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We began analyzing https://link.springer.com/article/10.1007/BF00403185, but it redirected us to https://link.springer.com/article/10.1007/BF00403185. The analysis below is for the second page.

Title[redir]:
An interleukin-1 receptor antagonist protein protects insulin-producing Beta cells against suppressive effects of interleukin-1β | Diabetologia
Description:
The cytokine interleukin-1β may have an important role in the autoimmune mediated damage of pancreatic Beta cells in insulin-dependent diabetes mellitus. In the present study we have investigated the effects of an interleukin-1 receptor antagonist protein, a blocker of the type I interleukin-1 receptor, on the suppressive actions of recombinant interleukin-1β on insulin-producing cells. Brief exposure (1–2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1β induced an 70–80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. When rat islets were cultured for 48 h in the presence of recombinant interleukin-1β (5 ng/ml) higher concentrations of interleukin-1 receptor antagonist protein (5000 ng/ml) were required to protect Beta-cell function. Interleukin-1 receptor antagonist protein also counteracted the inhibitory effects of recombinant interleukin-1β on the growth of the rat insulinoma cell line RINm5F. These data suggest that interleukin-1 receptor antagonist protein can protect insulin-producing cells from the deleterious effects of recombinant interleukin-1β, and that these cells possess type I interleukin-1 receptors.

Matching Content Categories {📚}

  • Games
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  • Science

Content Management System {📝}

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Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,486,609 visitors per month in the current month.

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Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

interleukin, receptor, interleukinβ, protein, article, cells, google, scholar, antagonist, pancreatic, islets, pubmed, effects, eizirik, bendtzen, privacy, cookies, insulinproducing, sandler, diabetes, recombinant, rat, insulin, content, data, publish, research, search, download, type, ngml, function, information, journal, diabetologia, beta, suppressive, tracey, exposure, cell, discover, welsh, gene, nature, medical, optional, personal, parties, policy, find,

Topics {✒️}

insulin-dependent diabetes mellitus protect insulin-producing cells insulin-producing cells cells possess type pancreatic beta cells protect beta-cell function recombinant interleukin-1β mouse pancreatic islets rat pancreatic islets interleukin-1β induces cytokine interleukin-1β human interleukin 1β privacy choices/manage cookies β-cell function interleukin-1 receptor insulin response pancreatic islets interleukin-1β interleukin-1 receptors decreased cell replication medical cell biology european economic area autoimmune mediated damage related subjects fahey iii tj main content log conditions privacy policy host inflammatory response medical department tta accepting optional cookies scope submit manuscript rat islets requires gene transcription 5 ng/ml 5000 ng/ml article eizirik journal finder publish type bendtzen rights search search eizirik dl protein synthesis article cite nielsen jh privacy policy mcdaniel ml personal data books a interleukin 1 optional cookies

