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Purpose: Given that mother plays the main nurturing role in a family unit and their unique influence on children's development, the current study aimed to examine the influence of maternal phubbing on children's problematic media use and the independent and interactive moderating role of children's negative affectivity and effortful control. Methods: Participants were 1986 children aged 3 to 6 years in Shanghai, China. Their mothers were asked to complete a series of questionnaires including parental phubbing scale, problematic media use measure, and child behavior questionnaire. To investigate the moderating influence of children's negative affectivity and effortful control, hierarchical linear regression analyses were conducted using SPSS 24.0. Simple slopes analyses and the Johnson-Neyman technique were further used to depict moderation effects. Results: Maternal phubbing was associated with higher levels of problematic media use in preschool children (ß = 0.18, p <.001, [0.14, 0.22]). Children's negative affectivity acts as a risk factor, exacerbating the adverse effects of maternal phubbing on children's problematic media use (ß = 0.05, t = 2.69, p < 0.05), whereas children's effortful control acts as a protective factor, buffering the link between maternal phubbing and children's problematic media use (ß = -0.10, t = -5.00, p < 0.001). Conclusion: These results suggest that interventions seeking to promote appropriate digital development in preschoolers should take the child's temperament into account and be complemented by active parental mediation and involvement.

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The COVID-19 pandemic has had an inestimable impact worldwide, challenging the daily lives and interactions of children and their families. In 2022, Shanghai implemented a three-month lockdown in response to an acceleration of positive cases during the pandemic period. This restrictive policy provided insight into the impact of the lockdown on children's social adjustment and the role of parent-child conflict during this process. Mothers of preschool-aged children participated in this study and completed the Chinese version of Child-Parent Relationship Scale (CPRS) and the Strengths and Difficulties Questionnaire (SDQ). Using Propensity Score Matching (PSM) method, two matched groups were formed: pre-lockdown group and post-lockdown group, with a total of 574 preschoolers (N = 297 in each group; Mage = 4.36, SD = 0.86) were recruited. The results showed that the lockdown directly impacted children's emotional symptoms. Additionally, the parent-child conflict mediated relationship between the lockdown and children's adjustment. Specifically, parent-child conflict deteriorated children's emotional symptoms, hyperactivity-attention problems, and prosocial behaviors. These findings highlight the significant impact of the severe lockdown on children's social adjustment and the role of parent-child interactions during this period.

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The pathogenesis of spinal cord injury (SCI) is complex. At present, there is no effective treatment for SCI, with most current interventions focused on improving the symptoms. Inflammation, apoptosis, autophagy, and oxidative stress caused by secondary SCI may instigate serious consequences in the event of SCI. The mammalian target of rapamycin (mTOR), as a key signaling molecule, participates in the regulation of inflammation, apoptosis, and autophagy in several processes associated with SCI. Quercetin can reduce the loss of myelin sheath, enhance the ability of antioxidant stress, and promote axonal regeneration. Moreover, quercetin is also a significant player in regulating the mTOR signaling pathway that improves pathological alterations following neuronal injury. Herein, we review the therapeutic effects of quercetin in SCI through its modulation of the mTOR signaling pathway and elaborate on how it can be a potential interventional agent for SCI.

