| 1. |
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| 2. |
- Björklund, A, et al.
(author)
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Reafferentation of the subcortically denervated hippocampus as a model for transplant-induced functional recovery in the CNS
- 1990
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In: Progress in Brain Research. - 0079-6123. ; 83, s. 411-426
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Research review (peer-reviewed)abstract
- Subcortical deafferentation of the hippocampal formation is known to induce profound behavioural deficits. Transplants of fetal septal or brainstem tissue are capable of restoring some aspects of normal physiological and behavioural function in subcortically deafferented (i.e. fimbria-fornix or septal lesioned) rats. Such grafts have been shown to re-establish extensive new afferent inputs to the denervated hippocampal formation. As shown for grafted cholinergic and noradrenergic neurons, the ingrowing axons form laminar innervation patterns which closely mimic those of the normal cholinergic and noradrenergic innervations. The ingrowth appears to be very precisely regulated by the denervated target: each neuron type produces distinctly different innervation patterns; the growth is inhibited by the presence of an intact innervation of the same type; and it is stimulated by additional denervating lesions. Both ultrastructually and electrophysiologically the graft-derived fibres have been seen to form extensive functional synaptic contacts. Biochemically, cholinergic septal grafts and noradrenergic locus coeruleus grafts restore transmitter synthesis and turnover in the reinnervated hippocampus. Intracerebral microdialysis has revealed that acetylcholine and noradrenaline release is restored to normal or supranormal levels in the graft-reinnervated hippocampus, and that the grafted neurons can be activated in a normal way from the host through behavioural activation induced by sensory stimulation or electrical stimulation of the lateral habenula. These results indicate that the grafted monoaminergic neurons can restore tonic regulatory neurotransmission at previously denervated synaptic sites even when they are implanted into the ectopic brain sites. Such functional reafferentation may be sufficient for at least partial restoration of function in the subcortically deafferented hippocampus.
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| 3. |
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| 4. |
- Dunnett, S. B, et al.
(author)
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Preface
- 2017
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In: Functional Neural Transplantation IV Translation to Clinical Application, Part B. - 0079-6123. - 9780128138793 ; 231
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Book chapter (other academic/artistic)
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| 5. |
- Dunnett, S., et al.
(author)
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Preface
- 2017
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In: Functional Neural Transplantation IV Translation to Clinical Application, Part A. - 0079-6123. ; 230
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Book chapter (other academic/artistic)
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| 6. |
- Ekerot, Carl-Fredrik, et al.
(author)
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Chapter 24 The control of forelimb movements by intermediate cerebellum
- 1997
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In: Progress in brain research. - 0079-6123. - 0444801049 ; 114, s. 423-429
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Book chapter (other academic/artistic)abstract
- In a series of studies, the functional organization of cerebellar regions contributing to the control of forelimb movements via the rubro- and corticospinal tracts has been characterized in the cat. The system consists of the cerebellar cortical C1, C3 and Y zones and their efferent intracerebellar nucleus, the interpositus anterior. Based on analyses of cutaneous and muscle afferent climbing fibre input, of corticonuclear connections and of limb movements controlled, a modular organization of this cerebellar control system is proposed. Each module consists of a number of cortical microzones, defined by their homogeneous climbing fibre input, and a group of neurones in nucleus interpositus anterior on which these microzones converge. The input to climbing fibres is multi-modal and originates from cutaneous A beta (tactile), A delta and C (nociceptive) fibres and from muscle afferents. The cutaneous receptive fields have spatial characteristics suggestive of a relation to elemental movements. For most climbing fibres, the spatial relationship between cutaneous and muscle afferent input is such that the muscle afferent input originates from muscles that, if activated, would tend to move the cutaneous receptive field of the climbing fibre towards a stimulus applied to the skin. By contrast, the limb movement controlled by the module often has the opposite direction, and would thus tend to move the cutaneous receptive field away from a stimulus applied to the skin. Functional implications of this organization for the involvement of these regions in acute and adaptive motor control of limb movements are discussed.
