ライフサイエンスコーパス: cerebral blood vessel

1 nvective transport in perivascular spaces of cerebral blood vessels.

2 peptide (Abeta) in the brain parenchyma and cerebral blood vessels.

3 y, we measured insoluble Abeta isolated from cerebral blood vessels.

4 ovide nitroxidergic innervation to forebrain cerebral blood vessels.

5 that delineate the architecture of activated cerebral blood vessels.

6 table to the deleterious effects of Abeta on cerebral blood vessels.

7 of nitroxidergic vasodilatory innervation of cerebral blood vessels.

8 tyrosine staining was observed in dermal and cerebral blood vessels.

9 amyloid deposits of the brain parenchyma and cerebral blood vessels.

10 lium-dependent dilatation of large and small cerebral blood vessels.

11 ight junctions and the outer basal lamina of cerebral blood vessels.

12 plaques differed structurally from those in cerebral blood vessels.

13 ic component of healthy pial and parenchymal cerebral blood vessels.

14 f fibrillar amyloid-beta protein (A beta) in cerebral blood vessels, a condition known as cerebral am

15 roduct of metabolism, has a strong impact on cerebral blood vessels, a phenomenon known as cerebrovas

16 amyloid beta (Abeta) in brain parenchyma and cerebral blood vessels, accompanied by cognitive decline

17 so exert direct effects on IL-1 receptors on cerebral blood vessels, activating cyclooxygenases and h

18 ve a role in infected erythrocyte binding to cerebral blood vessels and cerebral malaria.

19 Decreased pericyte-endothelium coupling in cerebral blood vessels and increased microglial activati

20 can disrupt the development and functions of cerebral blood vessels and lead to long-term cognitive i

21 TGF-beta1 induces amyloid-beta deposition in cerebral blood vessels and meninges of aged transgenic m

22 Abeta deposits, although a small fraction of cerebral blood vessels and neurofibrillary tangles were

23 Cocaine affects both cerebral blood vessels and neuronal activity in brain.

24 evealed preferential localization of MRG1 to cerebral blood vessels and of GK to hypothalamic neurons

25 activating Ang II type 1 (AT1) receptors on cerebral blood vessels and producing reactive oxygen spe

26 Astrocytes surround cerebral blood vessels and sense changes in oxygen avail

27 arkedly induced in cells associated with the cerebral blood vessels and the leptomeninges by immune s

28 ablished the relationship between changes in cerebral blood vessels and total cardiovascular risk.

29 as an increase in GFAP immunostaining around cerebral blood vessels, and an enhancement of OX-42 micr

30 sition in brain parenchyma as plaques and in cerebral blood vessels as cerebral amyloid angiopathy (C

31 This effect was specific for cerebral blood vessels, because acetylcholine-mediated d

32 wn to alter in the structure and function of cerebral blood vessels, but how these cerebrovascular ef

33 GF-beta1, Abeta accumulated substantially in cerebral blood vessels, but not in parenchymal plaques.

34 R in mature astrocytes, oligodendrocytes, or cerebral blood vessels, but we could detect the alpha(1A

35 may be the function of annular spaces around cerebral blood vessels, called perivascular spaces (PVS)

36 of the blood-brain barrier and reactivity of cerebral blood vessels, cellular mechanisms which accoun

37 rk to enhance MRI-derived velocity fields in cerebral blood vessel data sets.

38 particularly glia, are necessary for proper cerebral blood vessel development, and also reveal a nov

39 ular endothelium has no detectable effect on cerebral blood vessel development, whereas deletion of a

40 The relationship between changes in cerebral blood vessels diagnosed through MDCT angiograph

41 emonstrated that MAP is inversely related to cerebral blood vessel diameters (p-value < 0.05) globall

42 hip between mean arterial pressure (MAP) and cerebral blood vessels' diameters and tortuosity alterat

43 rovascular system to quantify alterations in cerebral blood vessels' diameters; 3) Calculation of mea

44 Dysfunctional endothelial cells can cause cerebral blood vessel dysfunction, alter blood-brain bar

45 Tight junctions are functional in cerebral blood vessels early in fetal development and co

46 inhibition of ICAM-1 expression on ischemic cerebral blood vessels (eg, 61% inhibition with 2 mg/kg

47 sels volume difference (AVVD) in delineating cerebral blood vessels from surrounding tissues compared

48 nfluence pattern and density of innervation, cerebral blood vessels from young (6 weeks) and old (24

49 o induce migraine attack without dilation of cerebral blood vessels, further confirming that Wolf's v

50 Cerebral blood vessels had thickened refractile basal la

51 ) along the paravascular spaces (PVS) around cerebral blood vessels has been controversial.

52 esence of the COX isoforms was determined in cerebral blood vessels immunocytochemically after the ex

53 cular mechanisms responsible for dilation of cerebral blood vessels in response to hypoxia are not fu

54 laques within the brain parenchyma and along cerebral blood vessels is a hallmark of Alzheimer's dise

55 beta amyloid peptide in neuritic plaques and cerebral blood vessels is a hallmark of Alzheimer's dise

56 Abeta) in senile plaques and in the walls of cerebral blood vessels is a key pathological feature of

57 Here, we show that loss of CD2AP in cerebral blood vessels is associated with cognitive decl

58 , where beta-amyloid (Abeta) deposits around cerebral blood vessels, is a major contributor of vascul

59 ase pathways in vivo; therefore, we compared cerebral blood vessels isolated from ovariectomized rats

60 mportant role in regulation of basal tone of cerebral blood vessels, it does not appear that basal sy

61 ontrol the unique permeability properties of cerebral blood vessels known as the blood-brain barrier

62 ine affects neuronal activity and constricts cerebral blood vessels, making it difficult to determine

63 Amylin amyloid formation in the wall of cerebral blood vessels may also induce failure of elimin

64 gested that impaired cholinergic dilation of cerebral blood vessels may play a role in the pathophysi

65 hypothesis, mitochondria were isolated from cerebral blood vessels obtained from ovariectomized fema

66 with amyloid-beta deposition in the damaged cerebral blood vessels of patients with cerebral amyloid

67 th extensive contacts with both synapses and cerebral blood vessels, participate in the increases in

68 e disease mechanism is the crucial role that cerebral blood vessels play in brain health, not only fo

69 In vivo two-photon imaging of cerebral blood vessels revealed sustained MA-induced vas

70 mount of glucose transporter type 1-positive cerebral blood vessels, reverted cerebral vasoreactivity

71 cranial structures (such as the meninges and cerebral blood vessels) suggests that sensory and nocice

72 In this study, we demonstrate using intact cerebral blood vessels that 17beta-estradiol rapidly act

73 Responses of cerebral blood vessels to nitric oxide (NO) are mediated

74 cerebral autoregulation (ie, the ability of cerebral blood vessels to react to changes in blood pres

75 AB fibrils were isolated from cerebral blood vessels using laser capture microdissecti

76 hed material from either brain parenchyma or cerebral blood vessels (using meninges as the source).

77 iol may also exert vasoprotective effects in cerebral blood vessels via stimulation of mitochondrial

78 tive transport in the perivascular spaces of cerebral blood vessels was also evident.

79 noreactive reinnervation on old transplanted cerebral blood vessels was significantly less dense comp

80 We addressed this issue using cerebral blood vessels where both the overall density an

81 Endothelium of the cerebral blood vessels, which constitutes the blood-brai