Explore the vast range of titles available.

This research examines how tourism development has impacted economic growth in a global city–Hong Kong. A large body of research has investigated national tourism-led growth in developed and developing countries. However, many such studies have overlooked how policies aimed at fostering the development of tourism affect the local economic development of global cities. The Chinese and Hong Kong governments liberalized their visa policies with the launch of the Individual Visit Scheme in 2003. Such liberalization has led to significantly more tourist arrival from China. Our autoregressive distributed lag model of tourism-related data from 2003 to 2019 provides strong evidence that more tourism can spur short-run economic growth. Yet, such tourism can lead to uncertain effects on local economic development in the longer run. Hong Kong’s transient tourism-led growth has almost entered the stagnation stage of the Tourism Area Life Cycle model. During such stagnation, jurisdictions like Hong Kong can expect limited long-term economic growth from their tourist sector. Our findings thus sound a warning for global cities looking to tourism to sustain longer-term economic growth.

Using a wireless single channel EEG device, we investigated the feasibility of using short-term frontal EEG as a means to evaluate the dynamic changes of mental workload. Frontal EEG signals were recorded from twenty healthy subjects performing four cognitive and motor tasks, including arithmetic operation, finger tapping, mental rotation and lexical decision task. Our findings revealed that theta activity is the common EEG feature that increases with difficulty across four tasks. Meanwhile, with a short-time analysis window, the level of mental workload could be classified from EEG features with 65%-75% accuracy across subjects using a SVM model. These findings suggest that frontal EEG could be used for evaluating the dynamic changes of mental workload.

Background The aims of this systematic review and meta-analysis are to examine the prevalence of adverse mental health outcomes, both short-term and long-term, among SARS patients, healthcare workers and the general public of SARS-affected regions, and to examine the protective and risk factors associated with these mental health outcomes. Methods We conducted a systematic search of the literature using databases such as Medline, Pubmed, Embase, PsycInfo, Web of Science Core Collection, CNKI, the National Central Library Online Catalog and dissertation databases to identify studies in the English or Chinese language published between January 2003 to May 2020 which reported psychological distress and mental health morbidities among SARS patients, healthcare workers, and the general public in regions with major SARS outbreaks. Results The literature search yielded 6984 titles. Screening resulted in 80 papers for the review, 35 of which were included in the meta-analysis. The prevalence of post-recovery probable or clinician-diagnosed anxiety disorder, depressive disorder, and post-traumatic stress disorder (PTSD) among SARS survivors were 19, 20 and 28%, respectively. The prevalence of these outcomes among studies conducted within and beyond 6 months post-discharge was not significantly different. Certain aspects of mental health-related quality of life measures among SARS survivors remained impaired beyond 6 months post-discharge. The prevalence of probable depressive disorder and PTSD among healthcare workers post-SARS were 12 and 11%, respectively. The general public had increased anxiety levels during SARS, but whether there was a clinically significant population-wide mental health impact remained inconclusive. Narrative synthesis revealed occupational exposure to SARS patients and perceived stigmatisation to be risk factors for adverse mental health outcomes among healthcare workers, although causality could not be determined due to the limitations of the studies. Conclusions The chronicity of psychiatric morbidities among SARS survivors should alert us to the potential long-term mental health complications of covid-19 patients. Healthcare workers working in high-risk venues should be given adequate mental health support. Stigmatisation against patients and healthcare workers should be explored and addressed. The significant risk of bias and high degree of heterogeneity among included studies limited the certainty of the body of evidence of the review.