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| 9. |
- Wieloch, Tadeusz
(author)
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Neurochemical Correlates to Selective Neuronal Vulnerability
- 1985. - C
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In: Molecular Mechanisms of Ischemic Brain Damage. - 0079-6123. - 0444806547 ; 63, s. 69-85
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Book chapter (peer-reviewed)abstract
- This chapter describes some of the special neurochemical features of the areas of the brain selectively vulnerable to ischemic and hypoglycemic insults. The chapter focuses on the neuronal connections to the vulnerable brain areas, on the distribution of receptors and transmitter content in the vulnerable areas, and on some current hypothesis of neuronal damage. Emphasis will be placed on a possible imbalance between excitation and inhibition of neurons as a factor in the development of neuronal necrosis, in particular the importance of excitatory transmitters, suggested to mediate ischemic and hypoglycemic brain damage. The amino acids glutamate and aspartate are major excitatory transmitters in the central neurons system. When present in high concentration they are neurotoxic and can play a role in the pathogenesis of several neurological diseases, such as temporal lobe epilepsy, Huntington's disease, and olivopontocerebellar dystrophy.
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| 10. |
- Wieloch, Tadeusz, et al.
(author)
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Protein phosphorylation and the regulation of mRNA translation following cerebral ischemia
- 1993. - C
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In: Neurobiology of Ischemic Brain Damage. - 0079-6123. - 9780444896032 ; 96, s. 179-191
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Book chapter (peer-reviewed)abstract
- This chapter discusses the changes in protein phosphorylation following ischemia, with particular reference to the regulation of the initiation of protein synthesis. Transient cerebral ischemia seems to induce a post-ischemic imbalance between protein kinase and protein phosphatase activities, leading to a net dephosphorylation of proteins in the vulnerable neurons. This imbalance may lead to the persistent changes in processes crucial for neuronal survival such as post-ischemic protein synthesis. The depression of protein synthesis after an ischemic insult most probably is because of a decreased guanine nucleotide exchange factor (GEF) activity, leading to a limited availability of eukaryotic initiation factors (eIF-2) for initiation complex formation. The inhibition of GEF activity in the vulnerable regions could in turn be because of dephosphorylation of GEF, possibly because of tyrosine phosphatase activation and a decreased casein kinase II activity. Post-ischemic inhibition of protein kinase C and calcium calmodulin kinase II may in addition depress eIF-4 activity leading to a selective translation of mRNA such as heat shock mRNA.
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| 21. |
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| 22. |
- Grillner, Sten, et al.
(author)
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Modeling a vertebrate motor system : pattern generation, steering and control of body orientation
- 2007
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 165, s. 221-234
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Research review (peer-reviewed)abstract
- The lamprey is one of the few vertebrates in which the neural control system for goal-directed locomotion including steering and control of body orientation is well described at a cellular level. In this report we review the modeling of the central pattern-generating network, which has been carried out based on detailed experimentation. In the same way the modeling of the control system for steering and control of body orientation is reviewed, including neuromechanical simulations and robotic devices.
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| 23. |
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| 24. |
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| 25. |
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| 26. |
- Jankowska, Elzbieta
(author)
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A neuronal system of movement control via muscle spindle secondaries
- 1989
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 80, s. 299-303
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Research review (peer-reviewed)abstract
- A recently discovered spinal interneuronal system of movement control is briefly described. It includes a population of midlumbar interneurones with a predominant monosynaptic input from secondary muscle spindle afferents but supplied with information via several other afferent and descending neuronal systems as well. The neurones are in direct contact with both motoneurones and other interneurones. The evidence in favour for their involvement in locomotion is briefly summarized. © 1989, Elsevier B.V.
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| 27. |
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| 28. |
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| 29. |
- Karlsson, Ann-Katrin, 1950
(author)
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Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs
- 2006
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In: Progress in Brain Research. - 0079-6123. ; 152, s. 1-8
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Research review (peer-reviewed)abstract
- Spinal cord injury and especially cervical spinal cord injury implies serious disturbances in autonomic nervous system function. The clinical effects of these disturbances are striking. In the acute phase, the autonomic imbalance and its effect on cardiovascular, respiratory system and temperature regulation may be life threatening. Serious complications such as over-hydration with the risk of pulmonary edema or hyponatremia are seen. The cord-injured person suffers from autonomic nervous system dysfunction also affecting bladder and bowel control, renal and sexual function. Paralytic ileus may cause vomiting and aspiration, which in turn interferes with respiratory function in those with cervical spinal cord injury. The cord-injured person is at risk to develop pressure sores from the moment of the accident. Two to three months post-injury the cord-injured person with a lesion level above the fifth thoracic segment may develop autonomic dysreflexia, characterised by sympathetically mediated vasoconstriction in muscular, skin, renal and presumably gastrointestinal vascular beds induced by an afferent peripheral stimulation below lesion level. The reaction might cause cerebrovascular complications and has effects on metabolism. Some of the autonomic disturbances are transient and a new balance is reached months post-injury, while others persist for life.
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| 35. |
- Nyberg, Fred, et al.
(author)
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Neuropeptides in hyperthermia
- 2007
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 277-293
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Research review (peer-reviewed)abstract
- Brain damage as a result of hyperthermia or heat-stress has been the focus of attention in many areas of neuroscience in recent years. Heat-induced alterations in structural components of the central nervous system (CNS) will obviously also influence the relevant transmitter systems, which may be involved in a variety of different behaviors. Indeed, many studies have indicated that excitatory amino acids, and monoaminergic and peptidergic systems are affected during hyperthermia. This chapter will address past and current research on various neuropeptides that have been implicated in the consequences of hyperthermia and various other heat disorders. However, considering the large and even increasing number of identified neuroactive peptides, it is necessary to limit this chapter to a few peptides or peptide systems, which have received particular attention in relation to hyperthermia. Among these are the opioid peptides, the tachykinins, calcitonin gene-related peptide (CGRP), and peptides belonging to the angiotensin system. Most of these neuropeptides are not only affected by hyperthermia and abnormal alterations in the body temperature but also are involved in the endogenous mechanisms of regulating body temperature. This review does not endeavor to fully cover the field but it does aim to give the reader an idea of how various neuropeptides may be involved in the control of body heat and how peptidergic systems are affected during various thermal changes, including both immediate and long-term consequences.
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| 36. |
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| 37. |
- Persson, Jonas, et al.
(author)
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Altered brain activity in healthy seniors : what does it mean?
- 2006
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In: Progress in Brain Research. - Amsterdam : Elsevier. - 0079-6123 .- 1875-7855. ; 157, s. 45-56
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Journal article (other academic/artistic)abstract
- Age-related performance decreases are frequently observed on various memory tasks. Recent brain imaging studies using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) suggest a link between altered patterns of brain activity in older adults and memory performance. Convergent neuroimaging evidence shows that older adults have decreased activity in multiple regions important for memory tasks. Such relative under-activation in older adults is likely related to age-related reductions in cognitive performance. Age-comparative neuroimaging studies have also provided convincing support for regional over-activation by older adults. Such findings indicate that the older brain can re-organize to better cope with cognitive and other challenges. Although over-activation may play a compensatory role when cognitive decline is limited, under-activation seems to be the typical pattern when cognitive impairment is in a more progressed state. This pattern of age-related changes suggests that compensation through over-activation is restricted to the early stages of cognitive impairment in aging.
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| 38. |
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| 39. |
- Petersson, M, et al.
(author)
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Cardiovascular effects of oxytocin
- 2002
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In: Progress in brain research. - : Elsevier. - 0079-6123. ; 139, s. 281-288
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Journal article (peer-reviewed)
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| 40. |
- Sharma, Hari Shanker, et al.
