An empirical study of software design practices

Software engineers have developed a large body of software design theory and folklore, much of which was never validated. The results of an empirical study of software design practices in one specific environment are presented. The practices examined affect module size, module strength, data coupling, descendant span, unreferenced variables, and software reuse. Measures characteristic of these practices were extracted from 887 FORTRAN modules developed for five flight dynamics software projects monitored by the Software Engineering Laboratory (SEL). The relationship of these measures to cost and fault rate was analyzed using a contingency table procedure. The results show that some recommended design practices, despite their intuitive appeal, are ineffective in this environment, whereas others are very effective

Designing with Ada for satellite simulation: A case study

A FORTRAN-operated and an Ada-oriented design for the same system are compared to learn whether an essentially different design was produced using Ada. The designs were produced by an experiment that involves the parallel development of software for a spacecraft dynamics simulator. Design differences are identified in the use of abstractions, system structure, and simulator operations. Although the designs were significantly different, this result may be influenced by some special characteristics discussed

Distributed top-k aggregation queries at large

Top-k query processing is a fundamental building block for efficient ranking in a large number of applications. Efficiency is a central issue, especially for distributed settings, when the data is spread across different nodes in a network. This paper introduces novel optimization methods for top-k aggregation queries in such distributed environments. The optimizations can be applied to all algorithms that fall into the frameworks of the prior TPUT and KLEE methods. The optimizations address three degrees of freedom: 1) hierarchically grouping input lists into top-k operator trees and optimizing the tree structure, 2) computing data-adaptive scan depths for different input sources, and 3) data-adaptive sampling of a small subset of input sources in scenarios with hundreds or thousands of query-relevant network nodes. All optimizations are based on a statistical cost model that utilizes local synopses, e.g., in the form of histograms, efficiently computed convolutions, and estimators based on order statistics. The paper presents comprehensive experiments, with three different real-life datasets and using the ns-2 network simulator for a packet-level simulation of a large Internet-style network

Direct Observation of Hyperfine Quenching of the (2)3p0 Level in Helium-Like Nickel

Journals published by the American Physical Society can be found at http://publish.aps.org/We report a clear demonstration of the effect of hyperfine quenching of a forbidden transition by direct comparison of the lifetimes of the 2 3P0 level in the heliumlike isotopes Ni-61(26+) and Ni-58(26+). We find the quenched lifetime of the 2 3P0 level in Ni-61(26+) to be 470(50) ps. From this we deduce the 2 3P0-2 3P1 energy splitting to be 2.33(15) eV. We also report a measurement of the lifetime of the 2 3P2 level in Ni-58(26+), which is found to be 70(3) ps

A mapping approach to synchronization in the "Zajfman trap": stability conditions and the synchronization mechanism

We present a two particle model to explain the mechanism that stabilizes a bunch of positively charged ions in an "ion trap resonator" [Pedersen etal, Phys. Rev. Lett. 87 (2001) 055001]. The model decomposes the motion of the two ions into two mappings for the free motion in different parts of the trap and one for a compressing momentum kick. The ions' interaction is modelled by a time delay, which then changes the balance between adjacent momentum kicks. Through these mappings we identify the microscopic process that is responsible for synchronization and give the conditions for that regime.Comment: 12 pages, 9 figures; submitted to Phys Rev

Prediction of relapse-free survival according to adjuvant chemotherapy and regulator of chromosome condensation 2 (RCC2) expression in colorectal cancer

Background There is a need for improved selection of patients for adjuvant chemotherapy after resection of non-metastatic colorectal cancer (CRC). Regulator of chromosome condensation 2 (RCC2) is a potential prognostic biomarker. We report on the establishment of a robust protocol for RCC2 expression analysis and prognostic tumour biomarker evaluation in patients who did and did not receive adjuvant chemotherapy. Materials and methods RCC2 was analysed in 2916 primary CRCs from the QUASAR2 randomised trial and two single-hospital Norwegian series. A new protocol using fluorescent antibody staining and digital image analysis was optimised. Biomarker value for 5-year relapse-free survival was analysed in relation to tumour stage, adjuvant chemotherapy and the molecular markers microsatellite instability, KRAS/BRAF(V600E)/TP53 mutations and CDX2 expression. Results Low RCC2 expression was scored in 41% of 2696 evaluable samples. Among patients with stage I-III CRC who had not received adjuvant chemotherapy, low RCC2 expression was an independent marker of inferior 5-year relapse-free survival in multivariable Cox models including clinicopathological factors and molecular markers (HR 1.45, 95% CI 1.09 to 1.94, p=0.012, N=521). RCC2 was not prognostic in patients who had received adjuvant chemotherapy, neither in QUASAR2 nor the pooled Norwegian series. The interaction between RCC2 and adjuvant chemotherapy for prediction of patient outcome was significant in stage III, and strongest among patients with microsatellite stable tumours (p(interaction)=0.028). Conclusions Low expression of RCC2 is a biomarker for poor prognosis in patients with stage I-III CRC and seems to be a predictive biomarker for effect of adjuvant chemotherapy.Peer reviewe

