Mobile phone addiction and academic burnout: the mediating role of technology conflict and the protective role of mindfulness.

With the rapid development of Internet technology, more and more college students are facing the threat of mobile phone addiction. However, the relationship and underlying mechanism between mobile phone addiction and academic burnout haven't been explored in depth. This study proves the mediating role of technology conflict and the moderating role of mindfulness in the relation between mobile phone addiction and academic burnout. 752 college students were recruited to complete the questionnaire of mobile phone addiction, technology conflict, mindfulness and academic burnout. Results showed that mobile phone addiction was significantly and positively associated with academic burnout, and this relationship could be mediated by technology conflict. Besides, the direct effect of mobile phone addiction on academic burnout and the indirect effect of technology conflict in this link were moderated by mindfulness. Both these two effects are stronger for college students with lower level of mindfulness. Our findings enrich our understanding of how and when mobile phone addiction was related to academic burnout. Educational professionals and parents should take timely measure to the academic burnout of college students suffering from mobile phone addiction, particularly for those with lower level of mindfulness.

Confining the Growth of AgNPs onto Epigallocatechin Gallate-Decorated Zein Nanoparticles for Constructing Potent Protein-Based Antibacterial Nanocomposites.

Sliver nanoparticles (AgNPs) have attracted tremendous interest as an alternative to commercially available antibiotics due to their low microbial resistance and broad-spectrum antimicrobial activity. However, AgNPs are highly reactive and unstable and are susceptible to fast oxidation. Synthesizing stable and efficient AgNPs using green chemistry principles remains a major challenge. To address this issue, we establish a facile route to form AgNP-doped zein nanoparticle core-satellite superstructures with ultralow minimum bactericidal concentration (MBC). In brief, polyphenol surface-functionalization of zein nanoparticles was performed, and the epigallocatechin gallate (EGCG) layer on zein nanoparticles served as a reducing-cum-stabilizing agent. We used EGCG-decorated zein nanoparticles (ZE) as a template to direct the nucleation and growth of AgNPs to develop metallized hybrid nanoparticles (ZE-Ag). The highly monodispersed core-satellite nanoparticles (∼150 nm) decorated with ∼4.9 nm AgNPs were synthesized successfully. The spatial restriction of EGCG by zein nanoparticles confined the nucleation and growth of AgNPs only on the surface of the particles, which prevented the formation of entangled clusters of polyphenols and AgNPs and concomitantly inhibited the coalescence and oxidation of AgNPs. Thus, this strategy improved the effective specific surface area of AgNPs, and as a result, ZE-Ag efficiently killed the indicator bacteria, Escherichia coli (E. coli) and Methicillin-resistant Staphylococcus aureus(MRSA) after 20 min of incubation, with MBCs of 2 and 4 µg/mL, respectively. This situation indicated that as-prepared core-satellite nanoparticles possessed potent short-term sterilization capability. Moreover, the simulated wound infection model also confirmed the promising application of ZE-Ag as an efficient antimicrobial composite. This work provides new insights into the synthesis and emerging application of AgNPs in food preservation, packaging, biomedicine, and catalysis.

How and when is academic stress associated with mobile phone addiction? The roles of psychological distress, peer alienation and rumination.

BACKGROUND: Mobile phone addiction has a high detection rate among adolescents and is thought to be related to academic stress. However, the underlying mechanisms in this relation were still unclear. The present study tested the mediating role of psychological distress and the moderating roles of peer alienation and rumination in the relationship between academic stress and mobile phone addiction. METHODS: A total of 742 middle school students were recruited to complete measures of academic stress, psychological distress, mobile phone addiction, peer alienation, rumination, and demographic variables. Regression-based statistical mediation and moderation were conducted using the PROCESS macro for SPSS. RESULTS: The results indicated that academic stress was significantly and positively associated with mobile phone addiction, and this link could be mediated by psychological distress. Moreover, this indirect effect was moderated by both peer alienation and rumination. Specifically, the mediating effect of psychological distress was stronger for adolescents with higher levels of peer alienation or adolescents with higher levels of rumination, as well as those with both higher levels of peer alienation and rumination. CONCLUSION: The findings of this study enrich our understanding of how and for whom academic stress is correlated with mobile phone addiction. Education experts and parents should pay special attention to adolescents suffering from academic stress, especially those with higher peer alienation and rumination, and help them get rid of mobile phone addiction.

