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Source: Neuroscience
Condition: Stroke
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Total 160 results found since Jan 2013.
Prevention of the Severity of Post-ischemic Inflammation and Brain Damage by Simultaneous Knockdown of Toll-like Receptors 2 and 4
This study thus shows that attenuation of the severity of TLR2- and TLR4-mediated post-stroke inflammation ameliorates ischemic brain damage.
Source: Neuroscience - February 6, 2018 Category: Neuroscience Source Type: research
Frequency-specific Effective Connectivity in Subjects with Cerebral Infarction as Revealed by NIRS Method
Publication date: 1 March 2018 Source:Neuroscience, Volume 373 Author(s): Qianying Liu, Bitian Wang, Ying Liu, Zeping Lv, Wenhao Li, Zengyong Li, Yubo Fan A connectivity-based approach can highlight the network reorganization in the chronic phases after stroke and contributes to the development of therapeutic interventions. Using dynamic Bayesian inference, this study aimed to assess the effective connectivity (EC) in various frequency bands through the near-infrared spectroscopy (NIRS) method in subjects with cerebral infarction (CI). A phase-coupling model was established based on phase information extracted using the w...
Source: Neuroscience - February 3, 2018 Category: Neuroscience Source Type: research
Necrostatin-1 Improves Long-term Functional Recovery Through Protecting Oligodendrocyte Precursor Cells After Transient Focal Cerebral Ischemia in Mice
This study demonstrated that pretreatment with Nec-1 significantly promoted OPCs survival, alleviated white matter injury, and improved cognitive function after transient cerebral ischemia. Nec-1 also inhibited the activation of RIPK1, RIPK3, MLKL, and P-MLKL in the subventricular zone (SVZ) and corpus callosum regions after MCAO. OPCs’ culture experiments confirmed that Nec-1 significantly reduced the necroptosis of OPCs, perhaps by inhibiting the expression of RIPK1, RIPK3, MLKL, and P-MLKL. Nec-1, an inhibitor of RIPK1, may reduce ischemic white matter damage and improve recovery of long-term neurological function fol...
Source: Neuroscience - December 27, 2017 Category: Neuroscience Source Type: research
RIP1K Contributes to Neuronal and Astrocytic Cell Death in Ischemic Stroke via Activating Autophagic-lysosomal Pathway
This study evaluates the contribution of RIP1K to ischemic stroke-induced neuronal and astrocytic cell death, and the activation of autophagic-lysosomal pathway. Using an in vitro oxygen and glucose deprivation (OGD) in primary cultured neurons or astrocytes and a permanent middle cerebral artery occlusion (pMCAO) model in rats or mice, we observed the role of RIP1K in the ischemic neuronal and astrocytic cell death and the underlying mechanisms by pharmacological or genetic inhibition of RIP1K. pMCAO or OGD condition led to an increase in RIP1K, RIP3K and RIP1K–RIP3K complex. RIP1K knockdown or necrostatin-1 (Nec-1, a s...
Source: Neuroscience - December 17, 2017 Category: Neuroscience Source Type: research
Cerebrovascular Gene Expression in Spontaneously Hypertensive Rats After Transient Middle Cerebral Artery Occlusion
In conclusion, these genes may be potential targets in future strategies for acute stroke treatments that can be used in patients with and without hypertension.
Source: Neuroscience - November 28, 2017 Category: Neuroscience Source Type: research
Sirtuin 6 protects the brain from cerebral ischemia/reperfusion injury through NRF2 activation
In this study, we investigated the effects of SIRT6 overexpression in regulating I/R injury in a mouse cerebral I/R model in vivo and in oxygen-glucose-deprivation/reoxygenation (OGD/R)-stimulated neuro-2a neuroblastoma cells in vitro. We found that cerebral I/R (1 h/24 h) resulted in decreased SIRT6 expression in the cerebral cortex (P < 0.01). SIRT6 overexpression in the brain by in vivo gene transfer enhanced the antioxidant NRF2 signaling (P < 0.05), reduced oxidative stress (P < 0.05), and attenuated cerebral I/R-induced brain tissue damage and neurological deficits (P <â€...
Source: Neuroscience - November 15, 2017 Category: Neuroscience Source Type: research
Cerebral Venous Collagen Remodeling in a Modified White Matter Lesions Animal Model
Publication date: 26 December 2017 Source:Neuroscience, Volume 367 Author(s): Jing Lin, Linfang Lan, Dilong Wang, Baoshan Qiu, Yuhua Fan To mimic the expected pathological changes of white matter lesions (WMLs) and increase the stability, we applied modified two-vessel occlusion (modified 2VO) (1-week interval bilateral carotid artery occlusion) in stroke-prone renovascular hypertensive rats (RHRSP) and established a modified WMLs model (RHRSP/modified 2VO) that compared their phenotypes with RHRSP and sham-operated rats. In addition, we tried to differentiate small veins from small arteries through the presence of smooth...
Source: Neuroscience - November 11, 2017 Category: Neuroscience Source Type: research
Inhibition of Nkcc1 promotes axonal growth and motor recovery in ischemic rats
In conclusion, bumetanide promoted post-stroke axonal sprouting together accompanied by an improved behavioral outcome possibly through restoring and maintaining neuronal chloride homeostasis and creating a recovery-promoting microenvironment by overcoming the axonal growth inhibition encountered after cerebral ischemia in rats.
