Evidence map›Paper›PMID 20130219›Full record

ReviewJournal of leukocyte biology2010

Inflammatory mechanisms in ischemic stroke: role of inflammatory cells.

Rong Jin, Guojun Yang, Guohong Li

Abstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 849 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
849citing papers in PubMed, 5 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

849 citing papers in PubMed, 5 syntheses or guidelines pooled it.

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789 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Rong JinDepartment of Neurosurgery, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
Guojun Yang
Guohong Li

Funding

Mechanisms of CD40/CD40L in vascular injury and repairR01HL087990 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI LI, GUOHONG · 2008 to 2013
$1.6M
NHLBI NIH HHS HL087990NHLBI NIH HHS R01 HL087990
6 · The paper itself

Abstract

Inflammation plays an important role in the pathogenesis of ischemic stroke and other forms of ischemic brain injury. Experimentally and clinically, the brain responds to ischemic injury with an acute and prolonged inflammatory process, characterized by rapid activation of resident cells (mainly microglia), production of proinflammatory mediators, and infiltration of various types of inflammatory cells (including neutrophils, different subtypes of T cells, monocyte/macrophages, and other cells) into the ischemic brain tissue. These cellular events collaboratively contribute to ischemic brain injury. Despite intense investigation, there are still numerous controversies concerning the time course of the recruitment of inflammatory cells in the brain and their pathogenic roles in ischemic brain injury. In this review, we provide an overview of the time-dependent recruitment of different inflammatory cells following focal cerebral I/R. We discuss how these cells contribute to ischemic brain injury and highlight certain recent findings and currently unanswered questions about inflammatory cells in the pathophysiology of ischemic stroke.

Indexed as

AnimalsAnti-Inflammatory AgentsBrain IschemiaHumansInflammationReperfusion InjuryStrokeAnti-Inflammatory Agents

Identifiers

PMID20130219
PMCPMC2858674

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.