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1 didate for the treatment of HIV-1-associated brain inflammation.
2  CNS glial cell type, also can contribute to brain inflammation.
3 opic effects of type 1 interferons in taming brain inflammation.
4 analysis in real time after triggering focal brain inflammation.
5 's disease (AD) is associated with prominent brain inflammation.
6 ion and in aging-associated microgliosis and brain inflammation.
7 ls including systemic inflammation and local brain inflammation.
8 of Plasmodium falciparum infection caused by brain inflammation.
9 ells lacking TCF1 and LEF1 fails to suppress brain inflammation.
10 pagation of tau in humans is associated with brain inflammation.
11 y gene expression and experimentally induced brain inflammation.
12  ferroptosis-induced cell death, and reduces brain inflammation.
13 lucidate the mechanisms of ChP regulation of brain inflammation.
14 glia-astrocyte positive feedback loop during brain inflammation.
15 nic (Tg4510) mouse model exhibiting elevated brain inflammation.
16 lar miRNA and TLR7 sensing in sepsis-induced brain inflammation.
17 egnancy on offspring behavioral outcomes and brain inflammation.
18  plasma EVs may be involved in posttraumatic brain inflammation.
19 e that neuronal STAT3 may directly influence brain inflammation.
20 ic seizures, which is preceded by persistent brain inflammation.
21 Q311X(A) mice with slow progression and mild brain inflammation.
22 trocyte-mediated microglia activation during brain inflammation.
23 rocytes and microglia play critical roles in brain inflammation.
24 ibit elevated expression of immune genes and brain inflammation.
25 e is temporally correlated with the onset of brain inflammation.
26 prevented PTB, neonatal mortality, and fetal brain inflammation.
27 el object recognition test, but not signs of brain inflammation.
28 ed the reparative capacity of NSCs following brain inflammation.
29  toxic amyloid-beta as well as regulation of brain inflammation.
30  on cognition, depressive-like behavior, and brain inflammation.
31 oimmune encephalomyelitis onset and enhanced brain inflammation.
32 (-/-) mice, which was accompanied by reduced brain inflammation.
33 ctively contributes to neuronal death during brain inflammation.
34 laques in APP/PS1 mice, as well as increased brain inflammation.
35 ight induce cerebral blood flow responses to brain inflammation.
36  insight into new therapeutic strategies for brain inflammation.
37 id MVs as a marker and therapeutic target of brain inflammation.
38 ers and is stable for months without causing brain inflammation.
39 f PGE2 EP4 receptor signaling in suppressing brain inflammation.
40 ir characteristic amoeboid morphology during brain inflammation.
41           We report here detection of active brain inflammation 3 months after successful inhibition
42                                   Such focal brain inflammation aggravates secondary brain injury by
43   We examined these samples for systemic and brain inflammation; amyloid-beta peptide (Abeta) and Ser
44 ry gene expression in a mouse model of acute brain inflammation and a mouse model of Alzheimer's dise
45 SPO PET as a potential biomarker to evaluate brain inflammation and anti-inflammatory therapies, a be
46 brain demyelination significantly attenuates brain inflammation and astrocyte reactivity.
47 , the activation of mast cell contributes to brain inflammation and brain injury.
48  of inflammatory cells, which can exacerbate brain inflammation and contribute to poor outcome.
49 (WNV) is a vectorborne pathogen that induces brain inflammation and death.
50 sensitive systems for detection of mammalian brain inflammation and disease.
51                                    Sustained brain inflammation and hyperactivation of inflammasome c
52 s a critical role for CD73 as a modulator of brain inflammation and immune function.
53 oited to develop therapies that can mitigate brain inflammation and improve the outcome after TBI.
54  widely recognized to play critical roles in brain inflammation and injury, although the responsible
55 ality and morbidity that are associated with brain inflammation and injury, but currently the only ef
56 a trigger astrocyte reactivity, resulting in brain inflammation and massive amyloid and tau pathologi
57 ficient naive CD4(+) T cells failed to cause brain inflammation and neurobehavioral disorders in Rag1
58 eferentially into the brain, contributing to brain inflammation and neurobehavioral disorders, thereb
59  their sensor Toll-like receptor 7 (TLR7) in brain inflammation and neurological dysfunction.
60 peripheral inflammation can exacerbate local brain inflammation and neuronal death.
61 copy (MRS) can be used to monitor changes in brain inflammation and neuronal integrity associated wit
62                               HypoMg-induced brain inflammation and oxidative stress were suppressed
63 -LOX mice was associated with an increase in brain inflammation and parasite burden.
64 caspase-1/11 deficient mice show deficits in brain inflammation and parasite control.
65 ain, as potential gatekeepers for modulating brain inflammation and pathology after stroke.
