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  4. Monthly Traffic Estimate
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We began analyzing https://journals.lww.com/hep/abstract/2013/05000/absence_of_receptor_interacting_protein_kinase_3.13.aspx, but it redirected us to https://journals.lww.com/hep/abstract/2013/05000/absence_of_receptor_interacting_protein_kinase_3.13.aspx. The analysis below is for the second page.

Title[redir]:
Hepatology
Description:
ptotic cell death pathway, is implicated in a variety of pathological conditions, we tested the hypothesis that ethanol-induced liver injury is RIP3-dependent and RIP1-independent. Increased expression of RIP3 was detected in livers of mice after chronic ethanol feeding, as well as in liver biopsies from patients with alcoholic liver disease. Chronic ethanol feeding failed to induce RIP3 in the livers of cytochrome P450 2E1 (CYP2E1)-deficient mice, indicating CYP2E1-mediated ethanol metabolism is critical for RIP3 expression in response to ethanol feeding. Mice lacking RIP3 were protected from ethanol-induced steatosis, hepatocyte injury, and expression of proinflammatory cytokines. In contrast, RIP1 expression in mouse liver remained unchanged following ethanol feeding, and inhibition of RIP1 kinase by necrostatin-1 did not attenuate ethanol-induced hepatocyte injury. Ethanol-induced apoptosis, assessed by terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling–positive nuclei and accumulation of cytokeratin-18 fragments in the liver, was independent of RIP3. Conclusion: CYP2E1-dependent RIP3 expression induces hepatocyte necroptosis during ethanol feeding. Ethanol-induced hepatocyte injury is RIP3-dependent, but independent of RIP1 kinase activity; intervention of this pathway could be targeted as a potential therapeutic strategy....

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Doi.org uses MYBB.

Traffic Estimate {📈}

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 600,420 visitors per month in the current month.

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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 has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

liver, rip, ethanolinduced, injury, hepatocyte, ethanol, aasld, expression, feeding, log, journal, kinase, access, hepatology, disease, subscribe, issue, alerts, abstract, apoptosis, mice, register, member, logo, browse, submit, protein, buy, cell, death, inhibition, necroptosis, pathway, ripdependent, livers, chronic, independent, copyright, american, association, study, diseases, text, subscribers, members, request, content, service, usa, privacy,

Topics {✒️}

receptor-interacting protein kinase ethanol-induced liver injury ethanol-induced hepatocyte injury alcoholic liver disease aasld members log ethanol-induced steatosis open access policy 3–mediated necroptosis ethanol-induced apoptosis individual subscribers log chronic ethanol feeding rip1 kinase activity hepatocyte injury institutional users access potential therapeutic strategy artificial intelligence training liver diseases full text access mice lacking rip3 liver biopsies rip1 kinase journal tables register subscribe ethanol feeding service request 800-638-3030 rip3-dependent rip3 expression liver rip1 expression increased expression journal website subscribe induce rip3 cyp2e1 major hallmarks pathological conditions cytochrome p450 2e1 deficient mice proinflammatory cytokines cytokeratin-18 fragments email inbox rights reserved data mining issue rip1-independent content expression rip3 pathway mice

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External Links {🔗}(68)

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