Here's how NCBI.NLM.NIH.GOV makes money* and how much!

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NCBI . NLM . NIH . GOV {}

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

We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC6534278/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC6534278/. The analysis below is for the second page.

Title[redir]:
The Coming Decade of Cell Death Research: Five Riddles - PMC
Description:
Active cell death, in its many forms, is a fundamental biological process, and its study over the past several decades has provided key insights into the molecular processes, functions, and consequences responsible. Here, we pose five questions, or ...

Matching Content Categories {๐Ÿ“š}

  • Science
  • Telecommunications
  • Education

Content Management System {๐Ÿ“}

What CMS is ncbi.nlm.nih.gov built with?

Custom-built

No common CMS systems were detected on Ncbi.nlm.nih.gov, and no known web development framework was identified.

Traffic Estimate {๐Ÿ“ˆ}

What is the average monthly size of ncbi.nlm.nih.gov audience?

๐ŸŒ  Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 6,694,437 visitors per month in the current month.

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How Does Ncbi.nlm.nih.gov Make Money? {๐Ÿ’ธ}

The income method remains a mystery to us.

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. Ncbi.nlm.nih.gov might have a hidden revenue stream, but it's not something we can detect.

Keywords {๐Ÿ”}

cell, death, cells, google, scholar, pubmed, doi, apoptosis, caspase, pmc, free, article, ripk, activation, necroptosis, membrane, promote, caspases, mitochondrial, pathway, function, proteins, process, pyroptosis, active, ferroptosis, apoptotic, gpx, pathways, gsdmd, development, dying, processes, state, momp, mlkl, cancer, expression, plasma, repair, animals, form, mechanisms, receptor, necrosis, infection, survival, inflammatory, response, receptors,

Topics {โœ’๏ธ}

caspase-8-c-flip proteolytic activity fadd-caspase-8-c-flip complex [google scholar] cao poly-unsaturated fatty acids pmc beta search cut inter-nucleosomal dna caspase-8-c-flip dimer google scholar p53-mediated hematopoietic stem requires nf-kb activation escrt-iii acts downstream anti-apoptotic bcl-2 proteins mitochondrial inter-membrane space pro-inflammatory โ€œfaddosomeโ€ complex nf-kb-induced inflammation nf-kb-induced mediators strain-dependent neurodevelopmental abnormalities infect wild-type animals similarly engage nf-kb early life post-birth promote nf-kb activation endoplasmic reticulum-induced stress total pubmed publications trigger nf-kb activation nf-kappab signaling puma-independent thymocyte apoptosis caspase-8-dependent apoptotic pathways amarante-mendes promote sting-dependent type dna-dependent inflammatory disease fas/cd95-induced chemokines free iron mtdna engages sting ๏ฟฝcaspase-independent cell deathโ€ vanden berghe dubensky tw jr caspase-11-induced gsdmd activity pore-forming protein gasdermin show increased virulence radiation-induced thymomagenesis nf-kb activity polyunsaturated fatty acids ripk1-dependent caspase-8 activation actin-mediated locomotion specific receptor antagonists apoptosis-induced compensatory proliferation limited mitochondrial permeabilization involves lysosomal permeabilization actively anti-inflammatory viruses produce proteins

Questions {โ“}

  • Apoptosis and Cancer: Force Awakens, Phantom Menace, or Both?
  • But is it essential?
  • But is it the cell death, itself, that controls infection?
  • How Do Cytotoxic Lymphocytes Kill Cancer Cells?
  • How dispensable is something that is essential?
  • How does cell death affect the physiology of surrounding cells, and of the body in general?
  • How final is engagement of active, cell death pathways, and are there consequences for survival after such engagement?
  • How many dastardly deeds can documenting doctors dictate?
  • How many ways can a cell actively die?
  • If a cell dies in the forest of the body, does it make a sound?
  • If, as has been suggested, HMGB1 and other DAMPs engage TLRs, why is necroptosis, which releases such DAMPs, insufficient to promote T cell immunity when NF-kB is not engaged in the dying cell?
  • Is NF-kB required in dying apoptotic cells for effective antigen presentation following engulfment?
  • Riddle #1: How deadly is death?
  • What are the stochastic differences between otherwise identical cells that define the persistent state, and is this state induced or does it exist prior to treatment?
  • What is it about a dying cell that triggers inflammation and immune responses?
  • What role does pyroptosis play in microbial infection?
  • What, then, is cell death โ€œfor?
  • When a clonal population of cells are faced with a death-inducing stimulus, why do some cells survive when their clonemates die, and are there consequences for this state of survival?
  • When is a toxin not toxic?

Social Networks {๐Ÿ‘}(6)

External Links {๐Ÿ”—}(203)

Analytics and Tracking {๐Ÿ“Š}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {๐Ÿ“š}

  • jQuery
  • jQuery module (jquery-3.6.0)
  • Zoom.js

Emails and Hosting {โœ‰๏ธ}

Mail Servers:

  • nihcesxway.hub.nih.gov
  • nihcesxway2.hub.nih.gov
  • nihcesxway3.hub.nih.gov
  • nihcesxway4.hub.nih.gov
  • nihcesxway5.hub.nih.gov

Name Servers:

  • dns1-ncbi.ncbi.nlm.nih.gov
  • dns2-ncbi.ncbi.nlm.nih.gov
  • lhcns1.nlm.nih.gov
  • lhcns2.nlm.nih.gov

CDN Services {๐Ÿ“ฆ}

  • Ncbi

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