Optimisation and Decision Support during the Conceptual Stage of Building Design

Merged with duplicate record 10026.1/726 on 28.02.2017 by CS (TIS)Modern building design is complex and involves many different disciplines operating in a fragmented manner. Appropriate computer-based decision support (DS) tools are sought that can raise the level of integration of different activities at the conceptual stage, in order to help create better designs solutions. This project investigates opportunities that exist for using techniques based upon the Genetic Algorithm (GA) to support critical activities of conceptual building design (CBD). Collective independent studies have shown that the GA is a powerful optimisation and exploratory search technique with widespread application. The GA is essentially very simple yet it offers robustness and domain independence. The GA efficiently searches a domain to exploit highly suitable information. It maintains multiple solutions to problems simultaneously and is well suited to non-linear problems and those of a discontinuous nature found in engineering design. The literature search first examines traditional approaches to supporting conceptual design. Existing GA techniques and applications are discussed which include pioneering studies in the field of detailed structural design. Broader GA studies are also reported which have demonstrated possibilities for investigating geometrical, topological and member size variation. The tasks and goals of conceptual design are studied. A rationale is introduced, aimed at enabling the GA to be applied in a manner that provides the most effective support to the designer. Numerical experiments with floor planning are presented. These studies provide a basic foundation for a subsequent design support system (DSS) capable of generating structural design concepts. A hierarchical Structured GA (SGA) created by Dasgupta et al [1] is investigated to support the generation of diverse structural design concepts. The SGA supports variation in the size, shape and structural configuration of a building and in the choice of structural frame type and floor system. The benefits and limitations of the SGA approach are discussed. The creation of a prototype DSS system, abritrarily called Designer-Pro (DPRO), is described. A detailed building design model is introduced which is required for design development and appraisal. Simplifications, design rationale and generic component modelling are mentioned. A cost-based single criteria optimisation problem (SCOP) is created in which other constraints are represented as design parameters. The thesis describes the importance of the object-oriented programming (OOP) paradigm for creating a versatile design model and the need for complementary graphical user interface (GUI) tools to provide human-computer interaction (HCI) capabilities for control and intelligent design manipulation. Techniques that increase flexibility in the generation and appraisal of concept are presented. Tools presented include a convergence plot of design solutions that supports cursor-interrogation to reveal the details of individual concepts. The graph permits study of design progression, or evolution of optimum design solutions. A visualisation tool is also presented. The DPRO system supports multiple operating modes, including single-design appraisal and enumerative search (ES). Case study examples are provided which demonstrate the applicability of the DPRO system to a range of different design scenarios. The DPRO system performs well in all tests. A parametric study demonstrates the potential of the system for DS. Limitations of the current approach and opportunities to broaden the study form part of the scope for further work. Some suggestions for further study are made, based upon newly-emerging techniques

The Vehicle, 1965, Vol. 7

Vol. 7 Table of Contents CommentaryElaine Lancepage 3 Lost Island and The Unseen SeaDaun Alan Leggpage 5 ElegyWilliam Mosierpage 6 AwayDavid Dixpage 7 DulceyRoberta Mathewspage 8 Alarum Tuam JonneDavid Walkerpage 11 Little BrotherSteve Gibbspage 13 River RunningDaun Alan Leggpage 15 PortraitRobert D. Thomaspage 16 The RockRoger Lewis Hudsonpage 17 Jarman HospitalElaine Lancepage 18 Of Domes and DiamondsDwight Ashbypage 19 Friday NightRoger J. Barrypage 20 MurderHelen Coxpage 23 Vigil SongDaun Alan Leggpage 24 Had You But Been the OneDavid Helmpage 25 To A Useless WeaponDarlene Brewerpage 25 Out of the NightPat Hartpage 26 La MortAdrian Beardpage 28 Mrs. Milton\u27s LamentBob Millerpage 30 Cockle CoveSusan McCabepage 31 Loss of VirtueJim Rinnertpage 32 The KeepsakeDwight Ashbypage 33 The RuinsRoger Lewis Hudsonpage 35 Ante Major OdysseyDaun Alan Leggpage 38 ReligionAnthony Barrettepage 39 All JoyJim Rinnertpage 40 SesameElaine Lancepage 40 CenterpieceDwight Ashbypage 41 A Great White WaveJohn Rhodespage 42 QueryElaine Lancepage 44 PistachioRita Salyerspage 45 FacadeKathleen McCormackpage 46 Winter Wisp AwaySteve Gibbspage 46 ScenarioDavid Dixpage 47 Damn-GodSteve Gibbspage 48 AccidentElaine Lancepage 48https://thekeep.eiu.edu/vehicle/1013/thumbnail.jp