Driver mutations are the genetic variants responsible for oncogenesis, but how specific somatic mutational events arise in cells remains poorly understood. Mutational signatures derive from the frequency of mutated trinucleotides in a given cancer sample, and they provide an avenue for investigating the underlying mutational processes that operate in cancer. Here we analyse somatic mutations from 7,815 cancer exomes from The Cancer Genome Atlas (TCGA) across 26 cancer types. We curate a list of 50 known cancer driver mutations by analysing recurrence in our cohort and annotations of known cancer-associated genes from the Cancer Gene Census, IntOGen database and Cancer Genome Interpreter. We then use these datasets to perform binary univariate logistic regression and establish the statistical relationship between individual driver mutations and known mutational signatures across different cancer types. Our analysis led to the identification of 39 significant associations between driver mutations and mutational signatures (P < 0.004, with a false discovery rate of < 5%). We first validate our methodology by establishing statistical links for known and novel associations between driver mutations and the mutational signature arising from Polymerase Epsilon proofreading deficiency. We then examine associations between driver mutations and mutational signatures for AID/APOBEC enzyme activity and deficient mismatch repair. We also identify negative associations (odds ratio < 1) between mutational signatures and driver mutations, and here we examine the role of aging and cigarette smoke mutagenesis in the generation of driver mutations in IDH1 and KRAS in brain cancers and lung adenocarcinomas respectively. Our study provides statistical foundations for hypothesised links between otherwise independent biological processes and we uncover previously unexplored relationships between driver mutations and mutagenic processes during cancer development. These associations give insights into how cancers acquire advantageous mutations and can provide direction to guide further mechanistic studies into cancer pathogenesis.

Since the Chinese government launched the Belt and Road Initiative, state-owned enterprises and private conglomerates have increased overseas investment. The massive outward foreign direct investment (OFDI) profoundly affects China’s regional development to varying degrees. Existing studies have mainly investigated the effect of foreign direct investment inflow on domestic investment (DI), but only a few studies have examined the impact of OFDI on DI. Though most researchers have indicated that OFDI activities can promote (or inhibit) DI in a particular country, they have overlooked how OFDI’s geographical distribution and motivation across the Chinese macro-regions have influenced DI. To fill these gaps, this paper examines the impact of such OFDI on DI in China and its macro-regions, using a province-level dataset from 2005 to 2021. It employs panel regression and rigorously tests the data using the generalised method of moments to address endogeneity issues. We also investigate the investment motivations of the top 100 Chinese multinationals with significant FDI outflows from 2015 to 2018. We find that OFDI has positively and markedly influenced DI in eastern coastal and central inland regions but not in western China. Though OFDI has positively affected DI in China, it may not hold in a regional context. Such OFDI seeks to enhance the efficiency of existing investment, expand domestic markets, and look for strategic assets. Our findings indicate that central and provincial governments could develop OFDI policies to cater to significant regional variations. Local governments should also consider the various OFDI motivations of Chinese multinationals and provide adequate support for developing and implementing local investment policies that encourage domestic firms to invest abroad.

Transposable elements (TEs) can influence human diseases by disrupting genome integrity, yet their quantification has been challenging due to the repetitive nature of these sequences across the genome. We develop LocusMasterTE, a method that integrates long-read with short-read RNA-seq to increase the accuracy of TE expression quantification. By incorporating fractional transcript per million values from long-read sequencing data into an expectation–maximization algorithm, LocusMasterTE reassigns multi-mapped reads, enhancing accuracy in short-read-based TE quantification. We validate the method with simulated and human datasets. LocusMasterTE may give new insights into TE functions through precise quantification.

Purpose This study aimed to compare the symptoms, unmet needs, and QoL reported by women at 6 months to <2 years and 2 to 5 years following surgery and adjuvant treatment for breast cancer. It also evaluated the relationships among symptoms, unmet needs, and QoL using structural equation modeling. Methods In this study, 113 and 137 survivors following breast cancer treatment 6 months to <2 years and 2 to 5 years, respectively, completed the Memorial Symptom Assessment Scale, the Supportive Care Needs Survey-34, and the Medical Outcomes Study 12-item Short Form Health Survey version 2.0 during their medical follow-up. Results The mean numbers of symptoms and unmet needs were 5.43 and 3.0, respectively, for survivors at <2 years, and 5.24 and 2.42, respectively, for survivors at 2 to 5 years following treatment. The most common reported symptoms were related primarily to physical domains. No significant differences were found between the two survivor groups on the MSAS scores. Survivors at <2 years reported significantly higher scores in Psychological and Health Care System/Information needs ( p  < 0.01), and lower composite scores in physical and mental QoL ( p  < 0.05) than those at 2 to 5 years post-treatment. Significant direct and indirect effects were found of symptom burden through unmet needs on survivors’ physical and mental QoL after adjustment for survival time, and the models showed a good fit. Conclusions Results suggest that breast cancer survivors continue to endure many symptoms independent of the survivorship period. The unmet needs mediate the relationship between symptom burden and survivors’ QoL.

