High Frequency Trading in Financial Markets

Financial markets have undergone tremendous changes in the last decades. Next to the automation of the trading process and the improvement in market quality, High Frequency Trading (HFT) plays a major role in financial markets. This thesis provides a background on the evolution of financial markets and the role of HFT in price discovery and the nature of its interaction with human traders

Humans versus Agents: Competition in Financial Markets of the 21st Century

Information systems have revolutionized the nature of markets. Traditionally, markets inherently comprised the strategic interaction of human traders only. Nowadays, however, automated trading agents are responsible for at least 60% of the US trading volume on financial stock markets. In this respect, financial markets of the 21st century are different to markets of previous centuries. Fuelled by discussions on their possible risks, there is a need for research on the effects of automated trading agents on market efficiency and on human traders. In order to systematically investigate these issues, we introduce a market framework for human-computer interaction. This framework is then applied in a case study on a financial market scenario. In particular, we plan to conduct a NeuroIS experiment in which we analyze overall market efficiency as well as the trading behavior and emotional responses of human traders when they interact with computerized trading agents

Integrated care for people with long-term mental and physical conditions in low- and middle-income countries: narrative review

Integrated care is defined as health services that are managed and delivered so that people receive a continuum of health promotion, disease prevention, diagnosis, treatment, disease-management, rehabilitation and palliative care services, coordinated across the different levels and sites of care within and beyond the health sector and, according to their needs, throughout the life course. This narrative review paper aims to describe the most relevant concepts and models of integrated care for people with chronic (or recurring) mental illness and comorbid physical health conditions, to assess the strength of evidence base for these models in high income countries (HICs) and in low- and middle-income countries (LMICs) through a conceptual overview and a structured narrative review, and to identify opportunities to further test the feasibility and impact of such integrated care models. The results of the review are presented in terms of; (i) the rationale for integrating care for people with mental disorders into chronic care; (ii) models of integrated care; (iii) evidence of the effects of integrating care in HICs and in LMICs; (iv) the key organisational challenges in LMICs to implement integrated chronic care; and (v) practical steps to realise a vision of integrated care in the future

What Ukraine Taught NATO about Hybrid Warfare

Russia’s invasion of Ukraine in 2022 forced the United States and its NATO partners to be confronted with the impact of hybrid warfare far beyond the battlefield. Targeting Europe’s energy security, Russia’s malign influence campaigns and malicious cyber intrusions are affecting global gas prices, driving up food costs, disrupting supply chains and grids, and testing US and Allied military mobility. This study examines how hybrid warfare is being used by NATO’s adversaries, what vulnerabilities in energy security exist across the Alliance, and what mitigation strategies are available to the member states. Cyberattacks targeting the renewable energy landscape during Europe’s green transition are increasing, making it urgent that new tools are developed to protect these emerging technologies. No less significant are the cyber and information operations targeting energy security in Eastern Europe as it seeks to become independent from Russia. Economic coercion is being used against Western and Central Europe to stop gas from flowing. China’s malign investments in Southern and Mediterranean Europe are enabling Beijing to control several NATO member states’ critical energy infrastructure at a critical moment in the global balance of power. What Ukraine Taught NATO about Hybrid Warfare will be an important reference for NATO officials and US installations operating in the European theater.https://press.armywarcollege.edu/monographs/1952/thumbnail.jp

Gain and loss of function variants in EZH1 disrupt neurogenesis and cause dominant and recessive neurodevelopmental disorders.

Genetic variants in chromatin regulators are frequently found in neurodevelopmental disorders, but their effect in disease etiology is rarely determined. Here, we uncover and functionally define pathogenic variants in the chromatin modifier EZH1 as the cause of dominant and recessive neurodevelopmental disorders in 19 individuals. EZH1 encodes one of the two alternative histone H3 lysine 27 methyltransferases of the PRC2 complex. Unlike the other PRC2 subunits, which are involved in cancers and developmental syndromes, the implication of EZH1 in human development and disease is largely unknown. Using cellular and biochemical studies, we demonstrate that recessive variants impair EZH1 expression causing loss of function effects, while dominant variants are missense mutations that affect evolutionarily conserved aminoacids, likely impacting EZH1 structure or function. Accordingly, we found increased methyltransferase activity leading to gain of function of two EZH1 missense variants. Furthermore, we show that EZH1 is necessary and sufficient for differentiation of neural progenitor cells in the developing chick embryo neural tube. Finally, using human pluripotent stem cell-derived neural cultures and forebrain organoids, we demonstrate that EZH1 variants perturb cortical neuron differentiation. Overall, our work reveals a critical role of EZH1 in neurogenesis regulation and provides molecular diagnosis for previously undefined neurodevelopmental disorders

Gain and loss of function variants in EZH1 disrupt neurogenesis and cause dominant and recessive neurodevelopmental disorders

Genetic variants in chromatin regulators are frequently found in neurodevelopmental disorders, but their effect in disease etiology is rarely determined. Here, we uncover and functionally define pathogenic variants in the chromatin modifier EZH1 as the cause of dominant and recessive neurodevelopmental disorders in 19 individuals. EZH1 encodes one of the two alternative histone H3 lysine 27 methyltransferases of the PRC2 complex. Unlike the other PRC2 subunits, which are involved in cancers and developmental syndromes, the implication of EZH1 in human development and disease is largely unknown. Using cellular and biochemical studies, we demonstrate that recessive variants impair EZH1 expression causing loss of function effects, while dominant variants are missense mutations that affect evolutionarily conserved aminoacids, likely impacting EZH1 structure or function. Accordingly, we found increased methyltransferase activity leading to gain of function of two EZH1 missense variants. Furthermore, we show that EZH1 is necessary and sufficient for differentiation of neural progenitor cells in the developing chick embryo neural tube. Finally, using human pluripotent stem cell-derived neural cultures and forebrain organoids, we demonstrate that EZH1 variants perturb cortical neuron differentiation. Overall, our work reveals a critical role of EZH1 in neurogenesis regulation and provides molecular diagnosis for previously undefined neurodevelopmental disorders

Novel Common Genetic Susceptibility Loci for Colorectal Cancer

BACKGROUND: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk. METHODS: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided. RESULTS: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0. CONCLUSIONS: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screenin