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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/s00109-003-0450-y.

Title:
Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes | Journal of Molecular Medicine
Description:
Pancreatic islet β-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. β-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes β-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to β-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block β-cell apoptosis could be a significant new development in type 1 and 2 diabetes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • Science

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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

We're unsure how the site profits.

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. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

google, scholar, pubmed, cas, diabetes, article, type, pancreatic, apoptosis, betacell, insulin, islet, kinase, mellitus, cells, human, rat, islets, interleukin, mandruppoulsen, clin, protein, med, diabetologia, expression, cell, factor, resistance, death, glucose, nitric, eizirik, betacells, donath, increased, oxide, biol, maedler, endocrinology, endocrinol, metab, chem, βcell, activation, disease, receptor, sci, beta, fatty, signaling,

Topics {✒️}

c-jun n-terminal kinase c-jun nh2-terminal kinase extracellular signal-regulated kinase mitogen-activated protein kinase glucose-induced beta-cell production hyperglycemia-induced beta-cell apoptosis immune-mediated beta-cell apoptosis terminal kinase activity nitric oxide-induced apoptosis cytokine-induced nf-kappab activation interleukin-1 beta-exposed human oxidative stress-mediated suppression regulated acute-phase proteins interleukin-1 beta-induced ceramide interferon-gamma-mediated toxicity tumor necrosis factor-alpha month download article/chapter tgf-beta signal transduction multicentre double-blind trial stimulating beta-cell production islet β-cell failure beta-cell maturation leads block β-cell apoptosis rat pancreatic beta-cells human beta-cells sorted cell-permeable peptide inhibitors anti-cd3 monoclonal antibody fadd/mort1 enhances deletion neonatal beta-cell apoptosis beta-cell inhibitory effect differentiating pancreatic beta-cells glutamic acid decarboxylase s58–s63 mohamed-ali reduced beta-cell mass c-jun nh rat insulin-producing cells high-density oligonucleotide arrays increased beta-cell apoptosis common bcl-2-inhibitable pathway uchscedu/misc/diabetes/bdc spontaneously diabetic biobreeding/worcester cytokine-induced insulin resistance fat-induced insulin resistance diet-induced insulin resistance tumor necrosis factor map kinase cascade c-reactive protein nf-kb dependent genes β-cell death beta-cell death

Questions {❓}

  • Cerasi E (1995) Insulin deficiency and insulin resistance in the pathogenesis of NIDDM: is a divorce possible?
  • Evans JL, Goldfine ID, Maddux BA, Grodsky GM (2003) Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?
  • Meier CA, Bobbioni E, Gabay C, Assimacopoulos-Jeannet F, Golay A, Dayer JM (2002) IL-1 receptor antagonist serum levels are increased in human obesity: a possible link to the resistance to leptin?
  • Pickup JC, Crook MA (1998) Is type II diabetes mellitus a disease of the innate immune system?
  • Syed MA, Barinas-Mitchell E, Pietropaolo SL, Zhang YJ, Henderson TS, Kelley DE, Korytkowski MT, Donahue RP, Tracy RP, Trucco M, Kuller LH, Pietropaolo M (2002) Is type 2 diabetes a chronic inflammatory/autoimmune disease?
  • Trudeau JD, Dutz JP, Arany E, Hill DJ, Fieldus WE, Finegood DT (2000) Neonatal beta-cell apoptosis: a trigger for autoimmune diabetes?
  • Type 1 diabetes mellitus as a disease of the β-cell (do not blame the immune system?
  • Which is the primary cause of NIDDM?

Schema {🗺️}

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         headline:Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes
         description:Pancreatic islet β-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. β-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes β-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to β-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block β-cell apoptosis could be a significant new development in type 1 and 2 diabetes.
         datePublished:2003-07-18T00:00:00Z
         dateModified:2003-07-18T00:00:00Z
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      headline:Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes
      description:Pancreatic islet β-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. β-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes β-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to β-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block β-cell apoptosis could be a significant new development in type 1 and 2 diabetes.
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         Mitogen-activated protein kinase
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         Internal Medicine
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External Links {🔗}(344)

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