Background: Neurodegenerative diseases (NDs) have posed significant challenges to public health, and it is crucial to understand their mechanisms in order to develop effective therapeutic strategies. Recent studies have highlighted the potential role of selenium in ND pathogenesis, as it plays a vital role in maintaining cellular homeostasis and preventing oxidative damage. However, a comprehensive analysis of the association between selenium and NDs is still lacking. Method: Five public databases, namely PubMed, Web of Science, EMBASE, Cochrane and Clinical Trials, were searched in our research. Random model effects were chosen, and Higgins inconsistency analyses (I²), Cochrane’s Q test and Tau2 were calculated to evaluate the heterogeneity. Result: The association of selenium in ND patients with Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) was studied. A statistically significant relationship was only found for AD patients (SMD = −0.41, 95% CI (−0.64, −0.17), p < 0.001), especially for erythrocytes. However, no significant relationship was observed in the analysis of the other four diseases. Conclusion: Generally, this meta-analysis indicated that AD patients are strongly associated with lower selenium concentrations compared with healthy people, which may provide a clinical reference in the future. However, more studies are urgently needed for further study and treatment of neurodegenerative diseases.

Background: The potential role of selenium in preventing chronic liver diseases remains controversial. This meta-analysis aimed to summarize the available evidence from observational studies and intervention trials that had evaluated the associations between body selenium status and chronic liver diseases. Methods: We comprehensively searched MEDLINE, Embase, Web of Science, and Cochrane Library from inception to April 2021. The study protocol was registered at PROSPERO (CRD42020210144). Relative risks (RR) for the highest versus the lowest level of selenium and standard mean differences (SMD) with 95% confidence intervals (CI) were pooled using random-effects models. Heterogeneity and publication bias were evaluated using the I² statistic and Egger’s regression test, respectively. Results: There were 50 studies with 9875 cases and 12975 population controls in the final analysis. Patients with hepatitis (SMD = −1.78, 95% CI: −2.22 to −1.34), liver cirrhosis (SMD = −2.06, 95% CI: −2.48 to −1.63), and liver cancer (SMD = −2.71, 95% CI: −3.31 to −2.11) had significantly lower selenium levels than controls, whereas there was no significant difference in patients with fatty liver diseases (SMD = 1.06, 95% CI: −1.78 to 3.89). Moreover, the meta-analysis showed that a higher selenium level was significantly associated with a 41% decrease in the incidence of significant advanced chronic liver diseases (RR = 0.59, 95% CI: 0.49 to 0.72). Conclusion: Our meta-analysis suggested that both body selenium status and selenium intake were negatively associated with hepatitis, cirrhosis, and liver cancer. However, the associations for fatty liver diseases were conflicting and need to be established in prospective trials.

Background: The prognostic value of human leukocyte antigen G (HLA-G) expression in gastrointestinal (GI) cancers remains controversial. Thus, this meta-analysis aimed to summarize available evidence from case-control or cohort studies that evaluated this association.Methods: The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched to identify relevant studies written in English published up to April 1, 2021, and with no initial date. Furthermore, the Google Scholar and Google databases were also searched manually for gray literature. The protocol for this meta-analysis was registered at PROSPERO (CRD42020213411). Pooled hazard ratios (HRs) or odds ratios (ORs) and 95% confidence intervals (CIs) were estimated for end points using fixed- and random-effects statistical models to account for heterogeneity. Publication bias was evaluated using a funnel plot, Begg’s and Egger’s tests, and the “trim and fill” method.Results: A total of 30 eligible articles with 5737 unique patients, including 12 studies on colorectal cancer (CRC), 6 on gastric cancer (GC), 5 on esophageal cancer (ESCC), 5 on hepatocellular carcinoma (HCC), and 2 on pancreatic adenocarcinoma (PC), were retrieved. Both univariate (HR = 2.01, 95% CI: 1.48 ~ 2.72) and multivariate (HR = 2.69, 95% CI: 2.03 ~ 3.55) analyses revealed that HLA-G expression was significantly correlated with poor overall survival (OS), regardless of the cancer type or antibody used. Subgroup analysis stratified by antibody showed that the 4H84 (I² = 45.8%, P = 0.101) antibodies could be trustworthy and reliable for detecting HLA-G expression in GI cancers. In addition, HLA-G expression was found to be correlated with adverse clinicopathological parameters such as clinical stage, nodal status, metastasis, and histological grade but not tumor status.Conclusion: Elevated HLA-G expression indicates a poor prognosis for GI cancer patients, and screening for this marker could allow for the early diagnosis and treatment of GI cancers to improve survival rates.

