[Sequential mediating role of digital participation and health lifestyle in the relationship between socioeconomic status and depression of older adults].

OBJECTIVE: To explore the potential mechanisms of the relationship between socioeconomic status (SES) and depression of Chinese older adults through the mediating role of digital participation and health lifestyle. METHODS: Using the nationally representative data from the China Family Panel Studies in 2020, 4 846 participants aged 60 years and older were analyzed in our study. We explored the potential mechanisms of the relationship between SES and depression of Chinese older adults in the digital era through a chain multiple mediating effects model. The KHB (The Karlson, Holm, and Breen) method was used to analyze the mediating role of digital participation and health lifestyle and the proportion of mediating effect between the two was also calculated. A series of robustness tests were further conducted and the fit of the model was checked by structural equation modeling. RESULTS: The mean age of the 4 846 older adults included in this study was (68.20±5.07) years, 48.06% of whom were female and 51.94% were male. The KHB results showed that both digital participation and health lifestyle could mediate the relationship between SES and depression of older adults (P < 0.000 1) and the mediating role of health lifestyle accounted for a greater proportion than digital participation. And our study mainly found three potential pathways of SES and depression of older adults, including: (1) SES → digital participation → health lifestyle → depression, (2) SES → health lifestyle → depression, and (3) SES → depression. Structural equation modeling tests proved the overall fit of the model in this study. CONCLUSION: Our findings showed that in the digital age, in addition to the direct relationship between SES and depression of older adults, and the health lifestyle as a mediator between the relationship, there is also a sequential mediating role of digital participation and health lifestyle to reduce the risk of depression. The findings suggest that we should pay more attention to the probability of the digital divide exacerbating health inequalities and socioeconomic inequalities accumulation in the digital age and promote the co-progress of digital literacy and health literacy among older adults.

Processing abnormalities in monetary outcome evaluations among male individuals with opioid use disorder: evidence from feedback-related negativity.

Background: Numerous studies have highlighted the pivotal role of alterations in the monetary reward system in the development and maintenance of substance use disorder (SUD). Although these alterations have been well documented in various forms of SUD, the electrophysiological mechanisms specific to opioid use disorder (OUD) remain underexplored. Understanding these mechanisms is critical for developing targeted interventions and advancing theories of addiction specific to opioid use.Objectives: To explore abnormalities in monetary reward outcome processing in males with OUD. We hypothesized that control individuals would show higher feedback-related negativity (FRN) to losses, unlike those in the OUD group, where FRN to losses and gains would not differ significantly.Methods: Fifty-seven participants (29 male individuals with OUD [heroin] and 28 male controls) were evaluated. A combination of the monetary incentive delay task (MIDT) and event-related potential (ERP) technology was used to investigate electrophysiological differences in monetary reward feedback processing between the OUD and healthy control groups.Results: We observed a significant interaction between group (control vs. OUD) and monetary outcome (loss vs. gain), indicated by p < .05 and η2p = 0.116. Specifically, control participants showed stronger negative FRN to losses than gains (p < .05), unlike the OUD group (p > .05).Conclusion: This study's FRN data indicate that males with OUD show altered processing of monetary rewards, marked by reduced sensitivity to loss. These findings offer electrophysiological insights into why males with OUD may pursue drugs despite potential economic downsides.

The sensor histidine kinase (SLN1) and acetyl-CoA carboxylase (ACC1) coordinately regulate the response of Neurospora crassa to the springtail Sinella curviseta (Collembola: Entomobryidae) attack.

IMPORTANCE: Understanding the regulatory pathways by which fungi respond to environmental signals through interlinked genes provides insights into the interactions between fungi and insects. The coordinated optimization of the regulatory networks is necessary for fungi to adapt to their habitats. We demonstrated that the synergistic regulation of sensor histidine kinase (SLN1) and acetyl-CoA carboxylase (ACC1) plays a critical role in regulating the fungal response to Sinella curviseta stress. Furthermore, we found that the enhanced production of trehalose, carotenoids, and 5-MTHF plays crucial role in the resistance to the fungivore. Our results provide insights into the understanding of the adaptation of N. crassa to environmental stimuli.

