Mediators of the relationship between self-control and pathological technology use: Negative affect and cognitive failures, but not self-efficacy

The widespread adoption of technologies such as smartphones, the Internet, and social media has been associated with the emergence of pathological technology use (e.g., Internet addiction). Prevalence rates of pathological technology use vary widely across age groups, cultures, and medium, although it is not uncommon for rates of mild to moderate pathological use to exceed 20%-30%. These relatively high prevalence rates have motivated researchers to identify the predictors of pathological use. The current study focuses on the relationship be- tween self-control and pathological technology use, and demonstrates that negative affect and cognitive failures, but not self-efficacy, partially mediate the association between self-control and pathological technology use. These findings re- veal some of the pathways by which poor self-control could lead to elevated levels of pathological technology use

Energy Insecurity among Families with Children

Energy insecurity (EI) reflects an inability to adequately meet basic household heating, cooling, and energy needs. EI is a pervasive and often-overlooked problem for low-income families with children. Conceptually, EI is a multi-dimensional construct that describes the interplay between structural conditions of housing and the costs of household energy. This brief describes the extent of economic EI, — disproportionate share of household income allocated to utility expenses among families with children, by family income, demographic characteristics, and geographical area, using the 2011 American Community Survey

Artificial intelligence-based conversational agents used for sustainable fashion: systematic literature review.

In the past five years, the textile industry has undergone significant transformations in response to evolving fashion trends and increased consumer garment turnover. To address the environmental impacts of fast fashion, the industry is embracing artificial intelligence (AI) and immersive technologies, particularly leveraging conversational agents as personalised guides for sustainable fashion practices. In this research paper, we conduct a systematic literature review to categorise techniques, platforms, and applications of conversational agents in promoting sustainability within the fashion industry. Additionally, the review aims to scrutinise the solutions offered, identify gaps in the existing literature, and provide insights into the effectiveness and limitations of these conversational agents. Utilising a predefined search strategy on IEEE Xplore, Google Scholar, SCOPUS, and Web of Science, 15 relevant articles were selected through a step-by-step procedure based on the guidelines of the PRISMA framework. The findings reveal a notable global interest in AI-powered conversational agents, with Italy emerging as a significant centre for research in this domain. The studies predominantly focus on consumer perceptions and intentions regarding the adoption of AI technologies, indicating a broader curiosity about how individuals incorporate such innovations into their daily lives. Moreover, a substantial proportion of the studies employs diverse methods, reflecting a comprehensive approach to understanding the functionality and performance of conversational agents in various contexts. While acknowledging the historical precedence of text-based agents, the review highlights a research gap related to embodied agents. The conclusion emphasises the need for continued exploration, particularly in understanding the broader impact of these technologies on creating sustainable and environmentally-friendly business models in the e-retail sector

Similarity-Aware Multimodal Prompt Learning for Fake News Detection

The standard paradigm for fake news detection mainly utilizes text information to model the truthfulness of news. However, the discourse of online fake news is typically subtle and it requires expert knowledge to use textual information to debunk fake news. Recently, studies focusing on multimodal fake news detection have outperformed text-only methods. Recent approaches utilizing the pre-trained model to extract unimodal features, or fine-tuning the pre-trained model directly, have become a new paradigm for detecting fake news. Again, this paradigm either requires a large number of training instances, or updates the entire set of pre-trained model parameters, making real-world fake news detection impractical. Furthermore, traditional multimodal methods fuse the cross-modal features directly without considering that the uncorrelated semantic representation might inject noise into the multimodal features. This paper proposes a Similarity-Aware Multimodal Prompt Learning (SAMPLE) framework. First, we incorporate prompt learning into multimodal fake news detection. Prompt learning, which only tunes prompts with a frozen language model, can reduce memory usage significantly and achieve comparable performances, compared with fine-tuning. We analyse three prompt templates with a soft verbalizer to detect fake news. In addition, we introduce the similarity-aware fusing method to adaptively fuse the intensity of multimodal representation and mitigate the noise injection via uncorrelated cross-modal features. For evaluation, SAMPLE surpasses the F1 and the accuracies of previous works on two benchmark multimodal datasets, demonstrating the effectiveness of the proposed method in detecting fake news. In addition, SAMPLE also is superior to other approaches regardless of few-shot and data-rich settings

Lipoxygenase Pathway Mediates Increases of Airway Resistance and Lung Inflation Induced by Exposure to Nanotitanium Dioxide in Rats

Nanotitanium dioxide particle (nTiO2) inhalation has been reported to induce lung parenchymal injury. After inhalation of nTiO2, we monitored changes in 5-lipoxygenase, endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) mRNA in rat lung tissue. Lung function parameters include specific airway resistance (SRaw), peak expiratory flow rate (PEF), functional residual capacity (FRC), and lung compliance (Cchord); blood white blood cell count (WBC), nitric oxide (NO), hydrogen peroxide, and lactic dehydrogenase (LDH); and lung lavage leukotriene C4, interleukin 6 (IL6), tumor necrotic factor α (TNFα), hydroxyl radicals, and NO. Leukotriene receptor antagonist MK571 and 5-lipoxygenase inhibitor MK886 were used for pharmacologic intervention. Compared to control, nTiO2 exposure induced near 5-fold increase in 5-lipoxygenase mRNA expression in lung tissue. iNOS mRNA increased while eNOS mRNA decreased. Lavage leukotriene C4; IL6; TNFα; NO; hydroxyl radicals; and blood WBC, NO, hydrogen peroxide, and LDH levels rose. Obstructive ventilatory insufficiency was observed. MK571 and MK886 both attenuated the systemic inflammation and lung function changes. We conclude that inhaled nTiO2 induces systemic inflammation, cytokine release, and oxidative and nitrosative stress in the lung. The lipoxygenase pathway products, mediated by oxygen radicals and WBC, play a critical role in the obstructive ventilatory insufficiency induced by nTiO2