66 nds provides a unique tool to assess diffuse brain inflammation and perilesional activity in progress
67 influx may be an effective therapy to reduce brain inflammation and promote myelin recovery in demyel
68 nti-inflammatory drugs (NSAIDs) could reduce brain inflammation and that NFP is an effective anti-inf
69              Evolving evidence suggests that brain inflammation and the buildup of proinflammatory cy
70  macrophages (Mi/MPhi) critically influences brain inflammation and the outcome after traumatic brain
71    These factors, in turn, promote liver and brain inflammation and the progression of liver fibrosis
72 e Sclerosis (MS), CVR may be diminished with brain inflammation and this may contribute to neurodegen
73 ere investigated on epileptiform discharges, brain inflammation, and BBB damage.
74  insulin resistance, brain oxidative stress, brain inflammation, and brain apoptosis, resulting in th
75 FB results in increased CSF cytokine levels, brain inflammation, and downregulation of the brain gluc
76 ides the most compelling evidence to date of brain inflammation, and more specifically microglial act
77 ssential in tempering microglial activation, brain inflammation, and neurodegeneration, with critical
78  breakdown of the blood-brain barrier (BBB), brain inflammation, and neurological dysfunction.
79 e to infection, prevented the development of brain inflammation, and protected mice from paralysis an
80 itment and their mechanisms of action during brain inflammation are not well understood.
81 mmation has not thus far clearly established brain inflammation as an early pathological event.
82 pendently, and significantly, attenuated the brain inflammation as indicated by the decreased density
83 hocyanidin B2 was also a potent inhibitor of brain inflammation as shown by reduction in astrocytosis
84  vivo, in a mouse model of EcoHIV-associated brain inflammation, as well as characterize its pharmaco
85 ng and attenuated lung injury and indices of brain inflammation at 10 days.
86 viated proinflammatory Mi/MPhi responses and brain inflammation burden after TBI.
87 tration of nitro-aspirin also attenuated the brain inflammation, but to a much lesser degree than NFP
88 te this issue, we established a new model of brain inflammation by injecting the Toll-like receptor 3
89  report in vivo detection of VCAM-1 in acute brain inflammation, by magnetic resonance imaging in a m
90  that systemic inflammation along with local brain inflammation can play a significant role in Alzhei
91                    We hypothesize that acute brain inflammation caused by neonatal infection reduces
92                                              Brain inflammation, changes in nicotinic receptor expres
93 mer's disease (AD) is found to have striking brain inflammation characterized by clusters of reactive
94 , compromised neuronal integrity, and robust brain inflammation characterized by extensive gliosis an
95                  Encephalitis is parenchymal brain inflammation, commonly due to herpes simplex virus
96                                              Brain inflammation contributes to the duration and recur
97 ink between cutaneous, systemic and possible brain inflammation could at least in part be driven by t
98                                           No brain inflammation, demyelination or right-turning behav
99 e subunit changes associated with persistent brain inflammation due to HIV-1; (2) determining whether
100 geted PET is a reliable tool for identifying brain inflammation during epileptogenesis.
101 liferating microglia as important drivers of brain inflammation during infection.
102 atory hypothesis is a paucity of evidence of brain inflammation during MDE.
103 ortem and in vivo imaging studies have shown brain inflammation early in these conditions, proportion
104  confirmed that the HHQK peptide reduces rat brain inflammation elicited after infusion of Abeta pept
105                                              Brain inflammation (encephalitis) in response to viral i
106 ts a systematic review of the data regarding brain inflammation evaluating microglia, astrocytes, cyt
107 nhibit NF-kappaB activation induced in acute brain inflammation even in the absence of MC1R.
108 er animals less sensitive to tissue loss and brain inflammation following experimental brain injury.
109      2019) reports that DAMP-induced sterile brain inflammation from stroke is associated with sympat
110 cific receptor Mrgprb2 regulates post-stroke brain inflammation from the meninges.
111              Therefore, neuronal loss during brain inflammation has always been assumed to be due to
112 tly, an intriguing link between TMEM106B and brain inflammation has been discovered, but how TMEM106B
113 hanism of this age-related susceptibility to brain inflammation has yet to be defined, but animal mod
114  BHB has been shown to modulate systemic and brain inflammation; however, its direct effects on micro
115 lates HSC lineage development to curb distal brain inflammation, implicating the bone marrow as a uni
116                                   We studied brain inflammation in 25 patients with early-onset amnes
117                         Accurately measuring brain inflammation in Alzheimer's disease (AD) is crucia
118                                              Brain inflammation in animal models of these diseases is
119                            Seizures initiate brain inflammation in glia and promote BBB damage that i
120 ion together with histological assessment of brain inflammation in infected animals revealed that cle
121               We applied 11C-ER176 to detect brain inflammation in mild cognitive impairment (MCI) ca
122 ainst the IL-2Ralpha chain, strongly reduces brain inflammation in multiple sclerosis patients.
