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bbb edema

X Liu, X Zhang, K Ma, R Zhang, P Hou, B Sun, S Yuan, Z Wang, Z Liu
Matrine is a quinolizidine alkaloid derived from the herb Radix Sophorae Flavescentis, and possesses anti-oxidant, anti-inflammatory and anti-tumoral properties. However, its effectiveness against subarachnoid hemorrhage (SAH) is not well known. In this study, we investigated the effects of matrine on early brain injury (EBI) and the related potential mechanisms following SAH in rats. Our results showed that matrine pretreatment partially alleviated SAH-induced EBI, including neurological deficit, severity of SAH grade, brain edema, and blood-brain barrier (BBB) disruption in rats...
September 30, 2016: Cellular and Molecular Biology
Hidehito Kimura, Masaaki Taniguchi, Tatsuya Mori, Kohkichi Hosoda, Eiji Kohmura
We present a rare case of a patient suffering temporary aphasia after an extracranial-to-intracranial (EC-IC) bypass surgery, which was shown as a transient hypointense lesion on diffusion-weighted imaging (DWI) with increased apparent diffusion coefficient (ADC) value, evidence of postoperative hyperperfusion. Postoperative hyperperfusion syndrome after EC-IC bypass causing temporary neurological deterioration has been reported rarely as isosignal intensity on DWI with hyperintense lesion on T2-weighted image and fluid-attenuated inversion recovery (FLAIR) image as an expression of vasogenic edema...
October 14, 2016: World Neurosurgery
Yash V Tiwari, Jianfei Lu, Qiang Shen, Bianca Cerqueira, Timothy Q Duong
Diffusion-weighted arterial spin labeling magnetic resonance imaging has recently been proposed to quantify the rate of water exchange (Kw) across the blood-brain barrier in humans. This study aimed to evaluate the blood-brain barrier disruption in transient (60 min) ischemic stroke using Kw magnetic resonance imaging with cross-validation by dynamic contrast-enhanced magnetic resonance imaging and Evans blue histology in the same rats. The major findings were: (i) at 90 min after stroke (30 min after reperfusion), group Kw magnetic resonance imaging data showed no significant blood-brain barrier permeability changes, although a few animals showed slightly abnormal Kw Dynamic contrast-enhanced magnetic resonance imaging confirmed this finding in the same animals...
October 14, 2016: Journal of Cerebral Blood Flow and Metabolism
Mingchang Li, Wei Wang, Haojian Mai, Xinmu Zhang, Jian Wang, Yufeng Gao, Yuefei Wang, Gang Deng, Ling Gao, Shuanhu Zhou, Qianxue Chen, Xin Wang
Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment. Currently, no clear measures can reduce brain nerve damage. The study of brain nerve protection after SAH is of great significance. We aim to evaluate the protective effects and the possible mechanism of methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary cortical neuron (PCNs) cellular model of SAH in vitro. We demonstrate that methazolamide accelerates the recovery of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or hemoglobin-treated PCNs and partially restores normal neuronal morphology...
October 12, 2016: Scientific Reports
Peter D Chang, Daniel S Chow, Peter H Yang, Christopher G Filippi, Angela Lignelli
OBJECTIVE: Recurrence of glioblastoma multiforme (GBM) arises from areas of microscopic tumor infiltration that have yet to disrupt the blood-brain barrier. We hypothesize that these microscopic foci of invasion cause subtle variations in the apparent diffusion coefficient (ADC) and FLAIR signal detectable with the use of computational big-data modeling. MATERIALS AND METHODS: Twenty-six patients with native GBM were studied immediately after undergoing gross total tumor resection...
October 11, 2016: AJR. American Journal of Roentgenology
Ulysse Gimenez, Adriana-T Perles-Barbacaru, Arnaud Millet, Florence Appaix, Michele El-Atifi, Karin Pernet-Gallay, Boudewijn van der Sanden, François Berger, Hana Lahrech
Monitoring glioma cell infiltration in the brain is critical for diagnosis and therapy. Using a new glioma Glio6 mouse model derived from human stem cells we show how diffusion tensor imaging (DTI) may predict glioma cell migration/invasion. In vivo multiparametric MRI was performed at one, two and three months of Glio6 glioma growth (Glio6 (n = 6), sham (n = 3)). This longitudinal study reveals the existence of a time window to study glioma cell/migration/invasion selectively. Indeed, at two months only Glio6 cell invasion was detected, while tumor mass formation, edema, blood-brain barrier leakage and tumor angiogenesis were detected later, at three months...