Colibactin is a secondary metabolite produced by bacteria present in the human gut and is implicated in the development of colorectal cancer. This genotoxin alkylates deoxyadenosines on opposite strands of host cell DNA to produce DNA interstrand cross-links. While cells have evolved multiple mechanisms to resolve (“unhook”) interstrand cross-links, little is known about which of these pathways promote resistance to colibactin. Here, we use Xenopus egg extracts to investigate replication-coupled repair of colibactin-induced interstrand cross-links. We show that replication fork stalling at a colibactin-induced interstrand cross-link activates the Fanconi anemia interstrand cross-link repair pathway, which unhooks the interstrand cross-link through nucleolytic incisions. These incisions generate a DNA double-strand break intermediate in one sister chromatid, which can be repaired by homologous recombination, and a monoadduct (“interstrand cross-link remnant”) in the other. Translesion synthesis past the colibactin-induced interstrand cross-link remnant depends on Pol η and the Pol κ-REV1-Pol ζ polymerase complex and introduces predominantly T>A point mutations at the sites of colibactin alkylation. Taken together, our work provides a molecular framework for understanding how cells tolerate a naturally occurring and clinically relevant interstrand cross-link. The bacterial genotoxin colibactin induces DNA interstrand cross-links which pose a barrier to DNA replication. Here, the authors use Xenopus egg extracts to show that the Fanconi anemia pathway is responsible for repairing these cross-links.

Emerging evidence of an altered gut microbiome in autism spectrum disorder (ASD) suggests a pathomechanism through the gut–brain axis despite the inconsistent microbiome profile reported across studies. One of the knowledge gaps in the existing ASD microbiota studies is the lack of systematic exploration of the role of comorbid functional gastrointestinal disorder (FGID) in the association of ASD and altered gut microbiome. Consequently, 92 ASD and 112 age-matched typically developing (TD) boys were profiled on general psychopathology, FGID status by Rome IV classification, and gut microbiota using 16S ribosomal RNA amplicon sequencing at the V4 hypervariable region. Compared to TD, a significant decrease in the within-sample abundance of taxa was observed in ASD, regardless of FGID status. The microbiota of ASD FGID+ and ASD FGID− clustered apart from the TD groups. The microbiota of ASD FGID+ also showed qualitative differences from that of ASD FGID− and had the highest-level Firmicutes: Bacteroidetes ratio, which was paralleled by elevated levels of anxiety and overall psychopathology. The altered gastrointestinal microbiota composition in ASD appeared to be independent of comorbid FGID. Further studies should address how FGID may mediate neuropsychiatric symptoms in ASD through inflammation along the microbiota–gut–brain axis.

Cancer genomes with mutations in the exonuclease domain of Polymerase Epsilon (POLE) present with an extraordinarily high somatic mutation burden. In vitro studies have shown that distinct POLE mutants exhibit different polymerase activity. Yet, genome-wide mutation patterns and driver mutation formation arising from different POLE mutants remains unclear. Here, we curated somatic mutation calls from 7,345 colorectal cancer samples from published studies and publicly available databases. These include 44 POLE mutant samples including 9 with whole genome sequencing data available. The POLE mutant samples were categorized based on the specific POLE mutation present. Mutation spectrum, associations of somatic mutations with epigenomics features and co-occurrence with specific driver mutations were examined across different POLE mutants. We found that different POLE mutants exhibit distinct mutation spectrum with significantly higher relative frequency of C>T mutations in POLE V411L mutants. Our analysis showed that this increase frequency in C>T mutations is not dependent on DNA methylation and not associated with other genomic features and is thus specifically due to DNA sequence context alone. Notably, we found strong association of the TP53 R213* mutation specifically with POLE P286R mutants. This truncation mutation occurs within the TT[C>T]GA context. For C>T mutations, this sequence context is significantly more likely to be mutated in POLE P286R mutants compared with other POLE exonuclease domain mutants. This study refines our understanding of DNA polymerase fidelity and underscores genome-wide mutation spectrum and specific cancer driver mutation formation observed in POLE mutant cancers.