Coordenação fiscal regional na área da Grande Baía:uma perspetiva de fluxo de talentos

Dissertação de Mestrado em Administração PúblicaEstudamos o papel da coordenação fiscal regional na promoção do fluxo de trabalhadores talentosos na Área da Grande Baía de Guangdong, Hong Kong e Macau (GBA). Num contexto de crescentes atividades transfronteiriças e maior integração regional, é crucial que os governos descubram até que ponto diferentes sistemas fiscais na Grande Baía impedem a circulação de talentos regionais. Primeiro, comparamos as leis fiscais relevantes para clarificar onde estão as diferenças. De seguida, determinamos o impacto do imposto de duas formas. Em primeiro lugar, para determinar o nível de rendimento líquido de impostos, simulamos a taxa efetiva de imposto usando um perfil do rendimento para trabalhadores talentosos. Depois, reportamos as conclusões de uma entrevista em grupo com profissionais, especialistas e professores, a fim de compreender melhor as nuances das diferenças em termos de tributação regional. Concluímos que as diferenças na tributação dos rendimentos do trabalho causam impactos negativos tanto na mobilidade do fator trabalho como na vontade de trabalhadores talentosos irem trabalhar para a parte continental da GBA. Certas medidas fiscais, com o objetivo de promover a circulação de talentos, provavelmente levarão a efeitos indesejados. No contexto de uma melhor coordenação fiscal regional, salientamos uma série de passos futuros para mitigar os impactos negativos dos impostos no fluxo regional de talento.We study the role of regional tax coordination in promoting the flow of talented workers in the Guangdong-Hong Kong-Macao Greater Bay Area (GBA). In a context of increasing crossboundary activities and greater regional integration, it is crucial for governments to determine to what extent different tax systems in the GBA hinder regional talent flow. We first compare the relevant tax laws to clarify where the differences lie. Then we determine the impact of taxes in two ways. First, to determine the after-taxes income level, we simulate the effective tax burden using an income profile of talented workers. Then, we report on a group interview with professionals and experts aimed at better understanding the nuances of differential regional taxation. We conclude that the differences in labour income taxation are deleterious both to labour mobility and to the personal willingness of talented workers to work on the mainland side of the GBA. Certain tax measures, with the purpose of promoting regional talent flow, are likely to lead to certain unintended effects, such as a social justice problem. In the context of better regional tax coordination, we highlight a number of future steps to mitigate the negative impacts of tax on regional talent flow.N/

A step into the world of Pakistanis: oral health education for Pakistani adults in Hong Kong

Includes bibliographical references (p. 32).Questionnaire in English and Urdu.published_or_final_versio

Initiation of warfarin is associated with decreased mortality in patients with infective endocarditis: A population-based cohort study.

The use of warfarin to prevent thromboembolism in patients with infective endocarditis (IE) remains controversial due to potentially increased bleeding risks. Population-based retrospective cohort study. Patients aged 18 or older and diagnosed with IE in Hong Kong between January 1st, 1997 and August 31st, 2020 were included. Patients with use of any anticoagulant 30 days before IE diagnosis were excluded. Patients initiated on warfarin within 14 days of IE diagnosis and patients without warfarin use were matched for baseline characteristics using 1:1 propensity score matching. Warfarin use within 14 days of IE diagnosis. Patients were followed up to 90 days for the outcomes of ischemic stroke, all-cause mortality, intracranial hemorrhage, and gastrointestinal bleeding. Cox regression was used to determine hazard ratios (HRs) [95 % confidence intervals (CIs)] between treatment groups. Fine-Gray competing risk regression with all-cause mortality as the competing event was performed as a sensitivity analysis. In addition to 90-day analyses, landmark analyses were performed at 30 days of follow-up. The matched cohort consisted of 675 warfarin users (57.0 % male, age 59 ± 16 years) and 675 warfarin non-users (53.5 % male, age 61 ± 19 years). Warfarin users had a 50 % decreased 90-day risk in all-cause mortality (HR:0.50 [0.39-0.65]), without significantly different 90-day risks of ischemic stroke (HR:1.04 [0.70-1.53]), intracranial hemorrhage (HR:1.25 [0.77-2.04]), and gastrointestinal bleeding (HR:1.04 [0.60-1.78]). Thirty-day landmark analysis showed similar results. Competing risk regression showed significantly higher 30-day cumulative incidence of intracranial hemorrhage in warfarin users (sub-HR:3.34 [1.34-8.31]), but not at 90-day (sub-HR:1.63 [0.95-2.81]). Results from Fine-Gray regression were otherwise congruent with those from Cox regression. Warfarin initiated within 14 days of IE diagnosis was associated with significantly decreased risks of mortality but higher risks of intracranial hemorrhage, with similar risks of ischemic stroke and gastrointestinal bleeding, compared with non-use of warfarin with 14 days of IE diagnosis. Question: Is warfarin, initiated within 14 days of a diagnosis of infective endocarditis (IE), efficacious and safe? In this propensity score-matched, population-based, prospective cohort study from Hong Kong, warfarin use within 14 days of IE diagnosis was associated with a 50 % decrease in the risk of all-cause mortality, albeit with higher risk of intracranial hemorrhage, and without significant differences in the risk of ischaemic stroke and gastrointestinal bleeding. Meaning: In patients with IE, warfarin use within 14 days of diagnosis may have mortality benefits, despite increased risks of intracranial hemorrhage. [Abstract copyright: Copyright © 2023. Published by Elsevier Ltd.