Schema {🗺️}

WebPage:
      mainEntity:
         headline:An interleukin-1 receptor antagonist protein protects insulin-producing Beta cells against suppressive effects of interleukin-1β
         description:The cytokine interleukin-1β may have an important role in the autoimmune mediated damage of pancreatic Beta cells in insulin-dependent diabetes mellitus. In the present study we have investigated the effects of an interleukin-1 receptor antagonist protein, a blocker of the type I interleukin-1 receptor, on the suppressive actions of recombinant interleukin-1β on insulin-producing cells. Brief exposure (1–2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1β induced an 70–80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. When rat islets were cultured for 48 h in the presence of recombinant interleukin-1β (5 ng/ml) higher concentrations of interleukin-1 receptor antagonist protein (5000 ng/ml) were required to protect Beta-cell function. Interleukin-1 receptor antagonist protein also counteracted the inhibitory effects of recombinant interleukin-1β on the growth of the rat insulinoma cell line RINm5F. These data suggest that interleukin-1 receptor antagonist protein can protect insulin-producing cells from the deleterious effects of recombinant interleukin-1β, and that these cells possess type I interleukin-1 receptors.
         datePublished:
         dateModified:
         pageStart:445
         pageEnd:448
         sameAs:https://doi.org/10.1007/BF00403185
         keywords:
            Interleukin-1β
            interleukin 1 receptor
            insulin secretion
            pancreatic islets
            RINm5F cells
            insulin-dependent diabetes mellitus
            Internal Medicine
            Metabolic Diseases
            Human Physiology
         image:
         isPartOf:
            name:Diabetologia
            issn:
               1432-0428
               0012-186X
            volumeNumber:34
            type:
               Periodical
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         publisher:
            name:Springer-Verlag
            logo:
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               type:ImageObject
            type:Organization
         author:
               name:D. L. Eizirik
               affiliation:
                     name:Uppsala University
                     address:
                        name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
                        type:PostalAddress
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               type:Person
               name:D. E. Tracey
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                     address:
                        name:Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, USA
                        type:PostalAddress
                     type:Organization
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               name:K. Bendtzen
               affiliation:
                     name:University Hospital
                     address:
                        name:Laboratory of Medical Immunology, Medical Department TTA, University Hospital, Copenhagen, Denmark
                        type:PostalAddress
                     type:Organization
               type:Person
               name:S. Sandler
               affiliation:
                     name:Uppsala University
                     address:
                        name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
                        type:PostalAddress
                     type:Organization
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      context:https://schema.org
ScholarlyArticle:
      headline:An interleukin-1 receptor antagonist protein protects insulin-producing Beta cells against suppressive effects of interleukin-1β
      description:The cytokine interleukin-1β may have an important role in the autoimmune mediated damage of pancreatic Beta cells in insulin-dependent diabetes mellitus. In the present study we have investigated the effects of an interleukin-1 receptor antagonist protein, a blocker of the type I interleukin-1 receptor, on the suppressive actions of recombinant interleukin-1β on insulin-producing cells. Brief exposure (1–2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1β induced an 70–80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. When rat islets were cultured for 48 h in the presence of recombinant interleukin-1β (5 ng/ml) higher concentrations of interleukin-1 receptor antagonist protein (5000 ng/ml) were required to protect Beta-cell function. Interleukin-1 receptor antagonist protein also counteracted the inhibitory effects of recombinant interleukin-1β on the growth of the rat insulinoma cell line RINm5F. These data suggest that interleukin-1 receptor antagonist protein can protect insulin-producing cells from the deleterious effects of recombinant interleukin-1β, and that these cells possess type I interleukin-1 receptors.
      datePublished:
      dateModified:
      pageStart:445
      pageEnd:448
      sameAs:https://doi.org/10.1007/BF00403185
      keywords:
         Interleukin-1β
         interleukin 1 receptor
         insulin secretion
         pancreatic islets
         RINm5F cells
         insulin-dependent diabetes mellitus
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
      isPartOf:
         name:Diabetologia
         issn:
            1432-0428
            0012-186X
         volumeNumber:34
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:D. L. Eizirik
            affiliation:
                  name:Uppsala University
                  address:
                     name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
                     type:PostalAddress
                  type:Organization
            type:Person
            name:D. E. Tracey
            affiliation:
                  name:The Upjohn Company
                  address:
                     name:Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:K. Bendtzen
            affiliation:
                  name:University Hospital
                  address:
                     name:Laboratory of Medical Immunology, Medical Department TTA, University Hospital, Copenhagen, Denmark
                     type:PostalAddress
                  type:Organization
            type:Person
            name:S. Sandler
            affiliation:
                  name:Uppsala University
                  address:
                     name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Diabetologia
      issn:
         1432-0428
         0012-186X
      volumeNumber:34
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      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Uppsala University
      address:
         name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
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      name:The Upjohn Company
      address:
         name:Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, USA
         type:PostalAddress
      name:University Hospital
      address:
         name:Laboratory of Medical Immunology, Medical Department TTA, University Hospital, Copenhagen, Denmark
         type:PostalAddress
      name:Uppsala University
      address:
         name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
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Person:
      name:D. L. Eizirik
      affiliation:
            name:Uppsala University
            address:
               name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
               type:PostalAddress
            type:Organization
      name:D. E. Tracey
      affiliation:
            name:The Upjohn Company
            address:
               name:Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, USA
               type:PostalAddress
            type:Organization
      name:K. Bendtzen
      affiliation:
            name:University Hospital
            address:
               name:Laboratory of Medical Immunology, Medical Department TTA, University Hospital, Copenhagen, Denmark
               type:PostalAddress
            type:Organization
      name:S. Sandler
      affiliation:
            name:Uppsala University
            address:
               name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
      name:Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, USA
      name:Laboratory of Medical Immunology, Medical Department TTA, University Hospital, Copenhagen, Denmark
      name:Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

External Links {🔗}(90)

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