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1.
Immun Inflamm Dis ; 11(8): e944, 2023 08.
Article in English | MEDLINE | ID: mdl-37647438

ABSTRACT

OBJECTIVE: To identify new trends and potential hotspots in research on rheumatoid arthritis-associated interstitial lung disease (RA-ILD). MATERIALS AND METHODS: The Web of Science (WOS) database was used to search for RA-ILD-related literature published between August 31, 2002 and August 31, 2022. CiteSpace 6.1.R3, VOSviewer version 1.6.17, Scimago Graphica, and Pajek V2.0 visualization software were used to conduct a comprehensive analysis and network visualization mapping of the authors, countries, institutions, journals, cited references, and keywords. RESULTS: A total of 2412 articles were retrieved, and the number of articles published has grown annually since 2002. Eric L. Matteson was the most prolific author, and the Mayo Clinic and UNITED STATES have the highest publishing volume and influence. Clinical Rheumatology is the journal with the most papers published. Rheumatology was the most cited journal. The citation clusters and keywords concentrated on the mechanism, treatment, and predictive and prognostic factors. CONCLUSION: Pathogenesis, treatment, and predictive and prognostic factors were among the RA-ILD research directions and hotspots. Antirheumatoid drugs, especially biologics and small molecule inhibitors, were among the most actively researched treatment options. The results of this study provides an in-depth understanding of the development of RA-ILD publications, aids researchers in understanding hotspots and trends and provides a new perspective for future RA-ILD research.


Subject(s)
Arthritis, Rheumatoid , Lung Diseases, Interstitial , Humans , Arthritis, Rheumatoid/complications , Databases, Factual , Health Personnel , Lung Diseases, Interstitial/etiology , Software
2.
Clin Rheumatol ; 42(3): 663-672, 2023 Mar.
Article in English | MEDLINE | ID: mdl-36369402

ABSTRACT

In order to provide a basis for the prevention of RA, this systematic review and meta-analysis evaluated the association between passive smoking and the risk of developing RA. We searched electronic databases, including PubMed, Cochrane Central Register of Controlled Trials, Web of Science, and Embase, for published literature from the establishment to March 2022. Then we included subject-related cohort studies and case-control studies, and two researchers independently screened and extracted relevant data. Finally, we performed a meta-analysis, cumulative meta-analysis, and dose-response meta-analysis using the Stata software and evaluated the included literature for the level of evidence. This meta-analysis included three case-control and three cohort studies. There was only a small amount of statistical heterogeneity among the studies (I2 = 34.9%). According to the study results, the risk of RA was 12% higher in passive smokers than in unexposed individuals. In subgroup analysis, a 12% increase in the prevalence of RA was observed in those exposed to passive smoking in adulthood. The developing RA rate was 34% higher in individuals exposed to passive smoking during childhood than in unexposed individuals. As time progressed and with the inclusion of extensive sample studies in the cumulative meta-analysis, the precision of the overall incidence effect values gradually increased. A dose-response meta-analysis showed no statistical significance that the risk of RA increased with the number of passive smoking years. Passive smoking may relate to the risk of RA, especially in childhood exposures.


Subject(s)
Arthritis, Rheumatoid , Tobacco Smoke Pollution , Humans , Tobacco Smoke Pollution/adverse effects , Arthritis, Rheumatoid/epidemiology , Arthritis, Rheumatoid/etiology , Cohort Studies , Incidence , Case-Control Studies
3.
J Tradit Chin Med ; 40(6): 917-921, 2020 12.
Article in English | MEDLINE | ID: mdl-33258342

ABSTRACT

OBJECTIVE: To establish an in vitro model of radiation-induced lung injury using rat lung alveolar macrophages (NR8383). METHODS: Using a medical electronic linear accelerator, cells were irradiated with either 0 Gy or 6 Gy X-rays. At 6, 12, 24, 30 and 48 h, the DNA damage index (8-OHdG) and lipid damage index (MDA) were measured in the two groups. We also determined the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and transforming growth factor-ß (TGF-ß). RESULTS: The levels of 8-OHdG and MDA in the 6 Gy irradiation group were higher than those in the 0 Gy group at 6, 12, 24, 30 and 48 h after irradiation. The levels reached the highest value -6 h after irradiation, and then gradually decreased. The levels of the inflammatory factors TNF-α, TGF-ß and IL-6 were higher in the 6 Gy irradiation group than those in the 0 Gy group at 6, 12, 24, 30 and 48 h after irradiation. CONCLUSION: Six Gy X-ray irradiated NR8383 cells can be used to establish an in-vitro model of radiation-induced lung injury. The levels of 8-OHdG, MDA, TNF-α, TGF-ß and IL-6 can be used as effective evaluation indicators.


Subject(s)
Lung Injury/etiology , Macrophages, Alveolar/radiation effects , Neoplasms/radiotherapy , Radiation Injuries/metabolism , Radiotherapy/adverse effects , Animals , Cell Line , Humans , Interleukin-6/genetics , Interleukin-6/metabolism , Lung Injury/genetics , Lung Injury/metabolism , Macrophages, Alveolar/metabolism , Models, Biological , Radiation Injuries/etiology , Radiation Injuries/genetics , Radiation, Ionizing , Rats , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism
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