Factors associated with cognitive impairment in patients with atrial fibrillation: A systematic review and meta-analysis.

BACKGROUND: Atrial fibrillation (AF) is associated with an increased risk of cognitive impairment. Therefore, exploring factors which may be associated with cognitive impairment is important. Correspondingly, this study aimed to systematically evaluate factors associated with cognitive impairment in AF patients by synthesizing relevant evidence. METHODS: A database search of the PubMed, Embase, Cochrane Library, Web of Science, CBM, CNKI, Wanfang, and VIP databases was conducted from inception until December 21, 2023. The effect size was expressed as a combined odds ratio (OR) and 95 % confidence interval (95 % CI). The heterogeneity was qualitatively analyzed by Cochran's Q test and quantified by the I2 statistic. RESULTS: A total of 7,128 studies were identified from the 8 databases, and 39 studies of 3,491,423 participants were included. A meta-analysis was performed on 19 influencing factors. Advanced age (OR=1.38, 95 % CI: 1.11-1.71), female sex (OR=2.19, 95 % CI: 1.18-4.06), smoking (OR=2.44, 95 % CI: 1.24-4.80), hypertension (OR=1.61, 95 % CI: 1.27-2.03), diabetes (OR=1.42, 95 % CI: 1.20-1.67), and hearing impairment (OR=1.37, 95 % CI: 1.05-1.81) were risk factors for cognitive impairment. A higher education level (OR=0.57, 95 % CI: 0.46-0.72), oral anticoagulants (OR=0.61, 95 % CI: 0.48-0.78), novel oral anticoagulants (OR=0.63, 95 % CI: 0.54-0.73), warfarin (OR=0.55, 95 % CI: 0.39-0.79), novel oral anticoagulants relative to warfarin (OR=0.88, 95 % CI: 0.81-0.97), catheter ablation (OR=0.74, 95 % CI: 0.58-0.94) and exercise (OR=0.66, 95 % CI: 0.61-0.72) were protective factors for cognitive impairment. CONCLUSIONS: Age, sex, education level, smoking, exercise, hypertension, diabetes, hearing impairment, anticoagulation therapy, and catheter ablation were associated with cognitive impairment in AF patients.

Association between the guardians' educational levels and unintentional injuries in children aged 6-18 in Shenzhen, China.

BACKGROUND: Unintentional injuries is the leading cause of death in children aged 6-18 in China. Previous studies on the association between the guardians' educational levels and unintentional injuries in children have been inconclusive, and it remains unclear among the Chinese population. Therefore, this study aimed to identify the association between guardians' educational levels and unintentional injuries in children aged 6-18 in Shenzhen, China. METHODS: This cross-sectional study enrolled 9,903 children aged 6-18 in Shenzhen in 2020 using a multistage cluster sampling method. Information on the children and guardians were collected, and unintentional injuries in the past year was examined by using two nested questions. Logistic regression analyses were used to test the association between the guardians' educational levels and unintentional injuries in children aged 6-18, and the crude odds ratios (ORs) and adjusted ORs with 95% confidence intervals (95% CI) were calculated. RESULTS: 275 of the 9,903 children reported experiencing at least one unintentional injuries in the past year, and the weighted incidence of unintentional injuries was 6.3% (95% CI: 5.8-6.8%) in children aged 6-18 in Shenzhen, China. The incidence of unintentional injuries differed significantly in the guardians' education levels (P < 0.05). After adjustment for the children's variables, multiple binary logistic regression analysis showed that compared to children whose guardians' educational levels were low, children whose guardians' educational levels were high (adjusted OR = 0.57, 95% CI: 0.37-0.87) and medium (adjusted OR = 0.56, 95% CI: 0.39-0.81) had a lower odds of unintentional injuries. Similar results were also observed when further adjustment for both the children's and guardians' variables. CONCLUSION: The overall incidence of unintentional injuries in children aged 6-18 in Shenzhen was low, and it was associated with the guardians' educational levels. Children whose guardians' educational levels were low should be given special concern to prevent unintentional injuries, and it is suggested to reduce the incidence of unintentional injuries in children by improving the guardians' educational levels.

One-Step Purification of IgE Epitope-Specific Antibody Using Immunomagnetic Beads and Highly Sensitive Detection of Bovine ß-Lactoglobulin for the Prediction of Milk Allergenicity in Foods.

