Analyzing PL/1 Legacy Ecosystems: An Experience Report

This paper presents a case study of analyzing a legacy PL/1 ecosystem that has grown for 40 years to support the business needs of a large banking company. In order to support the stakeholders in analyzing it we developed St1-PL/1 — a tool that parses the code for association data and computes structural metrics which it then visualizes using top-down interactive exploration. Before building the tool and after demonstrating it to stakeholders we conducted several interviews to learn about legacy ecosystem analysis requirements. We briefly introduce the tool and then present results of analysing the case study. We show that although the vision for the future is to have an ecosystem architecture in which systems are as decoupled as possible the current state of the ecosystem is still removed from this. We also present some of the lessons learned during our experience discussions with stakeholders which include their interests in automatically assessing the quality of the legacy code.

Analyzing the Role of αvβ8 Integrin in Glioma-Induced Angiogenesis

In this study we aimed to determine the functional roles for αvβ8 integrin in astrocytoma-induced angiogenesis. These studies originate from our analyses of αvβ8 integrin in developmental brain angiogenesis. αv and β8 knockout (KO) mice develop brain-specific vascular phenotypes that resemble vascular pathologies observed in the malignant astrocytoma, glioblastoma multiforme (GBM). Indeed, a murine xenograft model of astrocytoma suggested a role for the integrin in glioma-induced angiogenesis. Primary mouse astroglia were cultured from wild type (WT) and β8 KO neonates and were immortalized (HPV:E6/E7) and transformed (HRas:G12V). WT and β8 KO transformed astroglia were intracranially injected into athymic mice. WT tumors displayed pathological features of grade III astrocytomas, whereas β8 KO tumors resembled grade IV GBMs. KO tumors contained widespread edema and hemorrhage as well as pathological angiogenesis, as assessed by quantitation of microvascular density and blood vessel morphology. Additionally, exogenous expression of β8 integrin in β8 KO transformed astroglia resolved the pathologies observed in KO tumors giving further credence to the idea that loss of αvβ8 integrin expression correlates with tumorigenic potential of oncogene-transformed astroglia. To compliment our mouse model, several established human glioma cell lines were characterized for expression of αvβ8 integrin protein. Some of the cell lines displayed low expression of αvβ8 integrin, whereas others showed high levels, as compared to non-malignant human astrocytes. Intracranial implantation of high and low β8 integrin-expressing human glioma cell lines resulted in tumors exhibiting similar phenotypes to those observed in the mouse model; low expressers were marked by vascular pathologies indicative of β8 KO mouse tumors. Upon overexpression of β8 integrin in a low β8 integrin-expressing human glioma cell line, angiogenic pathologies were largely resolved. Moreover, intracranially injected αvHI- and αvLO-sorted GBM stem cells (GSCs) resulted in significantly different tumor sizes, where those GSCs endogenously expressing low levels of αv integrin formed two to three fold larger tumors. Furthermore, lentiviral knockdown of β8 integrin in transformed human astrocytes formed tumors that strikingly recapitulated the characteristics of the murine β8-/- tumors, exhibiting a significant increase in microvascular density leading to decreased overall survival. A paracrine mechanism was discovered involving endothelial cell homeostatic control governed by canonical TGFβ signaling initiated by αvβ8 integrin’s role in the latent cytokine’s activation. Diminished TGFβ signaling in tumor-associated endothelial cells promoted increased angiogenesis and decreased overall survival as a result of αvβ8 integrin’s loss on the tumor cell. Collectively, these data suggest an important functional role for αvβ8 integrin in glioma angiogenesis.

Analyzing diffuse scattering with supercomputers

Two new approaches to quantitatively analyze diffuse diffraction intensities from faulted layer stacking are reported. The parameters of a probability-based growth model are determined with two iterative global optimization methods: a genetic algorithm (GA) and particle swarm optimization (PSO). The results are compared with those from a third global optimization method, a differential evolution (DE) algorithm [Storn & Price (1997). J. Global Optim. 11, 341–359]. The algorithm efficiencies in the early and late stages of iteration are compared. The accuracy of the optimized parameters improves with increasing size of the simulated crystal volume. The wall clock time for computing quite large crystal volumes can be kept within reasonable limits by the parallel calculation of many crystals (clones) generated for each model parameter set on a super- or grid computer. The faulted layer stacking in single crystals of trigonal three-pointedstar- shaped tris(bicylco[2.1.1]hexeno)benzene molecules serves as an example for the numerical computations. Based on numerical values of seven model parameters (reference parameters), nearly noise-free reference intensities of 14 diffuse streaks were simulated from 1280 clones, each consisting of 96 000 layers (reference crystal). The parameters derived from the reference intensities with GA, PSO and DE were compared with the original reference parameters as a function of the simulated total crystal volume. The statistical distribution of structural motifs in the simulated crystals is in good agreement with that in the reference crystal. The results found with the growth model for layer stacking disorder are applicable to other disorder types and modeling techniques, Monte Carlo in particular.

How do sport clubs recruit volunteers? Analyzing and developing a typology of decision-making processes on recruiting volunteers in sport clubs.

Effective strategies for recruiting volunteers who are prepared to make a long-term commitment to formal positions are essential for the survival of voluntary sport clubs. This article examines the decision-making processes in relation to these efforts. Under the assumption of bounded rationality, the garbage can model is used to grasp these decision-making processes theoretically and access them empirically. Based on case study framework an in-depth analysis of recruitment practices was conducted in nine selected sport clubs. Results showed that the decision-making processes are generally characterized by a reactive approach in which dominant actors try to handle personnel problems of recruitment in the administration and sport domains through routine formal committee work and informal networks. In addition, it proved possible to develop a typology that deliver an overview of different decision-making practices in terms of the specific interplay of the relevant components of process control (top-down vs. bottom-up) and problem processing (situational vs. systematic).

