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Special Issue "Neurological Injuries’ Monitoring, Tracking and Treatment 2016"

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 2016)

Special Issue Editor

Guest Editor
Assoc. Prof. Dr. Xiaofeng Jia

Department of Neurosurgery, Orthopaedics, University of Maryland School of Medicine, Department of Biomedical Engineering, Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, 10 South Pine Street, MSTF RM 5-59, Baltimore, MD 21201, USA
Website | E-Mail
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 Issue Information

Dear Colleagues,

This Special Issue is the continuation of our 2015 Special Issue, “Neurological Injuries’ Monitoring, Tracking and Treatment” (http://www.mdpi.com/journal/ijms/special_issues/neurological-injuries-monitoring).

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

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


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 (9 papers)

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Research

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Open AccessArticle Developing and Evaluating a Flexible Wireless Microcoil Array Based Integrated Interface for Epidural Cortical Stimulation
Int. J. Mol. Sci. 2017, 18(2), 335; doi:10.3390/ijms18020335
Received: 6 December 2016 / Revised: 26 January 2017 / Accepted: 31 January 2017 / Published: 5 February 2017
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Abstract
Stroke leads to serious long-term disability. Electrical epidural cortical stimulation has made significant improvements in stroke rehabilitation therapy. We developed a preliminary wireless implantable passive interface, which consists of a stimulating surface electrode, receiving coil, and single flexible passive demodulated circuit printed by
[...] Read more.
Stroke leads to serious long-term disability. Electrical epidural cortical stimulation has made significant improvements in stroke rehabilitation therapy. We developed a preliminary wireless implantable passive interface, which consists of a stimulating surface electrode, receiving coil, and single flexible passive demodulated circuit printed by flexible printed circuit (FPC) technique and output pulse voltage stimulus by inductively coupling an external circuit. The wireless implantable board was implanted in cats’ unilateral epidural space for electrical stimulation of the primary visual cortex (V1) while the evoked responses were recorded on the contralateral V1 using a needle electrode. The wireless implantable board output stable monophasic voltage stimuli. The amplitude of the monophasic voltage output could be adjusted by controlling the voltage of the transmitter circuit within a range of 5–20 V. In acute experiment, cortico-cortical evoked potential (CCEP) response was recorded on the contralateral V1. The amplitude of N2 in CCEP was modulated by adjusting the stimulation intensity of the wireless interface. These results demonstrated that a wireless interface based on a microcoil array can offer a valuable tool for researchers to explore electrical stimulation in research and the dura mater-electrode interface can effectively transmit electrical stimulation. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessArticle Therapeutic Potential of Induced Neural Stem Cells for Parkinson’s Disease
Int. J. Mol. Sci. 2017, 18(1), 224; doi:10.3390/ijms18010224
Received: 30 December 2016 / Revised: 11 January 2017 / Accepted: 17 January 2017 / Published: 22 January 2017
Cited by 2 | PDF Full-text (5226 KB) | HTML Full-text | XML Full-text
Abstract
Parkinson’s disease (PD) is a chronic, neurodegenerative disorder that results from the loss of cells in the substantia nigra (SN) which is located in the midbrain. However, no cure is available for PD. Recently, fibroblasts have been directly converted into induced neural stem
[...] Read more.
Parkinson’s disease (PD) is a chronic, neurodegenerative disorder that results from the loss of cells in the substantia nigra (SN) which is located in the midbrain. However, no cure is available for PD. Recently, fibroblasts have been directly converted into induced neural stem cells (iNSCs) via the forced expression of specific transcription factors. Therapeutic potential of iNSC in PD has not been investigated yet. Here, we show that iNSCs directly converted from mouse fibroblasts enhanced functional recovery in an animal model of PD. The rotational behavior test was performed to assess recovery. Our results indicate that iNSC transplantation into the striatum of 6-hydroxydopamine (6-OHDA)-injected mice can significantly reduce apomorphine-induced rotational asymmetry. The engrafted iNSCs were able to survive in the striatum and migrated around the medial forebrain bundle and the SN pars compacta. Moreover, iNSCs differentiated into all neuronal lineages. In particular, the transplanted iNSCs that committed to the glial lineage were significantly increased in the striatum of 6-OHDA-injected mice. Engrafted iNSCs differentiated to dopaminergic (DA) neurons and migrated into the SN in the 6-OHDA lesion mice. Therefore, iNSC transplantation serves as a valuable tool to enhance the functional recovery in PD. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessArticle Glucocorticoids Protect Neonatal Rat Brain in Model of Hypoxic-Ischemic Encephalopathy (HIE)