Bovine ß-lactoglobulin (BLG) is a common allergen found in milk, and the immunoglobulin E (IgE) epitope plays a crucial role in cow milk allergy. Therefore, targeting the IgE epitope could be useful in accurately detecting BLG and assessing its allergenicity. However, producing an IgE epitope-specific antibody (IgE-EsAb) through traditional methods requires complex and time-consuming procedures. Here, IgE-EsAb was purified from rabbit anti-BLG sera by immunomagnetic beads in one step. Then, a sandwich ELISA (sELISA) based on the IgE-EsAb was developed to detect BLG and predict the potential milk allergenicity in foods. The obtained IgE-EsAb could specifically recognize the target IgE epitope of BLG and exhibited high affinity and specificity. The developed IgE-EsAb-based sELISA demonstrated an ultra-wide linear range of 3.9-1.28 × 105 ng/mL, with a limit of detection of 0.49 ng/mL for BLG. Additionally, the proposed immunoassay showed high specificity and recoveries (91.24-109.61%). The ability of the IgE-EsAb-based sELISA to evaluate the potential milk allergenicity in foods was validated using sera from cow milk allergy patients. These results suggest that immunomagnetic beads are an effective tool for rapidly obtaining the IgE-EsAb, and our proposed sELISA could be a reliable and user-friendly method for monitoring trace amounts of BLG and predicting the potential milk allergenicity of food samples.

The Nuclear Orphan Receptor Nur77 Alleviates Palmitate-induced Fat Accumulation by Down-regulating G0S2 in HepG2 Cells.

Excessive triglyceride accumulation in hepatocytes is the hallmark of obesity-associated nonalcoholic fatty liver disease (NAFLD). Elevated levels of the saturated free fatty acid palmitate in obesity are a major contributor to excessive hepatic lipid accumulation. The nuclear orphan receptor Nur77 is a transcriptional regulator and a lipotoxicity sensor. Using human HepG2 hepatoma cells, this study aimed to investigate the functional role of Nur77 in palmitate-induced hepatic steatosis. The results revealed that palmitate significantly induced lipid accumulation and suppressed lipolysis in hepatocytes. In addition, palmitate significantly suppressed Nur77 expression and stimulated the expression of peroxisome proliferator-activated receptor γ (PPARγ) and its target genes. Nur77 overexpression significantly reduced palmitate-induced expression of PPARγ and its target genes. Moreover, Nur77 overexpression attenuated lipid accumulation and augmented lipolysis in palmitate-treated hepatocytes. Importantly, G0S2 knockdown significantly attenuated lipid accumulation and augmented lipolysis in palmitate-treated hepatocytes, whereas G0S2 knockdown had no effect on the palmitate-induced expression of Nur77, PPARγ, or PPARγ target genes. In summary, palmitate suppresses Nur77 expression in HepG2 cells, and Nur77 overexpression alleviates palmitate-induced hepatic fat accumulation by down-regulating G0S2. These results display a novel molecular mechanism linking Nur77-regulated G0S2 expression to palmitate-induced hepatic steatosis.

Palmitate induces fat accumulation by activating C/EBPß-mediated G0S2 expression in HepG2 cells.

AIM: To determine the role of G0/G1 switch gene 2 (G0S2) and its transcriptional regulation in palmitate-induced hepatic lipid accumulation. METHODS: HepG2 cells were treated with palmitate, or palmitate in combination with CCAAT/enhancer binding protein (C/EBP)ß siRNA or G0S2 siRNA. The mRNA expression of C/EBPß, peroxisome proliferator-activated receptor (PPAR)γ and PPARγ target genes (G0S2, GPR81, GPR109A and Adipoq) was examined by qPCR. The protein expression of C/EBPß, PPARγ, and G0S2 was determined by Western blotting. Lipid accumulation was detected with Oil Red O staining and quantified by absorbance value of the extracted Oil Red O dye. Lipolysis was evaluated by measuring the amount of glycerol released into the medium. RESULTS: Palmitate caused a dose-dependent increase in lipid accumulation and a dose-dependent decrease in lipolysis in HepG2 cells. In addition, palmitate increased the mRNA expression of C/EBPß, PPARγ, and PPARγ target genes (G0S2, GPR81, GPR109A, and Adipoq) and the protein expression of C/EBPß, PPARγ, and G0S2 in a dose-dependent manner. Knockdown of C/EBPß decreased palmitate-induced PPARγ and its target genes (G0S2, GPR81, GPR109A, and Adipoq) mRNA expression and palmitate-induced PPARγ and G0S2 protein expression in HepG2 cells. Knockdown of C/EBPß also attenuated lipid accumulation and augmented lipolysis in palmitate-treated HepG2 cells. G0S2 knockdown attenuated lipid accumulation and augmented lipolysis, while G0S2 knockdown had no effects on the mRNA expression of C/EBPß, PPARγ, and PPARγ target genes (GPR81, GPR109A and Adipoq) in palmitate-treated HepG2 cells. CONCLUSION: Palmitate can induce lipid accumulation in HepG2 cells by activating C/EBPß-mediated G0S2 expression.