437 research outputs found
Despite the Place, Canāt Escape Gender and Race: Black Womenās Faculty Experiences at PWIs and HBCUs
RacerD: compositional static race detection
Automatic static detection of data races is one of the most basic problems in reasoning about concurrency. We present RacerDāa static program analysis for detecting data races in Java programs which is fast, can scale to large code, and has proven effective in an industrial software engineering scenario. To our knowledge, RacerD is the first inter-procedural, compositional data race detector which has been empirically shown to have non-trivial precision and impact. Due to its compositionality, it can analyze code changes quickly, and this allows it to perform continuous reasoning about a large, rapidly changing codebase as part of deployment within a continuous integration ecosystem. In contrast to previous static race detectors, its design favors reporting high-confidence bugs over ensuring their absence. RacerD has been in deployment for over a year at Facebook, where it has flagged over 2500 issues that have been fixed by developers before reaching production. It has been important in enabling the development of new code as well as fixing old code: it helped support the conversion of part of the main Facebook Android app from a single-threaded to a multi-threaded architecture. In this paper we describe RacerDās design, implementation, deployment and impact
Alternative mechanisms of structuring biomembranes: Self-assembly vs. self-organization
We study two mechanisms for the formation of protein patterns near membranes
of living cells by mathematical modelling. Self-assembly of protein domains by
electrostatic lipid-protein interactions is contrasted with self-organization
due to a nonequilibrium biochemical reaction cycle of proteins near the
membrane. While both processes lead eventually to quite similar patterns, their
evolution occurs on very different length and time scales. Self-assembly
produces periodic protein patterns on a spatial scale below 0.1 micron in a few
seconds followed by extremely slow coarsening, whereas self-organization
results in a pattern wavelength comparable to the typical cell size of 100
micron within a few minutes suggesting different biological functions for the
two processes.Comment: 4 pages, 5 figure
Factors regulating amino acid release from extrasplanchnic tissues in the rat. Interactions of alanine and glutamine
The effects of inhibition of gluconeogenesis on ketogenesis in starved and diabetic rats
Insulin and growth factors stimulate the phosphorylation of a Mr-22000 protein in 3T3-L1 adipocytes
SmartTrack: Efficient Predictive Race Detection
Widely used data race detectors, including the state-of-the-art FastTrack
algorithm, incur performance costs that are acceptable for regular in-house
testing, but miss races detectable from the analyzed execution. Predictive
analyses detect more data races in an analyzed execution than FastTrack
detects, but at significantly higher performance cost.
This paper presents SmartTrack, an algorithm that optimizes predictive race
detection analyses, including two analyses from prior work and a new analysis
introduced in this paper. SmartTrack's algorithm incorporates two main
optimizations: (1) epoch and ownership optimizations from prior work, applied
to predictive analysis for the first time; and (2) novel conflicting critical
section optimizations introduced by this paper. Our evaluation shows that
SmartTrack achieves performance competitive with FastTrack-a qualitative
improvement in the state of the art for data race detection.Comment: Extended arXiv version of PLDI 2020 paper (adds Appendices A-E) #228
SmartTrack: Efficient Predictive Race Detectio
Algorithms for optimizing drug therapy
BACKGROUND: Drug therapy has become increasingly efficient, with more drugs available for treatment of an ever-growing number of conditions. Yet, drug use is reported to be sub optimal in several aspects, such as dosage, patient's adherence and outcome of therapy. The aim of the current study was to investigate the possibility to optimize drug therapy using computer programs, available on the Internet. METHODS: One hundred and ten officially endorsed text documents, published between 1996 and 2004, containing guidelines for drug therapy in 246 disorders, were analyzed with regard to information about patient-, disease- and drug-related factors and relationships between these factors. This information was used to construct algorithms for identifying optimum treatment in each of the studied disorders. These algorithms were categorized in order to define as few models as possible that still could accommodate the identified factors and the relationships between them. The resulting program prototypes were implemented in HTML (user interface) and JavaScript (program logic). RESULTS: Three types of algorithms were sufficient for the intended purpose. The simplest type is a list of factors, each of which implies that the particular patient should or should not receive treatment. This is adequate in situations where only one treatment exists. The second type, a more elaborate model, is required when treatment can by provided using drugs from different pharmacological classes and the selection of drug class is dependent on patient characteristics. An easily implemented set of if-then statements was able to manage the identified information in such instances. The third type was needed in the few situations where the selection and dosage of drugs were depending on the degree to which one or more patient-specific factors were present. In these cases the implementation of an established decision model based on fuzzy sets was required. Computer programs based on one of these three models could be constructed regarding all but one of the studied disorders. The single exception was depression, where reliable relationships between patient characteristics, drug classes and outcome of therapy remain to be defined. CONCLUSION: Algorithms for optimizing drug therapy can, with presumably rare exceptions, be developed for any disorder, using standard Internet programming methods
The Transcription Factor Rfx3 Regulates Ī²-Cell Differentiation, Function, and Glucokinase Expression
OBJECTIVE: Pancreatic islets of perinatal mice lacking the transcription factor Rfx3 exhibit a marked reduction in insulin-producing beta-cells. The objective of this work was to unravel the cellular and molecular mechanisms underlying this deficiency. RESEARCH DESIGN AND METHODS: Immunofluorescence studies and quantitative RT-PCR experiments were used to study the emergence of insulin-positive cells, the expression of transcription factors implicated in the differentiation of beta-cells from endocrine progenitors, and the expression of mature beta-cell markers during development in Rfx3(-/-) and pancreas-specific Rfx3-knockout mice. RNA interference experiments were performed to document the consequences of downregulating Rfx3 expression in Min6 beta-cells. Quantitative chromatin immunoprecipitation (ChIP), ChIP sequencing, and bandshift experiments were used to identify Rfx3 target genes. RESULTS: Reduced development of insulin-positive cells in Rfx3(-/-) mice was not due to deficiencies in endocrine progenitors or beta-lineage specification, but reflected the accumulation of insulin-positive beta-cell precursors and defective beta-cells exhibiting reduced insulin, Glut-2, and Gck expression. Similar incompletely differentiated beta-cells developed in pancreas-specific Rfx3-deficient embryos. Defective beta-cells lacking Glut-2 and Gck expression dominate in Rfx3-deficent adults, leading to glucose intolerance. Attenuated Glut-2 and glucokinase expression, and impaired glucose-stimulated insulin secretion, were also induced by RNA interference-mediated inhibition of Rfx3 expression in Min6 cells. Finally, Rfx3 was found to bind in Min6 cells and human islets to two well-known regulatory sequences, Pal-1 and Pal-2, in the neuroendocrine promoter of the glucokinase gene. CONCLUSIONS: Our results show that Rfx3 is required for the differentiation and function of mature beta-cells and regulates the beta-cell promoter of the glucokinase gene
- ā¦