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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. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s000110050632.

Title:
Unregulated inflammation shortens human functional longevity | Inflammation Research
Description:
Systemic inflammation, represented in large part by the production of pro-inflammatory cytokines, is the response of humans to the assault of the non-self on the organism. Three distinct types of human ailments – namely autoimmunity, presenile dementia (Alzheimer
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Science
  • Non-Profit & Charity

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 8,150,568 visitors per month in the current month.

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

We don't see any clear sign of profit-making.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

inflammation, article, disease, unregulated, alzheimers, access, privacy, cookies, content, research, atherosclerosis, information, publish, search, systemic, response, autoimmunity, immune, data, log, journal, shortens, human, longevity, brod, proinflammatory, cytokines, local, inflammatory, open, discover, springer, optional, analysis, personal, parties, policy, find, track, functional, cite, explore, production, humans, hyperimmunity, acquired, system, hayflick, protein, brain,

Topics {✒️}

unregulated pro-inflammatory cytokines month download article/chapter pro-inflammatory cytokines unregulated systemic inflammation full article pdf privacy choices/manage cookies brain inflammatory response related subjects human ailments nominal longevity systemic inflammation european economic area scope submit manuscript inducing rapid turnover acquired immunity il-2 primary degenerative process driving-force role cardiovascular diseases focal plaques characterized conditions privacy policy organ-specific proteins inflammation context article brod acquired immune system accepting optional cookies local immunologic activation unregulated hyperimmunity journal finder publish check access instant access article log hayflick phenonmenon shortens inflammation article cite usage analysis privacy policy personal data cardiovascular disease books a immune system optional cookies alzheimer disease manage preferences immune response subscription content similar content information data protection essential cookies

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Unregulated inflammation shortens human functional longevity
         description: Systemic inflammation, represented in large part by the production of pro-inflammatory cytokines, is the response of humans to the assault of the non-self on the organism. Three distinct types of human ailments – namely autoimmunity, presenile dementia (Alzheimer's disease), or atherosclerosis - are initiated or worsened by systemic inflammation. Autoimmunity is unregulated hyperimmunity to organ-specific proteins, inducing rapid turnover of antigen-specific T cells of the acquired immune system with ultimate exhaustion and loss of acquired immunity IL-2 and IFN-γ; production and proliferative decline, conforming to the limited capacity of clonal division (Hayflick phenonmenon). In Alzheimer's disease (AD), the primary degenerative process of amyloid-beta (Aβ) protein precedes a cascade of events that ultimately leads to a local "brain inflammatory response". Unregulated systemic immune processes are secondary but important as a driving-force role in AD pathogenesis. Atherosclerosis, an underlying cause of myocardial infarction, stroke, and other cardiovascular diseases, consists of focal plaques characterized by cholesterol deposition, fibrosis, and inflammation. The presence of activated T lymphocytes and macrophages indicate a local immunologic activation in the atherosclerotic plaque that may be secondary to unregulated pro-inflammatory cytokines too. The premature hyperimmunity of autoimmunity, the local "brain inflammatory response" to Aβ protein in AD, and the immune response to fatty changes in vessels in atherosclerosis all signal the critical importance of unregulated systemic inflammation to common neurological and cardiovascular disease that shortens the nominal longevity of humans.
         datePublished:
         dateModified:
         pageStart:561
         pageEnd:570
         sameAs:https://doi.org/10.1007/s000110050632
         keywords:
            Key words: Inflammation – Immunosenescence – Autoimmunity – Alzheimer's disease - Atherosclerosis - Pro-inflammatory cytokines - Hayflick phenomenon
            Immunology
            Pharmacology/Toxicology
            Rheumatology
            Allergology
            Dermatology
            Neurology
         image:
         isPartOf:
            name: Inflammation Research
            issn:
               1420-908X
               1023-3830
            volumeNumber:49
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Birkhäuser Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:S.A. Brod
               affiliation:
                     name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected]
                     address:
                        name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected], , US
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ScholarlyArticle:
      headline:Unregulated inflammation shortens human functional longevity
      description: Systemic inflammation, represented in large part by the production of pro-inflammatory cytokines, is the response of humans to the assault of the non-self on the organism. Three distinct types of human ailments – namely autoimmunity, presenile dementia (Alzheimer's disease), or atherosclerosis - are initiated or worsened by systemic inflammation. Autoimmunity is unregulated hyperimmunity to organ-specific proteins, inducing rapid turnover of antigen-specific T cells of the acquired immune system with ultimate exhaustion and loss of acquired immunity IL-2 and IFN-γ; production and proliferative decline, conforming to the limited capacity of clonal division (Hayflick phenonmenon). In Alzheimer's disease (AD), the primary degenerative process of amyloid-beta (Aβ) protein precedes a cascade of events that ultimately leads to a local "brain inflammatory response". Unregulated systemic immune processes are secondary but important as a driving-force role in AD pathogenesis. Atherosclerosis, an underlying cause of myocardial infarction, stroke, and other cardiovascular diseases, consists of focal plaques characterized by cholesterol deposition, fibrosis, and inflammation. The presence of activated T lymphocytes and macrophages indicate a local immunologic activation in the atherosclerotic plaque that may be secondary to unregulated pro-inflammatory cytokines too. The premature hyperimmunity of autoimmunity, the local "brain inflammatory response" to Aβ protein in AD, and the immune response to fatty changes in vessels in atherosclerosis all signal the critical importance of unregulated systemic inflammation to common neurological and cardiovascular disease that shortens the nominal longevity of humans.
      datePublished:
      dateModified:
      pageStart:561
      pageEnd:570
      sameAs:https://doi.org/10.1007/s000110050632
      keywords:
         Key words: Inflammation – Immunosenescence – Autoimmunity – Alzheimer's disease - Atherosclerosis - Pro-inflammatory cytokines - Hayflick phenomenon
         Immunology
         Pharmacology/Toxicology
         Rheumatology
         Allergology
         Dermatology
         Neurology
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      isPartOf:
         name: Inflammation Research
         issn:
            1420-908X
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         name:Birkhäuser Verlag
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      author:
            name:S.A. Brod
            affiliation:
                  name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected]
                  address:
                     name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected], , US
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      name: Inflammation Research
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         1420-908X
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      name:Birkhäuser Verlag
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         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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      name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected]
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         name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected], , US
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            name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected]
            address:
               name:University of Texas Health Science Center at Houston, Department of Neurology, 7.044, P.O. Box 20708, Houston, TX 77225, Fax: 713 500-7041, e-mail: [email protected], , US
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External Links {🔗}(25)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

3.95s.