• Mission, scope, and focus

    The Association’s mission is to:
    • Build a closely connected, mutually beneficial network of active scientists who are actively doing experimental and translational stroke research;
    • Foster exchange of information on stroke models, experimental and translational stroke research among peers;
    • Coordinate hands-on training and promote Standard Operational Procedures (SOP) for stroke models;
    • Culture an environment that favors identifying and solving problems;
    • Improve the quality of experimental stroke research and facilitate a successful translation for ischemic stroke treatment.

    The Journal's focus and scope

    JESTM provides high quality tailored contents to stroke investigators. The scope of the journal covers original studies and reviews in experimental stroke and translational medical research. Special emphases are placed on new concepts and innovative research ideas in neuroprotection for acute ischemic stroke, and methodological improvements in stroke studies. JESTM differs from other stroke journals in the following aspects:
    • It encourages authors to submit articles with controversial/provocative ideas and negative results;
    • A unique article type "Innovative Research Idea" is available for accepting innovative research ideas, which is something similar to the abbreviated scientific part of a research proposal;
    • It accepts video articles and improved protocols;
    • The journal site provides a networking platform for building up professional connections;
    • It is both free and open-access.

Recent Articles

Chemokine receptor-like 2 is involved in ischemic brain injury

CCRL2 is involved in ischemic brain injury

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  • Robert M. Douglas Pediatrics, University of California-San Diego, La Jolla, CA, USA.
  • Alice H. Chen Pediatrics, University of California-San Diego, La Jolla, CA, USA.
  • Alejandra Iniguez Pediatrics, University of California-San Diego, La Jolla, CA, USA.
  • Juan Wang Pediatrics, University of California-San Diego, La Jolla, CA, USA.
  • Zhengxing Fu Physiology, University of California-San Diego, La Jolla, CA, USA.
  • Frank L. Powell Jr. Physiology, University of California-San Diego, La Jolla, CA, USA.
  • Gabriel G. Haddad Pediatrics, Neuroscience, University of California-San Diego, Rady Children’s Hospital-San Diego, San Diego, CA, USA.
  • Hang Yao Ph.D. Pediatrics, University of California-San Diego, La Jolla, CA, USA.

We examined the role of CCRL2 in ischemic brain injury using both in vitro and in vivo mouse stroke models. The expression of CCRL2 was enhanced at both the RNA and protein levels in cultured brain slices under ischemic conditions. Ischemia-induced cell death was reduced in brain slices derived from CCRL2 knockout (KO) mice in comparison with those from wild type (WT) mice. The infarct volume was smaller and neurological deficits were attenuated in CCRL2 KO mice when compared to WT mice subjected to a transient middle cerebral artery occlusion. Our data suggest that CCRL2 is involved in ischemia-induced brain injury in mice.