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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 82 (2002), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The motor signs of Parkinson's disease have been partly attributed to an overinhibition of the external globus pallidus (GP) that results from hyperactivity of striatopallidal GABA/enkephalinergic neurons. The goals of this study were to measure basal levels of extracellular fluid GABA in the GP of normal cats, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated parkinsonian cats and cats spontaneously recovered from MPTP-induced parkinsonism, and to examine the effects of opioid receptor activation on potassium (K+)-evoked GABA release in the GP in these animals. Basal GP GABA levels were increased 75% from normal in parkinsonian animals 1 week after MPTP administration and returned to control levels in recovered animals 6 weeks afterMPTP administration. No significant differences were observed in K+-evoked GABA release across conditions. The opioid receptor agonist [D-Ala2]-Met-Enkephalinamide (DALA) significantly attenuated K+-evoked GABA release in the GP of MPTP-treated symptomatic and recovered cats, but had no significant effect on GABA release in normal animals. These data show that basal GP GABA levels are elevated coincident with expression of parkinsonian signs and return to normal in animals that have functionally compensated for a nigrostriatal lesion. DALA-induced inhibition of pallidal GABA release after a dopamine-depleting lesion, suggests that enkephalin may attenuate GABA release in the GP specifically after striatal dopamine loss.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Desloratadine is a non-sedating, clinically effective, anti-allergic therapy that has been shown to exhibit anti-inflammatory properties that extend beyond its ability to antagonize histamine at H1-receptor sites. This latter effect has been shown in vitro to be both IgE-dependent and -independent.Objective In this study, we addressed the ability of desloratadine to inhibit the in vitro generation of interleukin (IL)-4 and IL-13 from human basophils while concurrently comparing its efficacy in preventing mediator release by these cells.Methods Basophil-enriched suspensions were treated with various concentrations of desloratadine for 15 min before stimulating with either anti-IgE antibody, calcium ionophore, IL-3 or phorbol ester. Histamine (fluorimetry), LTC4 (RIA) and IL-4 (ELISA) were all assayed using the same 4-h culture supernatants. IL-13 (ELISA) was measured in supernatants harvested after 20 h incubation. IL-4 mRNA expression (dilutional RT-PCR) was also examined.Results Desloratadine was found to be nearly six–seven times more potent in preventing the secretion of IL-4 and IL-13 induced by anti-IgE than it was at inhibiting the release of histamine and LTC4. These cytokines were equally inhibited by desloratadine following activation with ionomycin despite the lack of an effect on the histamine induced with ionomycin. Desloratadine had a lesser effect regarding inhibition of the IL-13 secreted in response to IL-3 and PMA. There was no evidence that desloratadine mediated its inhibitory effects by causing decreased cell viability. Finally, IL-4 mRNA accumulation was remarkably inhibited, by as much as 80%, following pretreatment with desloratadine.Conclusion While capable of inhibiting histamine and LTC4 release by human basophils, desloratadine is more effective at targeting the signals regulating IL-4 and IL-13 generation in these cells. This inhibitory effect on cytokine generation provides additional evidence that this antihistamine exerts anti-inflammatory properties.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The complex interactions between immune cells are partly mediated by different adhesion molecules, but little is known about their role in the systemic immunoinflammatory process following sensitization to food antigens in early infancy.Objective The aim of this study was to investigate the expression of intercellular adhesion molecule-1 (ICAM-1or CD54) and the α subunits of its ligands' lymphocyte function-associated antigen-1 (LFA-1) (αL subunit or CD11a) and Mac-1 (αM subunit or CD11b) on peripheral blood leucocytes in infants with cow's milk allergy (CMA) and in healthy controls.Methods Thirty-nine breastfed infants, aged from 0.6 to 8.3 months, and their lactating mothers were included in the study from delivery onwards. During follow-up, 25 infants developed CMA and 14 remained healthy. Expressions of CD54 and CD11b on peripheral blood leucocytes were evaluated by flow cytometry. In addition, the expression of CD11a on peripheral blood leucocytes was analysed by immunocytochemistry. Mothers' milk samples were collected and their leucocyte content was evaluated using a light microscope.Results The frequency of ICAM-1 expressing peripheral blood lymphocytes was significantly higher in patients with CMA than in healthy infants (P=0.03, Mann–Whitney U-test). Furthermore, the high proportion of ICAM-1-expressing cells was associated with gastrointestinal and multiorgan symptoms in the CMA infants. There was no significant difference in the expression of Mac-1 αM on lymphocytes in our study groups, but the LFA-1 αL expression seemed to be higher in the IgE-mediated CMA.Conclusion We suggest that the high expression of ICAM-1 on peripheral blood lymphocytes may reflect enhanced stimulation of T cells in vivo and their migration to the effector tissues in an early-phase of developing CMA. Furthermore, high ICAM-1 expression may be associated with the presence of multiorgan manifestations of CMA, whereas high LFA-1 expression may reflect the IgE-mediated disease.
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2015-07-23
    Description: Objectives To investigate researchers’ perceptions about the factors that influenced the policy and practice impacts (or lack of impact) of one of their own funded intervention research studies. Design Mixed method, cross-sectional study. Setting Intervention research conducted in Australia and funded by Australia's National Health and Medical Research Council between 2003 and 2007. Participants The chief investigators from 50 funded intervention research studies were interviewed to determine if their study had achieved policy and practice impacts, how and why these impacts had (or had not) occurred and the approach to dissemination they had employed. Results We found that statistically significant intervention effects and publication of results influenced whether there were policy and practice impacts, along with factors related to the nature of the intervention itself, the researchers’ experience and connections, their dissemination and translation efforts, and the postresearch context. Conclusions This study indicates that sophisticated approaches to intervention development, dissemination actions and translational efforts are actually widespread among experienced researches, and can achieve policy and practice impacts. However, it was the links between the intervention results, further dissemination actions by researchers and a variety of postresearch contextual factors that ultimately determined whether a study had policy and practice impacts. Given the complicated interplay between the various factors, there appears to be no simple formula for determining which intervention studies should be funded in order to achieve optimal policy and practice impacts.
    Keywords: Open access, Evidence based practice, Health policy, Research methods
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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