uu.seUppsala University Publications
Change search
Refine search result
1 - 9 of 9
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Falck-Ytter, Terje
    et al.
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    von Hofsten, Claes
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    How special is social looking in ASD: a review2011In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 189, p. 209-22Article, review/survey (Refereed)
    Abstract [en]

    This review is primarily concerned with the view that individuals with autism spectrum disorder (ASD) look less at the eyes and more at the mouth compared to typically developing (TD) individuals. Such performance in ASD could reflect that the eyes are not meaningful or that they are perceived as threatening, two ideas that may seem intuitively appealing. However, our review shows that despite the fact that the excess mouth/diminished eye gaze hypothesis fits with clinical common sense and initial data from adults, it does not-as a generalization across ages and contexts-fit with the emerging pattern of eye-tracking data. In adolescents and adults, there is only partial support for the excess mouth/diminished eye gaze hypothesis, and regarding children, most studies do not support this hypothesis. In particular, independent studies have found longer looking durations on the mouth in TD children than in children with ASD, and no difference for the eye area. We describe recent evidence that mouth fixations are functional responses related to (early) stages of normative language development. We conclude that although individuals with ASD often give less preferential attention to social objects and events (faces, people, and social actions) than TD individuals, the excess mouth/diminished eye gaze hypothesis of ASD is not generally supported. Therefore, this hypothesis needs to be reevaluated, as do related theories of social perception in ASD.

  • 2.
    Gredebäck, Gustaf
    et al.
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    von Hofsten, Claes
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Psychology.
    Taking an action perspective on infant’s object representations2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, no 164, p. 265-282Article in journal (Refereed)
  • 3.
    Nyberg, Fred
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Biological Research on Drug Dependence.
    Hallberg, Mathias
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Biological Research on Drug Dependence.
    Neuropeptides in hyperthermia2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 162, p. 277-293Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 4.
    Sharma, Hari Shanker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Interaction between amino acid neuro transmitters and opioid receptors in hyperthermia-induced brain pathology2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 162, p. 295-317Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 5.
    Sharma, Hari Shanker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Methods to produce hyperthermia-induced brain dysfunction2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 162, p. 173-199Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 6.
    Sharma, Hari Shanker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Preface: Nanoneuropharmacology and Nanoneurotoxicology2009In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 180, p. vii-ixArticle in journal (Refereed)
  • 7.
    Sharma, Hari Shanker
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Johanson, Conrad Earl
    Blood-cerebrospinal fluid barrier in hyperthermia2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 162, p. 459-478Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 8.
    Sharma, Hari Shanker
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Muresanu, Dafin F.
    Sharma, Aruna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Patnaik, Ranjana
    Vicente Lafuente, Jose
    Nanoparticles influence pathophysiology of spinal cord injury and repair2009In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 180, p. 155-180Article, review/survey (Refereed)
    Abstract [en]

    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.

  • 9.
    Sharma, Hari Shanker
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Sharma, Aruna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Nanoparticles aggravate heat stress induced cognitive deficits, blood-brain barrier disruption, edema formation and brain pathology2007In: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 162, p. 245-273Article, review/survey (Refereed)
    Abstract [en]

    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.

1 - 9 of 9
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf