Determinants of Income and Income Differentials between Blacks and Whites in the South

The problem with which this study is concerned is that of discrimination. Data from the United States Bureau of the Census is used to approach the problem through the concept of economic discrimination. This study has two purposes. First, it tests the hypothesis that blacks in the South have been subjected to significant economic discrimination, and, in turn, to give quantitative estimates of its magnitude if the hypothesis is accepted. The secondary purpose is to make a comparison of the relative importance of the independent variables for blacks and whites

Robustness against Power is PSPACE-complete

Power is a RISC architecture developed by IBM, Freescale, and several other companies and implemented in a series of POWER processors. The architecture features a relaxed memory model providing very weak guarantees with respect to the ordering and atomicity of memory accesses. Due to these weaknesses, some programs that are correct under sequential consistency (SC) show undesirable effects when run under Power. We call these programs not robust against the Power memory model. Formally, a program is robust if every computation under Power has the same data and control dependencies as some SC computation. Our contribution is a decision procedure for robustness of concurrent programs against the Power memory model. It is based on three ideas. First, we reformulate robustness in terms of the acyclicity of a happens-before relation. Second, we prove that among the computations with cyclic happens-before relation there is one in a certain normal form. Finally, we reduce the existence of such a normal-form computation to a language emptiness problem. Altogether, this yields a PSPACE algorithm for checking robustness against Power. We complement it by a matching lower bound to show PSPACE-completeness

AUTSEG: Automatic Test Set Generator for Embedded Reactive Systems

Part 2: Tools and FrameworksInternational audienceOne of the biggest challenges in hardware and software design is to ensure that a system is error-free. Small errors in reactive embedded systems can have disastrous and costly consequences for a project. Preventing such errors by identifying the most probable cases of erratic system behavior is quite challenging. In this paper, we introduce an automatic test set generator called AUTSEG. Its input is a generic model of the target system, generated using the synchronous approach. Our tool finds the optimal preconditions for restricting the state space of the model. It only works locally on significant subspaces. Our approach exhibits a simpler and efficient quasi-flattening algorithm than existing techniques and a useful compiled form to check security properties and reduce the combinatorial explosion problem of state space. To illustrate our approach, AUTSEG was applied to the case of a transportation contactless card

An empirical investigation into branch coverage for C programs using CUTE and AUSTIN

Automated test data generation has remained a topic of considerable interest for several decades because it lies at the heart of attempts to automate the process of Software Testing. This paper reports the results of an empirical study using the dynamic symbolic-execution tool. CUTE, and a search based tool, AUSTIN on five non-trivial open source applications. The aim is to provide practitioners with an assessment of what can be achieved by existing techniques with little or no specialist knowledge and to provide researchers with baseline data against which to measure subsequent work. To achieve this, each tool is applied 'as is', with neither additional tuning nor supporting harnesses and with no adjustments applied to the subject programs under test. The mere fact that these tools can be applied 'out of the box' in this manner reflects the growing maturity of Automated test data generation. However, as might be expected, the study reveals opportunities for improvement and suggests ways to hybridize these two approaches that have hitherto been developed entirely independently. (C) 2010 Elsevier Inc. All rights reserved

Locality and Singularity for Store-Atomic Memory Models

Robustness is a correctness notion for concurrent programs running under relaxed consistency models. The task is to check that the relaxed behavior coincides (up to traces) with sequential consistency (SC). Although computationally simple on paper (robustness has been shown to be PSPACE-complete for TSO, PGAS, and Power), building a practical robustness checker remains a challenge. The problem is that the various relaxations lead to a dramatic number of computations, only few of which violate robustness. In the present paper, we set out to reduce the search space for robustness checkers. We focus on store-atomic consistency models and establish two completeness results. The first result, called locality, states that a non-robust program always contains a violating computation where only one thread delays commands. The second result, called singularity, is even stronger but restricted to programs without lightweight fences. It states that there is a violating computation where a single store is delayed. As an application of the results, we derive a linear-size source-to-source translation of robustness to SC-reachability. It applies to general programs, regardless of the data domain and potentially with an unbounded number of threads and with unbounded buffers. We have implemented the translation and verified, for the first time, PGAS algorithms in a fully automated fashion. For TSO, our analysis outperforms existing tools

Fenofibrate Inhibits Cytochrome P450 Epoxygenase 2C Activity to Suppress Pathological Ocular Angiogenesis

Neovascular eye diseases including retinopathy of prematurity, diabetic retinopathy and age-related-macular-degeneration are major causes of blindness. Fenofibrate treatment in type 2 diabetes patients reduces progression of diabetic retinopathy independent of its peroxisome proliferator-activated receptor (PPAR)α agonist lipid lowering effect. The mechanism is unknown. Fenofibrate binds to and inhibits cytochrome P450 epoxygenase (CYP)2C with higher affinity than to PPARα. CYP2C metabolizes ω-3 long-chain polyunsaturated fatty acids (LCPUFAs). While ω-3 LCPUFA products from other metabolizing pathways decrease retinal and choroidal neovascularization, CYP2C products of both ω-3 and ω-6 LCPUFAs promote angiogenesis. We hypothesized that fenofibrate inhibits retinopathy by reducing CYP2C ω-3 LCPUFA (and ω-6 LCPUFA) pro-angiogenic metabolites. Fenofibrate reduced retinal and choroidal neovascularization in PPARα-/-mice and augmented ω-3 LCPUFA protection via CYP2C inhibition. Fenofibrate suppressed retinal and choroidal neovascularization in mice overexpressing human CYP2C8 in endothelial cells and reduced plasma levels of the pro-angiogenic ω-3 LCPUFA CYP2C8 product, 19,20-epoxydocosapentaenoic acid. 19,20-epoxydocosapentaenoic acid reversed fenofibrate-induced suppression of angiogenesis ex vivo and suppression of endothelial cell functions in vitro. In summary fenofibrate suppressed retinal and choroidal neovascularization via CYP2C inhibition as well as by acting as an agonist of PPARα. Fenofibrate augmented the overall protective effects of ω-3 LCPUFAs on neovascular eye diseases

Photoreceptor glucose metabolism determines normal retinal vascular growth

Abstract The neural cells and factors determining normal vascular growth are not well defined even though vision‐threatening neovessel growth, a major cause of blindness in retinopathy of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth. We here examined whether hyperglycemia and low adiponectin (APN) levels delayed normal retinal vascularization, driven primarily by dysregulated photoreceptor metabolism. In premature infants, low APN levels correlated with hyperglycemia and delayed retinal vascular formation. Experimentally in a neonatal mouse model of postnatal hyperglycemia modeling early ROP, hyperglycemia caused photoreceptor dysfunction and delayed neurovascular maturation associated with changes in the APN pathway; recombinant mouse APN or APN receptor agonist AdipoRon treatment normalized vascular growth. APN deficiency decreased retinal mitochondrial metabolic enzyme levels particularly in photoreceptors, suppressed retinal vascular development, and decreased photoreceptor platelet‐derived growth factor (Pdgfb). APN pathway activation reversed these effects. Blockade of mitochondrial respiration abolished AdipoRon‐induced Pdgfb increase in photoreceptors. Photoreceptor knockdown of Pdgfb delayed retinal vascular formation. Stimulation of the APN pathway might prevent hyperglycemia‐associated retinal abnormalities and suppress phase I ROP in premature infants

Retinal lipid and glucose metabolism dictates angiogenesis through the lipid sensor Ffar1

Tissues with high metabolic rates often use lipids, as well as glucose, for energy, conferring a survival advantage during feast and famine1. Current dogma suggests that high-energy–consuming photoreceptors depend on glucose2, 3. Here we show that the retina also uses fatty acid β-oxidation for energy. Moreover, we identify a lipid sensor, free fatty acid receptor 1 (Ffar1), that curbs glucose uptake when fatty acids are available. Very-low-density lipoprotein receptor (Vldlr), which is present in photoreceptors4 and is expressed in other tissues with a high metabolic rate, facilitates the uptake of triglyceride-derived fatty acid5, 6. In the retinas of Vldlr−/− mice with low fatty acid uptake6 but high circulating lipid levels, we found that Ffar1 suppresses expression of the glucose transporter Glut1. Impaired glucose entry into photoreceptors results in a dual (lipid and glucose) fuel shortage and a reduction in the levels of the Krebs cycle intermediate α-ketoglutarate (α-KG). Low α-KG levels promotes stabilization of hypoxia-induced factor 1a (Hif1a) and secretion of vascular endothelial growth factor A (Vegfa) by starved Vldlr−/− photoreceptors, leading to neovascularization. The aberrant vessels in the Vldlr−/− retinas, which invade normally avascular photoreceptors, are reminiscent of the vascular defects in retinal angiomatous proliferation, a subset of neovascular age-related macular degeneration (AMD)7, which is associated with high vitreous VEGFA levels in humans. Dysregulated lipid and glucose photoreceptor energy metabolism may therefore be a driving force in macular telangiectasia, neovascular AMD and other retinal diseases