Mom, dad, put down your phone and talk to me: how parental phubbing influences problematic internet use among adolescents.

BACKGROUND: The positive association of parental phubbing with internalising and externalising problems among adolescents has gained academic traction. To date, limited research has investigated the association of parental phubbing and adolescents' Problematic Internet Use (PIU). Furthermore, the mechanism underlying this association is largely unknown. These gaps limit our understanding of family-related issues affecting PIU among adolescents. The present study explores whether there is a relation between parental phubbing and PIU and investigates the mechanisms underlying this relation among adolescents. METHODS: The participants were 495 junior high schoolers aged 11-15 years. Participants completed questionnaires on their experiences with PIU, parental phubbing, parent-child relationships, and basic psychological needs satisfaction. RESULTS: The results showed a direct and indirect positive association between parental phubbing and PIU. Furthermore, parental phubbing indirectly influenced PIU and was mediated by the parent-child relationship and basic psychological needs satisfaction, respectively. Moreover, the parent-child relationship and basic psychological needs satisfaction were sequentially mediated. CONCLUSIONS: Our study highlights the crucial role of parents in the development of adolescent PIU and provides theoretical and practical guidelines for PIU prevention and intervention.

Process analysis of anaerobic fermentation of Phragmites australis straw and cow dung exposing to elevated chromium (VI) concentrations.

Anaerobic fermentation is considered as a cost-effective way of biomass waste disposal. Chromium (Cr) is one of the heavy metals that often been blamed for unsatisfactory operation or failure of anaerobic fermentation. The impact of Cr (added as K2Cr2O7) on mesophilic anaerobic fermentation of Phragmites australis straw and cow dung was demonstrated by investigating the biogas properties, process stability, substrate degradation and enzyme activities during the fermentation process. The results showed that 30, 100 and 500 mg/L Cr6+ addition increased the cumulative biogas yields by up to 19.00%, 14.85% and 7.68% respectively, and brought forward the daily biogas yield peak. Meanwhile, the methane (CH4) content in the 30 (52.47%) and 100 (40.57%) mg/L Cr6+-added groups were generally higher than the control group (37.70%). Higher pH values (close to pH 7) and lower oxidation-reduction potential (ORP) values in the Cr6+-added groups after the 15th day indicated the better process stability compared to the control group. Taking the whole fermentation process into account, the promoting effect of Cr6+ addition on biogas yields was mainly attributable to better process stability, the enhanced degradation of lignin and hemicellulose, the transformation of intermediates into VFA, the higher coenzyme F420 activities and the efficient generation of CH4. These results demonstrate that an appropriate addition of Cr6+ could enhance the anaerobic fermentation which support the regulations utilizing of the Cr6+ contaminated biowaste.

Celastrol stimulates hypoxia-inducible factor-1 activity in tumor cells by initiating the ROS/Akt/p70S6K signaling pathway and enhancing hypoxia-inducible factor-1α protein synthesis.

Celastrol, a tripterine derived from the traditional Chinese medicine plant Tripterygium wilfordii Hook F. ("Thunder of God Vine"), has been reported to have multiple effects, such as anti-inflammation, suppression of tumor angiogenesis, inhibition of tumor growth, induction of apoptosis and protection of cells against human neurodegenerative diseases. However, the mechanisms that underlie these functions are not well defined. In this study, we reported for the first time that Celastrol could induce HIF-1α protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1α protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. Celastrol did not influence HIF-1α transcription. Instead, Celastrol induced the accumulation of the HIF-1α protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1α translation. In addition, we found that the activation of Akt by Celastrol was transient. With increased exposure time, inhibition of Hsp90 chaperone function by Celastrol led to the subsequent depletion of the Akt protein and thus to the suppression of Akt activity. Moreover, in HepG2 cells, the accumulation of HIF-1α increased the expression of BNIP3, which induced autophagy. However, HIF-1α and BNIP3 did not influence the cytotoxicity of Celastrol because the main mechanism by which Celastrol kills cancer cells is through stimulating ROS-mediated JNK activation and inducing apoptosis. Furthermore, our data showed that the dose required for Celastrol to induce HIF-1α protein accumulation and enhance HIF-1α transcriptional activation was below its cytotoxic threshold. A cytotoxic dose of Celastrol for cancer cells did not display cytotoxicity in LO2 normal human liver cells, which indicated that the novel functions of Celastrol in regulating HIF-1 signaling and inducing autophagy might be used in new applications, such as in anti-inflammation and protection of cells against human neurodegenerative diseases. Future studies regarding these applications are required.

