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bbb edema

Yu Okuma, Hidenori Wake, Kiyoshi Teshigawara, Yu Takahashi, Tomohito Hishikawa, Takao Yasuhara, Shuji Mori, Hideo K Takahashi, Isao Date, Masahiro Nishibori
BACKGROUND: High mobility group box-1 (HMGB1) protein plays a key role in triggering inflammatory responses in many diseases. Our previous study showed that HMGB1 is found upstream of secondary damage in traumatic brain injury (TBI). We found that anti-HMGB1 monoclonal antibody (mAb) effectively decreased acute brain damage, including the disruption of the blood brain barrier, brain edema, and neurologic dysfunction. This effect of anti-HMGB1 mAb lasts for at least 1 week. In this study, we explored the subacute effects of anti-HMGB1 mAb after TBI...
November 1, 2018: World Neurosurgery
Juliane Gust, Agne Taraseviciute, Cameron J Turtle
Neurotoxicity is an important and common complication of chimeric antigen receptor-T cell therapies. Acute neurologic signs and/or symptoms occur in a significant proportion of patients treated with CD19-directed chimeric antigen receptor-T cells for B-cell malignancies. Clinical manifestations include headache, confusion, delirium, language disturbance, seizures and rarely, acute cerebral edema. Neurotoxicity is associated with cytokine release syndrome, which occurs in the setting of in-vivo chimeric antigen receptor-T cell activation and proliferation...
November 1, 2018: CNS Drugs
Jessica S Wallisch, Keri Janesko-Feldman, Henry Alexander, Ruchira M Jha, George W Farr, Paul R McGuirk, Anthony E Kline, Travis C Jackson, Marc F Pelletier, Robert S B Clark, Patrick M Kochanek, Mioara D Manole
BACKGROUND: Cerebral edema after cardiac arrest (CA) is associated with increased mortality and unfavorable outcome in children and adults. Aquaporin-4 mediates cerebral water movement and its absence in models of ischemia improves outcome. We investigated early and selective pharmacologic inhibition of aquaporin-4 in a clinically relevant asphyxial CA model in immature rats in a threshold CA insult that produces primarily cytotoxic edema in the absence of blood-brain barrier permeability...
October 26, 2018: Pediatric Research
Hirofumi Nishikawa, Lei Liu, Fumi Nakano, Fumihiro Kawakita, Hideki Kanamaru, Yoshinari Nakatsuka, Takeshi Okada, Hidenori Suzuki
Background and Purpose- Plasma levels of galectin-3-a matricellular protein-are increased after aneurysmal subarachnoid hemorrhage (SAH), but the functional significance remains undetermined. This study was conducted to evaluate whether modified citrus pectin (MCP; galectin-3 inhibitor) prevents post-SAH early brain injury, focusing on blood-brain barrier disruption. Methods- C57BL/6 male adult mice (n=251) underwent sham or filament perforation SAH modeling, followed by a random intracerebroventricular injection of vehicle or drug at 30 minutes post-modeling...
November 2018: Stroke; a Journal of Cerebral Circulation
Qing-Fang Chen, Yu-Ying Liu, Chun-Shui Pan, Jing-Yu Fan, Li Yan, Bai-He Hu, Xin Chang, Quan Li, Jing-Yan Han
Background and Purpose- tPA (tissue-type plasminogen activator) is the only recommended intravenous thrombolytic agent for ischemic stroke. However, its application is limited because of increased risk of hemorrhagic transformation beyond the time window. T541 is a Chinese compound medicine with potential to attenuate ischemia and reperfusion injury. This study was to explore whether T541-benefited subjects underwent tPA thrombolysis extending the time window. Methods- Male C57BL/6 N mice were subjected to carotid artery thrombosis by stimulation with 10% FeCl3 followed by 10 mg/kg tPA with/without 20 mg/kg T541 intervention at 4...
September 2018: Stroke; a Journal of Cerebral Circulation
Dian-Xu Yang, Yao Jing, Ying-Liang Liu, Zhi-Ming Xu, Fang Yuan, Ming-Liang Wang, Zhi Geng, Heng-Li Tian
Transient receptor potential vanilloid 1 (TRPV1) is widely expressed in the central nervous system and is activated by various stimuli. Inhibiting TRPV1 has neuroprotective effects in cerebral ischemia. However, the role of inhibiting TRPV1 to maintain blood-brain barrier (BBB) integrity following traumatic brain injury (TBI) remains unclear. Therefore, we investigated the effects of capsazepine-mediated TRPV1 inhibition on the BBB in a mouse model of TBI. Adult male C57BL/6 mice were subjected to controlled cortical impact injury and received capsazepine (1 µmol/kg body weight, twice daily, intraperitoneally) until sacrifice...