Adherence to a Mediterranean dietary pattern can protect against atherosclerosis in part by reducing intestinal permeability and gut microbial LPS production. Brussels chicory, a typical Mediterranean vegetable, has been shown to inhibit the formation of early-stage atherosclerosis in mice. We evaluated whether Brussels chicory affects advanced atherosclerosis progression, intestinal permeability, and gut microbial LPS production. Thirty-week-old male apoE-deficient mice with unstable atherosclerotic plaques in the brachiocephalic artery were fed the AIN-93G diet alone (control) or supplemented with 0.5% freeze-dried Brussels chicory for 20 wk. Plaque volume and features of plaque stability, plaque macrophage polarization, fecal and serum LPS concentrations, serum lipid profiles and inflammation-related cytokines, and gut microbial profiles were measured. Compared with the control treatment, Brussels chicory consumption did not significantly change plaque volume and serum lipid profiles. However, it increased plaque stability (P < 0.05), as evidenced by reduced necrotic core size (42.3%), and increased fibrous cap thickness (55.0%) and collagen content (68.4%). Moreover, Brussels chicory consumption reduced intestinal permeability (56.3%), fecal and serum LPS concentrations (52.2% and 39.4%), serum IL1β and TNFα (52.0% and 33.8%), promoted plaque macrophage polarization towards the M2-like phenotype, and altered gut microbial composition, the latter indicated by increased relative abundance of certain members of the Ruminococcaceae family, such as Ruminiclostridium_9, Ruminiclostridium_5, and Intestinimonas (P < 0.05). Spearman correlation analyses further showed that these bacterial genera were significantly correlated with intestinal permeability, fecal and serum LPS, serum proinflammatory cytokines, and several features of plaque stability. Brussels chicory might help stabilize atherosclerotic plaques in mice by reducing intestinal permeability and gut microbial LPS production. This study provides a promising approach to slow the progression of atherosclerosis.

Background: Poor cholesterol efflux capacity (CEC) has been proposed to be an independent risk factor for cardiovascular diseases. However, current evidence is inconsistent, especially in rheumatoid arthritis (RA) patients. This meta-analysis aims to identify whether CEC is impaired or altered by drug therapy in RA.Methods: The PubMed/MEDLINE, Embase, Cochrane Library andClinicalTrials.govdatabases were browsed to identify studies on CEC in RA patients. The searches mainly focused on studies in human subjects that were published before November 14, 2020, without any language restrictions. The effect size was pooled by the standardized mean differences and mean differences (SMD & MD) as well as the corresponding 95% confidence intervals (CIs) in a random or fixed effect model. Heterogeneity across the studies was tested using Cochran’s Q test andI²statistic. Newcastle-Ottawa Scale and the Downs and Black scale (D&B) were applied to evaluate the quality of included studies. The GRADE-system with its 4-grade evidence scale was used to assess the quality of evidence.Results: A total of 11 eligible articles, including 6 observational and 5 interventional studies, were retrieved. The pooled results showed that in patients with RA, CEC was not significantly different than in healthy controls (SMD: -0.34, 95% CI: − 0.83 to 0.14), whereas the plasma HDL-C levels was significantly lower (MD: -3.91, 95% CI: − 7.15 to − 0.68). Furthermore, in the before-after studies, the CEC of RA patients (SMD: 0.20, 95% CI: 0.02 to 0.37) increased, but the plasma HDL-C levels (MD: 3.63, 95% CI: − 0.13 to 7.39) remained at a comparable quantity after anti-rheumatic treatment comparing with the baseline. In addition, the funnel plot of included studies displayed a lightly asymmetry, while Egger’s and Begg’s test did not suggest the existence of publication bias. The quality of evidence was rated according to GRADE as moderate to very low.Conclusion: The current meta-analysis demonstrated that HDL-mediated CEC can be improved by the early control of inflammation and anti-rheumatic treatment in RA patients, which is independent of the plasma HDL-C levels. However, the results should be interpreted with caution because of low-quality and limited quantity of evidence. Future randomized controlled trials are needed to determine whether therapeutic strategies to enhance CEC in RA patients have beneficial effects for preventing CVD.