People-Specific Languages: a case for automated programming language generation by reverse-engineering programmer minds

The innovation of DSLs was the recognition that each application domain has its few idiomatic patterns of language use, found often in that domain and rarely in others. Capturing these idioms in the language design makes a DSL and yields gains in productivity, reliability and maintainability. Similarly, different groups of programmers have different predominant cognitive quirks. In this article I argue that programmers are attracted to some types of languages that resonate with their quirks and reluctant to use others that grate against them. Hence the question: could we tailor or evolve programming languages to the particular personality of their users? Due to the sheer diversity of personality types, any answer should be combined with automated language generation. The potential benefits include a leap in productivity and more social diversity in software engineering workplaces. The main pitfall is the risk of introducing new language barriers between people and decreased code reuse. However this may be avoidable by combining automated language generation with shared fundamental semantic building blocks

Heart Failure and Design of Potentially Therapeutic Mutants Relieving SERCA Inhibition: Expression and Analysis of Phospholamban Mutants

The CDC identifies heart disease as the leading cause of death in the U.S., and current treatments have variable success. Gene therapy is being investigated as an additional treatment option for heart disease. Various targets impacting calcium ion cycling and by consequence, cardiac contractility, are being studied as options for gene therapy. One molecular target in particular is the protein phospholamban (PLN), which is a small, hydrophobic protein located in the sarcoplasmic reticulum membrane of cardiac muscle, that has been linked to heart failure. Here, four PLN mutants were rationally designed, aiming for optimizing therapeutic potential. These mutants were analyzed using bioinformatics databases, and two of the mutants were successfully cloned, expressed, and purified. Results suggested these two mutants, R14E and Q26E, are predicted to fit the criteria for PLN therapeutic mutant design that were assessed. PLN mutants R14E and Q26E appear promising and further assessment of the impact and interaction of these mutants could offer insight into PLN’s role in heart failure, as well as provide potential targets for gene therapy

MGSim - Simulation tools for multi-core processor architectures

MGSim is an open source discrete event simulator for on-chip hardware components, developed at the University of Amsterdam. It is intended to be a research and teaching vehicle to study the fine-grained hardware/software interactions on many-core and hardware multithreaded processors. It includes support for core models with different instruction sets, a configurable multi-core interconnect, multiple configurable cache and memory models, a dedicated I/O subsystem, and comprehensive monitoring and interaction facilities. The default model configuration shipped with MGSim implements Microgrids, a many-core architecture with hardware concurrency management. MGSim is furthermore written mostly in C++ and uses object classes to represent chip components. It is optimized for architecture models that can be described as process networks.Comment: 33 pages, 22 figures, 4 listings, 2 table

Reiterative roles for FGF signaling in the establishment of size and proportion of the zebrafish heart

AbstractDevelopment of a functional organ requires the establishment of its proper size as well as the establishment of the relative proportions of its individual components. In the zebrafish heart, organ size and proportion depend heavily on the number of cells in each of its two major chambers, the ventricle and the atrium. Heart size and chamber proportionality are both affected in zebrafish fgf8 mutants. To determine when and how FGF signaling influences these characteristics, we examined the effect of temporally controlled pathway inhibition. During cardiac specification, reduction of FGF signaling inhibits formation of both ventricular and atrial cardiomyocytes, with a stronger impact on ventricular cells. After cardiomyocyte differentiation begins, reduction of FGF signaling can still result in a deficiency of ventricular cardiomyocytes. Consistent with two temporally distinct roles for FGF, we find that increased FGF signaling induces a cardiomyocyte surplus only before cardiac differentiation begins. Thus, FGF signaling first regulates heart size and chamber proportionality during cardiac specification and later refines ventricular proportion by regulating cell number after the onset of differentiation. Together, our data demonstrate that a single signaling pathway can act reiteratively to coordinate organ size and proportion