Evidence map›Paper›PMID 22105167›Full record

ArticleThe Journal of clinical investigation2011

On the origin of the liver.

Joshua R Friedman, Klaus H Kaestner

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Joshua R FriedmanDepartment of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Klaus H Kaestner

Funding

ZINC FINGER PROTEINS IN EARLY KIDNEY DEVELOPMENTP01DK049210 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI AHIMA, REXFORD S. · 1995 to 2016
$26.9M
MicroRNA in Liver Development and DiseaseR01DK079881 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI FRIEDMAN, JOSHUA R. · 2008 to 2012
$1.6M
NIDDK NIH HHS P01 DK049210NIDDK NIH HHS R01 DK079881
6 · The paper itself

Abstract

While it has been well established that the fetal liver originates from foregut endoderm, the identity of the mechanisms that maintain liver mass under both basal and injury conditions remains controversial. Dramatically different models have been proposed based on the experimental design employed. In this issue of the JCI, Malato and colleagues report their elegant new model for genetic lineage tracing of mature mouse hepatocytes using an adenoassociated virus-driven Cre recombinase. They show convincingly that maintenance of liver mass during normal turnover or in response to mild injury is achieved by mature hepatocytes, rather than cholangiocytes or specialized progenitor cells, as has been suggested by others.

Indexed as

AnimalsHepatocytesHomeostasisLiverLiver Regeneration

Identifiers

PMID22105167
PMCPMC3226340

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.