Ultraviolet radiation promotes the production of hispidin polyphenols by medicinal mushroom Inonotus obliquus.

Production of hispidin polyphenols in Inonotus obliquus is a stress-induced response triggered by environmental factors. As one of the important environmental factors, ultraviolet (UV) radiation plays regulatory roles in fungal growth and development. However, whether UV radiation regulates the formation of hispidin polyphenols remains to be established. In this study, we cultivated I. obliquus on solid medium and imposed intermittent UV radiation. We showed that UV exposure inhibited the growth of mycelia but increased the production of polyphenols. Further bioassays revealed that UV radiation also increased the catalytic activities of phenylalanine ammonia-lyase (PAL) and chalcone isomerase (CHI), up-regulated expression of genes related to redox, transcriptional regulation, and metabolism. In addition, the total extracts from the UV-irradiated group were more capable of scavenging DPPH and ABTS+ free radicals, especially at the later stage of culture. Thus, UV radiation, acting as one of the environmental factors, stimulated the accumulation of polyphenols in I. obliquus by regulating the activities of enzymes and the expression of genes related to growth and metabolism, and can be tentatively used as a feasible strategy to enhance the production of polyphenols in I. obliquus.

miR-4284 Promotes Cell Proliferation, Migration, and Invasion in Non-Small Cell Lung Cancer Cells and is Associated with Postoperative Prognosis.

PURPOSE: MicroRNA-4284 (miR-4284) was demonstrated to be aberrantly expressed and affected cell activities in some types of diseases, including cancer. However, the role of miR-4284 in non-small cell lung cancer (NSCLC) is largely unknown. The aim of this study was to investigate the expression and biological role of miR-4284 in NSCLC. PATIENTS AND METHODS: The qRT-PCR assay was applied to detect the expression of miR-4284 in NSCLC tissues and cell lines. Kaplan-Meier curve method and multiple Cox regression analyses were used to explore the prognostic factors for postoperative NSCLC patients. The CCK-8 assay was carried out to measure the proliferative abilities of A549 and H1299 cells. Transwell migration and invasion assays were used to determine the cell migratory and invasive capabilities of NSCLC cells. RESULTS: miR-4284 expression was upregulated in NSCLC tissues and cell lines. High expression of miR-4284 was correlated with poor differentiation, positive lymph node metastasis, and advanced TNM stages. In addition, postoperative patients with higher expression of miR-4284 exhibited a shorter overall survival time than those with lower expression of miR-4284. Moreover, the upregulation of miR-4284 accelerated cell proliferative, migratory, and invasive abilities of A549 and H1299 cells, while the downregulation of miR-4284 inhibited these cellular capabilities. CONCLUSION: miR-4284 was noticeably upregulated in NSCLC and associated with a poor prognosis of postoperative NSCLC patients. miR-4284 promoted the proliferation, migration, and invasion of A549 and H1299 cells. This study indicated that miR-4284 might serve as a prognostic biomarker and a potential therapeutic target for postoperative NSCLC patients.

Correction: High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma.

[This corrects the article DOI: 10.1371/journal.pone.0187356.].

SPC25 upregulation increases cancer stem cell properties in non-small cell lung adenocarcinoma cells and independently predicts poor survival.