September 15, 2016: NMR in Biomedicine
Kang-Ho Choi, Hyung-Seok Kim, Man-Seok Park, Eun-Bin Lee, Jung-Kil Lee, Joon-Tae Kim, Ja-Hae Kim, Min-Cheol Lee, Hong-Joon Lee, Ki-Hyun Cho
Cerebral edema from the disruption of the blood-brain barrier (BBB) after cerebral ischemia is a major cause of morbidity and mortality as well as a common event in patients with stroke. Caveolins (Cavs) are thought to regulate BBB functions. Here, we report for the first time that Cav-1 overexpression (OE) decreased brain edema from BBB disruption following ischemic insult. Edema volumes and Cav-1 expression levels were measured following photothrombosis and middle cerebral artery occlusion (MCAO). Endothelial cells that were transduced with a Cav-1 lentiviral expression vector were transplanted into rats...
September 29, 2016: Oncotarget
Chin-Yi Cheng, Yu-Chen Lee
Inflammation plays a crucial role in the pathophysiology of acute ischemic stroke. In the ischemic cascade, resident microglia are rapidly activated in the brain parenchyma and subsequently trigger inflammatory mediator release, which facilitates leukocyte-endothelial cell interactions in inflammation. Activated leukocytes invade the endothelial cell junctions and destroy the blood-brain barrier integrity, leading to brain edema. Toll-like receptors (TLRs) stimulation in microglia/macrophages through the activation of intercellular signaling pathways secretes various proinflammatory cytokines and enzymes and then aggravates cerebral ischemic injury...
2016: Evidence-based Complementary and Alternative Medicine: ECAM
Kouichi Itoh, Yasuhiro Ishihara, Rie Komori, Hiromi Nochi, Ruri Taniguchi, Yoichi Chiba, Masaki Ueno, Fuyuko Takata-Tsuji, Shinya Dohgu, Yasufumi Kataoka
Our previous study showed that treatment with levetiracetam (LEV) after status epilepticus (SE) termination by diazepam might prevent the development of spontaneous recurrent seizures via the inhibition of neurotoxicity induced by brain edema events. In the present study, we determined the possible molecular and cellular mechanisms of LEV treatment after termination of SE. To assess the effect of LEV against the brain alterations after SE, we focused on blood-brain barrier (BBB) dysfunction associated with angiogenesis and brain inflammation...
September 27, 2016: Brain Research
Martin Krueger, Wolfgang Härtig, Clara Frydrychowicz, Wolf C Mueller, Andreas Reichenbach, Ingo Bechmann, Dominik Michalski
Stroke-induced blood-brain barrier breakdown promotes complications like cerebral edema and hemorrhagic transformation, especially in association with therapeutical recanalization of occluded vessels. As arteries, capillaries and veins display distinct functional and morphological characteristics, we here investigated patterns of blood-brain barrier breakdown for each segment of the vascular tree in rodent models of embolic, permanent, and transient middle cerebral artery occlusion, added by analyses of human stroke tissue...
September 28, 2016: Journal of Cerebral Blood Flow and Metabolism
Budbazar Enkhjargal, Devin W McBride, Anatol Manaenko, Cesar Reis, Yasushi Sakai, Jiping Tang, John H Zhang
In this study, we investigated the role of vitamin D3 (VitD3) on endogenous osteopontin (OPN), a neuroprotective glycoprotein, after subarachnoid hemorrhage (SAH). The endovascular perforation SAH model in Sprague-Dawley rats was used to study the effect of intranasal VitD3 (30 ng/kg) before (Pre-SAH + VitD3) and after (Post-SAH + VitD3) subarachnoid hemorrhage. Vitamin D3 (30, 60, 120 ng/kg/day) increased more than one fold endogenous OPN expression in astrocytes and endothelial cells of rat brain...
September 26, 2016: Journal of Cerebral Blood Flow and Metabolism
Jose V Lafuente, G Bermudez, L Camargo-Arce, S Bulnes
Cerebral syndromes related to high altitude exposure are becoming more frequent as the number of trips to high altitudes has increased in the last decade. The commonest symptom is headache, followed by acute mountain sickness (AMS) and high-altitude cerebral edema (HACE), which can be fatal. The pathophysiology of these syndromes is not fully comprehended. The classical "tight-fit hypothesis" defends the fact that there are some anatomical variations that would obstruct the sinovenous outflow and worsen the vasogenic edema and intracranial hypertension reactive to hypoxia...
September 20, 2016: CNS & Neurological Disorders Drug Targets
Duk-Soo Kim, Su-Ji Min, Min-Ju Kim, Ji-Eun Kim, Tae-Cheon Kang
The blood-brain barrier (BBB) disruption during brain insults leads to vasogenic edema as one of the primary steps in the epileptogenic process. However, the signaling pathway concerning vasogenic edema formation has not been clarified. In the present study, status epilepticus (SE) resulted in vascular endothelial growth factor (VEGF) over-expression accompanied by loss of BBB integrity in the rat piriform cortex. Leptomycin B (LMB, an inhibitor of chromosome region maintenance 1) attenuated SE-induced vasogenic edema formation...
