Evidence map›Paper›PMID 34117991›Full record

ArticleInternational journal of hematology2021

Novel variant fibrinogen γp.C352R produced hypodysfibrinogenemia leading to a bleeding episode and failure of infertility treatment.

Masahiro Yoda, Takahiro Kaido, Tomu Kamijo, Chiaki Taira, Yumiko Higuchi, Shinpei Arai, Nobuo Okumura

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Article in International journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

7 authors at 1 institution in 1 country.

Masahiro YodaDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan.
Takahiro KaidoDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan.
Tomu KamijoDepartment of Medical Sciences, Graduate School of Medicine, Science and Technology, Shinshu University, Matsumoto, Japan.
Chiaki TairaDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan.
Yumiko HiguchiDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan.
Shinpei AraiDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan. arais@shinshu-u.ac.jp.ORCID http://orcid.org/0000-0003-2455-4350
Nobuo OkumuraDepartment of Clinical Laboratory Investigation, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, 390-8621, Japan.
Shinshu University · JP

Funding

Japan Society for the Promotion of Science JP20K07799
6 · The paper itself

Abstract

introductionWe identified a patient with a novel heterozygous variant fibrinogen, γp.C352R (Niigata II; N-II), who had a bleeding episode and failed infertility treatment and was suspected to have hypodysfibrinogenemia based on low and discordant fibrinogen levels (functional assay 0.33 g/L, immunological assay 0.91 g/L). We analyzed the mechanism of this rare phenotype of a congenital fibrinogen disorder. MATERIALS AND

methodsPatient plasma fibrinogen was purified and protein characterization and thrombin-catalyzed fibrin polymerization performed. Recombinant fibrinogen-producing Chinese hamster ovary (CHO) cells were established and the assembly and secretion of variant fibrinogen analyzed by ELISA and western blotting.

resultsPurified N-II plasma fibrinogen had a small lower molecular weight band below the normal γ-chain and slightly reduced fibrin polymerization. A limited proportion of p.C352R fibrinogen was secreted into the culture medium of established CHO cell lines, but the γ-chain of p.C352R was synthesized and variant fibrinogen was assembled inside the cells.

conclusionWe demonstrated that fibrinogen N-II, γp.C352R was associated with markedly reduced secretion of variant fibrinogen from CHO cells, that fibrin polymerization of purified plasma fibrinogen was only slightly affected, and that fibrinogen N-II produces hypodysfibrinogenemia in plasma.

Indexed as

AllelesMutationAfibrinogenemiaAmino Acid SubstitutionAnimalsBlood CoagulationBlood Coagulation TestsCatalysisCHO CellsCricetulusFibrinFibrinogenHemorrhageHumansInfertilityPolymerizationFGG protein, humanFibrinFibrinogenThrombinBleedingCongenital fibrinogen disordersFailure of infertility treatmentFibrinogen γ chainHypodysfibrinogenemia

Identifiers

PMID34117991
OpenAlexW3170024598

What OpenQuestion holds

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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.