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DOI . ORG {}

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

We began analyzing https://link.springer.com/article/10.1007/s00281-013-0364-x, but it redirected us to https://link.springer.com/article/10.1007/s00281-013-0364-x. The analysis below is for the second page.

Title[redir]:
Mechanisms regulating neutrophil survival and cell death | Seminars in Immunopathology
Description:
Neutrophils not only play a critical role as a first line of defense against bacteria and fungi infections but also contribute to tissue injury associated with autoimmune and inflammatory diseases. Neutrophils are rapidly and massively recruited from the circulation into injured tissues displaying an impressive arsenal of toxic weapons. Although effective in their ability to kill pathogens, these weapons were equally effective to induce tissue damage. Therefore, the inflammatory activity of neutrophils must be regulated with exquisite precision and timing, a task mainly achieved through a complex network of mechanisms, which regulate neutrophil survival. Neutrophils have the shortest lifespan among leukocytes and usually die via apoptosis although new forms of cell death have been characterized over the last few years. The lifespan of neutrophils can be dramatically modulated by a large variety of agents such as cytokines, pathogens, danger-associated molecular patterns as well as by pharmacological manipulation. Recent findings shed light about the complex mechanisms responsible for the regulation of neutrophil survival in different physiological, pathological, and pharmacological scenarios. Here, we provide an updated review on the current knowledge and new findings in this field and discuss novel strategies that could be used to drive the resolution of neutrophil-mediated inflammatory diseases.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is doi.org built with?

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?

đŸ™ïž Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,904,851 visitors per month in the current month.

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How Does Doi.org Make Money? {💾}

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

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

google, scholar, cas, pubmed, article, apoptosis, neutrophils, neutrophil, immunol, cell, death, human, rev, biol, nat, regulation, simon, mcl, role, inflammation, blood, mechanisms, med, leukoc, activation, inflammatory, expression, caspase, survival, immunity, differ, extracellular, kinase, function, doiblood, immune, caspases, ligand, bcl, doinri, trends, doicdd, mol, proteins, wang, resolution, haslett, annu, doijlb, doijit,

Topics {✒}

tnf-related apoptosis-inducing ligand granulocyte colony-stimulating factor month download article/chapter analĂ­a silvina trevani tnfalpha-mediated nf-kappab activation pi3-kinase-dependent bad phosphorylation granulocyte-derived hydrogen peroxide o'neill aj myeloid-derived suppressor cells viscum album agglutinin neisseria gonorrhoeae-mediated inhibition stimulating caspase-dependent turnover bcl-2-related a1 gene bad-mediated signalling pathway neutrophil-mediated inflammatory diseases reactive oxygen species cytokine-mediated neutrophil survival cytokine-mediated bax deficiency nf-kappab-dependent mechanism nf-kappab signaling pathways cell cycle-independent block extracellular signal-regulated kinase override pro-inflammatory signalling article gabelloni interferon-activated neutrophils store full article pdf bax-alpha-mediated regulation oxygen-dependent pathway reactive oxygen intermediates facultad de medicina mitochondria-dependent death pathway cyclin-dependent kinases 7 privacy choices/manage cookies leitch ae von andrian uh neutrophil apoptosis mediated regulating neutrophil apoptosis neutrophil extracellular traps infection-induced netosis c5a delays apoptosis de boer rj de graaff pm related subjects structural variations related bcl-2 family members francisella tularensis inhibits stimulation-induced apoptosis respiratory burst activation regulate neutrophil survival delay constitutive apoptosis

Questions {❓}

  • Brinkmann V, Zychlinsky A (2012) Neutrophil extracellular traps: is immunity the second function of chromatin?
  • Liles WC, Klebanoff SJ (1995) Regulation of apoptosis in neutrophils—fast track to death?

Schema {đŸ—ș}

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         description:Neutrophils not only play a critical role as a first line of defense against bacteria and fungi infections but also contribute to tissue injury associated with autoimmune and inflammatory diseases. Neutrophils are rapidly and massively recruited from the circulation into injured tissues displaying an impressive arsenal of toxic weapons. Although effective in their ability to kill pathogens, these weapons were equally effective to induce tissue damage. Therefore, the inflammatory activity of neutrophils must be regulated with exquisite precision and timing, a task mainly achieved through a complex network of mechanisms, which regulate neutrophil survival. Neutrophils have the shortest lifespan among leukocytes and usually die via apoptosis although new forms of cell death have been characterized over the last few years. The lifespan of neutrophils can be dramatically modulated by a large variety of agents such as cytokines, pathogens, danger-associated molecular patterns as well as by pharmacological manipulation. Recent findings shed light about the complex mechanisms responsible for the regulation of neutrophil survival in different physiological, pathological, and pharmacological scenarios. Here, we provide an updated review on the current knowledge and new findings in this field and discuss novel strategies that could be used to drive the resolution of neutrophil-mediated inflammatory diseases.
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      headline:Mechanisms regulating neutrophil survival and cell death
      description:Neutrophils not only play a critical role as a first line of defense against bacteria and fungi infections but also contribute to tissue injury associated with autoimmune and inflammatory diseases. Neutrophils are rapidly and massively recruited from the circulation into injured tissues displaying an impressive arsenal of toxic weapons. Although effective in their ability to kill pathogens, these weapons were equally effective to induce tissue damage. Therefore, the inflammatory activity of neutrophils must be regulated with exquisite precision and timing, a task mainly achieved through a complex network of mechanisms, which regulate neutrophil survival. Neutrophils have the shortest lifespan among leukocytes and usually die via apoptosis although new forms of cell death have been characterized over the last few years. The lifespan of neutrophils can be dramatically modulated by a large variety of agents such as cytokines, pathogens, danger-associated molecular patterns as well as by pharmacological manipulation. Recent findings shed light about the complex mechanisms responsible for the regulation of neutrophil survival in different physiological, pathological, and pharmacological scenarios. Here, we provide an updated review on the current knowledge and new findings in this field and discuss novel strategies that could be used to drive the resolution of neutrophil-mediated inflammatory diseases.
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External Links {🔗}(509)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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Emails and Hosting {✉}

Mail Servers:

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Name Servers:

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CDN Services {📩}

  • Crossref

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