In this study, we investigated the functional role and prognostic value of spindle pole body component 25 (SPC25) in non-small cell lung cancer (NSCLC). SPC25 expression profile in lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and normal lung tissues was examined by using data from the Cancer Genome Atlas (TCGA) and the Human Protein Atlas (HPA). LUAD A549 cells and LUSC H520 cells were used to investigate the influence of SPC25 on cancer stem cell (CSC) properties in terms of the proportion of CD133+ cells, tumorsphere formation and CSC markers, including CD133, ALDH1 and Sox2. Data mining was also performed in the Kaplan-Meier plotter and TCGA-NSCLC to assess the independent prognostic value of SPC25. Results showed SPC25 was significantly upregulated in LUAD and LUSC tissues compared with normal lung tissues. SPC25 overexpression significantly increased the CSC properties and invasion of A549 cells, but not H520 cells. In comparison, SPC25 knockdown impaired the CSC properties and invasion of A549 cells, but not H520 cells. Univariate and multivariate analysis confirmed that high SPC25 expression was an independent prognostic factor for poor overall survival (OS) (HR: 1.622, 95%CI: 1.207-2.178, p = .001) and recurrence-free survival (RFS) (HR: 1.726, 95%CI: 1.242-2.399, p = .001) in LUAD patients. However, no independent prognostic value of SPC25 was observed in LUSC patients even under the best cut-off model. Based on these findings, we infer that SPC25 upregulation can increase CSC properties in LUAD and independently predict poor survival in this histological subtype.

High ECT2 expression is an independent prognostic factor for poor overall survival and recurrence-free survival in non-small cell lung adenocarcinoma.

Different subtypes of non-small cell lung cancer (NSCLC) have distinct sites of origin, histologies, genetic and epigenetic changes. In this study, we explored the mechanisms of ECT2 dysregulation and compared its prognostic value in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). In addition, we also investigated the enrichment of ECT2 co-expressed genes in KEGG pathways in LUAD and LUSC. Bioinformatic analysis was performed based on data from the Cancer Genome Atlas (TCGA)-LUAD and TCGA-LUSC. Results showed that ECT2 expression was significantly upregulated in both LUAD and LUSC compared with normal lung tissues. ECT2 expression was considerably higher in LUSC than in LUAD. The level of ECT2 DNA methylation was significantly lower in LUSC than in LUAD. ECT2 mutation was observed in 5% of LUAD and in 51% of LUSC cases. Amplification was the predominant alteration. LUAD patients with ECT2 amplification had significantly worse disease-free survival (p = 0.022). High ECT2 expression was associated with unfavorable overall survival (OS) (p<0.0001) and recurrence-free survival (RFS) (p = 0.001) in LUAD patients. Nevertheless, these associations were not observed in patients with LUSC. The following univariate and multivariate analysis showed that the high ECT2 expression was an independent prognostic factor for poor OS (HR: 2.039, 95%CI: 1.457-2.852, p<0.001) and RFS (HR: 1.715, 95%CI: 1.210-2.432, p = 0.002) in LUAD patients, but not in LUSC patients. Among 518 genes co-expressed with ECT2 in LUAD and 386 genes co-expressed with ECT2 in LUSC, there were only 98 genes in the overlapping cluster. Some of the genes related KEGG pathways in LUAD were not observed in LUSC. These differences might help to explain the different prognostic value of ECT2 in LUAD and LUSC, which are also worthy of further studies.

[Chemical studies on roots of Ficus hirta].

Seventeen compounds were isolated from the 95% ethanolic extract of the root of Ficus hirta. Their structures were identified on the basis of physicochemical properties and spectral data analysis. The structures were elucidated as cyclomorusin (1), 3-O-[(6-O-E-sinapoyl)-beta-D-glucopyranosyl]-(1 --> 2)-beta-D-glucopyranoside (2), 3,5,4'-trihydroxy-6,7,3'-trimethoxyflavone (3), quercetin (4), tricin (5), acacetin (6), luteolin (7), apigenin (8), (E) -suberenol (9), meranzin hydrate (10), methyl eugenol (11), 3-methoxy-4-hydroxybenzoic acid (12), p-hydroxybenzoic acid (13), methyl chlorogenate (14), emodin (15), alpha-amyrin acetate (16), and beta-sitosterol emodin (17), respectively. Compounds 1-6, 9-15 were isolated from this plant for the first time.