Int. J. Mol. Sci. 2017, 18(1), 17; doi:10.3390/ijms18010017
Received: 20 September 2016 / Revised: 10 December 2016 / Accepted: 19 December 2016 / Published: 22 December 2016
Cited by 1 | PDF Full-text (1917 KB) | HTML Full-text | XML Full-text
Abstract
Hypoxic-ischemic encephalopathy (HIE) resulting from asphyxia in the peripartum period is the most common cause of neonatal brain damage and can result in significant neurologic sequelae, including cerebral palsy. Currently therapeutic hypothermia is the only accepted treatment in addition to supportive care for
[...] Read more.
Hypoxic-ischemic encephalopathy (HIE) resulting from asphyxia in the peripartum period is the most common cause of neonatal brain damage and can result in significant neurologic sequelae, including cerebral palsy. Currently therapeutic hypothermia is the only accepted treatment in addition to supportive care for infants with HIE, however, many additional neuroprotective therapies have been investigated. Of these, glucocorticoids have previously been shown to have neuroprotective effects. HIE is also frequently compounded by infectious inflammatory processes (sepsis) and as such, the infants may be more amenable to treatment with an anti-inflammatory agent. Thus, the present study investigated dexamethasone and hydrocortisone treatment given after hypoxic-ischemic (HI) insult in neonatal rats via intracerebroventricular (ICV) injection and intranasal administration. In addition, we examined the effects of hydrocortisone treatment in HIE after lipopolysaccharide (LPS) sensitization in a model of HIE and sepsis. We found that dexamethasone significantly reduced rat brain infarction size when given after HI treatment via ICV injection; however it did not demonstrate any neuroprotective effects when given intranasally. Hydrocortisone after HI insult also significantly reduced brain infarction size when given via ICV injection; and the intranasal administration showed to be protective of brain injury in male rats at a dose of 300 µg. LPS sensitization did significantly increase the brain infarction size compared to controls, and hydrocortisone treatment after LPS sensitization showed a significant decrease in brain infarction size when given via ICV injection, as well as intranasal administration in both genders at a dose of 300 µg. To conclude, these results show that glucocorticoids have significant neuroprotective effects when given after HI injury and that these effects may be even more pronounced when given in circumstances of additional inflammatory injury, such as neonatal sepsis. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessCommunication Serum Levels of Substance P and Mortality in Patients with a Severe Acute Ischemic Stroke
Int. J. Mol. Sci. 2016, 17(6), 991; doi:10.3390/ijms17060991
Received: 12 May 2016 / Revised: 7 June 2016 / Accepted: 15 June 2016 / Published: 22 June 2016
Cited by 2 | PDF Full-text (742 KB) | HTML Full-text | XML Full-text
Abstract
Substance P (SP), a member of tachykinin family, is involved in the inflammation of the central nervous system and in the appearance of cerebral edema. Higher serum levels of SP have been found in 18 patients with cerebral ischemia compared with healthy controls.
[...] Read more.
Substance P (SP), a member of tachykinin family, is involved in the inflammation of the central nervous system and in the appearance of cerebral edema. Higher serum levels of SP have been found in 18 patients with cerebral ischemia compared with healthy controls. The aim of our multi-center study was to analyze the possible association between serum levels of SP and mortality in ischemic stroke patients. We included patients with malignant middle cerebral artery infarction (MMCAI) and a Glasgow Coma Scale (GCS) lower than 9. Non-surviving patients at 30 days (n = 31) had higher serum concentrations of SP levels at diagnosis of severe MMCAI than survivors (n = 30) (p < 0.001). We found in multiple regression an association between serum concentrations of SP higher than 362 pg/mL and mortality at 30 days (Odds Ratio = 5.33; 95% confidence interval = 1.541–18.470; p = 0.008) after controlling for age and GCS. Thus, the major novel finding of our study was the association between serum levels of SP and mortality in patients suffering from severe acute ischemic stroke. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Review

