Objectives: Our aim was to establish whether alcohol protects against RA development and to determine whether this effect is influenced by alcohol dose, duration and serological status through systematically reviewing the literature and undertaking a meta-analysis.
Methods: We searched Medline/EMBASE (1946 to July 2012) using the terms rheumatoid arthritis.mp or arthritis, rheumatoid/ and alcohol.mp or ethanol/. Manuscript bibliographies were reviewed. Observational studies were included that were case-control/cohort, examined the relationship between alcohol and RA risk and reported or allowed the calculation of effect size data [odds ratios (ORs)/relative risks (RRs) with 95% CIs] in drinkers vs non-drinkers. A random-effects model was used to estimate pooled ORs/RRs. Dose-risk relationships were evaluated by trend tests. RESULTS. Nine studies (from 893 articles) met our inclusion criteria, comprising six case-control (3564 cases; 8477 controls) and three cohort studies (444 RA cases; 84 421 individuals). A significant protective effect of alcohol on RA risk was observed-summary OR for RA in drinkers vs non-drinkers 0.78 (95% CI 0.63, 0.96). This effect was confined to ACPA-positive RA-summary OR 0.52 (95% CI 0.36, 0.76), with no significant risk reduction seen for ACPA-negative RA-summary OR 0.74 (95% CI 0.53, 1.05). Subgroup analysis by study design identified a significant relationship in case-control but not cohort studies.
Conclusion: Alcohol intake is inversely associated with ACPA-positive RA, suggesting a protective effect. As this finding is confined to case-control studies further research is required with prospective cohort studies incorporating ACPA status to confirm this relationship.
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http://dx.doi.org/10.1093/rheumatology/kes376 | DOI Listing |
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Faculdade de Medicina, Universidade de São Paulo. Av. Dr. Arnaldo 455, 2º andar, sala 2216, Cerqueira Cesar. 01246-903 São Paulo SP Brasil.
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Key Laboratory of Bioactive Materials for the Ministry of Education, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, and Frontier of Science Center for Cell Response, Nankai University, Tianjin, 300071, China.
Nanozymes play a pivotal role in mitigating excessive oxidative stress, however, determining their specific enzyme-mimicking activities for intracellular free radical scavenging is challenging due to endo-lysosomal entrapment. In this study, we employ a genetic engineering strategy to generate ionizable ferritin nanocages (iFTn), enabling their escape from endo-lysosomes and entry into the cytoplasm. Specifically, ionizable repeated Histidine-Histidine-Glutamic acid (9HE) sequences are genetically incorporated into the outer surface of human heavy chain FTn, followed by the assembly of various chain-like nanostructures via a two-armed polyethylene glycol (PEG).
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