Evidence map›Paper›PMID 29483581›Full record

ArticleScientific reports2018

Quantitative Assessment of Liver Steatosis and Affected Pathways with Molecular Imaging and Proteomic Profiling.

Yasuyo Urasaki, Chi Zhang, Ji-Xin Cheng, Thuc T Le

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Akt3 Regulates the Tissue-Specific Response to Copaiba Essential Oil.International journal of molecular sciences · 2020
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  19. Adenosine Kinase Deficiency Increases Susceptibility to a Carcinogen.Journal of caffeine and adenosine research · 2019
    Article
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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

4 authors at 2 institutions in 1 country.

Yasuyo UrasakiDepartment of Biomedical Sciences, College of Medicine, Roseman University of Health Sciences, 10530 Discovery Drive, Las Vegas, NV, 89135, USA.
Chi ZhangDepartments of Electrical and Computer Engineering & Biomedical Engineering, College of Engineering, Boston University, 8 St. Mary's St, Boston, MA, 02215, USA.
Ji-Xin ChengDepartments of Electrical and Computer Engineering & Biomedical Engineering, College of Engineering, Boston University, 8 St. Mary's St, Boston, MA, 02215, USA. jxcheng@bu.edu.
Thuc T LeDepartment of Biomedical Sciences, College of Medicine, Roseman University of Health Sciences, 10530 Discovery Drive, Las Vegas, NV, 89135, USA. tle5@roseman.edu.
Boston University · USRoseman University of Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current assessment of non-alcoholic fatty liver disease (NAFLD) with histology is time-consuming, insensitive to early-stage detection, qualitative, and lacks information on etiology. This study explored alternative methods for fast and quantitative assessment of NAFLD with hyperspectral stimulated Raman scattering (SRS) microscopy and nanofluidic proteomics. Hyperspectral SRS microscopy quantitatively measured liver composition of protein, DNA, and lipid without labeling and sensitively detected early-stage steatosis in a few minutes. On the other hand, nanofluidic proteomics quantitatively measured perturbations to the post-translational modification (PTM) profiles of selective liver proteins to identify affected cellular signaling and metabolic pathways in a few hours. Perturbations to the PTM profiles of Akt, 4EBP1, BID, HMGCS2, FABP1, and FABP5 indicated abnormalities in multiple cellular processes including cell cycle regulation, PI3K/Akt/mTOR signaling cascade, autophagy, ketogenesis, and fatty acid transport. The integrative deployment of hyperspectral SRS microscopy and nanofluidic proteomics provided fast, sensitive, and quantitative assessment of liver steatosis and affected pathways that overcame the limitations of histology.

Indexed as

BH3 Interacting Domain Death Agonist ProteinFatty Acid-Binding ProteinsFatty LiverHumansHydroxymethylglutaryl-CoA SynthaseImmunoassayMolecular ImagingNonlinear Optical MicroscopyPhosphatidylinositol 3-KinasesProteomicsSignal TransductionBH3 Interacting Domain Death Agonist ProteinBID protein, humanFABP1 protein, humanFABP5 protein, humanFatty Acid-Binding ProteinsHMGCS2 protein, humanHydroxymethylglutaryl-CoA SynthasePhosphatidylinositol 3-Kinases

Identifiers

PMID29483581
PMCPMC5826939
OpenAlexW2805498581

What OpenQuestion holds

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LicenceCC BY
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.