Evidence map›Paper›PMID 26414230›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

Abnormal Expression of Urea Transporter Protein in a Rat Model of Hepatorenal Syndrome Induced by Succinylated Gelatin.

Weiping Song, Xiaolong Qi, Wenhui Zhang, Yingying Zhao, Yan Cao, Fei Wang, Changqing Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. 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
0.5field-weighted citation impact, top 29% 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, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Urea transport and clinical potential of urearetics.Current opinion in nephrology and hypertension · 2016
    Review
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 3 institutions in 1 country.

Weiping SongDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Xiaolong QiDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Wenhui ZhangLiver Cirrhosis Diagnosis and Therapeutic Center, 302 Hospital of the People's Liberation Army, Beijing, China (mainland).
Yingying ZhaoDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Yan CaoDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Fei WangDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Changqing YangDivision of Gastroenterology and Hepatology, Institute of Digestive Disease, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Tongji Hospital · CNTongji University · CN302 Military Hospital of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatorenal syndrome (HRS) is a serious complication of advanced chronic liver disease. Abdominal compartment syndrome (ACS) occurs with dysfunction of multiple organs when abdominal pressure increases. Here, we report on a novel model of ACS with ascites and a model of HRS in rats to observe the urea transporter protein (UT) expression in the 2 models. MATERIAL AND

methodsA liver cirrhosis model was induced by CCl4. After changes of liver histopathology were observed, rats were injected intraperitoneally with succinylated gelatin to establish a model of ACS and HRS. Then, changes in BUN, Cr, and renal histopathology were detected. Moreover, the UT in ACS and HRS were also quantified.

resultsThe surfaces of liver in the cirrhotic group became coarse, with visible small nodules and became yellow and greasy. The normal structure of the hepatic lobules were destroyed, and hyperplasia of fibrotic tissue and pseudo-lobe was observed. The levels of BUN and Cr were significantly increased in rats suffering from ACS and HRS, respectively, compared to their control groups. In addition, the mRNA levels of UT-A2 and UT-A3 decreased in rats with HRS compared to cirrhotic rats. However, there was no significant difference between the mRNA levels of UT-A2, UT-A3, and UT-B in rats with ACS vs. normal rats.

conclusionsIt is feasible to model ACS in rats by injecting succinylated gelatin into the abdominal cavity. Increasing the intra-abdominal pressure by succinylated gelatin is also a novel approach for modeling HRS in cirrhotic rats. Compared with control rats, there is an abnormal mRNA expression of UT in ACS rats and HRS rats.

Indexed as

AnimalsBlood Urea NitrogenCarbon TetrachlorideChemical and Drug Induced Liver InjuryDisease Models, AnimalGelatinHepatorenal SyndromeIntra-Abdominal HypertensionKidneyLiverLiver CirrhosisMaleMembrane Transport ProteinsPressureRatsRats, Sprague-DawleyCarbon TetrachlorideGelatinMembrane Transport ProteinsRNA, MessengerSuccinatessuccinylated gelatinUreaUrea Transporters

Identifiers

PMID26414230
PMCPMC4591985
OpenAlexW2220070606

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.