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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/bf01757696.

Title:
Pain due to nerve damage: Are inflammatory mediators involved | Inflammation Research
Description:
Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Technology & Computing

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

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 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

google, scholar, pubmed, pain, peripheral, nerve, hyperalgesia, neurosci, rat, levine, sympathetic, article, injury, inflammation, inflammatory, cells, neuropathic, neuropathy, taiwo, lett, role, macrophages, experimental, model, privacy, cookies, content, research, mediators, tracey, neurophysiol, products, sci, publish, search, damage, postganglionic, mechanisms, access, res, rats, nature, neurons, goetzl, usa, glia, data, information, log, journal,

Topics {✒️}

month download article/chapter sympathetic neuron-derived prostaglandins post-injury pain hypersensitivity directly-acting hyperalgesic agent voltage-sensitive na+ channels mediated byα2-adrenergic receptors noradrenaline-induced prostalgandin production inflammatory mediators involved privacy choices/manage cookies sciatic nerve injury full article pdf denervation-induced inflammation peripheral nerve injury nerve injury depends peripheral neuropathy produced sympathetic postganglionic neurons postganglionic sympathic terminals causalgiform pain produced peri-axonal inflammation sectioned peripheral nerve mediation byα2 adrenoreceptors dorsal horn neurons painful constriction neuropathy nerve growth factor postganglionic sympathetic neurones sympathetically maintained pain sustained graded pain cutaneous nociceptive threshold nociceptive peripheral neurons formalin-induced nociception norepinephrine-induced increase paravertebral sympathetic ganglia reflex sympathetic dystrophy experimental peripheral neuropathy european economic area scope submit manuscript related subjects mediating mechanical allodynia tumour necrosis factorα amino-terminal octapeptide chemotactic proinflammatory cytokines intravenous regional block ngf-induced hyperalgesia pain due primary afferent nociceptors clonidine relieves hyperalgesia conditions privacy policy sympathetic nervous system enzyme histochemical study damaged peripheral nerves

Questions {❓}

  • Epineurial peptides: a role in neuropathic pain?
  • Human monocytes/macrophages: NO or no NO?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Pain due to nerve damage: Are inflammatory mediators involved
         description:Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
         datePublished:
         dateModified:
         pageStart:407
         pageEnd:411
         sameAs:https://doi.org/10.1007/BF01757696
         keywords:
            Pain
            Hyperalgesia
            Neuropathy
            Nerve injury
            Inflammatory mediators
            Immunology
            Pharmacology/Toxicology
            Rheumatology
            Allergology
            Dermatology
            Neurology
         image:
         isPartOf:
            name:Inflammation Research
            issn:
               1420-908X
               1023-3830
            volumeNumber:44
            type:
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               PublicationVolume
         publisher:
            name:Birkhäuser-Verlag
            logo:
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               type:ImageObject
            type:Organization
         author:
               name:D. J. Tracey
               affiliation:
                     name:University of New South Wales
                     address:
                        name:School of Anatomy, University of New South Wales, Sydney, Australia
                        type:PostalAddress
                     type:Organization
               type:Person
               name:J. S. Walker
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                     name:University of New South Wales
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                        name:School of Anatomy, University of New South Wales, Sydney, Australia
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ScholarlyArticle:
      headline:Pain due to nerve damage: Are inflammatory mediators involved
      description:Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones. A better understanding of the mechanisms involved should lead to improved therapies for neuropathic pain.
      datePublished:
      dateModified:
      pageStart:407
      pageEnd:411
      sameAs:https://doi.org/10.1007/BF01757696
      keywords:
         Pain
         Hyperalgesia
         Neuropathy
         Nerve injury
         Inflammatory mediators
         Immunology
         Pharmacology/Toxicology
         Rheumatology
         Allergology
         Dermatology
         Neurology
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                     name:School of Anatomy, University of New South Wales, Sydney, Australia
                     type:PostalAddress
                  type:Organization
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      name:University of New South Wales
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         name:School of Anatomy, University of New South Wales, Sydney, Australia
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      name:University of New South Wales
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         name:School of Anatomy, University of New South Wales, Sydney, Australia
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      name:D. J. Tracey
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            name:University of New South Wales
            address:
               name:School of Anatomy, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:J. S. Walker
      affiliation:
            name:University of New South Wales
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               name:School of Anatomy, University of New South Wales, Sydney, Australia
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      name:School of Anatomy, University of New South Wales, Sydney, Australia
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External Links {🔗}(143)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.21s.