Causal relationship between breakfast skipping and myocardial infarction: Two-sample Mendelian randomization.

While observational studies suggest a connection between skipping breakfast and myocardial infarction (MI), the causal nature of this relationship is unclear. This study aims to investigate the genetic causal relationships between breakfast skipping and MI through Mendelian randomization (MR). Employing genetic data from a public genome-wide association study, this research focuses on genetic variations linked to breakfast skipping and MI. The primary analytical method was the inverse variance-weighted approach, complemented by additional methods like MR-Egger, weighted median, and mode analyses. It also includes heterogeneity and horizontal pleiotropy tests such as the Cochrane Q test, MR-Egger intercept, and MR-PRESSO tests, with a leave-one-out analysis for enhanced sensitivity assessment reliability. The study discovered a notable association between breakfast skipping and an increased risk of MI (odds ratios: 1.34, 95% confidence intervals: 1.03-1.76, P = .027). The test revealed no heterogeneity or multiplicity, and the sensitivity analysis confirmed the robustness of the results. Our MR analysis suggests that habitual breakfast skipping might elevate the likelihood of MI, underlining the importance of regular breakfast consumption in potentially mitigating heart attack risks.

[In vitro evaluation of cutaneous allergic reaction induced by chemicals using dendritic cells].

OBJECTIVE: To investigate the use of dendritic cells derived from mice bone marrow to evaluate the cutaneous allergic reaction induced by chemical sensitizers. METHODS: Dendritic cells derived from mice bone marrow were cultured and administrated with 2, 4-dinitrochlorobenzene (DNCB), nickel sulfate (NiSO4), sodium dodecyl sulfate (SDS) and hexyl cinnamic aldehyde (HCA), respectively. Cell membrane molecule CD86 and extracellular IL-1 beta, IL-6 and IL-12 were detected after 0, 1, 6, 12, 24, 36, 48 hour's administration, respectively. RESULTS: CD86 expression reached the highest level after exposure to DNCB for 48 h, and increased by about 279% compared with the control (P < 0.05), while it was lower than that of control after administrated with NiSO4 and HCA for 1 h and 6 h, and SDS for 36 h, respectively (P < 0.05). Extracellular IL-1 beta increased greatly after exposure to NiSO4 just for 1 h, with the maximum at 48 h (298 pg/ml, P < 0.05), and after exposure to HCA for 6 h, with maximum at 48 h (84 pg/ml, P < 0.05). However, it didn't fluctuate significantly after administrated with DNCB and SDS respectively, compared with the control. Extracellular IL-6 increased significantly after exposure to NiSO4 for 1 h, with the maximum at 24 h (2152 pg/ml, P < 0.05). After exposure to HCA, extracellular IL-6 reached the maximum at 1 h (1403 pg/ml), and then it was decreased quickly, but still higher than the control (P < 0.05), while it didn't change significantly after treatment with DNCB and SDS, compared with the control (P > 0.05). Extracellular IL-12 was not detected out among all the groups. CONCLUSION: Chemical sensitizer DNCB could induce the high expression of CD86 on DC membrane, and NiSO4 and HCA could induce DC to release IL-1 beta and IL-6. However, the irritant SDS had no such effect.