Prevalence of internet addiction disorder in Chinese university students: A comprehensive meta-analysis of observational studies

Background and aims: Internet addiction disorder (IAD) is common in university students. A number of studies have examined the prevalence of IAD in Chinese university students, but the results have been inconsistent. This is a meta-analysis of the prevalence of IAD and its associated factors in Chinese university students. Methods: Both English (PubMed, PsycINFO, and Embase) and Chinese (Wan Fang Database and Chinese National Knowledge Infrastructure) databases were systematically and independently searched from their inception until January 16, 2017. Results: Altogether 70 studies covering 122,454 university students were included in the meta-analysis. Using the random-effects model, the pooled overall prevalence of IAD was 11.3% (95% CI: 10.1%–12.5%). When using the 8-item Young Diagnostic Questionnaire, the 10-item modified Young Diagnostic Questionnaire, the 20-item Internet Addiction Test, and the 26-item Chen Internet Addiction Scale, the pooled prevalence of IAD was 8.4% (95% CI: 6.7%–10.4%), 9.3% (95% CI: 7.6%–11.4%), 11.2% (95% CI: 8.8%–14.3%), and 14.0% (95% CI: 10.6%–18.4%), respectively. Subgroup analyses revealed that the pooled prevalence of IAD was significantly associated with the measurement instrument (Q = 9.41, p = .024). Male gender, higher grade, and urban abode were also significantly associated with IAD. The prevalence of IAD was also higher in eastern and central of China than in its northern and western regions (10.7% vs. 8.1%, Q = 4.90, p = .027). Conclusions: IAD is common among Chinese university students. Appropriate strategies for the prevention and treatment of IAD in this population need greater attention

Compressive Sensing-Based Grant-Free Massive Access for 6G Massive Communication

The advent of the sixth-generation (6G) of wireless communications has given rise to the necessity to connect vast quantities of heterogeneous wireless devices, which requires advanced system capabilities far beyond existing network architectures. In particular, such massive communication has been recognized as a prime driver that can empower the 6G vision of future ubiquitous connectivity, supporting Internet of Human-Machine-Things for which massive access is critical. This paper surveys the most recent advances toward massive access in both academic and industry communities, focusing primarily on the promising compressive sensing-based grant-free massive access paradigm. We first specify the limitations of existing random access schemes and reveal that the practical implementation of massive communication relies on a dramatically different random access paradigm from the current ones mainly designed for human-centric communications. Then, a compressive sensing-based grant-free massive access roadmap is presented, where the evolutions from single-antenna to large-scale antenna array-based base stations, from single-station to cooperative massive multiple-input multiple-output systems, and from unsourced to sourced random access scenarios are detailed. Finally, we discuss the key challenges and open issues to shed light on the potential future research directions of grant-free massive access.Comment: Accepted by IEEE IoT Journa

Electrocardiographic features of immune checkpoint inhibitor-associated myocarditis.

Immune checkpoint inhibitors (ICIs) are associated with immune-related adverse events including myocarditis, whilst improving cancer-related outcomes. There is thus a clinical need to identify electrocardiographic manifestations of ICI-related myocarditis to guide clinical management. PubMed was searched for clinical studies and case reports describing electrocardiographic changes in patients with ICI-related myocarditis. A total of six clinical studies and 79 case reports were included. This revealed a range of presentations for patients on ICIs, including supraventricular arrhythmias, ventricular arrhythmias and heart block, and new changes of ST-T segment unrelated to coronary artery disease, ST-segment elevation or depression and T-wave abnormalities. Several patients showed low voltages in multiple leads and new onset Q-wave development. Patients with ICI-related myocarditis may develop new arrhythmia and ST-T changes, and infrequently low voltages in multiple leads. [Abstract copyright: Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

A Metabolomic Analysis Of Thiol Response For Standard And Modified N-Acetyl Cysteine Treatment Regimens In Patients With Acetaminophen Overdose

Abstract N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post‐start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post‐infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP‐metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP‐metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP‐induced ALI

Selective Differential Expression Of The Ribosomal Protein Genes El14 And Us19 In A Well-Differentiated Epithelial Cell Line Of Nasopharyngeal Carcinoma

Besides ribosome biogenesis and protein synthesis, ribosomal proteins (RP) are associated with congenital diseases and cancers. A small subset of ribosomal protein genes has shown expression pattern indicative of their association with nasopharyngeal carcinoma (NPC). Nevertheless, the list of RP genes that are NPC-associated factors is largely incomplete. Herein we report the expression patterns of eL14 and uS19 in NPC normal nasopharyngeal epithelium cell lines. Expression levels of eL14 and uS19 in the NPC-HK1 cell line was comparatively analysed with a normal nasopharyngeal cell line (NP69) using Reverse Transcription – Polymerase Chain Reaction (RT-PCR). We revealed that the transcript level of eL14 was significantly down-regulated in HK1 when compared to NP69. The expression behaviour of eL14 is demonstrated for the first time in the NPC context. In contrast, the transcript level of uS19 was up-regulated in NPC/HK1 compared to NP69, but not to a statistically significant extent. This study provides new evidence of differential expression of the ribosomal protein gene, eL14 in an NPC cell line derived from well-differentiated squamous cell carcinoma of human nasopharynx. It adds to the list of NPC-associated ribosomal protein genes amenable for development of biomarkers for improved molecular diagnosis of nasopharyngeal cancer

Zfp322a Regulates Mouse ES Cell Pluripotency and Enhances Reprogramming Efficiency