Jump to: Research

Open AccessReview The Temporal Pattern, Flux, and Function of Autophagy in Spinal Cord Injury
Int. J. Mol. Sci. 2017, 18(2), 466; doi:10.3390/ijms18020466
Received: 25 December 2016 / Revised: 16 February 2017 / Accepted: 17 February 2017 / Published: 21 February 2017
Cited by 1 | PDF Full-text (2107 KB) | HTML Full-text | XML Full-text
Abstract
Previous studies have indicated that autophagy plays a critical role in spinal cord injury (SCI), including traumatic spinal cord injury (TSCI) and ischemia-reperfusion spinal cord injury (IRSCI). However, while the understanding of mechanisms underlying autophagy in SCI has progressed, there remain several controversial
[...] Read more.
Previous studies have indicated that autophagy plays a critical role in spinal cord injury (SCI), including traumatic spinal cord injury (TSCI) and ischemia-reperfusion spinal cord injury (IRSCI). However, while the understanding of mechanisms underlying autophagy in SCI has progressed, there remain several controversial points: (1) temporal pattern results of autophagic activation after SCI are not consistent across studies; (2) effect of accumulation of autophagosomes due to the blockade or enhancement of autophagic flux is uncertain; (3) overall effect of enhanced autophagy remains undefined, with both beneficial and detrimental outcomes reported in SCI literature. In this review, the temporal pattern of autophagic activation, autophagic flux, autophagic cell death, relationship between autophagy and apoptosis, and pharmacological intervention of autophagy in TSCI (contusion injury, compression injury and hemisection injury) and IRSCI are discussed. Types of SCI and severity appear to contribute to differences in outcomes regarding temporal pattern, flux, and function of autophagy. With future development of specific strategies on autophagy intervention, autophagy may play an important role in improving functional recovery in patients with SCI. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessReview Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury
Int. J. Mol. Sci. 2017, 18(1), 129; doi:10.3390/ijms18010129
Received: 1 October 2016 / Revised: 31 December 2016 / Accepted: 4 January 2017 / Published: 11 January 2017
Cited by 2 | PDF Full-text (1212 KB) | HTML Full-text | XML Full-text
Abstract
Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain
[...] Read more.
Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians’ decision making in terms of which treatments to pursue. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessReview Brain Monitoring in Critically Neurologically Impaired Patients
Int. J. Mol. Sci. 2017, 18(1), 43; doi:10.3390/ijms18010043
Received: 14 November 2016 / Revised: 10 December 2016 / Accepted: 21 December 2016 / Published: 27 December 2016
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Abstract
Assessment of neurologic injury and the evolution of severe neurologic injury is limited in comatose or critically ill patients that lack a reliable neurologic examination. For common yet severe pathologies such as the comatose state after cardiac arrest, aneurysmal subarachnoid hemorrhage (aSAH), and
[...] Read more.
Assessment of neurologic injury and the evolution of severe neurologic injury is limited in comatose or critically ill patients that lack a reliable neurologic examination. For common yet severe pathologies such as the comatose state after cardiac arrest, aneurysmal subarachnoid hemorrhage (aSAH), and severe traumatic brain injury (TBI), critical medical decisions are made on the basis of the neurologic injury. Decisions regarding active intensive care management, need for neurosurgical intervention, and withdrawal of care, depend on a reliable, high-quality assessment of the true state of neurologic injury, and have traditionally relied on limited assessments such as intracranial pressure monitoring and electroencephalogram. However, even within TBI there exists a spectrum of disease that is likely not captured by such limited monitoring and thus a more directed effort towards obtaining a more robust biophysical signature of the individual patient must be undertaken. In this review, multimodal monitoring including the most promising serum markers of neuronal injury, cerebral microdialysis, brain tissue oxygenation, and pressure reactivity index to access brain microenvironment will be discussed with their utility among specific pathologies that may help determine a more complete picture of the neurologic injury state for active intensive care management and long-term outcomes. Goal-directed therapy guided by a multi-modality approach appears to be superior to standard intracranial pressure (ICP) guided therapy and should be explored further across multiple pathologies. Future directions including the application of optogenetics to evaluate brain injury and recovery and even as an adjunct monitoring modality will also be discussed. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessReview Stem Cells and Labeling for Spinal Cord Injury
