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Abstract The rapid growth of internet usage has led to increased cyberbullying among adolescents, with varying rates reported across countries. This study aimed to investigate the impact of cyber moral literacy on cyberbullying among late adolescents, examining both the mediating role of moral disengagement and the moderating effect of guilt on the relationship between cyber moral literacy and cyberbullying. Data were collected from 7837 late adolescent students (aged 18–21 years) at four universities in Sichuan Province, China. Scales measuring cyber moral literacy, cyberbullying, moral disengagement, and guilt were employed. Structural Equation Modeling was used to test hypothesized relationships. Cyber moral literacy showed a strong negative association with cyberbullying. The relationship between cyber moral literacy and cyberbullying was partially mediated by moral disengagement. Additionally, guilt moderated the direct relationship between cyber moral literacy and cyberbullying, with this negative relationship being stronger among individuals with high guilt compared to those with low guilt. The study highlights the complex interplay of moral, cognitive, and emotional factors in adolescent online behavior. The findings suggest that enhancing cyber moral literacy could be particularly effective in reducing cyberbullying, especially among individuals who experience higher levels of guilt. Additionally, addressing moral disengagement mechanisms could help strengthen the preventive effect of cyber moral literacy on cyberbullying. These insights contribute to our understanding of creating a more harmonious online environment for late adolescents.

Superconducting thin films have been a focal point for intensive research efforts since their reduced dimension allows for a wide variety of quantum phenomena. Many of these films, fabricated in UHV chambers, are highly vulnerable to air exposure, making it difficult to measure intrinsic superconducting properties such as zero resistance and perfect diamagnetism with ex situ experimental techniques. Previously, we developed a multifunctional scanning tunneling microscope (MSTM) containing in situ four-point probe (4PP) electrical transport measurement capability in addition to the usual STM capabilities [Ge et al., Rev. Sci. Instrum. 86, 053903 (2015)]. Here we improve thisMSTMvia development of both transmission and reflection two-coil mutual inductance techniques for in situ measurement of the diamagnetic response of a superconductor. This addition does not alter the original STM and 4PP functions of the MSTM. We demonstrate the performance of the two-coil mutual inductance setup on a 10-nm-thick NbN thin film grown on a Nb-doped SrTiO3(111) substrate. [ABSTRACT FROM AUTHOR]

Millions of infants and children are exposed to anesthesia every year during medical care. Sevoflurane is a volatile anesthetic that is frequently used for pediatric anesthesia. However, previous reports have suggested that the administration of sevoflurane promotes neurodegeneration, raising concerns regarding the safety of its usage. The present study aimed to investigate caffeic acid phenethyl ester (CAPE) and its protective effect against sevoflurane-induced neurotoxicity in neonatal rats. Rat pups were administered with CAPE at 10, 20 or 40 mg/kg body weight from postnatal day 1 (P1) to P15. The P7 rats were exposed to sevoflurane (2.9%) for 6 h. Control group rats received no sevoflurane or CAPE. Neuronal apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. The expression levels of caspases (caspase-3, -8 and -9), apoptotic pathway proteins [Bcl-2-associated X protein (Bax), B cell CCL/lymphoma 2 (Bcl-2), Bcl-2-like 1 (Bcl-xL), Bcl-2-associated agonist of cell death (Bad) and phosphorylated (p)-Bad], mitogen-activated protein kinases (MAPK) signaling pathway proteins [c-Jun N-terminal kinase (JNK), p-JNK, extracellular signal-regulated kinase (ERK)1/2, p-ERK1/2, p38, p-p38 and p-c-Jun] and the phosphoinositide 3-kinase (PI3K)/Akt cascade were evaluated by western blotting following sevoflurane and CAPE treatment. In addition, the expression of cleaved caspase-3 was analyzed by immunohistochemistry. CAPE significantly reduced sevoflurane-induced apoptosis, downregulated the expression levels of caspases and pro-apoptotic proteins (Bax and Bad) and elevated the expression levels of Bcl-2 and Bcl-xL when compared with sevoflurane treatment. Furthermore, CAPE appeared to modify the expression levels of MAPKs and activate the PI3K/Akt signaling pathway. Thus, the present study demonstrated that CAPE effectively inhibited sevoflurane-induced neuroapoptosis by modulating the expression and phosphorylation of apoptotic pathway proteins and MAPKs, and by regulating the PI3K/Akt pathway. [ABSTRACT FROM AUTHOR]