123 d monoclonal antibody against CD25, inhibits brain inflammation in multiple sclerosis, we observed th
124 eceptors by prostaglandin E2 (PGE2) promotes brain inflammation in neurodegenerative diseases, but th
125                     Astrocytes contribute to brain inflammation in neurological disorders but the mol
126 he present study, we used an animal model of brain inflammation in order to study a possible mechanis
127                                              Brain inflammation in patients with HE was evaluated by
128 n Ab against the IL-2R alpha-chain, inhibits brain inflammation in patients with multiple sclerosis,
129           Finally, PET can detect widespread brain inflammation in PD.
130 ammation, we investigated the development of brain inflammation in the T cell transfer model of chron
131 ic differences in cortical tissue sparing or brain inflammation in this experiment.
132 derived macrophage infiltration and enhanced brain inflammation in vivo.
133  systemic inflammation, in addition to local brain inflammation, in Alzheimer's disease (AD) progress
134 ave shown that TNF-alpha plays a key role in brain inflammation, including recruitment of inflammator
135      We investigated whether seizures induce brain inflammation independently on extracerebral factor
136 flammatory cytokines, in experimental murine brain inflammation induced by lipopolysaccharide.
137                 Using a mouse model of acute brain inflammation induced by local tumor necrosis facto
138 al cortex attenuated microglia activation in brain inflammation induced by systemic injection of lipo
139 g the CXC chemokine activity associated with brain inflammation inhibits neutrophil-mediated blood-br
140                                              Brain inflammation is considered a crucial etiopathogene
141                                              Brain inflammation is increasingly recognized as a criti
142 mented, how MIA in utero leads to persistent brain inflammation is not well understood.
143                                  Identifying brain inflammation is possible with the recent advance i
144 s effective at suppressing both systemic and brain inflammation, it may represent a novel therapeutic
145                           The development of brain inflammation largely contributes to neonatal brain
146 illing efficiency, but also long-term active brain inflammation, loss of myelin fibers and persistent
147 ing the liver and spleen, nor does it affect brain inflammation markers.
148  results suggest that persistent and diffuse brain inflammation may contribute to cognitive impairmen
149                                       Global brain inflammation might continuously shape the evolving
150 hionine provides further insights into heart-brain inflammation networking.
151 thionine provides further insight into heart-brain inflammation networking.
152 ven therapeutic efficacy in animal models of brain inflammation, neurodegenerative disorders and stro
153 ts into the roles of PGN as a determinant of brain inflammation, notably in multiple sclerosis (MS) a
154  stopped, the immune response was generated, brain inflammation occurred, virus was cleared, and mice
155 on, production of viral proteins, associated brain inflammation or in certain instances, antiretrovir
156  There were no differences in the amounts of brain inflammation or peak virus replication; however, I
157 DDs directly by inducing placental and fetal brain inflammation, or indirectly through affecting mate
158 ction of monocyte chemoattractant protein 1, brain inflammation, or mortality could not be accounted
159 n mediate interaction between peripheral and brain inflammation, our findings pinpoint the choroid pl
160 celerated recovery from weight loss, reduced brain inflammation, prevention of blood-brain barrier op
161 mokine family and that it may play a role in brain inflammation processes.
162 IB/SHIP1 pathway, resulting in a decrease of brain inflammation, protection of the blood-brain-barrie
163                             This hallmark of brain inflammation remains unexplained.
164 FDA-approved anti-inflammatory drugs reduced brain inflammation, restored LTP and long-term memory, a
165 mplement activation is implicated in driving brain inflammation, self-cell damage and progression of
166                                              Brain inflammation tended to be higher in LCR rats than
167             Wild-type (wt) MAV-1 causes less brain inflammation than an early region 3 (E3) null viru
168  astrocyte reactivity and astrocyte-mediated brain inflammation that is commonly observed in many neu
169 eonates at postnatal day 3 (P3) caused acute brain inflammation that was resolved within 72 h.
170 bservations in terms of BBB permeability and brain inflammation underline age susceptibility.
171 al cells (BECs) in fueling type I IFN-driven brain inflammation was demonstrated in brain endothelial
172                              Seizure-induced brain inflammation was evaluated by quantitative immunoh
173                                              Brain inflammation was measured by TaqMan RT-PCR amplifi
174                                              Brain inflammation was modeled by intravenous lipopolysa
175 /-) mice, lethality was markedly delayed and brain inflammation was significantly reduced, as demonst
176                                              Brain inflammation was suggested by MRS.
177  of global lipopolysaccharide (LPS)-mediated brain inflammation was used to induce global vascular ce
178 went dynamic PK PET for conditions involving brain inflammation were studied.
179    Autoimmune encephalitis (AE) is a form of brain inflammation where pathogenic autoantibodies bind
180 ilepsy characterized pathologically by focal brain inflammation with large numbers of infiltrating T
181                                              Brain inflammation, with an increased density of microgl
182  governing the emergence of so-called global brain inflammation would facilitate modulation of this i

 
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