[Source analysis of urea-N in Lake Taihu during summer].

To study the effect of urea nitrogen on the ecosystem of Lake Taihu, we conducted urea and various nitrogen analysis for the water samples collected from the lake and surrounding rivers during summer. The ecological index analysis of 82 sites in rivers and lake yielded the following results: (1) The urea nitrogen contents in Taihu ranged from 0.011 to 0.161 mg x L(-1), which was high in the northwest and low in the southeast, related to the main pollution sources distribution of its drainage basin. (2) The dissolved nitrogen was dominated by inorganic nitrogen and the ratio between ammonia nitrogen and nitrate nitrogen was 5: 1. The average percentage of urea nitrogen in total nitrogen, dissolved nitrogen, dissolved organic nitrogen and bioavailable nitrogen was respectively 2.28%, 5.91%, 15.86%, and 6.22%, which showed a significant ecological function in Taihu. (3) Urea nitrogen concentration in river was more than twice that in lake, and the lake river concentration was slightly higher than the river into the lake. (3) In Taihu, there was a transformation relationship between urea nitrogen and the nitrogen in other forms. It showed that urea nitrogen had a significant positive correlation with permanganate index and the other forms of nitrogen, and a significant negative correlation with dissolved oxygen. In addition, urea nitrogen was weakly and positively correlated with chlorophyll a, while closely related to the spatial distribution of benthos and zooplankton species. All the results above showed that urea nitrogen was the bridge of organic and inorganic nitrogen transformation, and was the sign of nitrogen cycle of Lake Taihu, which was controlled by the circulating rate. High nitrogen content (especially the organic nitrogen) and low dissolved oxygen content were the key contributors to the increased urea nitrogen content. In Taihu, the urea nitrogen content was affected by both exogenous input and endogenous release.

Reduction of in-stent restenosis risk on nickel-free stainless steel by regulating cell apoptosis and cell cycle.

High nitrogen nickel-free austenitic stainless steel (HNNF SS) is one of the biomaterials developed recently for circumventing the in-stent restenosis (ISR) in coronary stent applications. To understand the ISR-resistance mechanism, we have conducted a comparative study of cellular and molecular responses of human umbilical vein endothelial cells (HUVECs) to HNNF SS and 316L SS (nickel-containing austenitic 316L stainless steel) which is the stent material used currently. CCK-8 analysis and flow cytometric analysis were used to assess the cellular responses (proliferation, apoptosis, and cell cycle), and quantitative real-time PCR (qRT-PCR) was used to analyze the gene expression profile of HUVECs exposed to HNNF SS and 316L SS, respectively. Flow cytometry analysis revealed that 316L SS could activate the cellular apoptosis more efficiently and initiate an earlier entry into the S-phase of cell cycle than HNNF SS. At the molecular level, qRT-PCR results showed that the genes regulating cell apoptosis and autophagy were overexpressed on 316L SS. Further examination indicated that nickel released from 316L SS triggered the cell apoptosis via Fas-Caspase8-Caspase3 exogenous pathway. These molecular mechanisms of HUVECs present a good model for elucidating the observed cellular responses. The findings in this study furnish valuable information for understanding the mechanism of ISR-resistance on the cellular and molecular basis as well as for developing new biomedical materials for stent applications.

The histone deacetylase inhibitor vorinostat prevents TNFα-induced necroptosis by regulating multiple signaling pathways.

Histone deacetylase (HDAC) inhibitors are novel anticancer reagents that have recently been reported to have anti-inflammatory and neuroprotective effects; however, the mechanisms underlying their activities are largely undefined. The data from this study show that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) can protect L929 cells from TNFα-induced necroptosis. This effect involves multiple mechanisms, including the upregulation of cFLIPL expression, the enhanced activation of NFκB and p38 MAPK, and the inactivation of JNK. In addition, SAHA could initiate cell autophagy by inhibiting Akt and mTOR, which also play important roles in protecting cells from necroptosis. Because cell necroptosis is important for inflammation-related deterioration and neurodegenerative disease, our results indicate that preventing cell necrosis may be an important mechanism through which HDAC inhibitor compounds exert their anti-inflammatory or neuroprotective effects.

Metastasis-associated gene, mag-1 improves tumour microenvironmental adaptation and potentiates tumour metastasis.