FAM111A regulates replication origin activation and cell fitness

FAM111A is a replisome-associated protein and dominant mutations within its trypsin-like peptidase domain are linked to severe human developmental syndrome, the Kenny–Caffey syndrome. However, FAM111A functions remain unclear. Here, we show that FAM111A facilitates efficient activation of DNA replication origins. Upon hydroxyurea treatment, FAM111A-depleted cells exhibit reduced single-stranded DNA formation and a better survival rate. Unrestrained expression of FAM111A WT and patient mutants causes accumulation of DNA damage and cell death, only when the peptidase domain remains intact. Unrestrained expression of FAM111A WT also causes increased single-stranded DNA formation that relies on S phase entry, FAM111A peptidase activity but not its binding to proliferating cell nuclear antigen. Altogether, these data unveil how FAM111A promotes DNA replication under normal conditions and becomes harmful in a disease context

Sofosbuvir and Ribavirin Therapy for Children Aged 3 to <12 Years With Hepatitis C Virus Genotype 2 or 3 Infection.

Currently, the only approved hepatitis C virus (HCV) treatment for children aged <12 years is pegylated interferon plus ribavirin. In an open-label study, we evaluated the safety and efficacy of sofosbuvir plus ribavirin for 12 weeks in children aged 3 to <12 years chronically infected with genotype 2 or for 24 weeks in patients with genotype 3. Patients aged 3 to <6 years weighing <17 kg received sofosbuvir 150 mg, and patients aged 3 to <6 years weighing ≥17 kg and all patients aged 6 to <12 years received sofosbuvir 200 mg once daily. Intensive pharmacokinetic sampling conducted in each age group confirmed the appropriateness of sofosbuvir doses. For all patients, ribavirin dosing was determined by baseline weight (up to 1,400 mg/day, two divided doses). The primary efficacy endpoint was sustained virologic response 12 weeks after therapy (SVR12). Fifty-four patients were enrolled (41 aged 6 to <12 years and 13 aged 3 to <6 years). Most were treatment naïve (98%) and infected perinatally (94%). All but one patient achieved SVR12 (53/54, 98%; 95% confidence interval, 90%-100%). The patient who did not achieve SVR12 was a 4-year-old who discontinued treatment after 3 days because of "abnormal drug taste." The most commonly reported adverse events in patients aged 6 to <12 years were vomiting (32%) and headache (29%), and those in patients aged 3 to <6 years were vomiting (46%) and diarrhea (39%). One 3-year-old patient had a serious adverse event of accidental ribavirin overdose requiring hospitalization for monitoring; this patient completed treatment and achieved SVR12. Conclusion: Sofosbuvir plus ribavirin was well tolerated and highly effective in children aged 3 to <12 years with chronic HCV genotype 2 or 3 infection

NR2B phosphorylation at tyrosine 1472 contributes to brain injury in a rodent model of neonatal hypoxia-ischemia.

Background and purposeThe NR2B subunit of the N-methyl-d-aspartate (NMDA) receptor is phosphorylated by the Src family kinase Fyn in brain, with tyrosine (Y) 1472 as the major phosphorylation site. Although Y1472 phosphorylation is important for synaptic plasticity, it is unknown whether it is involved in NMDA receptor-mediated excitotoxicity in neonatal brain hypoxia-ischemia (HI). This study was designed to elucidate the specific role of Y1472 phosphorylation of NR2B in neonatal HI in vivo and in NMDA-mediated neuronal death in vitro.MethodsNeonatal mice with a knockin mutation of Y1472 to phenylalanine (YF-KI) and their wild-type littermates were subjected to HI using the Vannucci model. Brains were scored 5 days later for damage using cresyl violet and iron staining. Western blotting and immunoprecipitation were performed to determine NR2B tyrosine phosphorylation. Expression of NADPH oxidase subunits and superoxide production were measured in vivo. NMDA-induced calcium response, superoxide formation, and cell death were evaluated in primary cortical neurons.ResultsAfter neonatal HI, YF-KI mice have reduced expression of NADPH oxidase subunit gp91phox and p47phox and superoxide production, lower activity of proteases implicated in necrotic and apoptotic cell death, and less brain damage when compared with the wild-type mice. In vitro, YF-KI mutation diminishes superoxide generation in response to NMDA without effect on calcium accumulation and inhibits NMDA and glutamate-induced cell death.ConclusionsUpregulation of NR2B phosphorylation at Y1472 after neonatal HI is involved in superoxide-mediated oxidative stress and contributes to brain injury