Evidence map›Paper›PMID 27796576›Full record

ArticlePflugers Archiv : European journal of physiology2016

Cardiac inotropy, lusitropy, and Ca

Zai Hao Zhao, Jae Boum Youm, Yue Wang, Jeong Hoon Lee, Jae Hwi Sung, Joon-Chul Kim, Sun Hee Woo, Chae Hun Leem, Sung Joon Kim, Lan Cui and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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  6. Neuronal nitric oxide synthase modulation of intracellular CaPflugers Archiv : European journal of physiology · 2017
    Article
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

11 authors at 7 institutions in 4 countries.

Zai Hao ZhaoDepartment of Physiology & Biomedical Sciences, Ischemic/hypoxic disease institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Jongno Gu,, Seoul, 110-799, South Korea.
Jae Boum YoumDepartment of Physiology, College of Medicine, Inje University, Busan, South Korea.
Yue WangDepartment of Physiology & Biomedical Sciences, Ischemic/hypoxic disease institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Jongno Gu,, Seoul, 110-799, South Korea.
Jeong Hoon LeeCollege of Medicine/Asan Medical Center, University of Ulsan, Ulsan, South Korea.
Jae Hwi SungDepartment of Physiology & Biomedical Sciences, Ischemic/hypoxic disease institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Jongno Gu,, Seoul, 110-799, South Korea.
Joon-Chul KimCollege of Pharmacy, Chungnam National University, Daejeon, South Korea.
Sun Hee WooCollege of Pharmacy, Chungnam National University, Daejeon, South Korea.
Chae Hun LeemCollege of Medicine/Asan Medical Center, University of Ulsan, Ulsan, South Korea.
Sung Joon KimDepartment of Physiology & Biomedical Sciences, Ischemic/hypoxic disease institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Jongno Gu,, Seoul, 110-799, South Korea.
Lan CuiYan Bian University Hospital, Yanji, Ji Lin, China. lancui@ybu.edu.cn.
Yin Hua ZhangDepartment of Physiology & Biomedical Sciences, Ischemic/hypoxic disease institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Jongno Gu,, Seoul, 110-799, South Korea. yinzhang87@gmail.com.
Seoul National University · KRChungnam National University · KRYanbian University Hospital · CNAsan Medical Center · KRInje University · KRNew Generation University College · ETUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatty acid (FA)-dependent oxidation is the predominant process for energy supply in normal heart. Impaired FA metabolism and metabolic insufficiency underlie the failing of the myocardium. So far, FA metabolism in normal cardiac physiology and heart failure remains undetermined. Here, we evaluate the mechanisms of FA and major metabolic substrates (termed NF) on the contraction, relaxation, and Ca

Indexed as

Calcium SignalingMyocardial ContractionAnimalsBicarbonatesCalcium Channels, L-TypeCells, CulturedFatty AcidsHeart VentriclesMaleMyocytes, CardiacRatsRats, Sprague-DawleyBicarbonatesCalcium Channels, L-TypeFatty AcidsCardiac myocyteContractionIntracellular Ca2+ transientMetabolic substratesMyofilament Ca2+ sensitivitypHRelaxation

Identifiers

PMID27796576
PMCPMC5138277
OpenAlexW2542513780

What OpenQuestion holds

Textmetadata
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.