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

3 ovide nitroxidergic innervation to forebrain cerebral blood vessels.

4 that delineate the architecture of activated cerebral blood vessels.

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

6 of nitroxidergic vasodilatory innervation of cerebral blood vessels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Cerebral blood vessels had thickened refractile basal la

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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