Embryonic stem (ES) cells derived from the inner cell mass (ICM) of blastocysts are characterised by their ability to self-renew and their potential to differentiate into many different cell types. Recent studies have shown that zinc finger proteins are crucial for maintaining pluripotent ES cells. Mouse zinc finger protein 322a (Zfp322a) is expressed in the ICM of early mouse embryos. However, little is known regarding the role of Zfp322a in the pluripotency maintenance of mouse ES cells. Here, we report that Zfp322a is required for mES cell identity since depletion of Zfp322a directs mES cells towards differentiation. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays revealed that Zfp322a binds to Pou5f1 and Nanog promoters and regulates their transcription. These data along with the results obtained from our ChIP-seq experiment showed that Zfp322a is an essential component of mES cell transcription regulatory network. Targets which are directly regulated by Zfp322a were identified by correlating the gene expression profile of Zfp322a RNAi-treated mES cells with the ChIP-seq results. These experiments revealed that Zfp322a inhibits mES cell differentiation by suppressing MAPK pathway. Additionally, Zfp322a is found to be a novel reprogramming factor that can replace Sox2 in the classical Yamanaka's factors (OSKM). It can be even used in combination with Yamanaka's factors and that addition leads to a higher reprogramming efficiency and to acceleration of the onset of the reprogramming process. Together, our results demonstrate that Zfp322a is a novel essential component of the transcription factor network which maintains the identity of mouse ES cells

Current Evidence for a Role of the Kynurenine Pathway of Tryptophan Metabolism in Multiple Sclerosis

The kynurenine pathway (KP) is the major metabolic pathway of the essential amino acid tryptophan (TRP). Stimulation by inflammatory molecules, such as interferon-γ (IFN-γ), is the trigger for induction of the KP, driving a complex cascade of production of both neuroprotective and neurotoxic metabolites, and in turn, regulation of the immune response and responses of brain cells to the KP metabolites. Consequently, substantial evidence has accumulated over the past couple of decades that dysregulation of the KP and the production of neurotoxic metabolites are associated with many neuroinflammatory and neurodegenerative diseases, including Parkinson's disease, AIDS-related dementia, motor neurone disease, schizophrenia, Huntington's disease, and brain cancers. In the past decade, evidence of the link between the KP and multiple sclerosis (MS) has rapidly grown and has implicated the KP in MS pathogenesis. KP enzymes, indoleamine 2,3-dioxygenase (IDO-1) and tryptophan dioxygenase (highest expression in hepatic cells), are the principal enzymes triggering activation of the KP to produce kynurenine from TRP. This is in preference to other routes such as serotonin and melatonin production. In neurological disease, degradation of the blood-brain barrier, even if transient, allows the entry of blood monocytes into the brain parenchyma. Similar to microglia and macrophages, these cells are highly responsive to IFN-γ, which upregulates the expression of enzymes, including IDO-1, producing neurotoxic KP metabolites such as quinolinic acid. These metabolites circulate systemically or are released locally in the brain and can contribute to the excitotoxic death of oligodendrocytes and neurons in neurological disease principally by virtue of their agonist activity at N-methyl-d-aspartic acid receptors. The latest evidence is presented and discussed. The enzymes that control the checkpoints in the KP represent an attractive therapeutic target, and consequently several KP inhibitors are currently in clinical trials for other neurological diseases, and hence may make suitable candidates for MS patients. Underpinning these drug discovery endeavors, in recent years, several advances have been made in how KP metabolites are assayed in various biological fluids, and tremendous advancements have been made in how specimens are imaged to determine disease progression and involvement of various cell types and molecules in MS.22 page(s

AluScan: a method for genome-wide scanning of sequence and structure variations in the human genome

<p>Abstract</p> <p>Background</p> <p>To complement next-generation sequencing technologies, there is a pressing need for efficient pre-sequencing capture methods with reduced costs and DNA requirement. The Alu family of short interspersed nucleotide elements is the most abundant type of transposable elements in the human genome and a recognized source of genome instability. With over one million Alu elements distributed throughout the genome, they are well positioned to facilitate genome-wide sequence amplification and capture of regions likely to harbor genetic variation hotspots of biological relevance.</p> <p>Results</p> <p>Here we report on the use of inter-Alu PCR with an enhanced range of amplicons in conjunction with next-generation sequencing to generate an Alu-anchored scan, or 'AluScan', of DNA sequences between Alu transposons, where Alu consensus sequence-based 'H-type' PCR primers that elongate outward from the head of an Alu element are combined with 'T-type' primers elongating from the poly-A containing tail to achieve huge amplicon range. To illustrate the method, glioma DNA was compared with white blood cell control DNA of the same patient by means of AluScan. The over 10 Mb sequences obtained, derived from more than 8,000 genes spread over all the chromosomes, revealed a highly reproducible capture of genomic sequences enriched in genic sequences and cancer candidate gene regions. Requiring only sub-micrograms of sample DNA, the power of AluScan as a discovery tool for genetic variations was demonstrated by the identification of 357 instances of loss of heterozygosity, 341 somatic indels, 274 somatic SNVs, and seven potential somatic SNV hotspots between control and glioma DNA.</p> <p>Conclusions</p> <p>AluScan, implemented with just a small number of H-type and T-type inter-Alu PCR primers, provides an effective capture of a diversity of genome-wide sequences for analysis. The method, by enabling an examination of gene-enriched regions containing exons, introns, and intergenic sequences with modest capture and sequencing costs, computation workload and DNA sample requirement is particularly well suited for accelerating the discovery of somatic mutations, as well as analysis of disease-predisposing germline polymorphisms, by making possible the comparative genome-wide scanning of DNA sequences from large human cohorts.</p