1 Ocak 2017 Dergi makalesi Açık Erişim

Doeppner, Thorsten R.; Doehring, Maria; Kaltwasser, Britta; Majid, Arshad; Lin, Fengyan; Bahr, Mathias; Kilic, Ertugrul; Hermann, Dirk M.

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    "creators": [
      {
        "name": "Doeppner, Thorsten R."
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      {
        "affiliation": "Oberhavel Kliniken, Dept Internal Med, Oranienburg, Germany", 
        "name": "Doehring, Maria"
      }, 
      {
        "affiliation": "Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany", 
        "name": "Kaltwasser, Britta"
      }, 
      {
        "affiliation": "Univ Sheffield, Sheffield Inst Translat Neurosci, Sheffield, S Yorkshire, England", 
        "name": "Majid, Arshad"
      }, 
      {
        "affiliation": "Jilin Univ, Affiliated Hosp 1, Ctr Canc, Changchun, Jilin, Peoples R China", 
        "name": "Lin, Fengyan"
      }, 
      {
        "affiliation": "Univ Gottingen, Dept Neurol, Sch Med, Gottingen, Germany", 
        "name": "Bahr, Mathias"
      }, 
      {
        "affiliation": "Istanbul Medipol Univ, Regenerat & Restorat Med Res Ctr, Istanbul, Turkey", 
        "name": "Kilic, Ertugrul"
      }, 
      {
        "affiliation": "Univ Duisburg Essen, Sch Med, Dept Neurol, Essen, Germany", 
        "name": "Hermann, Dirk M."
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    "description": "In view of the failure of pharmacological therapies, alternative strategies promoting post-stroke brain repair are needed. Post-conditioning is a potentially promising therapeutic strategy, which induces acute neuroprotection against ischemic injury. To elucidate longer lasting actions of ischemic post-conditioning, mice were exposed to a 60-min stroke and post-conditioning by an additional 10-min stroke that was induced 10 min after reperfusion onset. Animals were sacrificed 24 h or 28 days post-stroke. Post-conditioning reduced infarct volume and neurological deficits 24 h poststroke, enhancing blood-brain barrier integrity, reducing brain leukocyte infiltration, and reducing oxidative stress. On the molecular level, post-conditioning yielded increased Hsp70 expression, whereas nuclear factor (NF)-kappa B and proteasome activities were decreased. Reduced infarct volume and proteasome inhibition were reversed by Hsp70 knockdown, suggesting a critical role of the Hsp70 proteasome pathway in ischemic post-conditioning. The survival-promoting effects of ischemic post-conditioning, however, were not sustainable as neuroprotection and neurological recovery were lost 28 days post-stroke. Although angioneurogenesis was not increased by post-conditioning, the favorable extracellular milieu facilitated intracerebral transplantation of neural progenitor cells 6 h post-stroke, resulting in persisted neuroprotection and neurological recovery. Thus, post-conditioning might support brain repair processes, but in view of its transient, neuroprotection is unlikely useful as stroke therapy in its current form.", 
    "doi": "10.1007/s12035-016-0137-3", 
    "has_grant": false, 
    "journal": {
      "issue": "8", 
      "pages": "6061-6073", 
      "title": "MOLECULAR NEUROBIOLOGY", 
      "volume": "54"
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    "license": {
      "id": "cc-by"
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    "publication_date": "2017-01-01", 
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    "resource_type": {
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      "title": "Dergi makalesi", 
      "type": "publication"
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    "title": "Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation"
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