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We are analyzing https://link.springer.com/article/10.1007/s00401-005-0016-x.

Title:
Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats | Acta Neuropathologica
Description:
Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Education
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What CMS is link.springer.com built with?

Custom-built

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What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,016 visitors per month in the current month.

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Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

pubmed, google, scholar, cas, article, interleukin, spinal, cord, injury, receptor, type, brain, neurosci, expression, rat, interleukinbeta, inflammatory, ilri, res, research, traumatic, wang, access, rothwell, rats, sci, astrocytes, science, cytokines, privacy, cookies, content, adult, university, levison, factor, induction, necrosis, mice, data, publish, search, xiaoming, response, microglia, open, receptors, cell, activation, ilbeta,

Topics {✒️}

month download article/chapter corticotropin-releasing factor-producing neurons interleukin-1beta converting enzyme/caspase-1 acute-phase cytokines il-1beta cytokine-induced sickness behaviour pei-hua lu lipopolysaccharide-induced sickness behaviour hypothalamic corticotropin-releasing factor mild hypoxic/ischemic injury related subjects real-time quantitative pcr inflammatory pain hypersensitivity tumour necrosis factor-alpha tumor necrosis factor-alpha spinal cord injury xiao-ming xu interleukin neuroimmunology rig-i 10 mm-long cord segment interleukin-1beta promotes repair gm-csf promotes proliferation rat spinal cord spinal cord contusion proinflammatory cytokines interleukin-1beta full article pdf posttraumatic inflammation responses albrecht pj post-injury compared experimental traumatic injury tumor necrosis factor il1beta signaling pathway interleukin-1beta-mediated induction privacy choices/manage cookies secondary injury mechanisms interleukin−1 receptor antagonist il-1ri deficient mice article wang spinal cord inflammatory cytokine mrnas central inflammatory response reduced inflammatory response ohio state university key inflammatory mediator pro-inflammatory cytokines focal cerebral ischaemia fibroblast growth factor-2 astroglial growth factor il-1 receptor family type 2 receptors pan-pan yu multiple proinflammatory mediators

Questions {❓}

  • Vitkovic L, Bockaert J, Jacque C (2000) “Inflammatory” cytokines: neuromodulators in normal brain?

Schema {🗺️}

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         headline:Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats
         description:Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
         datePublished:2006-02-03T00:00:00Z
         dateModified:2006-02-03T00:00:00Z
         pageStart:220
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            IL-1
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            Neurosciences
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                     address:
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                        name:Kentucky Spinal Cord Injury Research Center, Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, USA
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      headline:Upregulation of type I interleukin−1 receptor after traumatic spinal cord injury in adult rats
      description:Post-traumatic inflammation response has been implicated in secondary injury mechanisms after spinal cord injury (SCI). Interleukin-1 (IL-1) is a key inflammatory mediator that is increasingly expressed after SCI. The action of IL-1 is mediated through its functional receptor, type I interleukin-1 receptor (IL-1RI). However, whether this receptor is expressed after SCI remains to be elucidated. In the present study, the temporospatial expression of IL-1RI was detected in rats that received a moderate contusive SCI (a 10 g rod dropped at a height of 12.5 mm) at the ninth to tenth thoracic vertebral level using a widely used New York University impact device. Our study demonstrated that IL-1RI was slightly increased at 4 h post-injury compared to the normal or sham-operated controls, reached the peak at 8 h at mRNA level (4.44-fold, P<0.01) and 1 d at protein level (2.62-fold, P<0.01). IL-1RI remained at its elevated levels for a relatively long duration (4 h–7 days). Spatially, IL-1RI was observed throughout the entire length of a 10 mm-long cord segment containing the injury epicenter. Colocalization of IL-1RI was found in neurons, oligodendrocytes, astrocytes, and activated microglia. Our results suggest that the elevated expression of IL-1RI after SCI may contribute to posttraumatic inflammation responses of IL-1.
      datePublished:2006-02-03T00:00:00Z
      dateModified:2006-02-03T00:00:00Z
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         Spinal cord injury Rat
         IL-1
         IL-1 receptor
         Pathology
         Neurosciences
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                     name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
                     type:PostalAddress
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                  address:
                     name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
                     type:PostalAddress
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                  name:University of Louisville School of Medicine
                  address:
                     name:Kentucky Spinal Cord Injury Research Center, Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, USA
                     type:PostalAddress
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            type:Person
            name:Pei-Hua Lu
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                  name:Shanghai Second Medical University
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                     name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
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         name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
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      address:
         name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
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      address:
         name:Kentucky Spinal Cord Injury Research Center, Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, USA
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            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
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      name:Jian-Guo Hu
      affiliation:
            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
               type:PostalAddress
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      name:Lan Yin
      affiliation:
            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Li Wang
      affiliation:
            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Xiao-Ming Xu
      affiliation:
            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:University of Louisville School of Medicine
            address:
               name:Kentucky Spinal Cord Injury Research Center, Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Pei-Hua Lu
      affiliation:
            name:Shanghai Second Medical University
            address:
               name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Laboratory Science, Affiliated Hospital of Nantong University, Nantong, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
      name:Kentucky Spinal Cord Injury Research Center, Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, USA
      name:Department of Neurobiology, Shanghai Second Medical University, Shanghai, People’s Republic of China
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