Int. J. Mol. Sci. 2017, 18(1), 6; doi:10.3390/ijms18010006
Received: 30 September 2016 / Revised: 9 December 2016 / Accepted: 12 December 2016 / Published: 26 December 2016
Cited by 1 | PDF Full-text (3486 KB) | HTML Full-text | XML Full-text
Abstract
Spinal cord injury (SCI) is a devastating condition that usually results in sudden and long-lasting locomotor and sensory neuron degeneration below the lesion site. During the last two decades, the search for new therapies has been revolutionized with the improved knowledge of stem
[...] Read more.
Spinal cord injury (SCI) is a devastating condition that usually results in sudden and long-lasting locomotor and sensory neuron degeneration below the lesion site. During the last two decades, the search for new therapies has been revolutionized with the improved knowledge of stem cell (SC) biology. SCs therapy offers several attractive strategies for spinal cord repair. The transplantation of SCs promotes remyelination, neurite outgrowth and axonal elongation, and activates resident or transplanted progenitor cells across the lesion cavity. However, optimized growth and differentiation protocols along with reliable safety assays should be established prior to the clinical application of SCs. Additionally, the ideal method of SCs labeling for efficient cell tracking after SCI remains a challenging issue that requires further investigation. This review summarizes the current findings on the SCs-based therapeutic strategies, and compares different SCs labeling approaches for SCI. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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Open AccessReview Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke
Int. J. Mol. Sci. 2016, 17(12), 1967; doi:10.3390/ijms17121967
Received: 5 October 2016 / Revised: 8 November 2016 / Accepted: 17 November 2016 / Published: 25 November 2016
Cited by 5 | PDF Full-text (3459 KB) | HTML Full-text | XML Full-text
Abstract
After an acute ischemic stroke (AIS), inflammatory processes are able to concomitantly induce both beneficial and detrimental effects. In this narrative review, we updated evidence on the inflammatory pathways and mediators that are investigated as promising therapeutic targets. We searched for papers on
[...] Read more.
After an acute ischemic stroke (AIS), inflammatory processes are able to concomitantly induce both beneficial and detrimental effects. In this narrative review, we updated evidence on the inflammatory pathways and mediators that are investigated as promising therapeutic targets. We searched for papers on PubMed and MEDLINE up to August 2016. The terms searched alone or in combination were: ischemic stroke, inflammation, oxidative stress, ischemia reperfusion, innate immunity, adaptive immunity, autoimmunity. Inflammation in AIS is characterized by a storm of cytokines, chemokines, and Damage-Associated Molecular Patterns (DAMPs) released by several cells contributing to exacerbate the tissue injury both in the acute and reparative phases. Interestingly, many biomarkers have been studied, but none of these reflected the complexity of systemic immune response. Reperfusion therapies showed a good efficacy in the recovery after an AIS. New therapies appear promising both in pre-clinical and clinical studies, but still need more detailed studies to be translated in the ordinary clinical practice. In spite of clinical progresses, no beneficial long-term interventions targeting inflammation are currently available. Our knowledge about cells, biomarkers, and inflammatory markers is growing and is hoped to better evaluate the impact of new treatments, such as monoclonal antibodies and cell-based therapies. Full article
(This article belongs to the Special Issue Neurological Injuries’ Monitoring, Tracking and Treatment 2016)
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