The relationship between health literacy and problematic internet use in Chinese college students: The mediating effect of subject well-being and moderating effect of social support.

BACKGROUND: The issue of problematic Internet use (PIU) amongst college students is emerging as a major concern for mental health. Factors such as health literacy, subjective well-being and the extent of social support may be critical in preventing PIU. However, the complex relationship between these factors has not been extensively explored in research. METHODS: A national cross-sectional study based on multistage random sampling was conducted in China in 2022. The subjects for this study were 7669 college students who completed a set of questionnaires assessing their health literacy, subjective well-being, PIU and social support. A structural equation model (SEM) was utilised for exploring the mediating effect of subjective well-being, and the PROCESS macro was used to test the moderating effect of social support. RESULTS: After controlling for demographic factors, a significantly negative correlation was found between health literacy and PIU, and subjective well-being partially mediated this relationship. In addition, social support was negatively related to PIU and could moderate the relationship between health literacy and subjective well-being and between subjective well-being and PIU. LIMITATIONS: This is a cross-sectional study, and the results cannot inform the causality between these variables. CONCLUSION: Results revealed that the relationship between health literacy and PIU was partially mediated by subjective well-being in college students. The correlation between health literacy and subjective well-being and between subjective well-being and PIU were moderated by social support. Thus, future interventions for college students' PIU should be facilitated by improving health literacy, subjective well-being and social support.

Predictors of quitting support from nonsmoking mothers for smoking fathers: a cross-sectional study from Chinese pupils' families.

BACKGROUND: Quitting support from smokers' partners can predict quit attempts and smoking abstinence but research on factors that predict such support has been limited. To add more evidence for partner support and the improved interventions for smoking cessation, we analyzed some new potential predictors of quitting support from smokers' spouses. METHOD: This cross-sectional study was conducted in in 2022 and 2023, selecting the students' families in which fathers smoked and mothers didn't smoke from grade 1-5 of 13 primary schools in Qingdao, China. Parents who met the criteria completed the online questionnaires and 1018 families were included in the analysis. We measured personal information related to smokers and their spouses such as age, education and nicotine dependence, and variables related to family and marital relationship such as family functioning, perceived responsiveness and power in decision-making of quitting smoking. Quitting support from smokers' spouses was measured by Partner Interaction Questionnaire and generalized linear model was used to explore the potential predictors of partner support. RESULTS: In this study, the mean age of smokers was 39.97(SD = 5.57) and the mean age of smokers' spouses was 38.24(SD = 4.59). The regression analysis showed that for smokers and their spouses, the older age groups showed the lower ratio of positive/negative support(P < 0.05) and smokers with high education showed the less positive and negative partner support(P < 0.05). Nicotine dependence was positively associated with negative support (ß = 0.120, P < 0.01), and perceived responsiveness (ß = 0.124, P < 0.05) as well as family functioning (ß = 0.059, P < 0.05) was positively associated with positive support. These three factors were associated with ratio of positive/negative support(P < 0.05). In addition, power of smoker's spouse in decision-making of quitting smoking was positively associated with the positive (ß = 0.087, P < 0.001) and negative support (ß = 0.084, P < 0.001). CONCLUSIONS: Nicotine dependence, family functioning, power in decision-making of quitting smoking and perceived responsiveness were found to be the predictors of quitting support from smokers' spouses. By incorporating predictors of partner support and integrating some established theories that can improve family functioning and marital relationships, smoking cessation interventions can be further improved.

Effects of smoke-free government policy in Qingdao, China: Evidence from the path analysis.

Smoke-free government(SFG), as a key tobacco control measure, has been added in Healthy China 2030 blueprint and Qingdao started the establishment of the demonstrative SFG in 2020.This study examined the effects of SFG policy on smoking and smoke-free(SF) environment after establishing the demonstrative SFG. This cross-sectional survey selected participants by simple random sampling from party and government agencies in Qingdao (N = 3625) and the participants filled in questionnaires online from November 31 to December 15, 2020. We utilized AMOS to set up models to analyze the direct and indirect effects of SFG policy. The findings showed that knowledge of SFG policy was positively associated with SF environment(ß = 0.29, P<0.001) and negatively associated with smoking(ß = -0.14,P<0.001). Knowledge of SFG policy had indirect effects on SF environment through four channels: independent mediation of discouraging smoking and attitude towards SFG policy, as well as chain mediation of these two factors, and perception of tobacco hazards and discouraging smoking, with indirect effects accounting for 33.5% of the total effect. Knowledge of SFG policy had indirect effects on smoking reduction via SF environment and two chain mediation: SF environment and attitude towards SFG policy, perception of tobacco hazards and intention to quit smoking, with indirect effects accounting for 50.2% of the total effect. The results provided the evidence that SFG policy not only had positive effects on creating SF environment but also on reducing smoking. The efficient policy infiltration to individuals played a vital role in the establishment of SFG. Attitude towards SFG policy, discouraging smoking and SF environment were the potential mediators for SFG policy. Findings in this study added more evidence related to effect mechanism of SFG policy and had a positive influence on promoting the implementation SFG policies for China and other countries.

