Evidence map›Paper›PMID 31542866›Full record

ArticleMolecular biology reports2019

Effect of single nucleotide polymorphisms in SEPS1 and SEPP1 on expression in the protein level in metabolic syndrome in subjects with cardiovascular disease.

Mojgan Gharipour, Khadija Ouguerram, El-Hassane Nazih, Mansoor Salehi, Mehrdad Behmanesh, Rouzbeh Razavi, Amin Gharipour, Minoo Diantkhah, Masoumeh Sadeghi

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Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

9 authors at 6 institutions in 4 countries.

Mojgan GharipourIsfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran.ORCID http://orcid.org/0000-0001-7397-1172
Khadija OuguerramUMR PHAN, INRA & Université de Nantes, IMAD, CRNH-Ouest, Nantes, France. khadija.ouguerram@univ-nantes.fr.
El-Hassane NazihIUML-Institut Universitaire Mer et Littoral-FR3473 CNRS, MMS-EA2160, Nantes, France.
Mansoor SalehiDepartment of Genetics and Molecular Biology Medical School, Isfahan University of Medical Sciences, Isfahan, Iran.
Mehrdad BehmaneshDepartment of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Rouzbeh RazaviDepartment of Management and Information Systems, Kent State University, Kent, OH, USA.
Amin GharipourDepartment of Accounting, Finance and Economics, Griffith University, Gold Coast Campus, Australia.
Minoo DiantkhahIsfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran.
Masoumeh SadeghiCardiac Rehabilitation Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran.
Isfahan University of Medical Sciences · IRCentre National de la Recherche Scientifique · FRDigestive Health Research Institute · FRGriffith University · AUKent State University · USTarbiat Modares University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MetS) results from the interaction between environmental and genetic factors. Several previous studies considered the role of selenium in developing MetS. Two selenoproteins, selenoprotein S (SelS), and the Selenoprotein P (SePP) play an important role in antioxidative defense and therefore susceptibility to MetS. The involvement of SNPs in SEPP1 and SEPS1 have not been studied in MetS subjects. This study aims to investigate the association between the risk of MetS and four polymorphisms SEPS1 (rs28665122, rs4965373), SEPP1 (rs7579, rs3877899) in an Iranian population. The sample of this case-control study consisted of 132 Iranian patients with cardiovascular disease (71 MetS and 65 non-MetS subjects) from December 2015 to March 2016. Demographic data, medical history, and para-clinical were measured, and Taqman probes were used for allelic discrimination. The level of the SelS and the SePP were measured by the ELIZA method. No significant differences were found in the genotype frequencies of SEPS1 (rs4965373, rs28665122), SEPP1 (rs7579, rs3877899) in patients with MetS and the non-MetS group. The mean of SelS in MetS subjects with SEPS1 (rs4965373) GG genotype is significantly lower than the non-MetS group (4496.99 ± 3688.5 vs. 6148.6 ± 1127.0, P = 0.009). The mean of SePP in MetS subjects with SEPP1 (rs3877899) GG genotype is significantly lower than the non-MetS group (40.73 ± 8.44 vs.83.91 ± 21.33, P = 0.002). The mean of SePP in MetS subjects with SEPP1 (rs7579) GG genotype is lower than the non-MetS group (55.52 ± 16.7 vs. 109.48 ± 29.78, P = 0.01). In summary, the results of this study does not indicate significant differences in the SEPP1 (rs7579, rs3877899) and SEPS1 (rs4965373, rs28665122) genotypes between MetS and non-MetS subjects. However, the results show that the mean of expression of SelS and SePP decreased in the subjects with SEPP1 (rs7579) GG and SEPP1 (rs3877899) GG.

Indexed as

Cardiovascular DiseasesMetabolic SyndromeCase-Control StudiesFemaleHumansMaleMembrane ProteinsMiddle AgedPolymorphism, Single NucleotideSelenoprotein PSelenoproteinsMembrane ProteinsSELENOP protein, humanSelenoprotein PSelenoproteinsSELENOS protein, humanCardiovascular diseaseGeneMetabolic syndromePolymorphismsSelSSePPSEPP1SEPS1

Identifiers

PMID31542866
OpenAlexW2973373393

What OpenQuestion holds

Textmetadata
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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.