Source: Neuroscience - October 18, 2017 Category: Neuroscience Source Type: research
Disrupted structural and functional connectivity networks in ischemic stroke patients
Publication date: 19 November 2017 Source:Neuroscience, Volume 364 Author(s): Jingna Zhang, Ye Zhang, Li Wang, Linqiong Sang, Jun Yang, Rubing Yan, Pengyue Li, Jian Wang, Mingguo Qiu Local lesions caused by stroke may result in extensive structural and functional reorganization in the brain. Previous studies of this phenomenon have focused on specific brain networks. Here, we aimed to discover abnormalities in whole-brain networks and to explore the decoupling between structural and functional connectivity in patients with stroke. Fifteen ischemic stroke patients and 23 normal controls (NCs) were recruited in this study. ...
Source: Neuroscience - October 11, 2017 Category: Neuroscience Source Type: research
Effects of crenolanib, a nonselective inhibitor of PDGFR, in a mouse model of transient middle cerebral artery occlusion
In this study, we investigated the effects of PDGFR inhibition in a mouse model of transient middle cerebral artery occlusion (MCAO). We blocked the pathway using a nonselective PDGFR inhibitor, crenolanib, during the acute post-MCAO phase (days 1–3) or during the sub-acute phase (days 7–9). Downregulating the PDGFR signaling pathway with crenolanib from day 1 to day 3 after MCAO significantly decreased the migration of neuroblasts from the SVZ to the peri-infarct region, decreased angiogenesis, and lowered expression of vascular endothelial growth factor, stromal cell-derived factor-1, and monocyte chemotactic protein...
Source: Neuroscience - October 10, 2017 Category: Neuroscience Source Type: research
Microglia-mediated BAFF –BAFFR ligation promotes neuronal survival in brain ischemia injury
Publication date: 5 November 2017 Source:Neuroscience, Volume 363 Author(s): Kai Li, Wei Yu, Rangjuan Cao, Zhihua Zhu, Guoqing Zhao The innate immune responses of brain to vascular occlusion are primarily orchestrated by activated microglia. However, the roles of microglia in inflammatory responses to brain ischemic injuries are controversial. Here, we report a new mechanism by which microglia confer protective effects on ischemic neuronal cells. We found that under ischemic condition, the B-cell-activating factor (BAFF) was vastly upregulated in microglia and this upregulation could at least be attributed to JAK-STAT sig...
Source: Neuroscience - September 24, 2017 Category: Neuroscience Source Type: research
Vascular expression of angiopoietin1, α5β1 integrin and tight junction proteins is tightly regulated during vascular remodeling in the post-ischemic brain
Publication date: 24 October 2017 Source:Neuroscience, Volume 362 Author(s): Jialan Sun, Liming Yu, Shu Huang, Xiaoyin Lai, Richard Milner, Longxuan Li The post-stroke angiogenic response is accompanied by changes of tight junctions (TJs) of the blood–brain barrier (BBB). However, the precise dynamic change of TJ proteins (TJPs) in the different stages of stroke-induced vascular remodeling and the molecules mediating these processes have yet to be fully defined. To investigate the temporal relationship between changes in TJPs, the pro-angiogenic factor α5β1 integrin and the anti-permeability factor Ang1 in cerebral ve...
Source: Neuroscience - September 14, 2017 Category: Neuroscience Source Type: research
Gabapentin prevents cortical spreading depolarization-induced disinhibition
Publication date: 11 October 2017 Source:Neuroscience, Volume 361 Author(s): Masoud Mesgari, Johanna Krüger, Christopher Theo Riemer, Maryam Khaleghi Ghadiri, Stjepana Kovac, Ali Gorji Cortical spreading depolarization (CSD) has an important role in brain diseases such as stroke, subarachnoid hemorrhage, migraine with aura, and epilepsy. Several anti-epileptic drugs (AEDs) are used to treat paroxysmal brain diseases and are thus known to suppress CSD. One of these AEDs is gabapentin (GBP) which has been traditionally used for treatment of some CSD-related neurological diseases. We applied intra- and extracellular recordi...
Source: Neuroscience - September 2, 2017 Category: Neuroscience Source Type: research
Heat stress-induced neuroinflammation and aberration in monoamine levels in hypothalamus are associated with temperature dysregulation
In conclusion, the data suggest that SHS induces neuroinflammation in HTH, which is associated with monoamines and Glu imbalances, leading to thermoregulatory disruption.
Source: Neuroscience - July 15, 2017 Category: Neuroscience Source Type: research
Sevoflurane postconditioning attenuates reactive astrogliosis and glial scar formation after ischemia –reperfusion brain injury
This study was designed to investigate the effect of sevoflurane postconditioning on astrogliosis and glial scar formation in ischemic stroke model both in vivo and in vitro. The results showed that 2.5% of sevoflurane postconditioning could significantly reduce infarction volume and improve neurologic deficits. And it could also decrease the expression of the glial scar marker glial fibrillary acidic protein (GFAP), neurocan and phosphacan in the peri-infarct region and markedly reduce the thickness of glial scar after ischemia/reperfusion (I/R). Consistent with the in vivo data, in the oxygen and glucose deprivation/reox...
Source: Neuroscience - June 2, 2017 Category: Neuroscience Source Type: research