MiR-128-3p alleviates TNBS-induced colitis through inactivating TRAF6/NF-κB signaling pathway in rats.

miR-128-3p is reported to involve in pathogenesis of several autoimmune diseases, yet the role of miR-128-3p in inflammatory bowel disease (IBD) remains unknown. To investigate miR-128-3p in IBD, experimental colitis animal model was generated by 2,4,6-Trinitrobenzenesulfonic acid solution (TNBS). miR-128-3p agomir was used to overexpress miR-128-3p in rats. Histological assessment and myeloperoxidase activity were conducted to evaluate the TNBS-induced colitis. Effect of miR-128-3p overexpression on levels of TNF-α, IL-1ß, ICAM-1, and MCP-1 was tested by ELISA assay. The target of miR-128-3p was predicted and further confirmed by dual-luciferase reporter assay. The expressions of TRAF6, p-NF-κB, and NF-κB were determined by western blot. The miR-128-3p level was significantly decreased in rats with TNBS-induced colitis. miR-128-3p could alleviate TNBS-induced colitis and inhibit production of inflammatory factors. We found TRAF6 was a direct target of miR-128-3p using bioinformatics and luciferase assay. By western blot, we discovered miR-128-3p activates NF-κB by targeting TRAF6. Our data reveal a novel mechanism that a decreased miR-128-3p level in TNBS-induced colitis could inhibit production of inflammatory factors, which activates NF-κB signaling by targeting TRAF6. Our findings might provide a novel therapeutic target for drug design and development for IBD therapeutics.

Role of TLR4/NF-κB pathway in the damage of acute hypobaric hypoxia to small intestinal mucosa in rats.

The purpose of this study was to investigate the effect of acute hypobaric hypoxia (HH) exposure on small intestinal mucosa in rats and its underling mechanism. The pathological changes of rat small intestine mucosa were detected by HE staining. The expressions of TLR4 and NF-κB in the small intestine were detected by immunohistochemistry (IHC). The levels of Zonulin, TNF-α, IL-1ß, and IL-6 in the serum were detected by ELISA. The proportion of natural killer (NK) cells and dendritic cell population in the small intestine was analyzed by flow cytometry. The mRNA and protein levels of TLR4, NF-κB, occludin, HIF-1α, and iNOS were detected by RT-qPCR and Western blot, respectively. Compared with the Control group, the HH groups had different degrees of injury in intestinal mucosa. Meanwhile, in the HH groups, it was also found the increased levels of Zonulin, TNF-α, IL-1ß and IL-6 in the serum, the increased CD4+/CD8+T cells ratio and small intestine NK cells population, the increased mRNA and protein expression levels of small intestine TLR4, NF-κB, HIF-1α and iNOS, and the decreased mRNA and protein expression levels of occludin. Acute HH may damage the intestinal mucosa of rats by inducing TLR4/NF-κB pathway overexpression.

Evaluation of Nanoparticles Emitted from Printers in a Clean Chamber, a Copy Center and Office Rooms: Health Risks of Indoor Air Quality.

Indoor air quality has great impact on the human health. An increasing number of studies have shown that printers could release particulate matters and pose adverse effects on indoor air quality. In this study, a thorough investigation was designed to assess the aerosol printer particle total number concentration (TNC) and size distribution in normal office environment, one copy center, and a clean chamber. Particle analyzers, SMPS, OPS, and CPC3007 were used to monitor the total printing process. In normal office environment, 37 laser printers out of all surveyed 55 printers were classified as high particle emitters. Comparing to laser printers, 5 inkjet printers showed no particle emission. Particle emission level in a copy center increased slightly with TNC elevating to about 2 times of the aerosol background. Simulating test in a clean chamber indicated that printer-emitted particles were dominated by particles in nanoscale (diameter of particle, D(p) < 100 nm). These particles in a sealed clean chamber attenuated so slowly that it still held at high level with the concentration of 1.5 x 10(4) particles/cm3 after printing for 2.5 hours. Our present results demonstrate that printers indeed release particulates which keeping at a high concentration level in the indoor environment. Special care should be taken to this kind of widely applied machines and effective controls of particle emission at printing processes are necessary.

