Evidence map›Paper›PMID 36545833›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2023

Role of post-ischemic phase-dependent modulation of anti-inflammatory M2-type macrophages against rat brain damage.

Yoshitaka Kurashiki, Hiroshi Kagusa, Kenji Yagi, Tomoya Kinouchi, Manabu Sumiyoshi, Takeshi Miyamoto, Kenji Shimada, Keiko T Kitazato, Yoshihiro Uto, Yasushi Takagi

Open access · greenAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 41% of its field
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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Trial
  2. Review
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

10 authors at 1 institution in 1 country.

Yoshitaka KurashikiDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Hiroshi KagusaDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Kenji YagiDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.ORCID 0000-0001-9392-5827
Tomoya KinouchiDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Manabu SumiyoshiDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Takeshi MiyamotoDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Kenji ShimadaDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Keiko T KitazatoDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Yoshihiro UtoDepartment of Life Systems, Institute of Technology and Science, Tokushima University Graduate School, Japan.
Yasushi TakagiDepartment of Neurosurgery, Institute of Biomedical Sciences, Tokushima University Graduate School, Japan.
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia triggers inflammatory changes, and early complications and unfavorable outcomes of endovascular thrombectomy for brain occlusion promote the recruitment of various cell types to the ischemic area. Although anti-inflammatory M2-type macrophages are thought to exert protective effects against cerebral ischemia, little has been clarified regarding the significance of post-ischemic phase-dependent modulation of M2-type macrophages. To test our hypothesis that post-ischemic phase-dependent modulation of macrophages represents a potential therapy against ischemic brain damage, the effects on rats of an M2-type macrophage-specific activator, Gc-protein macrophage-activating factor (GcMAF), were compared with vehicle-treated control rats in the acute (day 0-6) or subacute (day 7-13) phase after ischemia induction. Acute-phase GcMAF treatment augmented both anti-inflammatory CD163

Indexed as

Brain InjuriesBrain IschemiaAnimalsAnti-Inflammatory AgentsBrainCerebral InfarctionMacrophagesRatsAnti-Inflammatory AgentsArginase-1cerebral ischemiainterleukin-4macrophage modulationpost-ischemic phase

Identifiers

PMID36545833
PMCPMC10063836
OpenAlexW4312094380

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.