in a transgenic animal model.

32 was observed in CAA-vessels with evidence of microhemorrhage in aged APPsw transgenic mice, but not d

33 l amyloid but increased vascular amyloid and microhemorrhage in amyloid precursor protein (APP) trans

34 cerbated cerebral amyloid angiopathy-related microhemorrhage in APP23/ABCA1-/- mice.

35 In the healthy GC there was no evidence of microhemorrhage in participants that had only simple cap

36 chronic, passive immunization on VAbeta and microhemorrhage in PDAPP mice by comparing antibodies wi

37 itary abnormalities, with a low incidence of microhemorrhage in the chronic phase.

38 Brain microhemorrhages in CM suggest a clotting disorder, but

39 Vasculitis associated with microhemorrhages in the brain dominates the pathological

40 e effects, including meningoencephalitis and microhemorrhage, in WT mice and a transgenic mouse model

41 GzmB deficiency also reduced microhemorrhage, inflammation, and fibroblast accumulati

42 existing plaque but manifested a significant microhemorrhage liability.

43 rsely affecting cerebral amyloid angiopathy, microhemorrhages, myelination, or neuromuscular function

44 d cerebral cortical hemorrhagic infarctions, microhemorrhages, neuronal ischemia, and microvascular i

45 Comparisons of microhemorrhage number, size, and magnetic susceptibilit

46 he increased vascular amyloid deposition and microhemorrhage observed with unmodified IgG.

47 Safety (lack of edema or microhemorrhage) of FUS was also improved during alert c

48 Seventy-seven percent (451 of 585) of the microhemorrhages on susceptibility-weighted images had a

49 e patients, MRI of the brain showed multiple microhemorrhages predominantly in the splenium of the co

50 pecificity and exposure levels on VAbeta and microhemorrhage rates have not been well established, no

51 s were analyzed to determine the presence of microhemorrhage related to branched dilated microvessels

52 face were often abnormal morphologically and microhemorrhages sometimes occurred.

53 further highlights a role of microinfarcts, microhemorrhages, strategic white matter tracts, loss of

54 The incidence of microhemorrhage was increased in the high-dose 3D6 group

55 Microhemorrhage was observed in all vaccinated APPSw/NOS

56 Microhemorrhage was present in the majority of participa

57 The longitudinal evolution of microhemorrhages was monitored in a subset of patients b

58 r 266 or 3D6 would exacerbate CAA-associated microhemorrhage, we treated aged PDAPP mice with either

59 VAbeta and microhemorrhage were assessed using concomitant Abeta im

60 on, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiot

61 In these patients, a smaller number of microhemorrhages were identified at follow-up imaging co

62 Microhemorrhages were identified by two radiologists ind

63 Among the 603 patients, cerebral microhemorrhages were identified in 43 patients, with si

64 Further, microhemorrhages were increased by 3D6 in the APP/PS1/co

65 Cerebral microhemorrhages were observed in a small percentage of

66 ficantly fewer vascular amyloid deposits and microhemorrhages were observed in mice administered the

67 the incidence and severity of CAA-associated microhemorrhage when PDAPP transgenic mice were treated

68 can significantly mitigate the incidence of microhemorrhage while still preventing or reducing VAbet

69 HIP rats have brain microhemorrhages, white matter injury, and neurologic de

70 This resulted in microhemorrhages with release of neurotoxic hemoglobin-d

71 age-dependent increase in CAA and associated microhemorrhage, with the APPsw model having an earlier