Metastasis is a major cause of death from malignant diseases, and the underlying mechanisms are still largely not known. A detailed probe into the factors which may regulate tumour invasion and metastasis contributes to novel anti-metastatic therapies. We previously identified a novel metastasis-associated gene 1 (mag-1) by means of metastatic phenotype cloning. Then we characterized the gene expression profile of mag-1 and showed that it promoted cell migration, adhesion and invasion in vitro. Importantly, the disruption of mag-1 via RNA interference not only inhibited cellular metastatic behaviours but also significantly reduced tumour weight and restrained mouse breast cancer cells to metastasize to lungs in spontaneous metastatic assay in vivo. Furthermore, we proved that mag-1 integrates dual regulating mechanisms through the stabilization of HIF-1α and the activation of mTOR signalling pathway. We also found that mag-1-induced metastatic promotion could be abrogated by mTOR specific inhibitor, rapamycin. Taken together, the findings identified a direct role that mag-1 played in metastasis and implicated its function in cellular adaptation to tumour microenvironment.

Evaluating cell migration in vitro by the method based on cell patterning within microfluidic channels.

Cell migration is an early-stage and critical step for cancer metastasis. The most common approach to monitor this process is wound-healing assay. However, this traditional method has some unavoidable limitations. We observed that simply scratching the monolayer of cultured cells might cause local cell damage around the injury line. The cells along the scratched border seemed to be irritated and exhibited abnormal distribution of cytoskeleton reassembly with protruding "cell islands" and "pseudopodia" during wound healing, which might potentially affect the assessment of cell migration behavior. Herein, we applied a microfluidic device that mechanically constrained cells seeded in a designed pattern inside microchannels, and monitored cell movement in a way of mimicking the natural microenvironment of cancerous tissues. We illustrated the capacity of this simple method to probe cellular migration behaviors and to screen some biological active agents that reflected in their influence on cellular motility.

A novel RGD-toxin protein, Lj-RGD3, from the buccal gland secretion of Lampetra japonica impacts diverse biological activities.

RGD (Arg-Gly-Asp) motif toxin proteins from snake venoms, saliva glands secretion of leech or tick have typical characteristics of inhibiting platelet aggregation, angiogenesis, and tumor growth. Here we report cloning and characterization of a novel RGD-toxin protein from the buccal gland of Lampetra japonica. In an attempt to study the activities of anticoagulant in the buccal gland secretion of L. japonica, we established buccal gland cDNA library and identified a gene encoding a predicted protein of 118 amino acids with 3 RGD motifs. The predicted protein was named Lj-RGD3. We generated the cDNA of Lj-RGD3 and obtained the recombinant protein rLj-RGD3. The polyclonal antibodies against rLj-RGD3 recognized the native Lj-RGD3 protein in buccal gland secretion in Western blot analyses. The biological function studies reveal that rLj-RGD3 inhibited human platelet aggregation in a dose-dependent manner with IC(50) value at 5.277 µM. In addition, rLj-RGD3 repressed bFGF-induced angiogenesis in the chick chorioallantoic membrane model. rLj-RGD3 also inhibited the adhesion of ECV304 cells to vitronectin. Furthermore, rLj-RGD3 induced apoptosis and significantly inhibited proliferation, migration, and invasion evoked by bFGF in ECV304 cells. Taken together, these results suggested that rLj-RGD3 is a novel RGD-toxin protein possessing typical functions of the RGD-toxin protein.

A smart-card-enabled privacy preserving E-prescription system.

Within the overall context of protection of health care information, privacy of prescription data needs special treatment. First, the involvement of diverse parties, especially nonmedical parties in the process of drug prescription complicates the protection of prescription data. Second, both patients and doctors have privacy stakes in prescription, and their privacy should be equally protected. Third, the following facts determine that prescription should not be processed in a truly anonymous manner: certain involved parties conduct useful research on the basis of aggregation of prescription data that are linkable with respect to either the patients or the doctors; prescription data has to be identifiable in some extreme circumstances, e.g., under the court order for inspection and assign liability. In this paper, we propose an e-prescription system to address issues pertaining to the privacy protection in the process of drug prescription. In our system, patients' smart cards play an important role. For one thing, the smart cards are implemented to be portable repositories carrying up-to-date personal medical records and insurance information, providing doctors instant data access crucial to the process of diagnosis and prescription. For the other, with the secret signing key being stored inside, the smart card enables the patient to sign electronically the prescription pad, declaring his acceptance of the prescription. To make the system more realistic, we identify the needs for a patient to delegate his signing capability to other people so as to protect the privacy of information housed on his card. A strong proxy signature scheme achieving technologically mutual agreements on the delegation is proposed to implement the delegation functionality.