Pangea: A Workbench for Statically Analyzing Multi-Language Software Corpora

Software corpora facilitate reproducibility of analyses, however, static analysis for an entire corpus still requires considerable effort, often duplicated unnecessarily by multiple users. Moreover, most corpora are designed for single languages increasing the effort for cross-language analysis. To address these aspects we propose Pangea, an infrastructure allowing fast development of static analyses on multi-language corpora. Pangea uses language-independent meta-models stored as object model snapshots that can be directly loaded into memory and queried without any parsing overhead. To reduce the effort of performing static analyses, Pangea provides out-of-the box support for: creating and refining analyses in a dedicated environment, deploying an analysis on an entire corpus, using a runner that supports parallel execution, and exporting results in various formats. In this tool demonstration we introduce Pangea and provide several usage scenarios that illustrate how it reduces the cost of analysis.

Familial aggregation, candidate genes and genome scans: Analyzing the role of genetics in stroke

The genetic etiology of stroke likely reflects the influence of multiple loci with small effects, each modulating different pathophysiological processes. This research project utilized three analytical strategies to address the paucity of information related to the identification and characterization of genetic variation associated with stroke in the general population. ^ First, the general contribution of familial factors to stroke susceptibility was evaluated in a population-based sample of unrelated individuals. Increased risk of subclinical cerebral infarction was observed among individuals with a positive parental history of stroke. This association did not appear to be mediated by established stroke risk factors, specifically blood pressure levels or hypertension status. ^ The need to identify specific gene variation associated with stroke in the general population was addressed by evaluating seven candidate gene polymorphisms in a population-based sample of unrelated individuals. Three polymorphisms were significantly associated with increased subclinical cerebral infarction or incident clinical ischemic stroke risk. These relationships include the G-protein β3 subunit 825C/T polymorphism and clinical stroke in Whites, the lipoprotein lipase S/X447 polymorphism and subclinical and clinical stroke in men, and the angiotensin I-converting enzyme Ins/Del polymorphism and subclinical stroke in White men. These associations did not appear to be obfuscated by the stroke risk factors adjusted for in the analysis models specifically blood pressure levels or anti-hypertensive medication use. ^ The final research strategy considered, on a genome-wide scale, the idea that genetic variation may contribute to the occurrence of hypertension or stroke through a common etiologic pathway. Genomic regions were identified for which significant evidence of heterogeneity was observed among hypertensive sibpairs stratified by family history of stroke information. Regions identified on chromosome 15 in African Americans, and chromosome 13 in Whites and African Americans, suggest the presence of genes influencing hypertension and stroke susceptibility. ^ Insight into the role of genetics in stroke is useful for the potential early identification of individuals at increased risk for stroke and improved understanding of the etiology of the disease. The ultimate goal of these endeavors is to guide the development of therapeutic intervention and informed prevention to provide a lasting and positive impact on public health. ^

Forecasting and Analyzing Economic Activity with Coincident and Leading Indexes: The Case of Connecticut

We develop coincident and leading employment indexes for the Connecticut economy. Four employment-related variables enter the coincident index while five employment-related variables enter the leading index. The peaks and troughs in the leading index lead the peaks and troughs in the coincident index by an average of 3 and 9 months. Finally, we use the leading index in vector-autoregressive (VAR) and Bayesian vector-autoregressive (BVAR) models to forecast the coincident index, nonfarm employment, and the unemployment rate.

Analyzing the function of myogenin in adult satellite cells through the construction of a myogenin conditional allele

Although mechanisms regulating the formation of embryonic skeletal muscle are well characterized, less is known about muscle formation in postnatal life. This disparity is unfortunate because the largest increases in skeletal muscle mass occur after birth. Adult muscle stem cells (satellite cells) appear to recapitulate the events that occur in embryonic myoblasts. In particular, the myogenic basic helix-loop-helix factors, which have crucial functions in embryonic muscle development, are assumed to have similar roles in postnatal muscle formation. Here, I test this assumption by determining the role of the myogenic regulator myogenin in postnatal life. Myogenin-null mice die at birth, necessitating the generation of floxed alleles of myogenin and the use of cre-recombinase lines to delete myogenin. Removing myogenin before embryonic muscle development resulted in myofiber deficiencies identical to those observed in myogenin-null mice. However, mice in which myogenin was deleted following embryonic muscle development had normal skeletal muscle, except for modest alterations in MRF4 and MyoD expression. Notably, myogenin-deleted mice were 30% smaller than controls, suggesting that myogenin's absence disrupted general body growth. These results suggest that skeletal muscle growth in postnatal life is controlled by mechanisms distinct from those occurring in embryonic muscle development. ^

Analyzing the effectiveness of Kinderworld's food program on lowering & controlling childhood obesity

This is an analysis of previously collected data at Kinderworld Child Care and Early Learning Center, as part of an evaluation done to determine the program's effectiveness in reducing/controlling childhood obesity. Kinderworld is a private, for-profit organization that provides healthy, nutritious meals and snacks to children under the guidelines of the Child and Adult Care Food Program, and is reimbursed by the Texas Department of Agriculture on a fixed price-per-meal basis. The primary goal of the program is to reduce childhood obesity. Previous studies have shown a link between obesity and diet. Other, similar programs have shown success in reducing obesity among children with a healthy diet and exercise. The results from the outcome evaluation indicated that time spent in the center was positively related to higher proportions of healthy-weight children, and inversely related to BMI levels. ^