Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  Molecular Medicine Reports

• Publication date

  2014-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.3892/mmr.2014.2075PMID 24676712
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2012influential reference
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