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BACKGROUND: Docetaxel has been approved by USFDA as a first-line treatment for castration-resistant prostate cancer (CRPC) patients. Patients receiving androgen deprivation therapy along with docetaxel result in superior survival, lower serum prostate specific antigen (PSA) level, and better quality of life. However, a significant proportion of these patients ultimately develop resistance to docetaxel within months. Caffeic acid phenethyl ester (CAPE), one of the main bioactive components extracted from the propolis, has been reported to be effective for repressing the tumor growth, the migration and invasion of prostate cancer (PCa) cells, as well as the downstream signaling and stability of androgen receptor (AR). We hence determined if combination treatment of docetaxel with CAPE can suppress the proliferation and the survival of docetaxel-resistant PCa cells. METHODS: We established docetaxel-resistant PC/DX25 and DU/DX50 CRPC cell lines from PC-3 and DU-145 human PCa cells, respectively. Proliferation assay, MTT assay, flow cytometry with Annexin V staining, Comet Assay, and nude mice xenograft model were applied to determine the effects of combination treatment on cell proliferation and survival of the docetaxel-resistant PCa cells. Micro-Western Array (MWA) and qRT-PCR were used to investigate the molecular mechanism lying underneath. RESULTS: Combination treatment effectively suppressed the proliferation, survival and tumor growth of docetaxel-resistant PCa cells both in vitro and in nude mice. Comet assay and flow cytometry indicated that combination treatment induced apoptosis in docetaxel-resistant PCa cells. MWA and Western blotting assay revealed that combination treatment suppressed protein expression of Bcl-2, AKT2, c-Myc, apoptosis and caspase activation inhibitor (AVEN), pyruvate kinase M2 (PKM2) but increased protein expression of Bax, caspase 3, cytochrome c, glucose-6-phosphate dehydrogenase (G6PD) and acylglycerol kinase (AGK). Overexpression of Bcl-2 in the docetaxel-resistant PCa cells enhanced cell proliferation of docetaxel-resistant PCa cells under combination treatment. Analysis with qRT-PCR suggested that combination treatment decreased cholesterol biosynthesis genes DHCR24 (24-dehydrocholesterol reductase) and LSS (lanosterol synthase) but increased genes involved in glycolysis and TCA cycle. CONCLUSIONS: Combination treatment of docetaxel with CAPE effectively suppressed the proliferation and survival of docetaxel-resistant PCa cells via inhibition of Bcl-2 and c-Myc as well as induction of metabolism interference. Combination treatment can be beneficial for patients with docetaxel-resistant PCa.

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We established the NHRI-HN1 cell line from a mouse tongue tumor induced by 4-nitroquinoline 1-oxide (4-NQO)/arecoline, with further selection for cell stemness via in vitro sphere culture, to evaluate potential immunotherapies for oral squamous cell carcinoma (OSCC) in East and Southeast Asia. In vivo and in vitro phenotypic characterization, including tumor growth, immune modulator administration, gene expression, morphology, migration, invasion, and sphere formation assays, were conducted. NHRI-HN1 cells are capable of generating orthotopic tumors in syngeneic mice. Interestingly, immune stimulation via CpG oligodeoxynucleotide (CpG-ODN) dramatically reduced the tumor growth in NHRI-HN1 cell-injected syngeneic mice. The pathways enriched in genes that were differentially expressed in NHRI-HN1 cells when compared to non-tumorigenic cells were similar to those that were identified when comparing human OSCC and non-tumorous tissues. NHRI-HN1 cells have characteristics of epithelial-mesenchymal transition (EMT), including enhanced migration and invasion. NHRI-HN1 cells showed aggressive cell growth and sphere formation. The blockage of extracellular signal-regulated kinase (ERK) activation suppressed cell migration and reduced stemness characteristics in NHRI-HN1 cells, similar to human OSCC cell lines. Our data suggest that NHRI-HN1 cells, showing tumorigenic characteristics of EMT, cancer stemness, and ERK activation, are sufficient in modeling human OSCC and also competent for use in investigating oral cancer immunotherapies.

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Deoxyribonuclease I (DNase I) is an endonuclease responsible for the destruction of chromatin during apoptosis. However, its role in diabetes remains unclear. The aim of the current study was to investigate the role of DNase I combined with high glucose levels in ß­cell apoptosis. Human samples were collected and the DNase I activity was examined. High glucose­cultured INS­1 cells were transfected with DNase I small interfering RNA (siRNA) and the cell apoptosis was examined by western blotting and flow cytometry. Cell viability was analyzed by the Cell Counting Kit­8 assay. Cell apoptosis resulting from 50 mU/µl DNase I was also observed by flow cytometry, terminal deoxynucleotidyl transferase dUTP nick­end labeling stain and western blotting. Compared with healthy controls, the serum DNase I activity of patients with diabetes was significantly increased (P<0.05). In addition, DNase I expression was observed to be significantly increased in human pancreatic tissues. The addition of high glucose upregulated the cell apoptotic rate, whereas DNase I knockdown significantly reduced apoptosis in cells treated with high glucose. In addition, the western blotting results indicated that caspase­3 was increased subsequent to treatment of cells with 30 mM high glucose, however, this increase can be reversed by transfection with DNase I siRNA (P<0.05). Compared with cells cultured in normal conditions and high glucose, 50 mU/µl DNase I was able to significantly increase the cell apoptotic rate and level of caspase-3. DNase I activity was observed to be increased in type 2 diabetes, and high glucose combined with increased DNase I is suggested to aggravate ß-cell apoptosis.

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