High-Content Screening for Assessing Nanomaterial Toxicity.

With rapid development of novel nanomaterials (NMs), the state of the art technologies with high efficiency and high-throughput characteristics had been applied for nanosafety evaluation. High-content screening (HCS), a cell-based multi-parametric image analysis technique, was adopted in the evaluation of eight different NMs in this study. A set of different endpoints including reactive oxygen species (ROS) production, Ca2+ transient, mitochondrial membrane potential (MMP) and cellular pH levels were checked in human bronchial epithelial (16HBE) cells after incubating with NMs for 24 hours. All NMs induced significant increase of intracellular ROS levels in 16HBE cells, although the decrease of cell viability was only found in Ag and ZnO NMs-treated cells. MMP level had a dose-response decrease in Ag, ZnO and CeO2 NMs-treated cells, while showed a significant increase in TiO2 NMs-treated cells. All tested NMs showed significant up-regulation of cellular lysosomal pH levels. However, none of NMs caused significant changes in cellular Ca2+ level at 24-hour time point. HCS allows for efficient and reliable screening of multiple responses of cells simultaneously within one screen test, which can avoid the problematic interpretation of investigations when carried on a single toxicological endpoint. Therefore, the present data provide insight and inspiration that HCS is an effective and powerful method for image-based assessments with a broad set of biological endpoints in toxicity evaluation of nanomaterials.

Silver nanoparticles activate endoplasmic reticulum stress signaling pathway in cell and mouse models: The role in toxicity evaluation.

Silver nanoparticles (AgNPs) attract considerable public attention both for their antimicrobial properties and their potential adverse effects. In the present study, endoplasmic reticulum (ER) stress was used as a sensitive and early biomarker to evaluate the toxic potential of AgNPs in three different human cell lines in vitro and in vivo in mice. In 16HBE cells, the activation of ER stress signaling pathway was observed by upregulated expression including xbp-1s, chop/DDIT3, TRIB3, ADM2, BIP, Caspase-12, ASNS and HERP at either the mRNA and/or protein levels. However, these changes were not observed in HUVECs or HepG2 cells. Furthermore, mice experiments showed that different tissues had various sensitivities to AgNPs following intratracheal instillation exposure. The lung, liver and kidney showed significant ER stress responses, however, only the lung and kidney exhibited apoptosis by TUNEL assay. The artery and tracheal tissues had lower ER stress and apoptosis after exposure. The lowest observable effect concentrations (LOEC) were proposed based on evaluation of AgNP induced ER stress response in cell and mouse models. In summary, preliminary evaluation of AgNP toxicity by monitoring the ER stress signaling pathway provides new insights toward the understanding the biological impacts of AgNPs. The adverse effects of exposure to AgNPs may be avoided by rational use within the safe dose.

Endoplasmic reticulum stress induced by zinc oxide nanoparticles is an earlier biomarker for nanotoxicological evaluation.

Zinc oxide nanoparticles (ZnO NPs) have been widely used in cosmetics and sunscreens, advanced textiles, self-charging and electronic devices; the potential for human exposure and the health impact at each stage of their manufacture and use are attracting great concerns. In addition to pulmonary damage, nanoparticle exposure is also strongly correlated with the increase in incidences of cardiovascular diseases; however, their toxic potential remains largely unclear. Herein, we investigated the cellular responses and endoplasmatic reticulum (ER) stress induced by ZnO NPs in human umbilical vein endothelial cells (HUVECs) in comparison with the Zn2+ ions and CeO2 NPs. We found that the dissolved zinc ion was the most significant factor for cytotoxicity in HUVECs. More importantly, ZnO NPs at noncytotoxic concentration, but not CeO2 NPs, can induce significant cellular ER stress response with higher expression of spliced xbp-1, chop, and caspase-12 at the mRNA level, and associated ER marker proteins including BiP, Chop, GADD34, p-PERK, p-eIF2α, and cleaved Caspase-12 at the protein levels. Moreover, ER stress was widely activated after treatment with ZnO NPs, while six of 84 marker genes significantly increased. ER stress response is a sensitive marker for checking the interruption of ER homeostasis by ZnO NPs. Furthermore, higher dosage of ZnO NPs (240 µM) quickly rendered ER stress response before inducing apoptosis. These results demonstrate that ZnO NPs activate ER stress-responsive pathway and the ER stress response might be used as an earlier and sensitive end point for nanotoxicological study.