Family cohesion and adaptability reduces mobile phone addiction: the mediating and moderating roles of automatic thoughts and peer attachment.

With the popularity of mobile Internet devices, the incidence of mobile phone addiction has been increasing, which has aroused the concern of all sectors of society. Due to the difficulty of eliminating the risk factors of mobile phone addiction, it's significant for researchers to examine the function and underlying mechanisms of positive environmental factors in reducing individuals' mobile phone addiction. Thus, the current study aimed to examine the relationship between family cohesion and adaptability and mobile phone addiction among university students and analyzed the mediating role of automatic thoughts as well as the moderating role of peer attachment in this link. The sample consisted of 958 Chinese university students. Participants completed self-report questionnaires assessing family cohesion and adaptability, mobile phone addiction, automatic thoughts, and peer attachment. PROCESS model 8 was significant (the total effect model (F (5, 952) = 19.64, R2 = 0.09, p < 0.001)). Results indicated that family cohesion and adaptability could not only negatively predict mobile phone addiction directly, but also indirectly through the mediating effect of automatic thoughts. Moreover, both the direct association between family cohesion and adaptability and mobile phone addiction as well as the indirect effect of automatic thoughts were moderated by peer attachment. Findings emphasized the beneficial role of peer attachment on the effect of family cohesion and adaptability on automatic thoughts and mobile phone addiction.

TR score: A noninvasive model to predict histological stages in patients with primary biliary cholangitis.

Introduction: The aim of this study was to develop a noninvasive prediction model for histological stages in PBC that is simple, easy to implement, and highly accurate. Methods: A total of 114 patients with PBC were included in this study. Demographic, laboratory data and histological assessments were collected. The independent predictors of histological stages were selected to establish a noninvasive serological model. The scores of 22 noninvasive models were calculated and compared with the established model. Results: This study included 99 females (86.8%) and 15 males (13.2%). The number of patients in Scheuer's stage 1, 2, 3 and 4 was 33 (29.0%), 34 (29.8%), 16 (14.0%), and 31 (27.2%), respectively. TBA and RDW are independent predictors of PBC histological stages. The above indexes were used to establish a noninvasive model-TR score. When predicting early histological change (S1) or liver fibrosis and cirrhosis (S3-S4), the AUROC of TR score were 0.887 (95% CI, 0.809-0.965) and 0.893 (95% CI, 0.816-0.969), higher than all of the other 22 models included in this study. When predicting cirrhosis (S4), its AUROC is still as high as 0.921 (95% CI, 0.837-1.000). Conclusion: TR score is an easy, cheap and stable noninvasive model, without complex calculation formulas and tools, and shows good accuracy in diagnosing the histological stages of PBC.

Cathelicidin-WA Facilitated Intestinal Fatty Acid Absorption Through Enhancing PPAR-γ Dependent Barrier Function.

The molecular mechanisms underlying the cellular uptake of long-chain fatty acids and the regulation of this process have been debated in recent decades. Here, we established an intestinal barrier dysfunction model in mice and Caco2 cell line by Lipopolysaccharide (LPS), and evaluated the fatty acid uptake capacity of the intestine. We found that LPS stimulation restricted the absorption of long chain fatty acid (LCFA), while Cathelicidin-WA (CWA) pretreatment facilitated this physiological process. At the molecular level, our results demonstrated that the stimulatory effects of CWA on intestinal lipid absorption were dependent on cluster determinant 36 and fatty acid transport protein 4, but not fatty acid-binding protein. Further, an enhanced intestinal barrier was observed in vivo and in vitro when CWA alleviated the fatty acid absorption disorder induced by LPS stimulation. Mechanistically, peroxisome proliferator-activated receptor (PPAR-γ) signaling was considered as a key pathway for CWA to enhance LCFA absorption and barrier function. Treatment with a PPAR-γ inhibitor led to impaired intestinal barrier function and suppressed LCFA uptake. Moreover, once PPAR-γ signaling was blocked, CWA pretreatment could not maintain the stability of the intestinal epithelial cell barrier or LCFA uptake after LPS stimulation. Collectively, these findings suggested that PPAR-γ may serve as a target for specific therapies aimed at alleviating fatty acid uptake disorder, and CWA showed considerable potential as a new PPAR-γ agonist to strengthen intestinal barrier function against fatty acid malabsorption.

