Evidence map›Paper›PMID 29599128›Full record

ArticleBioscience reports2018

Internal biliary drainage superior to external biliary drainage in improving gut mucosa barrier because of goblet cells and mucin-2 up-regulation.

Xuechan Tang, Weiping Ma, Weirong Zhan, Xin Wang, Huan Dong, Hongjing Zhao, Lin Yang, Cuiying Ji, Qing Han, Chenguang Ji and 2 more

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

5 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  5. 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

12 authors at 3 institutions in 2 countries.

Xuechan TangDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Weiping MaDepartment of Gastroenterology, the Han Dan Central Hospital, 59 Congtai North Road, Gaokai District, Handan 056000, Hebei Province, China.
Weirong ZhanDepartment of Laboratory Medicine, Department of Biotechnology, School of Medical Science, School of Applied Science, Royal Melbourne Institute of Technology University, Plenty Road, Bundoora VIC 3083, Australia.
Xin WangDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Huan DongDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Hongjing ZhaoDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Lin YangDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Cuiying JiDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Qing HanDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Chenguang JiDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Hongqun LiuDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China.
Na WangDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, 215 Heping West Road, Xinhua District, Shijiazhuang 050000, Hebei Province, China wangna1975@126.com.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CNRMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Backgroud: Obstructive jaundice increases intestinal permeability, but the pathological mechanisms remain obscure, which results in debates about the necessity of performing preoperative biliary drainage in patients with obstructive jaundice. Mucin-2 (MUC2) and goblet cells regulated by bile acids play an important role in maintaining the function of intestinal mucosal barrier. The present study was to investigate the role of goblet cells and MUC2 in obstructive jaundice and evaluate the effect of biliary drainage on intestinal permeability. STUDY

designWe enrolled patients with malignant biliary obstruction and controls. We also did animal studies with four groups of rats: sham operation, obstructive jaundice, internal biliary drainage, and external biliary drainage. Histopathological analysis, biochemical measurement, and electron microscopy examination were done on pertinent samples.

resultsCompared with the control group, the small intestinal mucosa was significantly damaged; goblet cells and MUC2 were significantly decreased and serum endotoxin level was significantly increased in patients and rats with obstructive jaundice. Biliary drainage, especially internal biliary drainage, significantly increased goblet cells and MUC2 and attenuated the damage of small intestinal mucosa.

conclusionsIn obstructive jaundice condition, goblet cells and MUC2 were reduced which were involved in the damage of intestinal mucosa barrier; biliary drainage increased goblet cells and MUC2, repaired mucosa layer and restored the intestinal mucosa barrier function.

Indexed as

AgedAnimalsBile Acids and SaltsDrainageFemaleGoblet CellsHumansIntestinal MucosaIntestinesJaundice, ObstructiveMaleMiddle AgedMucin-2PermeabilityRatsBile Acids and SaltsMUC2 protein, humanMucin-2External biliary drainageGoblet cellInternal biliary drainageIntestinal mucosal barrierMucin-2Obstructive jaundice

Identifiers

PMID29599128
PMCPMC6435503
OpenAlexW2795119846

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.