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Titlebook: Brain Edema XVI; Translate Basic Scie Richard L. Applegate,Gang Chen,John H. Zhang Book 2016 Springer International Publishing Switzerland

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發(fā)表于 2025-3-21 19:17:50 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
期刊全稱(chēng)Brain Edema XVI
期刊簡(jiǎn)稱(chēng)Translate Basic Scie
影響因子2023Richard L. Applegate,Gang Chen,John H. Zhang
視頻videohttp://file.papertrans.cn/191/190169/190169.mp4
發(fā)行地址Presents the latest progress in basic sciences, translational research and clinical management strategies relating to brain edema and neurological disorders/injuries.Written by leading world authoriti
學(xué)科分類(lèi)Acta Neurochirurgica Supplement
圖書(shū)封面Titlebook: Brain Edema XVI; Translate Basic Scie Richard L. Applegate,Gang Chen,John H. Zhang Book 2016 Springer International Publishing Switzerland
影響因子In this book, leading world authorities on brain edema and neurological disorders/injuries and experts in preconditioning join forces to discuss the latest progress in basic sciences, translational research, and clinical management strategies relating to these conditions. The range of topics covered is wide, including microglia, energy metabolism, trace metals and ion channels, vascular biology, cellular treatment, hemorrhagic stroke, novel technological advances, anesthesia and medical gases, pediatric brain edema, neuroimaging, behavioral assessment, clinical trials, peripheral to central signaling pathways, preconditioning translation, and animal models for preconditioning and brain edema research. The book comprises presentations from Brain Edema 2014, the joint meeting of the 16th International Conference on Brain Edema and Cellular Injury and the 3rd Symposium on Preconditioning for Neurological Disorders, held in Los Angeles on September 27–30, 2014.
Pindex Book 2016
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書(shū)目名稱(chēng)Brain Edema XVI影響因子(影響力)




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Lecture Notes in Computer Science unruptured and non-hemorrhagic bAVMs demonstrate microscopic evidence of hemosiderin in the vascular wall. In bAVM mouse models, vascular mural cell coverage is reduced in the AVM lesion, accompanied by vascular leakage and microhemorrhage. In this review, we discuss possible signaling pathways involved in abnormal vascular development in bAVM.
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發(fā)表于 2025-3-22 02:39:41 | 只看該作者
Vascular Integrity in the Pathogenesis of Brain Arteriovenous Malformation unruptured and non-hemorrhagic bAVMs demonstrate microscopic evidence of hemosiderin in the vascular wall. In bAVM mouse models, vascular mural cell coverage is reduced in the AVM lesion, accompanied by vascular leakage and microhemorrhage. In this review, we discuss possible signaling pathways involved in abnormal vascular development in bAVM.
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發(fā)表于 2025-3-22 05:33:58 | 只看該作者
Book 2016atest progress in basic sciences, translational research, and clinical management strategies relating to these conditions. The range of topics covered is wide, including microglia, energy metabolism, trace metals and ion channels, vascular biology, cellular treatment, hemorrhagic stroke, novel techn
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https://doi.org/10.1007/978-94-015-8541-5about mannitol. More recently, administration of hypertonic saline has transitioned from boluses to continuous infusions. The rationale for and data supporting the use of continuous infusions are presented.
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發(fā)表于 2025-3-22 16:04:10 | 只看該作者
A Three-Level Approach to Ontology Mergingtricular area, suggestive of blood-cerebrospinal fluid (CSF) barrier disruption. Our data suggest that the periventricular area may be compromised first in conditions of inflammation and hypoxia. Voxel-based analysis could be used in future studies assessing subtle blood-CSF or BBB disruption.
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發(fā)表于 2025-3-22 17:24:42 | 只看該作者
Dexmont Pe?a,Ricardo Sánchez,Arturo Berronesview, we discuss the dual role of peripheral immune cells in stroke-related brain injury and neuroprotection. Furthermore, we report new data from our laboratory that supports the important role of peripheral cells and their interaction with the brain endothelium for the establishment of the protective phenotype in preconditioning.
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發(fā)表于 2025-3-22 21:13:01 | 只看該作者
Kavitha Yaddanapudi,Robert A. Mitchell Ph.D.has taken place in the last decade. This report describes our experiences with a murine model of SAH. We aim to standardize and optimize the procedures to establish a relatively stable animal model for SAH research.
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