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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
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  13. Hosting Providers
  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s10072-011-0828-5, but it redirected us to https://link.springer.com/article/10.1007/s10072-011-0828-5. The analysis below is for the second page.

Title[redir]:
The role of glutamate in neuronal ischemic injury: the role of spark in fire | Neurological Sciences
Description:
Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.

Matching Content Categories {📚}

  • Education
  • Science
  • Insurance

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,479,999 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We see no obvious way the site makes money.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

google, scholar, pubmed, article, cas, glutamate, brain, ischemic, cell, ischemia, cerebral, neuronal, calcium, neurosci, receptor, stroke, res, death, nmda, role, excitotoxicity, neurons, sci, biol, pharmacol, focal, neurochem, injury, release, effects, chem, neuroprotective, receptors, neuroprotection, metabotropic, antagonist, ischaemia, cortical, intracellular, mitochondrial, activation, neurotoxicity, acad, effect, rat, treatment, wang, apoptosis, usa, caspase,

Topics {✒️}

n-methyl-d-aspartic acid receptor n-methyl-d-aspartate-mediated neurotoxicity n-methyl-d-aspartic acid-receptors n-methyl-d-aspartate receptor month download article/chapter g-aminobutyric acid studied 3-dihydroxy-6-nitro-7-sulfamoyl-benzo dantrolene-sensitive calcium channels l-type ca2+ channels plasma-stable peptidomimetic inhibitors randomized placebo-controlled trial diaspirin cross-linked hemoglobin kainic acid-induced neurodegeneration calpain-mediated mglur1alpha truncation ampa receptor-mediated excitotoxicity brain-permeable dual blocker cain/cabin1 activates calcineurin long-term secondary prevention l-type calcium channels glutamate-induced neuronal toxicity ligand-operated calcium channels short-term forebrain ischemia synoptically-released zinc contributes mitochondrial nitric-oxide synthase kainate-induced oxidative lesions combined oxygen–glucose deprivation s-100b serum levels glutamate-induced cell death full article pdf calcium-dependent protease calpain metabotropic glutamate receptor nmda receptor subtypes postsynaptic density proteins synthase pdz domain extracellular oxidative/nitrosative stress nmda-induced neurotoxicity ca2+ release channel protein synthesis requirement interleukin-1 receptor antagonist de deyn pp 13 l-type ca privacy choices/manage cookies excitotoxic neuronal death ampa receptor trafficking actin filament depolymerization nmda receptor activities nmda receptor activity oxygen–glucose deprivation metabotropic glutamate receptors neurological disorders

Questions {❓}

  • Blomgren K, Zhu C, Wang X et al (2001) Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia–ischemia: a mechanism of “pathological apoptosis”?

Schema {🗺️}

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         headline:The role of glutamate in neuronal ischemic injury: the role of spark in fire
         description:Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.
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      headline:The role of glutamate in neuronal ischemic injury: the role of spark in fire
      description:Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.
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External Links {🔗}(586)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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Emails and Hosting {✉️}

Mail Servers:

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Name Servers:

  • josh.ns.cloudflare.com
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CDN Services {📦}

  • Crossref

5.3s.