October 23, 2018: Journal of Neurotrauma
Tianyang Xi, Feng Jin, Ying Zhu, Jialu Wang, Ling Tang, Yanzhe Wang, David S Liebeskind, Fabien Scalzo, Zhiyi He
Previous studies have reported that miR-27a-3p is down-regulated in the serum of patients with intracerebral hemorrhage (ICH).Yet the implication of miR-27a-3p down-regulation in post-ICH complications remains elusive. Here, we verified miR-27a-3p levels in the serum of ICH patients by real-time PCR and observed that miR-27a-3p is also significantly reduced in the serum of these patients. We then further investigated the effect of miR-27a-3p on post-ICH complications by intraventricular administration of a miR-27a-3p mimic in rats with collagenase-induced ICH...
October 18, 2018: Journal of Biological Chemistry
You-Dong Zhou, Li Cai
BACKGROUND: Inhibition of calpain activity provides neuroprotection in multiple central nervous system injury, but the role and mechanism of calpain in subarachnoid hemorrhage (SAH) remain unclear. This study was undertaken to determine the effects of inhibition of calpain on neurological deficit and neuronal apoptosis following experimental SAH. METHODS: The endovascular perforation model of SAH was produced in male Sprague-Dawley rats. Rats were administered calpeptin 50μg, intracerebroventricular injection, 30 minutes before induction of SAH...
October 15, 2018: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Yanrong Zhu, Ke Wang, Zhiqiang Ma, Dong Liu, Yang Yang, Meng Sun, Aidong Wen, Yuewen Hao, Shanbo Ma, Fang Ren, Zhenlong Xin, Yue Li, Shouyin Di, Juntian Liu
Sepsis-induced brain injury is frequently encountered in critically ill patients with severe systemic infection. Butein (3,4,2',4'-tetrahydroxychalcone) has been demonstrated as the neuro-protective agent via reducing inflammation and oxidative stress on neurons. Moreover, activation of silent information regulator 1 (SIRT1) inhibits apoptosis, oxidation and inflammation thus alleviating sepsis-induced multiorgan injuries. In present study, we show that butein administrated intraperitoneally (10 mg/kg) saved mice from sepsis-induced lethality by increasing 7-day survival rate after cecal ligation and puncture (CLP) surgery...
October 15, 2018: Toxicology and Applied Pharmacology
Pengfei Wang, Yueyu Hu, Danhua Yao, Yousheng Li
BACKGROUND/AIMS: the pathogenesis of sepsis-associated encephalopathy (SAE) is multifactorial, involving neurotransmitter alterations, inflammatory cytokines, oxidative damage, mitochondrial dysfunction, apoptosis, and other factors. Mitochondria are major producers of reactive oxygen species, resulting in cellular injury. Omi/HtrA2 is a proapoptotic mitochondrial serine protease involved in caspase-dependent cell death; it is translocated from mitochondria to the cytosol after an apoptotic insult...
2018: Cellular Physiology and Biochemistry
Weilin Xu, Xiaoyang Lu, Jingwei Zheng, Tao Li, Liansheng Gao, Cameron Lenahan, Anwen Shao, Jianmin Zhang, Jun Yu
Neuronal apoptosis is an important factor accounting for the poor outcomes of intracerebral hemorrhage (ICH). This study first showed that inhibition of activating transcription factor 6 (ATF6) could alleviate secondary brain injury through anti-apoptosis after ICH in rats. Melatonin, ATF6 and CCAAT/enhancer-binding protein homologous protein (CHOP) siRNAs were applied in this study. Brain edema, neurological functions, blood-brain barrier (BBB) integrity were evaluated at 24 h after ICH. Western blot analysis was used to evaluate the protein level of target proteins (ATF6, CHOP, Bip, Bcl-2, Bax, and cleaved caspase-3)...
2018: Frontiers in Neuroscience
Suraj Sulhan, Kristopher A Lyon, Lee A Shapiro, Jason H Huang
Traumatic Brain Injury (TBI) is the most frequent cause of death and disability in young adults and children in the developed world, occurring in over 1.7 million persons and resulting in 50,000 deaths in the United States alone. The Centers for Disease Control and Prevention estimate that between 3.2 and 5.3 million persons in the United States live with a TBI-related disability, including several neurocognitive disorders and functional limitations. Following the primary mechanical injury in TBI, literature suggests the presence of a delayed secondary injury involving a variety of neuroinflammatory changes...
September 27, 2018: Journal of Neuroscience Research
Matthew D Howe, Liang Zhu, Lauren H Sansing, Nicole R Gonzales, Louise D McCullough, Nancy J Edwards
Background: Intracerebral hemorrhage (ICH) is a stroke subtype associated with high disability and mortality. There is a clinical need for blood-based biomarkers that can aid in diagnosis, risk stratification, and prognostication. Given their role in the pathophysiology of ICH, we hypothesized markers of blood-brain barrier disruption and fibrosis would associate with neurologic deterioration and/or long-term functional outcomes. We also hypothesized these markers may be unique in patients with ICH due to cerebral amyloid angiopathy (CAA) vs...
