Evidence map›Paper›PMID 24877088›Full record

ArticleBioMed research international2014

Complete cell killing by applying high hydrostatic pressure for acellular vascular graft preparation.

Atsushi Mahara, Naoki Morimoto, Takahiro Sakuma, Toshiya Fujisato, Tetsuji Yamaoka

Abstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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  11. Simple and efficient method for consecutive inactivation-cryopreservation of porcine skin grafts.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 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

5 authors.

Atsushi MaharaDepartment of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, Fujishiro-dai, Suita, Osaka 565-8565, Japan.ORCID 0000-0002-4075-6019
Naoki MorimotoDepartment of Plastic and Reconstructive Surgery, Kansai Medical University, 2-5-1 Shin-machi, Hirakata City, Osaka 573-1010, Japan.
Takahiro SakumaDepartment of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, Fujishiro-dai, Suita, Osaka 565-8565, Japan.
Toshiya FujisatoDepartment of Biomedical Engineering, Osaka Institute of Technology, 5-16-1 Omiya, Asahi-ku, Osaka 535-8585, Japan.
Tetsuji YamaokaDepartment of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, Fujishiro-dai, Suita, Osaka 565-8565, Japan.ORCID 0000-0003-0225-2407

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pressure treatment has been developed in tissue engineering application. Although the tissue scaffold prepared by a ultrahydrostatic pressure treatment has been reported, an excessive pressure has a potential to disrupt a structure of extracellular matrix through protein denaturation. It is important to understand the suitable low-pressure condition and mechanisms for cell killing. In this study, cellular morphology, mitochondria activity, and membrane permeability of mammalian cells with various pressure treatments were investigated with in vitro models. When the cells were treated with a pressure of 100 MPa for 10 min, cell morphology and adherence were the same as an untreated cells. Dehydrogenase activity in mitochondria was almost the same as untreated cells. On the other hand, when the cells were treated with the pressure of more than 200 MPa, the cells did not adhere, and the dehydrogenase activity was completely suppressed. However, green fluorescence was observed in the live/dead staining images, and the cells were completely stained as red after above 500 MPa. That is, membrane permeability was disturbed with the pressure treatment of above 500 MPa. These results indicated that the pressure of 200 MPa for 10 min was enough to induce cell killing through inactivation of mitochondria activity.

Indexed as

Blood Vessel ProsthesisAnimalsCell DeathHumansHuman Umbilical Vein Endothelial CellsHydrostatic PressureMiceNIH 3T3 CellsTissue Engineering

Identifiers

PMID24877088
PMCPMC4022071

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Registered trials

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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.