Evidence map›Paper›PMID 35837536›Full record

ArticleInfection and drug resistance2022

How Does

Yang-Kun Wang, Jun-Ling Zhou, Nian-Long Meng, Chao-Ya Zhu, Su-Nan Wang, Xiao-Dong Chen

Open access · goldAbstract read
In one paragraph

Article in Infection and drug resistance, 2022. 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
3.5field-weighted citation impact, top 7% 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, 19 citations in OpenAlex.

  1. Article
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  3. Correlation analysis ofFrontiers in cellular and infection microbiology · 2026
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  12. Article
  13. Histopathological Features ofJournal of inflammation research · 2022
    Article
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 4 institutions in 1 country.

Yang-Kun WangDepartment of Pathology, Foresea Life Insurance Guangzhou General Hospital, Guangzhou, 511300, People's Republic of China.
Jun-Ling ZhouShenzhen Nanshan District People's Hospital, Shenzhen, 518067, People's Republic of China.
Nian-Long MengDepartment of Pathology, The 989th Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Luoyang, Henan, 471031, People's Republic of China.
Chao-Ya ZhuDepartment of Pathology, Third Affiliated Hospital, Zhengzhou University, Zhengzhou, 450052, People's Republic of China.
Su-Nan WangShenzhen Polytechnic, Shenzhen, 518055, People's Republic of China.
Xiao-Dong ChenDepartment of Pathology, Foresea Life Insurance Guangzhou General Hospital, Guangzhou, 511300, People's Republic of China.
Chinese People's Liberation Army · CNShenzhen Polytechnic · CNShenzhen Sixth People's Hospital · CNThird Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the occurrence and development of gastric mucosal atrophy due to Methods: Detailed histological observations and immunohistochemical examinations were conducted via 197 endoscopic biopsies and endoscopic submucosal dissection specimens of gastric mucosal atrophic lesions with gastric Hp infection. Detailed observation was made of columnar cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix. Results: The infection of the gastric mucosa by Hp firstly led to the proliferative disorder of stem cells in the normal proliferative region of the gastric mucosa. This caused substantial propagation of cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix, as a means to replenish the damaged surface mucus cells. However, the propagation of stem cells in the proliferative region was insufficient for downward migration, and the normal physiological process of differentiation into fundic/pyloric gland cells was disrupted, resulting in glandular atrophy of the intrinsic layer of the gastric mucosa. Persistent Hp infection and disruption of stem cell proliferation in the proliferative region subsequently resulted in extensive segmental hyperplasia of the gastric mucosa and glandular atrophy of the lamina propria. Conclusion: The occurrence, development, and histomorphological features of gastric mucosal atrophy due to gastric Hp infection provide a reliable pathological basis for precise treatment by clinicians and are of great significance for controlling the development of gastric cancer.

Indexed as

gastric tumorHelicobacter pylorihistopathologyimmunohistochemistrymucosal atrophy

Identifiers

PMID35837536
PMCPMC9273833
OpenAlexW4284662717

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.