Evidence map›Paper›PMID 30542414›Full record

ArticleExperimental and therapeutic medicine2018

sTLR4/sMD-2 complex alleviates LPS-induced acute lung injury by inhibiting pro-inflammatory cytokines and chemokine CXCL1 expression.

Jie Meng, Yan Zou, Jifei Chen, Fengxian Qin, Xiang Chen, Xiaoli Chen, Shengming Dai

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  12. Evidence-based complementary and alternative medicine : eCAM · 2020
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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

7 authors at 1 institution in 1 country.

Jie MengMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Yan ZouMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Jifei ChenMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Fengxian QinMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Xiang ChenMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Xiaoli ChenMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Shengming DaiMedical Science Laboratory, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China.
Fourth Affiliated Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of Toll-like receptor 4 (TLR4) and its accessory proteins myeloid differentiation protein 2 (MD-2) can trigger immune and inflammatory activities, and contribute to developing chronic inflammatory diseases. The formation of the TLR4/MD-2 complex after binding to lipopolysaccharide (LPS) leads to the activation of downstream signaling pathway. The present study was designed to reveal the effect of the soluble form of the extracellular TLR4 domain and MD-2 (sTLR4/sMD-2) complex lacking the intracellular and transmembrane domains on various aspects of LPS-induced inflammation

Indexed as

ALICXCL1cytokineLPSsTLR4/sMD-2 complexTHP-1

Identifiers

PMID30542414
PMCPMC6257829
OpenAlexW2889741856

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.