Evidence map›Paper›PMID 24932583›Full record

ArticlePloS one2014

Dysplastic hepatocytes develop nuclear inclusions in a mouse model of viral hepatitis.

Priyanka Thakur, Folami Lamoke, Joanna M Chaffin, Manuela Bartoli, Jeffrey R Lee, Michael B Duncan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
0.2field-weighted citation impact, top 40% 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, 10 citations in OpenAlex.

  1. Article
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  4. Cannabinoid receptor 1 knockout alleviates hepatic steatosis by downregulating perilipin 2.Laboratory investigation; a journal of technical methods and pathology · 2020
    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

6 authors at 2 institutions in 1 country.

Priyanka ThakurSection of Gastroenterology/Hepatology, Department of Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America.
Folami LamokeDepartment of Pharmacology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Department of Ophthalmology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America.
Joanna M ChaffinDepartment of Pathology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America.
Manuela BartoliDepartment of Pharmacology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Department of Ophthalmology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America.
Jeffrey R LeeDepartment of Pathology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Georgia Regents University Cancer Center, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia, United States of America.
Michael B DuncanSection of Gastroenterology/Hepatology, Department of Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Georgia Regents University Cancer Center, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America; Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, United States of America.
Augusta University · USGeorgia Regents Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viral hepatitis resulting in chronic liver disease is an important clinical challenge and insight into the cellular processes that drive pathogenesis will be critical in order to develop new diagnostic and therapeutic options. Nuclear inclusions in viral and non-viral hepatitis are well documented and have diagnostic significance in some disease contexts. However, the origins and functional consequences of these nuclear inclusions remain elusive. To date the clinical observation of nuclear inclusions in viral and non-viral hepatitis has not been explored at depth in murine models of liver disease. Herein, we report that in a transgenic model of hepatitis B surface antigen mediated hepatitis, murine hepatocytes exhibit nuclear inclusions. Cells bearing nuclear inclusions were more likely to express markers of cell proliferation. We also established a correlation between these inclusions and oxidative stress. N-acetyl cysteine treatment effectively reduced oxidative stress levels, relieved endoplasmic reticulum (ER) stress, and the number of nuclear inclusions we observed in the transgenic mice. Our results suggest that the presence of nuclear inclusions in hepatocytes correlates with oxidative stress and cellular proliferation in a model of antigen mediated hepatitis.

Indexed as

AldehydesAnimalsBiomarkersCell DeathCell NucleusCell Nucleus SizeCellular SenescenceDisease Models, AnimalEndoplasmic ReticulumGlycogenHepatitisHepatitis B Surface AntigensHepatocytesIntranuclear Inclusion BodiesMice, Inbred C57BLMice, Transgenic4-hydroxy-2-nonenalAldehydesBiomarkersGlycogenHepatitis B Surface AntigensProliferating Cell Nuclear Antigen

Identifiers

PMID24932583
PMCPMC4059674
OpenAlexW2058739763

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.