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Neurological Injuries’ Monitoring, Tracking and Treatment 2017

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2017) | Viewed by 12466

Special Issue Editor

1. Department of Neurosurgery, Orthopaedics, Anatomy & Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA
2. Department of Biomedical Engineering, Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Interests: brain monitoring and therapeutic hypothermia; peripheral nerve injury and regeneration; translational therapeutic model for neurological injuries; development and characterization of biomaterials for bone and peripheral nerve regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2016 Special Issue, “Neurological Injuries’ Monitoring, Tracking and Treatment 2016”.

Despite recent advancements, the monitoring and tracking of neurological injuries are still major hindrances in the development of neurological injury therapies. Current monitoring methodologies have been largely limited to post-injury evaluation and prognostication. Induced hypothermia improves both survival and neurological outcome in cardiac arrest survivors; however, the monitoring methodologies to guide hypothermia therapy and improve its efficiency are not currently satisfying. Among the most exciting research areas, stem cell biology recently burst out and holds significant promise in the repair of neurological injuries. However, the role and effect of stem cell therapy still remain un-elucidated. The goal of this Special Issue is to provide a summary of the field, describe its impact, as well as to introduce the recent advances in the Neurological Injuries’ Monitoring, Tracking and Treatment. We invite authors to submit original research and review articles related with neurological injury; mainly brain injury after cardiac arrest, stroke, and traumatic brain injury, but also spinal cord injury as well. We are interested in articles that explore the advances in neuroengineering and latest technologies in monitoring and tracking neurological injury from translational model to clinical evaluation, such as electrophysiological monitoring and the optogenesis technique. This Special Issue will address novel therapeutic intervention in humans and also in animal models, including therapeutic hypothermia and stem cell therapy. 

Dr. Xiaofeng Jia
Guest Editor

Manuscript Submission Information

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Keywords

  • brain injury
  • cardiac arrest
  • stroke
  • traumatic brain injury
  • spinal cord injury
  • brain monitoring
  • electrophysiology
  • therapeutic hypothermia
  • stem cell
  • optogenesis
  • translational model
  • functional outcome
  • neuroengineering
  • clinical evaluation

Published Papers (2 papers)

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3154 KiB  
Article
Antarctic Krill Oil Diet Protects against Lipopolysaccharide-Induced Oxidative Stress, Neuroinflammation and Cognitive Impairment
by Ji Yeon Choi, Jun Sung Jang, Dong Ju Son, Hyung-Sik Im, Ji Yeong Kim, Joung Eun Park, Won Rak Choi, Sang-Bae Han and Jin Tae Hong
Int. J. Mol. Sci. 2017, 18(12), 2554; https://doi.org/10.3390/ijms18122554 - 28 Nov 2017
Cited by 42 | Viewed by 7067
Abstract
Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer’s disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and [...] Read more.
Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer’s disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from Euphausia superba (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). We examined whether krill oil diet (80 mg/kg/day for one month) prevents amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections in AD mice model and found that krill oil treatment inhibited the LPS-induced memory loss. We also found that krill oil treatment inhibited the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and decreased reactive oxygen species (ROS) and malondialdehyde levels. Krill oil also suppresses IκB degradation as well as p50 and p65 translocation into the nuclei of LPS-injected mice brain cells. In association with the inhibitory effect on neuroinflammation and oxidative stress, krill oil suppressed amyloid beta (1–42) peptide generation by the down-regulating APP and BACE1 expression in vivo. We found that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) dose-dependently decreased LPS-induced nitric oxide and ROS generation, and COX-2 and iNOS expression as well as nuclear factor-κB activity in cultured microglial BV-2 cells. These results suggest that krill oil ameliorated impairment via anti-inflammatory, antioxidative, and anti-amyloidogenic mechanisms. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2017)
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4802 KiB  
Article
GPE Promotes the Proliferation and Migration of Mouse Embryonic Neural Stem Cells and Their Progeny In Vitro
by Cristina Almengló, Pablo Devesa, Jesús Devesa and Víctor M. Arce
Int. J. Mol. Sci. 2017, 18(6), 1280; https://doi.org/10.3390/ijms18061280 - 16 Jun 2017
Cited by 11 | Viewed by 4815
Abstract
This study was designed to investigate a possible role of the N-terminal tripeptide of insulin-like growth factor-1 (IGF-I), Gly-Pro-Glu (GPE), physiologically generated in neurons following IGF-I-specific cleavage, in promoting neural regeneration after an injury. Primary cultures of mouse neural stem cells (NSCs), obtained [...] Read more.
This study was designed to investigate a possible role of the N-terminal tripeptide of insulin-like growth factor-1 (IGF-I), Gly-Pro-Glu (GPE), physiologically generated in neurons following IGF-I-specific cleavage, in promoting neural regeneration after an injury. Primary cultures of mouse neural stem cells (NSCs), obtained from 13.5 Days post-conception (dpc) mouse embryos, were challenged with either GPE, growth hormone (GH), or GPE + GH and the effects on cell proliferation, migration, and survival were evaluated both under basal conditions and in response to a wound healing assay. The cellular pathways activated by GPE were also investigated by using specific chemical inhibitors. The results of the study indicate that GPE treatment promotes the proliferation and the migration of neural stem cells in vitro through a mechanism that involves the activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase PI3K-Akt pathways. Intriguingly, both GPE effects and the signaling pathways activated were similar to those observed after GH treatment. Based upon the results obtained from this study, GPE, as well as GH, may be useful in promoting neural protection and/or regeneration after an injury. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2017)
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