ライフサイエンスコーパス: brain inflammation

1 e is temporally correlated with the onset of brain inflammation.

2 ed the reparative capacity of NSCs following brain inflammation.

3 prevented PTB, neonatal mortality, and fetal brain inflammation.

4 toxic amyloid-beta as well as regulation of brain inflammation.

5 on cognition, depressive-like behavior, and brain inflammation.

6 oimmune encephalomyelitis onset and enhanced brain inflammation.

7 el object recognition test, but not signs of brain inflammation.

8 (-/-) mice, which was accompanied by reduced brain inflammation.

9 ctively contributes to neuronal death during brain inflammation.

10 ight induce cerebral blood flow responses to brain inflammation.

11 insight into new therapeutic strategies for brain inflammation.

12 id MVs as a marker and therapeutic target of brain inflammation.

13 ers and is stable for months without causing brain inflammation.

14 f PGE2 EP4 receptor signaling in suppressing brain inflammation.

15 ir characteristic amoeboid morphology during brain inflammation.

16 CNS glial cell type, also can contribute to brain inflammation.

17 opic effects of type 1 interferons in taming brain inflammation.

18 's disease (AD) is associated with prominent brain inflammation.

19 We report here detection of active brain inflammation 3 months after successful inhibition

20 We examined these samples for systemic and brain inflammation; amyloid-beta peptide (Abeta) and Ser

21 , the activation of mast cell contributes to brain inflammation and brain injury.

22 of inflammatory cells, which can exacerbate brain inflammation and contribute to poor outcome.

23 (WNV) is a vectorborne pathogen that induces brain inflammation and death.

24 sensitive systems for detection of mammalian brain inflammation and disease.

25 s a critical role for CD73 as a modulator of brain inflammation and immune function.

26 widely recognized to play critical roles in brain inflammation and injury, although the responsible

27 ality and morbidity that are associated with brain inflammation and injury, but currently the only ef

28 peripheral inflammation can exacerbate local brain inflammation and neuronal death.

29 copy (MRS) can be used to monitor changes in brain inflammation and neuronal integrity associated wit

30 -LOX mice was associated with an increase in brain inflammation and parasite burden.

31 ain, as potential gatekeepers for modulating brain inflammation and pathology after stroke.

32 nds provides a unique tool to assess diffuse brain inflammation and perilesional activity in progress

33 nti-inflammatory drugs (NSAIDs) could reduce brain inflammation and that NFP is an effective anti-inf

34 Evolving evidence suggests that brain inflammation and the buildup of proinflammatory cy

35 ere investigated on epileptiform discharges, brain inflammation, and BBB damage.

36 insulin resistance, brain oxidative stress, brain inflammation, and brain apoptosis, resulting in th

37 FB results in increased CSF cytokine levels, brain inflammation, and downregulation of the brain gluc

38 ides the most compelling evidence to date of brain inflammation, and more specifically microglial act

39 ssential in tempering microglial activation, brain inflammation, and neurodegeneration, with critical

40 e to infection, prevented the development of brain inflammation, and protected mice from paralysis an

41 itment and their mechanisms of action during brain inflammation are not well understood.

42 mmation has not thus far clearly established brain inflammation as an early pathological event.

43 pendently, and significantly, attenuated the brain inflammation as indicated by the decreased density

44 tration of nitro-aspirin also attenuated the brain inflammation, but to a much lesser degree than NFP

45 te this issue, we established a new model of brain inflammation by injecting the Toll-like receptor 3

46 report in vivo detection of VCAM-1 in acute brain inflammation, by magnetic resonance imaging in a m

47 that systemic inflammation along with local brain inflammation can play a significant role in Alzhei

48 We hypothesize that acute brain inflammation caused by neonatal infection reduces

49 Brain inflammation, changes in nicotinic receptor expres

50 mer's disease (AD) is found to have striking brain inflammation characterized by clusters of reactive

51 , compromised neuronal integrity, and robust brain inflammation characterized by extensive gliosis an

52 Encephalitis is parenchymal brain inflammation, commonly due to herpes simplex virus

53 Brain inflammation contributes to the duration and recur

54 No brain inflammation, demyelination or right-turning behav

55 e subunit changes associated with persistent brain inflammation due to HIV-1; (2) determining whether

56 geted PET is a reliable tool for identifying brain inflammation during epileptogenesis.