Antimicrobial peptide KR-32 alleviates Escherichia coli K88-induced fatty acid malabsorption by improving expression of fatty acid transporter protein 4 (FATP4)1.

Bacterial infection causes nutrient malabsorption in small intestine. KR-32, a kind of synthetic antimicrobial peptide, has the bacteriostatic effect. In the present study, 2 experiments were designed to analyze the effects of KR-32 on fat absorption of piglets with or without Escherichia coli infection. In Exp. 1, 12 weaning piglets (21 d old) were allocated to 2 groups: piglets with an intraperitoneal (i.p.) injection of antimicrobial peptide KR-32 (APK) and piglets with an i.p. injection of an equivalent volume (1 mL) of phosphate-buffered saline (PBS) (CON-1). Results showed that after 7 d of growth, KR-32 did not significantly change growth performance and apparent total tract digestibility (ATTD) of feed nutrients of normal pigs. To confirm whether KR-32 affects those of enterotoxigenic Escherichia coli (ETEC) K88-challenged pigs, we performed Exp. 2, in which 18 piglets (28 d old) were divided into the following 3 groups: 1) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of 0.6 mg/kg KR-32 (K88 + APK); 2) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of an equivalent volume (1 mL) of PBS (K88); and 3) piglets with an oral administration of fresh Luria-Bertani broth (50 mL) followed by an i.p. injection of an equivalent volume of PBS (CON-2). Results showed that ETEC K88 challenge led to poor ADFI, ADG, and G:F in piglets; decreased ATTD of feed nutrients, especially CP and ether extract (EE); and intestinal morphology disorder. After i.p. injection of KR-32, ADG and ATTD of CP and EE were greatly increased, G:F was significantly reduced (P < 0.05), and, especially, ATTD of EE returned to a normal level compared with group CON-2. Fatty acid absorption also highly increased after KR-32 injection. Then we focused on fat digestion and fatty acid uptake. The pH in the intestine and pancreas lipase showed no difference among the 3 treatment groups, whereas fatty acid transporter protein 4 (FATP4) expression was remarkably improved (P < 0.05) and the epithelial barrier was recovered after i.p. injection of KR-32. In conclusion, KR-32, given to ETEC K88-challenged piglets, improved growth performance, ATTD of EE, fatty acid absorption, and intestinal morphology, which indicated that KR-32 was likely to improve the expression of FATP4 and by repairing the epithelial barrier, thereby alleviating fatty acid malabsorption.

Porcine lactoferrin-derived peptide LFP-20 modulates immune homoeostasis to defend lipopolysaccharide-triggered intestinal inflammation in mice.

The performance of immune system is vital for defending the body from pathogens, and it plays a crucial role in health homoeostasis. In a previous study, we have shown that LFP-20, a twenty-amino acid antimicrobial peptide in the N terminus of porcine lactoferrin, modulated inflammatory response in colitis. Here, we further investigated the effects of LFP-20 on immune homoeostasis to elucidate the mechanism of its anti-inflammation action. A lipopolysaccharide (LPS)-triggered systemic inflammatory response mice model was established. On the basis of observed mucosal lesions and apoptosis in small intestine, we found increased macrophage and neutrophil infiltration in ileum after LPS stimulation. Expectedly, LFP-20 pre-treatment attenuated the LPS-mediated immune disorders in ileum. Moreover, the flow cytometry results indicated pre-treatment with LFP-20 sustained the balance of CD3+CD8+ T cells, B cells and natural killer cells in LPS-triggered immune disturbance. Simultaneously, we demonstrated LFP-20 modulated the secretion of both activated Th1-related IL-12p70, interferon-γ, TNF-α and Th2-related IL-4, IL-5 and IL-6. Furthermore, we found LFP-20 facilitated a balanced Th1 and Th2 response, which triggered cellular defence mechanisms and induced B cells to produce opsonising antibodies belonging to certain IgG subclasses to defend against LPS stimulation. Collectively, our study indicated pre-treatment with LFP-20 could defend against LPS-triggered systemic inflammatory response in mice via modulating immune homoeostasis.