Identification of Genes and Key Pathways Associated with the Pathophysiology of Lung Cancer and Atrial Fibrillation.

Background: Lung cancer is a malignant tumor originating from respiratory epithelial cells in the bronchi, bronchioles, and alveoli, often associated with atrial fibrillation; However, there is a lack of in-depth understanding of its genetic basis and molecular mechanisms. Our goal is to study the genes and signaling networks associated with cancer and atrial fibrillation. Materials and methods: We obtained microarray datasets for lung tumors from the Gene Expression Omnibus (GEO) database and AF for this investigation: GSE30219, GSE79768, and screened the candidate specimens in both microarrays for differential genes at P < .05 using GEO2R. The outcomes were also examined using the Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Gene and Gene Combinations (KEGG) pathway analysis methods. Using STRING and Cytoscape, protein interaction networks (PPI) were analyzed and visualized. The Molecular Complex Detection (MOCDE) plugin is responsible for filtering important compounds. Candidate genes are then screened by the cytoHubba plugin according to MCC criteria. After taking the intersection of the Hub genes by the Wayne diagram, the ROC curves were plotted separately by combining the data from one lung cancer dataset GSE19804, two AF datasets GSE41177/GSE14975 in the GEO database. Results: An aggregate of 49 co-expressed differentially expressed genes (co-DEGs) were discovered in lung cancer/AF and healthy controls. Most co-DEGs were found in neutrophil activation, where they were linked to immunological response and interactions between cytokines and cytokine receptors, according to GO and KEGG pathway analyses. Furthermore, due of their significant connectedness in both the lung carcinoma and AF datasets, we chose six key genes. They are MNDA, HP, LYZ, S100A9, S100A8, and S100A12, among others. Conclusions: The findings of this research indicate that the onset of lung cancer and AF depends on a small number of distinctive genes. We investigated the functional enrichment, differential gene expression, and PPI of DEGs in lung cancer and AF, and the results offer fresh perspectives on the discovery of prospective biomarkers and priceless therapeutic precursors in these two diseases.

Spirituality as a Mediator Between Social Support and Benefit Finding Among Advanced Cancer Patients.

BACKGROUND: Social support and benefit finding (BF) are important for cancer patients. The relationship between social support and BF has not been studied sufficiently in patients with advanced cancer, and the mechanism through which social support might influence BF is unclear. OBJECTIVE: This study aimed to investigate the relationship between social support and BF in Chinese patients with advanced cancer as mediated by their perceptions of spirituality. METHODS: This was a correlation study with a cross-sectional design. We recruited advanced-cancer patients (n = 208) from China. Patients' sociodemographic and clinical characteristics were collected, and they were asked to complete the Benefit Finding Scale, the Multidimensional Scale of Perceived Social Support, and the Spiritual Attitude and Involvement List. RESULTS: Social support was associated with greater spirituality and greater BF ( P < .01). Spirituality was positively correlated with BF ( P < .01). Results from mediation analysis identified that both the indirect effect of social support on BF via spirituality (indirect effect, 0.268; 95% confidence interval, 0.147-0.419) and its direct effect on BF (direct effect, 0.233; 95% confidence interval, 0.031-0.429) were statistically significant, suggesting a partial mediatory effect of spirituality between social support and BF. CONCLUSIONS: Our findings supported a positive association between social support and BF among Chinese advanced-cancer patients. The mediatory role of spirituality should provide a new perspective for augmentation of BF in these patients. IMPLICATIONS FOR PRACTICE: Interventions that help enhance social support and spirituality in patients with advanced cancer could facilitate their BF.

Maresin-2 alleviates allergic airway inflammation in mice by inhibiting the activation of NLRP3 inflammasome, Th2 type immune response and oxidative stress.

Asthma is a chronic inflammatory disease of the respiratory system. Maresin-2 (MaR2) is biosynthesized from docosahexaenoic acid (DHA) by macrophages, display strong anti-inflammatory and pro-resolving activity. To investigate the therapeutic effect and mechanism of MaR2 on asthmatic mice induced by ovalbumin (OVA) in conjunction with the adjuvant aluminum hydroxide. Twenty four female BALB/c mice were randomly divided into control, OVA, OVA + MaR2, and OVA + dexamethasone (Dexa) groups. MaR2 or Dexa were given as a treatment for OVA-induced asthma. Serum, bronchoalveolar alveolar lavage fluid (BALF) and lung tissue were collected for further analysis. The Pathological changes of lung tissue, proportion of inflammatory cells in BALF, levels of inflammatory cytokines in BALF or serum, oxidative stress indices, and the protein concentration of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 in lung tissues were evaluated. Compared with the OVA group, both OVA + MaR2 and OVA + Dexa group had reduced inflammation and mucus secretion in lung tissue, number of inflammatory cells in BALF, levels of related inflammatory cytokines in serum or BALF, and expressions of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 proteins in lung tissue. In addition, the oxidative stress was alleviated as indicated by decreased MDA, and elevated SOD and GSH. MaR2 has an obvious protective effect on OVA-induced bronchial asthma in mice, in a similar manner as Dexa. The mechanism may be related to the inhibition of the Th2 type immune response, the NLRP3 inflammasome activation and oxidative stress.

Potato pomace: An efficient resource for Monascus pigments production through solid-state fermentation.

Monascus pigments are the important natural additives in food industrial production. To obtain more economic pigments production processes, the present study was performed to evaluate the feasibility of using pomace resource as substrate for pigments production. Petri dish fermentation was designed to seek the optimal process parameters, and the value of red, yellow and total pigments per dry fermented substrate could achieve 654.6, 1268.1 and 1922.7 OD units/g, respectively. Shallow tray fermentation experiments were used for investigating the potential industrial production of pigments using potato pomace as sole carbon. The final total pigments of 200 g and 1000 g shallow tray experiments could reach 1886.9 and 1737.4 OD units/g. The results in this work indicating that potato pomace could be an efficient and low cost substrate for the production of Monascus pigments, and will supply a valuable reference for the comprehensive utilization of potato resources and seeking the economical natural pigments process.

The Protective Effects of Maresin 1 in the OVA-Induced Asthma Mouse Model.

Asthma is a chronic inflammatory disease that cannot be cured. Maresin 1 (MaR1) is a specific lipid synthesized by macrophages that exhibits powerful anti-inflammatory effects in various inflammatory diseases. The goal of this study was to evaluate the effect of MaR1 on allergic asthma using an ovalbumin- (OVA-) induced asthma model. Thirty BALB/c mice were randomly allocated to control, OVA, and MaR1 + OVA groups. Mice were sacrificed 24 hours after the end of the last challenge, and serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for further analysis. Western blotting was used to measure the protein level of IκBα, the activation of the NF-κB signaling pathway, and the expression of NF-κB downstream inflammatory cytokines. Quantitative real-time polymerase chain reactions (qRT-PCRs) were used to evaluate the expression levels of COX-2 and ICAM-1 in lung tissues. We found that high doses of MaR1 were most effective in preventing OVA-induced inflammatory cell infiltration and excessive mucus production in lung tissue, reducing the number of inflammatory cells in the BALF and inhibiting the expression of serum or BALF-associated inflammatory factors. Furthermore, high-dose MaR1 treatment markedly suppressed the activation of the NF-κB signaling pathway, the degradation of IκBα, and the expression of inflammatory genes downstream of NF-κB, such as COX-2 and ICAM-1, in the OVA-induced asthma mouse model. Our findings indicate that MaR1 may play a critical role in OVA-induced asthma and may be therapeutically useful for the management of asthma.