57 atory hypothesis is a paucity of evidence of brain inflammation during MDE.

58 confirmed that the HHQK peptide reduces rat brain inflammation elicited after infusion of Abeta pept

59 Brain inflammation (encephalitis) in response to viral i

60 nhibit NF-kappaB activation induced in acute brain inflammation even in the absence of MC1R.

61 er animals less sensitive to tissue loss and brain inflammation following experimental brain injury.

62 Therefore, neuronal loss during brain inflammation has always been assumed to be due to

63 hanism of this age-related susceptibility to brain inflammation has yet to be defined, but animal mod

64 Brain inflammation in animal models of these diseases is

65 Seizures initiate brain inflammation in glia and promote BBB damage that i

66 ion together with histological assessment of brain inflammation in infected animals revealed that cle

67 ainst the IL-2Ralpha chain, strongly reduces brain inflammation in multiple sclerosis patients.

68 d monoclonal antibody against CD25, inhibits brain inflammation in multiple sclerosis, we observed th

69 eceptors by prostaglandin E2 (PGE2) promotes brain inflammation in neurodegenerative diseases, but th

70 he present study, we used an animal model of brain inflammation in order to study a possible mechanis

71 n Ab against the IL-2R alpha-chain, inhibits brain inflammation in patients with multiple sclerosis,

72 Finally, PET can detect widespread brain inflammation in PD.

73 ic differences in cortical tissue sparing or brain inflammation in this experiment.

74 systemic inflammation, in addition to local brain inflammation, in Alzheimer's disease (AD) progress

75 ave shown that TNF-alpha plays a key role in brain inflammation, including recruitment of inflammator

76 We investigated whether seizures induce brain inflammation independently on extracerebral factor

77 flammatory cytokines, in experimental murine brain inflammation induced by lipopolysaccharide.

78 g the CXC chemokine activity associated with brain inflammation inhibits neutrophil-mediated blood-br

79 Brain inflammation is considered a crucial etiopathogene

80 Brain inflammation is increasingly recognized as a criti

81 Identifying brain inflammation is possible with the recent advance i

82 s effective at suppressing both systemic and brain inflammation, it may represent a novel therapeutic

83 The development of brain inflammation largely contributes to neonatal brain

84 illing efficiency, but also long-term active brain inflammation, loss of myelin fibers and persistent

85 ing the liver and spleen, nor does it affect brain inflammation markers.

86 ven therapeutic efficacy in animal models of brain inflammation, neurodegenerative disorders and stro

87 stopped, the immune response was generated, brain inflammation occurred, virus was cleared, and mice

88 There were no differences in the amounts of brain inflammation or peak virus replication; however, I

89 ction of monocyte chemoattractant protein 1, brain inflammation, or mortality could not be accounted

90 n mediate interaction between peripheral and brain inflammation, our findings pinpoint the choroid pl

91 celerated recovery from weight loss, reduced brain inflammation, prevention of blood-brain barrier op

92 mokine family and that it may play a role in brain inflammation processes.

93 IB/SHIP1 pathway, resulting in a decrease of brain inflammation, protection of the blood-brain-barrie

94 This hallmark of brain inflammation remains unexplained.

95 Wild-type (wt) MAV-1 causes less brain inflammation than an early region 3 (E3) null viru

96 eonates at postnatal day 3 (P3) caused acute brain inflammation that was resolved within 72 h.

97 bservations in terms of BBB permeability and brain inflammation underline age susceptibility.

98 Seizure-induced brain inflammation was evaluated by quantitative immunoh

99 Brain inflammation was measured by TaqMan RT-PCR amplifi

100 Brain inflammation was modeled by intravenous lipopolysa

101 /-) mice, lethality was markedly delayed and brain inflammation was significantly reduced, as demonst

102 Brain inflammation was suggested by MRS.

103 of global lipopolysaccharide (LPS)-mediated brain inflammation was used to induce global vascular ce

104 went dynamic PK PET for conditions involving brain inflammation were studied.

105 ilepsy characterized pathologically by focal brain inflammation with large numbers of infiltrating T