2018: Frontiers in Neurology
James M Jones, Marc A DePaul, Cynthia R Gregory, Bradley T Lang, Hua Xie, Meihua Zhu, Michael J Rutten, Robert W Mays, Sarah A Busch, Shibani Pati, Kenton W Gregory
Following spinal cord injury (SCI), inflammation amplifies damage beyond the initial insult, providing an opportunity for targeted treatments. An ideal protective therapy would reduce both edema within the lesion area and the activation/infiltration of detrimental immune cells. Previous investigations demonstrated the efficacy of intravenous injection of multi-potent adult progenitor cells (MAPC® ) to modulate immune response following SCI, leading to significant improvements in tissue sparing, locomotor and urological functions...
November 2, 2018: Journal of Neurotrauma
Eva Kjer Oernbo, Kasper Lykke, Annette Buur Steffensen, Kathrin Töllner, Christina Kruuse, Martin Fredensborg Rath, Wolfgang Löscher, Nanna MacAulay
BACKGROUND: Cerebral edema can cause life-threatening increase in intracranial pressure. Besides surgical craniectomy performed in severe cases, osmotherapy may be employed to lower the intracranial pressure by osmotic extraction of cerebral fluid upon intravenous infusion of mannitol or NaCl. A so-called rebound effect can, however, hinder continuous reduction in cerebral fluid by yet unresolved mechanisms. METHODS: We determined the brain water and electrolyte content in healthy rats treated with osmotherapy...
September 25, 2018: Fluids and Barriers of the CNS
Hidenori Suzuki, Masashi Fujimoto, Fumihiro Kawakita, Lei Liu, Yoshinari Nakatsuka, Fumi Nakano, Hirofumi Nishikawa, Takeshi Okada, Hideki Kanamaru, Kyoko Imanaka-Yoshida, Toshimichi Yoshida, Masato Shiba
Subarachnoid hemorrhage (SAH) by a rupture of cerebral aneurysms remains the most devastating cerebrovascular disease. Early brain injury (EBI) is increasingly recognized to be the primary determinant for poor outcomes, and also considered to cause delayed cerebral ischemia (DCI) after SAH. Both clinical and experimental literatures emphasize the impact of global cerebral edema in EBI as negative prognostic and direct pathological factors. The nature of the global cerebral edema is a mixture of cytotoxic and vasogenic edema, both of which may be caused by post-SAH induction of tenascin-C (TNC) that is an inducible, non-structural, secreted and multifunctional matricellular protein...
September 22, 2018: Journal of Neuroscience Research
Yu-Wei Han, Xiu-Juan Liu, Ying Zhao, Xiao-Ming Li
Vasogenic brain edema after subarachnoid hemorrhage (SAH) is an independent risk factor for death and poor prognosis. Disruption of the blood-brain barrier (BBB) is the main cause of vasogenic brain edema induced by SAH. Oleanolic acid (OA) is a natural pentacyclic triterpenoid with various biological functions. Previous studies have shown that prophylactic administration of OA could prevent the BBB disruption in autoimmune encephalomyelitis mice. In this context, we speculate that OA may play a neuroprotective role by protecting the integrity of the BBB and reducing vasogenic cerebral edema after SAH...
September 19, 2018: European Journal of Pharmacology
Esmeralda K Bosma, Cornelis J F van Noorden, Reinier O Schlingemann, Ingeborg Klaassen
Breakdown of the blood-brain barrier (BBB) or inner blood-retinal barrier (BRB), induced by pathologically elevated levels of vascular endothelial growth factor (VEGF) or other mediators, can lead to vasogenic edema and significant clinical problems such as neuronal morbidity and mortality, or vision loss. Restoration of the barrier function with corticosteroids in the brain, or by blocking VEGF in the eye are currently the predominant treatment options for brain edema and diabetic macular edema, respectively...
September 20, 2018: Fluids and Barriers of the CNS
Xiaohui Li, Xinjun Wang, Jingwei Xie, Bo Liang, Jianheng Wu
Glioblastoma multiforme (GBM) is the most primary brain tumor, specially characterized with the damage of blood-brain barrier (BBB). The Ang-(1-7) was proven to have an inhibitory effect on glioblastoma growth. However, its role on blood-brain barrier (BBB) and the underlying molecular mechanism remains unclear. In this study, Ang-(1-7) significantly relieved the damage of blood-brain barrier in rats with intracranial U87 gliomas as evaluated by magnetic resonance imaging (MRI). Furthermore, its treatment attenuated BBB permeability, tumor growth and edema formation...
September 18, 2018: Pathology Oncology Research: POR
Mayanka Kamboj, Amir Kazory
Over the last decades, there have been major advancements in the field of renal replacement therapy (RRT) with utilization of newer technologies and advent of various modalities. Once exclusively used for treatment of renal failure and its metabolic consequences, the science of RRT has expanded to include non-renal indications such as treatment of fluid overload in patients with refractory heart failure. Hepatic encephalopathy due to sudden rise in serum ammonia level in the setting of acute liver failure represents an underexplored area in which RRT can potentially be helpful...
September 18, 2018: Blood Purification
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