The relationship of self-efficacy to catastrophizing and depressive symptoms in community-dwelling older adults with chronic pain: A moderated mediation model

Self-efficacy has been consistently found to be a protective factor against psychological distress and disorders in the literature. However, little research is done on the moderating effect of self-efficacy on depressive symptoms in the context of chronic pain. This cross-sectional study aimed to examine if pain self-efficacy attenuated the direct relationship between pain intensity and depressive symptoms, as well as their indirect relationship through reducing the extent of catastrophizing when feeling pain (moderated mediation). 664 community-dwelling Chinese older adults aged 60–95 years who reported chronic pain for at least three months were recruited from social centers. They completed a battery of questionnaires on chronic pain, pain self-efficacy, catastrophizing, and depressive symptoms in individual face-to-face interviews. Controlling for age, gender, education, self-rated health, number of chronic diseases, pain disability, and pain self-efficacy, pain catastrophizing was found to partially mediate the connection between pain intensity and depressive symptoms. Furthermore, the relationship between pain intensity and depressive symptoms was moderated by pain self-efficacy. Self-efficacy was also found to moderate the relationship between pain intensity and catastrophizing and the moderated mediation effect was confirmed using bootstrap analysis. The results suggested that with increasing levels of self-efficacy, pain intensity’s direct effect on depressive symptoms and its indirect effect on depressive symptoms via catastrophizing were both reduced in a dose-dependent manner. Our findings suggest that pain self-efficacy is a significant protective factor that contributes to psychological resilience in chronic pain patients by attenuating the relationship of pain intensity to both catastrophizing and depressive symptoms

Spatial analysis of the impact of urban geometry and socio-demographic characteristics on COVID-19, a study in Hong Kong

The World Health Organization considered the widespread of COVID-19 over the world as a pandemic. There is still a lack of understanding of its origin, transmission, and treatment methods. Understanding the influencing factors of the COVID-19 can help mitigate its spread, but little research on the spatial factors has been conducted. Therefore, this study explores the effects of urban geometry and socio-demographic factors on the COVID-19 cases in Hong Kong. For each patient, the places they visited during the incubation period before going to hospital were identified, and matched with corresponding attributes of urban geometry (i.e., building geometry, road network, greenspace) and socio-demographic factors (i.e., demographic, educational, economic, household and housing characteristics) based on the coordinates. The local cases were then compared with the imported cases using the stepwise logistic regression, the logistic regression with case-control of time, and the least absolute shrinkage and selection operator regression to identify factors influencing local disease transmission. Results show that the building geometry, road network and certain socio-economic characteristics are significantly associated with COVID-19 cases. In addition, the results indicate that urban geometry is playing a more important role than the socio-demographic characteristics in affecting the COVID-19 incidences. These findings provide a useful reference to the government and the general public as to the spatial vulnerability of the COVID-19 transmission and to take appropriate preventive measures in high-risk areas

Concomitant Hepatorenal Dysfunction and Malnutrition in Valvular Heart Surgery:Long-Term Prognostic Implications for Death and Heart Failure