Whitefield News

File includes January 2015 Volume 2, Issue 7 February 2015 Volume 2, Issue 8 March 2015 Volume 2, Issue 9 April 2015 Volume 2, Issue 10 May 2015 Volume 2, Issue 11 June 2015 Volume 2, Issue 12 July 2015 Volume 3, Issue 1 August 2015 Volume 3, Issue 2 September 2015, Volume 3, Issue 3 October 2015, Volume 3, Issue 4 November 2015, Volume 3, Issue 5 December 2015, Volume 3, Issue

Adjunctive rifampicin for Staphylococcus aureus bacteraemia (ARREST): a multicentre, randomised, double-blind, placebo-controlled trial.

BACKGROUND: Staphylococcus aureus bacteraemia is a common cause of severe community-acquired and hospital-acquired infection worldwide. We tested the hypothesis that adjunctive rifampicin would reduce bacteriologically confirmed treatment failure or disease recurrence, or death, by enhancing early S aureus killing, sterilising infected foci and blood faster, and reducing risks of dissemination and metastatic infection. METHODS: In this multicentre, randomised, double-blind, placebo-controlled trial, adults (≥18 years) with S aureus bacteraemia who had received ≤96 h of active antibiotic therapy were recruited from 29 UK hospitals. Patients were randomly assigned (1:1) via a computer-generated sequential randomisation list to receive 2 weeks of adjunctive rifampicin (600 mg or 900 mg per day according to weight, oral or intravenous) versus identical placebo, together with standard antibiotic therapy. Randomisation was stratified by centre. Patients, investigators, and those caring for the patients were masked to group allocation. The primary outcome was time to bacteriologically confirmed treatment failure or disease recurrence, or death (all-cause), from randomisation to 12 weeks, adjudicated by an independent review committee masked to the treatment. Analysis was intention to treat. This trial was registered, number ISRCTN37666216, and is closed to new participants. FINDINGS: Between Dec 10, 2012, and Oct 25, 2016, 758 eligible participants were randomly assigned: 370 to rifampicin and 388 to placebo. 485 (64%) participants had community-acquired S aureus infections, and 132 (17%) had nosocomial S aureus infections. 47 (6%) had meticillin-resistant infections. 301 (40%) participants had an initial deep infection focus. Standard antibiotics were given for 29 (IQR 18-45) days; 619 (82%) participants received flucloxacillin. By week 12, 62 (17%) of participants who received rifampicin versus 71 (18%) who received placebo experienced treatment failure or disease recurrence, or died (absolute risk difference -1·4%, 95% CI -7·0 to 4·3; hazard ratio 0·96, 0·68-1·35, p=0·81). From randomisation to 12 weeks, no evidence of differences in serious (p=0·17) or grade 3-4 (p=0·36) adverse events were observed; however, 63 (17%) participants in the rifampicin group versus 39 (10%) in the placebo group had antibiotic or trial drug-modifying adverse events (p=0·004), and 24 (6%) versus six (2%) had drug interactions (p=0·0005). INTERPRETATION: Adjunctive rifampicin provided no overall benefit over standard antibiotic therapy in adults with S aureus bacteraemia. FUNDING: UK National Institute for Health Research Health Technology Assessment

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Tale of a Death Exaggerated::How Keynesian Policies Survived the 1970s

It has become a commonplace to divide the post-war period into ‘Keynesian’ and ‘post-Keynesian’ eras, usually with the break point in the 1970s. This article challenges that periodisation and the arguments that underpin it. It is argued that Keynesianism did not die in the 1970s, but survived, if somewhat mutated, into the twenty first century. This proposition is then used to challenge exaggerated views about the scale of the crisis of the 1970s