September 19, 2016: Brain Research
Jennifer M Colón, Jorge D Miranda
Spinal cord injury (SCI) is a condition without a cure, affecting sensory and/or motor functions. The physical trauma to the spinal cord initiates a cascade of molecular and cellular events that generates a non-permissive environment for cell survival and axonal regeneration. Among these complex set of events are damage of the blood-brain barrier, edema formation, inflammation, oxidative stress, demyelination, reactive gliosis and apoptosis. The multiple events activated after SCI require a multi-active drug that could target most of these events and produce a permissive environment for cell survival, regeneration, vascular reorganization and synaptic formation...
August 2016: Neural Regeneration Research
Bin Zhao, Xiaoke Wang, Jun Zheng, Hailiang Wang, Jun Liu
Considerable evidence has demonstrated that metformin can activate 5'-AMP-activated protein kinase (AMPK) signaling pathway, which plays a critical role in protection of endothelial cell permeability. Hence, the present study evaluated the effects of metformin on blood brain barrier permeability and AQP4 expression in vitro, and assessed the effects of metformin treatment on tumor-induced brain edema in vivo. Hypoxia or VEGF exposure enhanced bEnd3 endothelial cell monolayer permeability and attenuated the expression of tight junction proteins including Occludin, Claudin-5, ZO-1, and ZO-2...
2016: American Journal of Translational Research
So Y Cheon, Kyoung J Cho, So Y Kim, Eun H Kam, Jong E Lee, Bon-Nyeo Koo
Conditions of increased oxidative stress including cerebral ischemia can lead to blood-brain barrier dysfunction via matrix metalloproteinase (MMP). It is known that MMP-9 in particular is released from brain endothelial cells is involved in the neuronal cell death that occurs after cerebral ischemia. In the intracellular signaling network, apoptosis signal-regulating kinase 1 (ASK1) is the main activator of the oxidative stress that is part of the pathogenesis of cerebral ischemia. ASK1 also promotes apoptotic cell death and brain infarction after ischemia and is associated with vascular permeability and the formation of brain edema...
2016: Frontiers in Cellular Neuroscience
Jui-Tai Chen, Yi-Ling Lin, Ta-Liang Chen, Yu-Ting Tai, Cheng-Yu Chen, Ruei-Ming Chen
Following brain injury, a sequence of mechanisms leads to disruption of the blood-brain barrier (BBB) and subsequent cerebral edema, which is thought to begin with activation of bradykinin. Our previous studies showed that ketamine, a widely used intravenous anesthetic agent, can suppress bradykinin-induced cell dysfunction. This study further aimed to evaluate the protective effects of ketamine against bradykinin-induced disruption of the mouse cerebrovascular endothelial cell (MCEC)-constructed tight junction barrier and the possible mechanisms...
August 10, 2016: Toxicology
Conrad Johanson, Nancy Johanson
Robust modeling of CNS transport integrates molecular fluxes at the microvascular blood-brain barrier and epithelial choroid plexus blood-CSF barrier. Normal activity of solute transporters, channels and aquaporins, in the cerebral endothelium and choroidal epithelium, sets the microenvironment composition for neurons and glia. Conversely, perturbed transport/permeability at the barrier interfaces causes interstitial fluid dyshomeostasis (e.g. edema) arising in neural disorders. Critically-important transependymal solute/water distribution between brain and CSF needs more attention...
September 15, 2016: CNS & Neurological Disorders Drug Targets
Gustav Folmer Genét, Peter Bentzer, Sisse Rye Ostrowski, Pär Ingemar Johansson
Traumatic brain injury and hemorrhagic shock is associated with blood-brain barrier (BBB) breakdown and edema formation. Recent animal studies have shown that fresh frozen plasma (FFP) resuscitation reduces brain swelling and improves endothelial function compared to isotonic NaCl (NS). The aim of this study was to investigate whether pooled and pathogen-reduced plasma (OctaplasLG(®) [OCTA]; Octapharma, Stockholm, Sweden) was comparable to FFP with regard to effects on brain water content, BBB permeability, and plasma biomarkers of endothelial glycocalyx shedding and cell damage...
October 13, 2016: Journal of Neurotrauma
Su-Ji Min, Tae-Cheon Kang
Brain-blood barrier (BBB) disruption results in vasogenic edema, which is involved in the pathogenesis of epilepsy. Following status epilepticus (SE), up-regulated transient receptor potential canonical channel-3 (TRPC3), a Ca(2+)-permeable cation channels in endothelial cells, is relevant to vasogenic edema formation in the rat piriform cortex. In addition, pyrazole-3 (Pyr-3, a TRPC3 inhibitor) attenuated SE-induced vasogenic edema. However, the upstream regulators of TRPC3 expression in vasogenic edema formation have been unclear...
September 10, 2016: Neuroscience
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