(author)
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Blood-cerebrospinal fluid barrier in hyperthermia
- 2007
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 459-478
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Research review (peer-reviewed)abstract
- The blood-CSF barrier (BCSFB) in choroid plexus works with the blood-brain barrier (BBB) in cerebral capillaries to stabilize the fluid environment of neurons. Dysfunction of either transport interface, i.e., BCSFB or BBB, causes augmented fluxes of ions, water and proteins into the CNS. These barrier disruptions lead to problems with edema and other compromised homeostatic mechanisms. Hyperthermic effects on BCSFB permeability and transport are not as well known as for BBB. However, it is becoming increasingly appreciated that elevated prostaglandin synthesis from fever/heat activation of cyclooxygenases (COXs) in the BCSFB promotes water and ion transfer from plasma to the ventricles; this harmful fluid movement into the CSF-brain interior can be attenuated by agents that inhibit the COXs. Moreover, new functional data from our laboratory animal model indicate that the BCSFB (choroidal epithelium) and the CSF-bordering ependymal cells are vulnerable to whole body hyperthermia (WBH). This is evidenced from the fact that rats subjected to 4h of heat stress (38 degrees C) showed a significant increase in the translocation of Evans blue and (131)Iodine from plasma to cisternal CSF, and manifested blue staining of the dorsal surface of the hippocampus and caudate nucleus. Degeneration of choroidal epithelial cells and underlying ependyma, a dilated ventricular space and damage to the underlying neuropil were frequent. A disrupted BCSFB is associated with a marked increase in edema formation in the hippocampus, caudate nucleus, thalamus and hypothalamus. Taken together, these findings suggest that the breaching of the BCSFB in hyperthermia significantly contributes to cell and tissue injuries in the CNS.
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| 41. |
- Sharma, Hari Shanker
(author)
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Interaction between amino acid neuro transmitters and opioid receptors in hyperthermia-induced brain pathology
- 2007
-
In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 295-317
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Research review (peer-reviewed)abstract
- This review is focused on the possible interaction between amino acid neurotransmitters and opioid receptors in hyperthermia-induced brain dysfunction. A balance between excitatory and inhibitory amino acids appears to be necessary for normal brain function. Increased excitotoxicity and a decrease in inhibitory amino acid neurotrarismission in hyperthermia are associated with brain pathology and cognitive impairment. This is supported by recent data from our laboratory that show a marked increase in glutamate and aspartate and a decrease in GABA and glycine in several brain areas following heat stress at the time of brain pathology. Blockade of multiple opioid receptors with naloxone restored the heat stress-induced decline in GABA and glycine and thwarted the elevation of glutamate and aspartate in the CNS. In naloxone-treated stressed animals, cognitive dysfunction and brain pathology are largely absent. Taken together, these new findings suggest that an intricate balance between excitatory and inhibitory amino acids is important for brain function in heat stress. In addition, opioid receptors play neuromodulatory roles in amino acid neurotransmission in hyperthermia.
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| 42. |
- Sharma, Hari Shanker
(author)
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Methods to produce hyperthermia-induced brain dysfunction
- 2007
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 173-199
-
Research review (peer-reviewed)abstract
- The recent increase in the frequency and intensity of killer heat waves across the globe has aroused worldwide medical attention to exploring therapeutic strategies to attenuate heat-related morbidity and/or mortality. Death due to heat-related illnesses often exceeds >50% of heat victims. Those who survive are crippled with lifetime disabilities and exhibit profound cognitive, sensory, and motor dysfunction akin to premature neurodegeneration. Although more than 50% of the world populations are exposed to summer heat waves; our understanding of detailed underlying mechanisms and the suitable therapeutic strategies have still not been worked out. One of the basic reasons behind this is the lack of a reliable experimental model to simulate clinical hyperthermia. This chapter describes a suitable animal model to induce hyperthermia in rats (or mice) comparable to the clinical situation. The model appears to be useful for studying the effects of heat-related illnesses on changes in various organs and systems, including the central nervous system (CNS). Since hyperthermia is often associated with profound brain dysfunction, additional methods to examine some crucial parameters of brain injury, e.g., blood-brain barrier (BBB) breakdown and brain edema formation, are also described.
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| 43. |
- Sharma, Hari Shanker, et al.
