Idiosyncratic Risk and Short Interest Analysis for Canadian Large Cap Stocks

While previous studies have focused on the relation between idiosyncratic risk and short interest in US stock markets, we test whether the Canadian market shows the same symptoms in costs limiting arbitrage. In order to measure arbitrage cost, we use idiosyncratic risk and use it as a proxy to determine the cost level. To prevent any ambiguity and bias in our result, we use commonly recognized indexes to measure both transaction and holding costs. Consistent with the similar study conducted in U.S., we find that high Short Interest Canadian stocks appear to have higher idiosyncratic risk that is significant enough to affect investors’ decisions

Defining functional classes of Barth syndrome mutation in humans

The X-linked disease Barth syndrome (BTHS) is caused by mutations in TAZ; TAZ is the main determinant of the final acyl chain composition of the mitochondrial-specific phospholipid, cardiolipin. To date, a detailed characterization of endogenous TAZ has only been performed in yeast. Further, why a given BTHS-associated missense mutation impairs TAZ function has only been determined in a yeast model of this human disease. Presently, the detailed characterization of yeast tafazzin harboring individual BTHS mutations at evolutionarily conserved residues has identified seven distinct loss-of-function mechanisms caused by patient-associated missense alleles. However, whether the biochemical consequences associated with individual mutations also occur in the context of human TAZ in a validated mammalian model has not been demonstrated. Here, utilizing newly established monoclonal antibodies capable of detecting endogenous TAZ, we demonstrate that mammalian TAZ, like its yeast counterpart, is localized to the mitochondrion where it adopts an extremely protease-resistant fold, associates non-integrally with intermembrane space-facing membranes and assembles in a range of complexes. Even though multiple isoforms are expressed at the mRNA level, only a single polypeptide that co-migrates with the human isoform lacking exon 5 is expressed in human skin fibroblasts, HEK293 cells, and murine heart and liver mitochondria. Finally, using a new genome-edited mammalian BTHS cell culture model, we demonstrate that the loss-of-function mechanisms for two BTHS alleles that represent two of the seven functional classes of BTHS mutation as originally defined in yeast, are the same when modeled in human TAZ

The Maker\u27s CubeSat: Increasing Student-lab Capabilities in the Design, Integration & Test of the Alpha CubeSat

Alpha is a 1U CubeSat developed at Cornell University that deploys a ChipSat-equipped free-flying light sail into LEO. While the payload is rather unique, the spacecraft that deploys it is designed to be adaptable and scalable to future student-led missions. Technology demonstrations include a 3D-printed chassis, entirely commercial off-the-shelf (COTS) electronics, an Iridium modem that bypasses the need for ground-station hardware, and magnetorquer-only spin-stabilization and pointing. This paper details the driving factors behind Alpha’s novel architecture with a focus on the affordable methods developed for design verification and optimization. Drawing inspiration from the maker community, the lab acquired a suite of tools that dramatically increased in-house integration and test capabilities. Lessons are shared from training multiple generations of students on these tools, along with the best-practices developed for student assembly of flight hardware

Non-linear PID predictive controller

A new class of nonlinear PID controllers are derived for nonlinear systems using a Nonlinear Generalised Predictive Control (NGPC) approach. First the disturbance decoupling ability of the nonlinear generalised predictive controller is discussed. For a nonlinear system where the disturbance cannot be decoupled, a nonlinear observer is designed to estimate the offset. By selecting the nonlinear gain function in the observer, it is shown that the closed-loop system under optimal generalised predictive control with the nonlinear observer is asymptotically stable. It is pointed out that this composite controller is equivalent to a nonlinear controller with integral action. As a special case, for a nonlinear system with a low relative degree, the proposed nonlinear controller reduces to a nonlinear PI or PID predictive controller, which consists of a nonlinear PI or PID controller and a prediction controller. The design method is illustrated by an example nonlinear mechanical system

Mechanisms of NOD-like Receptor-Associated Inflammasome Activation

A major function of a subfamily of NLR (nucleotide-binding domain, leucine rich repeat containing or NOD-like receptor) proteins is in inflammasome activation, which has been implicated in a multitude of disease models and human diseases. This work will highlight key progress in understanding the mechanisms which activates the best studied NLRs (NLRP3, NLRC4, NAIP and NLRP1) and in uncovering new inflammasome NLRs

Inflammasomes and Metabolic Disorders: Old Genes in Modern Diseases

Modern medical and hygienic practices have greatly improved human health and longevity; however, increased human lifespan occurs concomitantly with the emergence of metabolic and age-related diseases. Studies over the past decade have strongly linked host inflammatory responses to the etiology of several metabolic diseases including atherosclerosis, type 2 diabetes (T2D), obesity and gout. A common immunological factor to these diseases is the activation of the inflammasome and release of pro-inflammatory cytokines that promote disease progression. Here we review the molecular mechanism(s) of inflammasome activation in response to metabolic damage associated molecular patterns (DAMPs) and discuss potential targets for therapeutic intervention

Mechanisms of NOD-like Receptor-Associated Inflammasome Activation

A major function of a subfamily of NLR (nucleotide-binding domain, leucine rich repeat containing or NOD-like receptor) proteins is in inflammasome activation, which has been implicated in a multitude of disease models and human diseases. This work will highlight key progress in understanding the mechanisms which activates the best studied NLRs (NLRP3, NLRC4, NAIP and NLRP1) and in uncovering new inflammasome NLRs

The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

Inflammasome activation leads to caspase-1 activation, which causes the maturation cleavage of pro-IL-1β and pro-IL-18. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field

A role for the NLRP3 inflammasome in metabolic diseases—did Warburg miss inflammation?

The inflammasome is a protein complex that is comprised of an intracellular sensor that is typically an NLR protein, the pro-protein, procaspase-1 and adaptor molecule ASC. Inflammasome activation leads to caspase-1 maturation and the processing of its substrate, IL-1β and IL-18. Although initially the inflammasome was described as a complex that affects infection and inflammation, recent evidence suggests that inflammasome activation influences a host of metabolic disorders including atherosclerosis, type 2 diabetes, gout and obesity. Another aspect regarding inflammation in general and inflammasome in specific is that the activation process has a profound effect on aerobic glycolysis, or the Warburg effect. How the Warburg effect might be link to inflammation and inflammasome activation is a novel concept to contemplate