Electron-Transfer from H-2 and Ar to Stored Multiply Charged Argon Ions Produced by Synchrotron Radiation

Journals published by the American Physical Society can be found at http://publish.aps.org/The rate coefficients for electron transfer from Ar and H-2 to Ar(q+) ions (3 less-than-or-equal-to q less-than-or-equal-to 6) have been measured using an ion-storage technique in a Penning ion trap. The ions were produced in the trap by K-shell photoionization of Ar atoms, using broadband synchrotron x-ray radiation. K-electron removal resulted in vacancy cascading, yielding a distribution of argon-ion charge states peaked near Ar4+. The stored ion gas had an initial temperature near 480 K. The basic data determining the rate coefficients k(Ar(q+)) are the storage time constants of each charge state in the trap, in the presence of a measured pressure of target gas. The results of the measurements (in units of 10(-9) cm3 s-1) are k(Ar3+, H-2) = 4.3(0.7), k(Ar3+, Ar) = 1.6(0.2), k(Ar4+, H-2) = 5.2(0.6), k(Ar4+, Ar) = 2.5(0.3), k(Ar5+, H-2) = 5.9(0.7), k(Ar5+, Ar) = 2.9(0.3), k(Ar6+, H-2) = 8.5(l.2), and k(Ar6+, Ar) = 2.5(0.3)

Histological and Somatic Mutational Profiles of Mismatch Repair Deficient Endometrial Tumours of Different Aetiologies

SIMPLE SUMMARY: Endometrial cancers can arise due to an error in DNA mending known as mismatch repair. This can happen because of an error in the cancer itself (somatic) or due to an inherited error (Lynch syndrome). Treatment trials have considered endometrial cancers caused by either of these errors as identical. As it is easier to recruit people with Lynch syndrome, they may be overrepresented in this group despite being less numerous in clinical practice. This would not be an issue if somatic and Lynch syndrome-related endometrial cancers were similar at a molecular level. The data presented herein, however, indicates that these two routes to mismatch repair, although sharing many similarities, lead to endometrial cancers with distinct molecular and pathological features. This may explain the range of outcomes observed in clinical trials of endometrial cancers with mismatch repair errors. ABSTRACT: Background: Mismatch repair deficient (MMRd) tumours may arise from somatic events acquired during carcinogenesis or in the context of Lynch syndrome (LS), an inherited cancer predisposition condition caused by germline MMR pathogenic variants. Our aim was to explore whether sporadic and hereditary MMRd endometrial cancers (EC) display distinctive tumour biology. Methods: Clinically annotated LS-EC were collected. Histological slide review was performed centrally by two specialist gynaecological pathologists. Mutational analysis was by a bespoke 75- gene next-generation sequencing panel. Comparisons were made with sporadic MMRd EC. Multiple correspondence analysis was used to explore similarities and differences between the cohorts. Results: After exclusions, 135 LS-EC underwent independent histological review, and 64 underwent mutational analysis. Comparisons were made with 59 sporadic MMRd EC. Most tumours were of endometrioid histological subtype (92% LS-EC and 100% sporadic MMRd EC, respectively, p = NS). Sporadic MMRd tumours had significantly fewer tumour infiltrating lymphocytes (p ≤ 0.0001) and showed more squamous/mucinous differentiation than LS-EC (p = 0.04/p = 0.05). PTEN mutations were found in 88% sporadic MMRd and 61% LS-EC, respectively (p < 0.001). Sporadic MMRd tumours had significantly more mutations in PDGFRA, ALK, IDH1, CARD11, CIC, MED12, CCND1, PTPN11, RB1 and KRAS, while LS-EC showed more mutations affecting SMAD4 and ARAF. LS-EC showed a propensity for TGF-β signalling disruption. Cluster analysis found that wild type PTEN associates predominantly with LS-EC, whilst co-occurring mutations in PTEN, PIK3CA and KRAS predict sporadic MMRd EC. Conclusions: Whilst MMRd EC of hereditary and sporadic aetiology may be difficult to distinguish by histology alone, differences in infiltrating immune cell counts and mutational profile may predict heterogenous responses to novel targeted therapies and warrant further study