BACKGROUND: Strategies to improve long-term prediction of heart failure and death in valvular surgery are urgently needed because of an increasing number of procedures globally. This study sought to report the prevalence, changes, and prognostic implications of concomitant hepatorenal dysfunction and malnutrition in valvular surgery. METHODS AND RESULTS: In 909 patients undergoing valvular surgery, 3 groups were defined based on hepatorenal function (the modified model for end-stage liver disease excluding international normalized ratio score) and nutritional status (Controlling Nutritional Status score): normal hepatorenal function and nutrition (normal), hepatorenal dysfunction or malnutrition alone (mild), and concomitant hepatorenal dysfunction and malnutrition (severe). Overall, 32%, 46%, and 19% of patients were classified into normal, mild, and severe groups, respectively. Over a 4.1-year median follow-up, mild and severe groups in-curred a higher risk of mortality (hazard ratio [HR], 3.17 [95% CI, 1.40–7.17] and HR, 9.30 [95% CI, 4.09– 21.16], respectively), cardiovascular death (subdistribution HR, 3.29 [95% CI, 1.14– 9.52] and subdistribution HR, 9.29 [95% CI, 3.09– 27.99]), heart failure hospitalization (subdistribution HR, 2.11 [95% CI, 1.25– 3.55] and subdistribution HR, 3.55 [95% CI, 2.04– 6.16]), and adverse outcomes (HR, 2.11 [95% CI, 1.25– 3.55] and HR, 3.55 [95% CI, 2.04– 6.16]). Modified model for end-stage liver disease excluding international normalized ratio and controlling nutritional status scores improved the predictive ability of European System for Cardiac Operative Risk Evaluation (area under the curve: 0.80 versus 0.73, P<0.001) and Society of Thoracic Surgeons score (area under the curve: 0.79 versus 0.72, P=0.004) for all-cause mortality. One year following surgery (n=707), patients with persistent concomitant hepatorenal dysfunction and malnutrition (severe) experienced worse outcomes than those without.  CONCLUSIONS: Concomitant hepatorenal dysfunction and malnutrition was frequent and strongly linked to heart failure and mortality in valvular surgery

MicroRNAs in pulmonary arterial remodeling

Pulmonary arterial remodeling is a presently irreversible pathologic hallmark of pulmonary arterial hypertension (PAH). This complex disease involves pathogenic dysregulation of all cell types within the small pulmonary arteries contributing to vascular remodeling leading to intimal lesions, resulting in elevated pulmonary vascular resistance and right heart dysfunction. Mutations within the bone morphogenetic protein receptor 2 gene, leading to dysregulated proliferation of pulmonary artery smooth muscle cells, have been identified as being responsible for heritable PAH. Indeed, the disease is characterized by excessive cellular proliferation and resistance to apoptosis of smooth muscle and endothelial cells. Significant gene dysregulation at the transcriptional and signaling level has been identified. MicroRNAs are small non-coding RNA molecules that negatively regulate gene expression and have the ability to target numerous genes, therefore potentially controlling a host of gene regulatory and signaling pathways. The major role of miRNAs in pulmonary arterial remodeling is still relatively unknown although research data is emerging apace. Modulation of miRNAs represents a possible therapeutic target for altering the remodeling phenotype in the pulmonary vasculature. This review will focus on the role of miRNAs in regulating smooth muscle and endothelial cell phenotypes and their influence on pulmonary remodeling in the setting of PAH

Expression of Fraser syndrome genes in normal and polycystic murine kidneys

BACKGROUND: Fraser syndrome (FS) features renal agenesis and cystic kidneys. Mutations of FRAS1 (Fraser syndrome 1)and FREM2 (FRAS1-related extracellular matrix protein 2)cause FS. They code for basement membrane proteins expressed in metanephric epithelia where they mediate epithelial/mesenchymal signalling. Little is known about whether and where these molecules are expressed in more mature kidneys. METHODS: In healthy and congenital polycystic kidney (cpk)mouse kidneys we sought Frem2 expression using a LacZ reporter gene and quantified Fras family transcripts. Fras1 immunohistochemistry was undertaken in cystic kidneys from cpk mice and PCK (Pkhd1 mutant) rats (models of autosomal recessive polycystic kidney disease) and in wildtype metanephroi rendered cystic by dexamethasone. RESULTS: Nascent nephrons transiently expressed Frem2 in both tubule and podocyte epithelia. Maturing and adult collecting ducts also expressed Frem2. Frem2 was expressed in cpk cystic epithelia although Frem2 haploinsufficiency did not significantly modify cystogenesis in vivo. Fras1 transcripts were significantly upregulated, and Frem3 downregulated, in polycystic kidneys versus the non-cystic kidneys of littermates. Fras1 was immunodetected in cpk, PCK and dexamethasone-induced cystepithelia. CONCLUSIONS: These descriptive results are consistent with the hypothesis that Fras family molecules play diverse roles in kidney epithelia. In future, this should be tested by conditional deletion of FS genes in nephron segments and collecting ducts