(author)
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Nanoparticles aggravate heat stress induced cognitive deficits, blood-brain barrier disruption, edema formation and brain pathology
- 2007
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 245-273
-
Research review (peer-reviewed)abstract
- Our knowledge regarding the influence of nanoparticles on brain function in vivo during normal or hyperthermic conditions is still lacking. Few reports indicate that when nanoparticles enter into the central nervous system (CNS) they may induce neurotoxicity. On the other hand, nanoparticle-induced drug delivery to the brain enhances neurorepair processes. Thus, it is likely that the inclusion of nanoparticles in body fluid compartments alters the normal brain function and/or its response to additional stress, e.g., hyperthermia. New data from our laboratory show that nanoparticles derived from metals (e.g., Cu, Ag or Al, approximately 50-60nm) are capable of inducing brain dysfunction in normal animals and aggravating the brain pathology caused by whole-body hyperthermia (WBH). Thus, normal animals treated with nanoparticles (for 1 week) exhibited mild cognitive impairment and cellular alterations in the brain. Subjection of these nanoparticle-treated rats to WBH resulted in profound cognitive and motor deficits, exacerbation of blood-brain barrier (BBB) disruption, edema formation and brain pathology compared with naive animals. These novel observations suggest that nanoparticles enhance brain pathology and cognitive dysfunction in hyperthermia. The possible mechanisms of nanoparticle-induced exacerbation of brain damage in WBH and its functional significance in relation to our current knowledge are discussed in this review.
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| 44. |
- Sharma, Hari Shanker, et al.
(author)
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Nanoparticles influence pathophysiology of spinal cord injury and repair
- 2009
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In: Progress in Brain Research. - Amsterdam : Elsevier. - 0079-6123 .- 1875-7855. - 9780444534316 ; 180, s. 155-180
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Research review (peer-reviewed)abstract
- Spinal cord injury (SCI) is a serious clinical problem for which no suitable therapeutic strategies have been worked out so far. Recent studies suggest that the SCI and its pathophysiological responses could be altered by systemic exposure to nanoparticles. Thus, SCI when made in animals intoxicated with engineered nanoparticles from metals or silica dust worsened the outcome. On the other hand, drugs tagged with titanium (TiO2) nanoparticles or encapsulated in liposomes could enhance their neuroprotective efficacy following SCI. Thus, to expand our knowledge on nanoparticle-induced alterations in the spinal cord pathophysiology further research is needed. These investigations will help to develop new strategies to achieve neuroprotection in SCI, for example, using nanodrug delivery. New results from our laboratory showed that nanoparticle-induced exacerbation of cord pathology following trauma can be reduced when the suitable drugs tagged with TiO2 nanowires were administered into the spinal cord as compared to those drugs given alone. This indicates that nanoparticles depending on the exposure and its usage could induce both neurotoxicity and neuroprotection. This review discusses the potential adverse or therapeutic utilities of nanoparticles in SCI largely based on our own investigations. In addition, possible mechanisms of nanoparticle-induced exacerbation of cord pathology or enhanced neuroprotection following nanodrug delivery is described in light of recently available data in this rapidly emerging field of nanoneurosciences.
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| 45. |
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| 46. |
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| 47. |
- Wiens, Stefan
(author)
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Subliminal emotion perception in brain imaging: Findings, issues, and recommendations.
- 2006
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In: Understanding Emotions. - : Elsevier. - 9780444521828 ; 156, s. 105-21
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Book chapter (peer-reviewed)abstract
- Many theories of emotion propose that emotional input is processed preferentially due to its relevance for the organism. Further, because consciousness has limited capacity, these considerations imply that emotional input ought to be processed even if participants are perceptually unaware of the input (subliminal perception). Although brain imaging has studied effects of unattended, suppressed (in binocular rivalry), and visually masked emotional pictures, conclusions regarding subliminal perception have been mixed. The reason is that subliminal perception demands a concept of an awareness threshold or limen, but there is no agreement on how to define and measure this threshold. Although different threshold concepts can be identified in psychophysics (signal detection theory), none maps directly onto perceptual awareness. Whereas it may be tempting to equate unawareness with the complete absence of objective discrimination ability (d′=0), this approach is incompatible with lessons from blindsight and denies the subjective nature of consciousness. This review argues that perceptual awareness is better viewed as a continuum of sensory states than a binary state. When levels of awareness are characterized carefully in terms of objective discrimination and subjective experience, findings can be informative regarding the relative independence of effects from awareness and the potentially moderating role of awareness in processing emotional input. Thus, because the issue of a threshold concept may never be resolved completely, the emphasis is to not prove subliminal perception but to compare effects at various levels of awareness.
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| 48. |
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| 49. |
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