Evidence map›Paper›PMID 28916727›Full record

ArticleThe Journal of biological chemistry2017

Inflammatory responses induce an identity crisis of alveolar macrophages, leading to pulmonary alveolar proteinosis.

Risa Ebina-Shibuya, Mitsuyo Matsumoto, Makoto Kuwahara, Kyoung-Jin Jang, Manabu Sugai, Yoshiaki Ito, Ryo Funayama, Keiko Nakayama, Yuki Sato, Naoto Ishii and 8 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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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

18 authors at 5 institutions in 2 countries.

Risa Ebina-ShibuyaFrom the Department of Biochemistry.
Mitsuyo MatsumotoFrom the Department of Biochemistry.
Makoto Kuwaharathe Department of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Kyoung-Jin Jangthe Department of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Yoshidakonoe-machi, Sakyo-ku, Kyoto 606-8501, Japan.
Manabu Sugaithe Department of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Yoshidakonoe-machi, Sakyo-ku, Kyoto 606-8501, Japan.
Yoshiaki Itothe Cancer Stem Cells and Biology Programme, Cancer Science Institute of Singapore, National University of Singapore, Singapore 117599, Singapore.
Ryo FunayamaDepartment of Cell Proliferation, United Center for Advanced Research and Translational Medicine.
Keiko NakayamaDepartment of Cell Proliferation, United Center for Advanced Research and Translational Medicine.
Yuki SatoFrom the Department of Biochemistry.
Naoto IshiiDepartment of Immunology, and.
Yasunobu Okamurathe Graduate School of Information Sciences, Tohoku University, Aoba 6-3-09, Aramaki, Sendai, Miyagi 980-8579, Japan.
Kengo Kinoshitathe Graduate School of Information Sciences, Tohoku University, Aoba 6-3-09, Aramaki, Sendai, Miyagi 980-8579, Japan.
Kohei Kometanithe RIKEN Center for Integrative Medical Sciences, Suehiro-cho 1-7-22, Yokohama Tsurumi-ku, Kanagawa 230-0045, Japan, and.
Tomohiro Kurosakithe RIKEN Center for Integrative Medical Sciences, Suehiro-cho 1-7-22, Yokohama Tsurumi-ku, Kanagawa 230-0045, Japan, and.
Akihiko MutoFrom the Department of Biochemistry.
Masakazu Ichinosethe Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, Seiryo-machi 1-1, Sendai, Miyagi 980-8574, Japan.
Masakatsu Yamashitathe Department of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Kazuhiko IgarashiFrom the Department of Biochemistry, igarashi@med.tohoku.ac.jp.ORCID 0000-0002-2470-2475
Tohoku University · JPEhime University · JPRIKEN Center for Integrative Medical Sciences · JPUniversity of Fukui · JPNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary alveolar proteinosis (PAP) is a severe respiratory disease characterized by dyspnea caused by accumulation of surfactant protein. Dysfunction of alveolar macrophages (AMs), which regulate the homeostasis of surfactant protein, leads to the development of PAP; for example, in mice lacking BTB and CNC homology 2 (Bach2). However, how Bach2 helps prevent PAP is unknown, and the cell-specific effects of Bach2 are undefined. Using mice lacking

Indexed as

Gene Expression RegulationImmunity, InnateAnimalsBasic-Leucine Zipper Transcription FactorsBiomarkersCell LineageCells, CulturedChromatin ImmunoprecipitationDendritic CellsDNA-Binding ProteinsGene Expression ProfilingHeterozygoteLungLymphocyte ActivationLymphocyte DepletionMacrophages, AlveolarBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsBiomarkersDNA-Binding ProteinsRag2 protein, mouseimmunologyinflammationmacrophagepulmonary surfactanttranscription factor

Identifiers

PMID28916727
PMCPMC5672035
OpenAlexW2755217176

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.