Causality in Quantiles and Dynamic Stock Return-Volume Relations

This paper investigates the causal relations between stock return and volume based on quantile regressions. We first define Granger non-causality in all quantiles and propose testing non-causality by a sup-Wald test. Such a test is consistent against any deviation from non-causality in distribution, as opposed to the existing tests that check only noncausality in certain moment. This test is readily extended to test non-causality in different quantile ranges, and the testing results enable us to identify the quantile range for which causality is relevant. In the empirical studies of 3 major stock market indices, we find that, while the conventional test suggests no causality in mean, there are strong evidences that lagged volume Granger causes return in all but some middle quantiles. In particular, the causal effects have opposite signs at lower and upper quantiles and are stronger at more extreme quantiles. These relations form (symmetric) V shapes across quantiles. They also show that the dispersion of the return distribution increases with volume so that volume has a positive effect on return volatility. It is also shown that the quantile causal effects of lagged return on volume are mainly negative.Granger non-causality in quantiles, quantile causal effect, quantile regression, return-volume relation, sup-Wald test

Potential roles of microRNAs and ROS in colorectal cancer: diagnostic biomarkers and therapeutic targets

As one of the most commonly diagnosed cancers worldwide, colorectal adenocarcinoma often occurs sporadically in individuals aged 50 or above and there is an increase among younger patients under 50. Routine screenings are recommended for this age group to improve early detection. The multifactorial etiology of colorectal cancer consists of both genetic and epigenetic factors. Recently, studies have shown that the development and progression of colorectal cancer can be attributed to aberrant expression of microRNA. Reactive oxygen species (ROS) that play a key role in cancer cell survival, can also lead to carcinogenesis and cancer exacerbations. Given the rapid accumulating knowledge in the field, an updated review regarding microRNA and ROS in colorectal cancer is necessary. An extensive literature search has been conducted in PubMed/Medline databases to review the roles of microRNAs and ROS in colorectal cancer. Unique microRNA expression in tumor tissue, peripheral blood, and fecal samples from patients with colorectal cancer is outlined. Therapeutic approaches focusing on microRNA and ROS in colorectal cancer treatment is also delineated. This review aims to summarize the newest knowledge on the pathogenesis of colorectal cancer in the hopes of discovering novel diagnostic biomarkers and therapeutic techniques

Continuing Use of SNS Games for the Growth of Social Network Services

By using Social Network Services (SNSs) as platforms, game developers have gathered a huge user base, and the entertainment these games provide has further enlarged the SNS user base. However, there are signs that this symbiotic growth is slowing down. We developed a model and tested 14 hypotheses. Our main findings are: Although SNSs are “social,” “social norms” do not have much impact on the intention to use the games continually. Although users generally are not addicted to SNS games, the creation of addiction is an effective way to achieve continuance

Cyclic deformation of FCC crystals

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1995.Includes bibliographical references (leaves 83-86).by Chuang-Chia Lin.M.S

Loss of vesicular dopamine release precedes tauopathy in degenerative dopaminergic neurons in a Drosophila model expressing human tau.

While a number of genome-wide association studies have identified microtubule-associated protein tau as a strong risk factor for Parkinson's disease (PD), little is known about the mechanism through which human tau can predispose an individual to this disease. Here, we demonstrate that expression of human wild-type tau is sufficient to disrupt the survival of dopaminergic neurons in a Drosophila model. Tau triggers a synaptic pathology visualized by vesicular monoamine transporter-pHGFP that precedes both the age-dependent formation of tau-containing neurofibrillary tangle-like pathology and the progressive loss of DA neurons, thereby recapitulating the pathological hallmarks of PD. Flies overexpressing tau also exhibit progressive impairments of both motor and learning behaviors. Surprisingly, contrary to common belief that hyperphosphorylated tau could aggravate toxicity, DA neuron degeneration is alleviated by expressing the modified, hyperphosphorylated tau(E14). Together, these results show that impairment of VMAT-containing synaptic vesicle, released to synapses before overt tauopathy may be the underlying mechanism of tau-associated PD and suggest that correction or prevention of this deficit may be appropriate targets for early therapeutic intervention

Submandibular Cavernous Hemangiomas with Multiple Phleboliths Masquerading as Sialolithiasis

Vasoformative tumors (almost exclusively hemangiomas) are the most common lesions of the major salivary glands during infancy and early childhood. They are more common in the parotid gland but are particularly rare in the submandibular gland. Changes in blood flow dynamics within hemangiomas result in thrombus formation and phleboliths. Hemangiomas of the salivary glands in adults are histologically unlike those in infants, the former being characteristically of the cavernous variant. Most cavernous hemangiomas require surgery since they do not show a tendency to regress. A case of an adult man with cavernous hemangioma affecting the submandibular salivary gland that clinically simulated sialolithiasis is presented to alert surgeons to the possibility of such a lesion. We describe the clinical course and review the literature

