Here's how DOI.ORG makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

DOI . ORG {}

Detected CMS Systems:

  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. Social Networks
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. Hosting Providers
  13. CDN Services

We began analyzing https://journals.lww.com/transplantjournal/fulltext/2009/08150/c_jun_terminal_kinase_2_gene_deleted_mice.5.aspx, but it redirected us to https://journals.lww.com/transplantjournal/fulltext/2009/08150/c_jun_terminal_kinase_2_gene_deleted_mice.5.aspx. The analysis below is for the second page.

Title[redir]:
Transplantation
Description:
-type and jnk-2 βˆ’/βˆ’ animals were subjected to hepatic ischemia reperfusion insults in two models: a total hepatic ischemia model involving timed Pringle maneuver, and a partial hepatic ischemia model involving selective occlusion of the portal pedicle supplying the left hepatic lobe. Optimal durations of injury were calibrated for each model. After 24 hr, animals were killed, and blood and tissues were collected for alanine aminotransferase, histologic injury scoring, and other analyses. Before total or partial hepatic ischemia reperfusion insults, some animals were subject to HO-1 inhibition with chromium mesoporphyrin IX or Kupffer cell depletion with liposomal clodronate. Bone marrow-derived monocytes were grown from hemopoietic progenitors taken from wild-type and jnk-2 βˆ’/βˆ’ mice before stimulation with lipopolysaccharide and measurement of tumour necrosis factor-Ξ± production. Results. Jnk-2 βˆ’/βˆ’ animals were protected from hepatic ischemia reperfusion injury. HO-1 expression and activity was elevated in jnk-2 βˆ’/βˆ’ animals (2.2-fold; P=0.006). Most HO-1 was expressed in Kupffer cells. Inhibition of HO-1 in jnk-2 βˆ’/βˆ’ animals led to the loss of protection from ischemia. Depletion of Kupffer cells using liposomal clodronate led to loss of hepatic HO-1 expression and much more severe injury in wild-type and jnk-2 βˆ’/βˆ’ animals. In vitro studies of cultured macrophages demonstrated reduced tumour necrosis factor-Ξ± secretion after lipopolysacharride stimulus, an effect lost after HO-1 inhibition....

Matching Content Categories {πŸ“š}

  • Science
  • Animals & Wildlife
  • Crafts

Content Management System {πŸ“}

What CMS is doi.org built with?


Doi.org is based on MYBB.

Traffic Estimate {πŸ“ˆ}

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

🌍 Impressive Traffic: 500k - 1M visitors per month


Based on our best estimate, this website will receive around 600,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {πŸ’Έ}

We're unsure how the site profits.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org has a revenue plan, but it's either invisible or we haven't found it.

Keywords {πŸ”}

jnk, animals, wildtype, ischemia, hepatic, injury, cells, fig, min, cjun, model, crmp, kupffer, cell, liver, insults, inhibition, iri, total, expression, ischemic, alt, data, hemeoxygenase, deletion, histologic, necrosis, mice, protected, demonstrated, previously, bmdms, induction, clodronate, apoptosis, experiments, shown, mortality, terminal, kinase, reperfusion, subjected, led, macrophages, livers, tnfΞ±, journal, transplantation, secretion, factor,

Topics {βœ’οΈ}

abcam mouse anti-Ξ²-actin c-jun terminal kinase-2 rabbit polyclonal anti-phospho-cjun c-jun binding sites rabbit anti-rat biotinylated bone marrow-derived monocytes pe-conjugated anti-f4/80 reduce tnf-Ξ± secretion rabbit polyclonal anti-ho-1 rat anti-mouse f4/80 d-jnki-1 affect targets modulates t-cell activation stress-activated protein kinases biotinylated anti-mouse gr1 effective kupffer-cell ablation hematoxylin-eosin stained slides sex-matched wild-type insufficient wild-type survivors phospho c-jun previous inhibitor studies lps-induced tnf-Ξ± tnf-Ξ± signaling selective gene deletion advanced donor age total hepatic ischemia permit selective occlusion confers direct cytoprotection human pringle maneuver chromium mesoporphyrin ix caspase luminometric assay wild-type animals died il-1Ξ² secretion antiinflammatory il-10 secretion wild-type animals led untreated wild-type cells western blotting confirmed journal authors submit ischemia reperfusion injury kupffer-cell ablation macrophage ablation resulted tnf-Ξ± induction home office regulations 4=pan-lobular necrosis wild-type ho-1 intact cell type led upstream mesenteric congestion kupffer cell distribution kupffer cell morphology 3=perivenular hepatocyte injury termed β€œmarginal livers

Social Networks {πŸ‘}(5)

External Links {πŸ”—}(131)

Analytics and Tracking {πŸ“Š}

  • Comscore
  • Google Analytics
  • Google Tag Manager

Libraries {πŸ“š}

  • Bootstrap
  • FontAwesome
  • jQuery
  • Zoom.js

Emails and Hosting {βœ‰οΈ}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {πŸ“¦}

  • Cookielaw
  • Jsdelivr
  • Scite
  • Wolterskluwer

4.78s.