Evidence map›Paper›PMID 23073658›Full record

ArticleMolecular medicine (Cambridge, Mass.)2013

Augmenter of liver regeneration (ALR) is a novel biomarker of hepatocellular stress/inflammation: in vitro, in vivo and in silico studies.

Yoram Vodovotz, John Prelich, Claudio Lagoa, Derek Barclay, Ruben Zamora, Noriko Murase, Chandrashekhar R Gandhi

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. The impact of augmenter of liver regeneration in blunt liver trauma: An experimental model analysis.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2024
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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

7 authors at 2 institutions in 1 country.

Yoram VodovotzDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
John Prelich
Claudio Lagoa
Derek Barclay
Ruben Zamora
Noriko Murase
Chandrashekhar R Gandhi
University of Pittsburgh · USVA Pittsburgh Healthcare System · US

Funding

ROLE OF STELLATE CELLS IN LIVER FAILURER01DK054411 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GANDHI, CHANDRASHEKHAR R · 1998 to 2006
$1.7M
Mechanisms of Alcoholic Liver DiseaseR21AA020846 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GANDHI, CHANDRASHEKHAR R · 2012 to 2013
$344k
BLRD VA I01 BX001174NIAAA NIH HHS R21 AA020846NIAAA NIH HHS R21AA020846NIDDK NIH HHS R01 DK054411NIDDK NIH HHS R01-DK54411
6 · The paper itself

Abstract

The liver is a central organ involved in inflammatory processes, including the elaboration of acute-phase proteins. Augmenter of liver regeneration (ALR) protein, expressed and secreted by hepatocytes, promotes liver regeneration and maintains viability of hepatocytes. ALR also stimulates secretion of inflammatory cytokines (tumor necrosis factor [TNF]-α and interleukin [IL]-6) and nitric oxide from Kupffer cells. We hypothesized that ALR may be involved in modulating inflammation induced by various stimuli. We found that hepatic ALR levels are elevated at 24 h, before or about the same time as an increase in the mRNA expression of TNF-α and IL-6, after portacaval shunt surgery in rats. Serum ALR also increased, but significantly only on d 4 when pathological changes in the liver become apparent. In rats, serum ALR was elevated after intraperitoneal administration of lipopolysaccharide alone and in a model of gram-negative sepsis. Serum ALR increased before alanine aminotransferase (ALT) in endotoxemia and in the same general time frame as TNF-α and IL-6 in the bacterial sepsis model. Furthermore, mathematical prediction of tissue damage correlated strongly with alterations in serum ALR in a mouse model of hemorrhagic shock. In vitro, monomethyl sulfonate, TNF-α, actinomycin D and lipopolysaccharide all caused increased release of ALR from rat hepatocytes, which preceded the loss of cell viability and/or inhibition of DNA synthesis. ALR may thus serve as a potential diagnostic marker of hepatocellular stress and/or acute inflammatory conditions.

Indexed as

Computer SimulationStress, PhysiologicalAnimalsBiomarkersDisease Models, AnimalGene Expression RegulationHepatocytesInflammationInterleukin-6LipopolysaccharidesLiverMaleMiceOxidoreductases Acting on Sulfur Group DonorsProteinsRatsBiomarkersGFER protein, ratInterleukin-6LipopolysaccharidesOxidoreductases Acting on Sulfur Group DonorsProteinsRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID23073658
PMCPMC3563711
OpenAlexW194360514

What OpenQuestion holds

Textmetadata
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.