Associations of single and multiple vitamin exposure with childhood eczema: data from the national health and nutrition examination survey.

Aim: The association between vitamins and eczema has garnered attention, yet few studies have evaluated the effects of co-exposure to multiple vitamins on this condition. This study aims to assess the association of vitamin mixtures with eczema in children. Methods: This cross-sectional study analyzed data from 2,244 children aged 6-17 years from the National Health and Nutrition Examination Surveys. Eczema served as the primary outcome. Six serum vitamins, namely, vitamins A, B6, B12, C, D, and E, were the main variables. Weighted multivariate logistic regression was adopted to analyze the association between each serum vitamin and eczema. Odds ratios (OR) with a 95% confidence interval (CI) were calculated. Bayesian kernel machine regression (BKMR) analysis and the quantile g-computation (qgcomp) model were used to evaluate the association of co-exposure to multiple vitamins with eczema. Results: In total, 10.83% of children (n = 243) developed eczema. After adjusting for confounding factors, we observed that compared with the reference group (vitamin B12 with second quartile), the OR for eczema was 0.604 (95% CI: 0.373-0.978, P = 0.041) for the first quartile of vitamin B12. Both BKMR analysis and the qgcomp model consistently showed that co-exposure to the six vitamins was positively correlated with the risk of eczema, with vitamin B6 contributing most to the overall effect. In BKMR analyses, we observed an interaction between vitamins B6 and B12 concerning eczema risk. Conclusion: Co-exposure to vitamins A, C, B6, B12, D, and E was found to be associated with an increased risk of eczema in children, with vitamin B6 as the greatest positive contributor driving the overall effect.

Advancements in elucidating the pathogenesis of actinic keratosis: present state and future prospects.

Solar keratosis, also known as actinic keratosis (AK), is becoming increasingly prevalent. It is a benign tumor that develops in the epidermis. Individuals with AK typically exhibit irregular, red, scaly bumps or patches as a result of prolonged exposure to UV rays. These growths primarily appear on sun-exposed areas of the skin such as the face, scalp, and hands. Presently, dermatologists are actively studying AK due to its rising incidence rate in the United States. However, the underlying causes of AK remain poorly understood. Previous research has indicated that the onset of AK involves various mechanisms including UV ray-induced inflammation, oxidative stress, complex mutagenesis, resulting immunosuppression, inhibited apoptosis, dysregulated cell cycle, altered cell proliferation, tissue remodeling, and human papillomavirus (HPV) infection. AK can develop in three ways: spontaneous regression, persistence, or progression into invasive cutaneous squamous cell carcinoma (cSCC). Multiple risk factors and diverse signaling pathways collectively contribute to its complex pathogenesis. To mitigate the risk of cancerous changes associated with long-term UV radiation exposure, prompt identification, management, and prevention of AK are crucial. The objective of this review is to elucidate the primary mechanisms underlying AK malignancy and identify potential treatment targets for dermatologists in clinical settings.

Identification of lncRNAs and Their Regulatory Relationships with mRNAs in Response to Cryptococcus neoformans Infection of THP-1 Cells.

Aims: Cryptococcosis is an invasive fungal disease that is associated with an increasing prevalence along with a very high fatality and is primarily caused by Cryptococcus. However, its mechanism to cause pathogenicity is not yet completely understood. In this study, we aim to screen the lncRNA markers in human monocytic (THP-1) cells infected by Cryptococcus neoformans (C. neoformans) through high-throughput sequencing technology and to explore its effects on biological functions. Methods: We initially conducted an lncRNA microarray analysis of the THP-1 cells infected by C. neoformans and normal THP-1 cells. Based upon these data, RT-qPCR was used to verify the expressions of the selected lncRNAs and mRNAs. We then performed functional and pathway enrichment analyses. Lastly, target prediction was performed by using the lncRNA target tool which was based on the differentially expressed lncRNAs. Results: We determined 81 upregulated and 96 downregulated lncRNAs using microarray. In addition, the profiling data showed 42 upregulated and 57 downregulated genes and discovered that neuroactive ligand-receptor interaction, tyrosine metabolism, and phenylalanine metabolism are extremely impaired in the regulation of C. neoformans infection. GO enrichment analysis of the 99 differentially expressed mRNAs exhibited that these modules showed different signaling pathways and biological mechanisms like protein binding and metal ion binding. Moreover, lncRNAs and mRNAs were analyzed for their coexpression relations. A qRT-PCR analysis confirmed that the expression of the top 10 differently expressed mRNA and lincRNA. The expressions of the lncRNAs after C. neoformans infection in THP-1 cells were detected by RNA-sequence, suggesting that microarray analysis could reveal lncRNAs having functional significance that might be linked with the progression of patients. Conclusion: The current study analyzed the differential lncRNAs and mRNAs in C. neoformans infection and predicted the corresponding pathways and their correlations that can offer new potential insights into the mechanistic basis of this condition.