Control Design for Signal Transduction Networks

Signal transduction networks of biological systems are highly complex. How to mathematically describe a signal transduction network by systematic approaches to further develop an appropriate and effective control strategy is attractive to control engineers. In this paper, the synergism and saturation system (S-systems) representations are used to describe signal transduction networks and a control design idea is presented. For constructing mathematical models, a cascaded analysis model is first proposed. Dynamic analysis and controller design are simulated and verified

A Rough Penalty Genetic Algorithm for Multicast Routing in Mobile Ad Hoc Networks

Multicast routing is an effective way to transmit messages to multiple hosts in a network. However, it is vulnerable to intermittent connectivity property in mobile ad hoc network (MANET) especially for multimedia applications, which have some quality of service (QoS) requirements. The goal of QoS provisioning is to well organize network resources to satisfy the QoS requirement and achieve good network delivery services. However, there remains a challenge to provide QoS solutions and maintain end-to-end QoS with user mobility. In this paper, a novel penalty adjustment method based on the rough set theory is proposed to deal with path-delay constraints for multicast routing problems in MANETs. We formulate the problem as a constrained optimization problem, where the objective function is to minimize the total cost of the multicast tree subject to QoS constraints. The RPGA is evaluated on three multicast scenarios and compared with two state-of-the-art methods in terms of cost, success rate, and time complexity. The performance analyses show that this approach is a self-adaptive method for penalty adjustment. Remarkably, the method can address a variety of constrained multicast routing problems even though the initial routes do not satisfy all QoS requirements

CAPIH: A Web interface for comparative analyses and visualization of host-HIV protein-protein interactions

<p>Abstract</p> <p>Background</p> <p>The Human Immunodeficiency Virus type one (HIV-1) is the major causing pathogen of the Acquired Immune Deficiency Syndrome (AIDS). A large number of HIV-1-related studies are based on three non-human model animals: chimpanzee, rhesus macaque, and mouse. However, the differences in host-HIV-1 interactions between human and these model organisms have remained unexplored.</p> <p>Description</p> <p>Here we present CAPIH (Comparative Analysis of Protein Interactions for HIV-1), the first web-based interface to provide comparative information between human and the three model organisms in the context of host-HIV-1 protein interactions. CAPIH identifies genetic changes that occur in HIV-1-interacting host proteins. In a total of 1,370 orthologous protein sets, CAPIH identifies ~86,000 amino acid substitutions, ~21,000 insertions/deletions, and ~33,000 potential post-translational modifications that occur only in one of the four compared species. CAPIH also provides an interactive interface to display the host-HIV-1 protein interaction networks, the presence/absence of orthologous proteins in the model organisms in the networks, the genetic changes that occur in the protein nodes, and the functional domains and potential protein interaction hot sites that may be affected by the genetic changes. The CAPIH interface is freely accessible at <url>http://bioinfo-dbb.nhri.org.tw/capih</url>.</p> <p>Conclusion</p> <p>CAPIH exemplifies that large divergences exist in disease-associated proteins between human and the model animals. Since all of the newly developed medications must be tested in model animals before entering clinical trials, it is advisable that comparative analyses be performed to ensure proper translations of animal-based studies. In the case of AIDS, the host-HIV-1 protein interactions apparently have differed to a great extent among the compared species. An integrated protein network comparison among the four species will probably shed new lights on AIDS studies.</p

Urinary Macrophage Migration Inhibitory Factor Serves as a Potential Biomarker for Acute Kidney Injury in Patients with Acute Pyelonephritis

Conventional markers of kidney function that are familiar to clinicians, including the serum creatinine and blood urea nitrogen levels, are unable to reveal genuine injury to the kidney, and their use may delay treatment. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine, and the predictive role and pathogenic mechanism of MIF deregulation during kidney infections involving acute kidney injury (AKI) are not currently known. In this study, we showed that elevated urinary MIF levels accompanied the development of AKI during kidney infection in patients with acute pyelonephritis (APN). In addition to the MIF level, the urinary levels of interleukin (IL)-1β and kidney injury molecule (KIM)-1 were also upregulated and were positively correlated with the levels of urinary MIF. An elevated urinary MIF level, along with elevated IL-1β and KIM-1 levels, is speculated to be a potential biomarker for the presence of AKI in APN patients