Resource allocation and scheduling of multiple composite web services in cloud computing using cooperative coevolution genetic algorithm

In cloud computing, resource allocation and scheduling of multiple composite web services is an important and challenging problem. This is especially so in a hybrid cloud where there may be some low-cost resources available from private clouds and some high-cost resources from public clouds. Meeting this challenge involves two classical computational problems: one is assigning resources to each of the tasks in the composite web services; the other is scheduling the allocated resources when each resource may be used by multiple tasks at different points of time. In addition, Quality-of-Service (QoS) issues, such as execution time and running costs, must be considered in the resource allocation and scheduling problem. Here we present a Cooperative Coevolutionary Genetic Algorithm (CCGA) to solve the deadline-constrained resource allocation and scheduling problem for multiple composite web services. Experimental results show that our CCGA is both efficient and scalable.

Why adopt now? Multiple case studies and survey studies comparing small, medium and large firms

While a number of factors have been highlighted in the innovation adoption literature, little is known about whether different factors are related to innovation adoption in differently-sized firms. We used preliminary case studies of small, medium and large firms to ground our hypotheses, which were then tested using a survey of 94 firms. We found that external stakeholder pressure and non-financial readiness were related to innovation adoption in SMEs; but that for large firms, adoption was related to the opportunity to innovate. It may be that the difficulties of adopting innovations, including both the financial cost and the effort involved, are too great for SMEs to overcome unless there is either a compelling need (external pressure) or enough in-house capability (non-financial readiness). This suggests that SMEs are more likely to have innovation “pushed” onto them while large firms are more likely to “pull” innovations when they have the opportunity.

CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein

The CDKN2A gene encodes p16 (CDKN2A), a cell-cycle inhibitor protein which prevents inappropriate cell cycling and, hence, proliferation. Germ-line mutations in CDKN2A predispose to the familial atypical multiple-mole melanoma (FAMMM) syndrome but also have been seen in rare families in which only 1 or 2 individuals are affected by cutaneous malignant melanoma (CMM). We therefore sequenced exons 1alpha and 2 of CDKN2A using lymphocyte DNA isolated from index cases from 67 families with cancers at multiple sites, where the patterns of cancer did not resemble those attributable to known genes such as hMLH1, hMLH2, BRCA1, BRCA2, TP53 or other cancer susceptibility genes. We found one mutation, a mis-sense mutation resulting in a methionine to isoleucine change at codon 53 (M531) of exon 2. The individual tested had developed 2 CMMs but had no dysplastic nevi and lacked a family history of dysplastic nevi or CMM. Other family members had been diagnosed with oral cancer (2 persons), bladder cancer (1 person) and possibly gall-bladder cancer. While this mutation has been reported in Australian and North American melanoma kindreds, we did not observe it in 618 chromosomes from Scottish and Canadian controls. Functional studies revealed that the CDKN2A variant carrying the M531 change was unable to bind effectively to CDK4, showing that this mutation is of pathological significance. Our results have confirmed that CDKN2A mutations are not limited to FAMMM kindreds but also demonstrate that multi-site cancer families without melanoma are very unlikely to contain CDKN2A mutations.

Beyond MOF constraints : multiple constraint set metamodelling for lifecycle management

The management of models over time in many domains requires different constraints to apply to some parts of the model as it evolves. Using EMF and its meta-language Ecore, the development of model management code and tools usually relies on the meta- model having some constraints, such as attribute and reference cardinalities and changeability, set in the least constrained way that any model user will require. Stronger versions of these constraints can then be enforced in code, or by attaching additional constraint expressions, and their evaluations engines, to the generated model code. We propose a mechanism that allows for variations to the constraining meta-attributes of metamodels, to allow enforcement of different constraints at different lifecycle stages of a model. We then discuss the implementation choices within EMF to support the validation of a state-specific metamodel on model graphs when changing states, as well as the enforcement of state-specific constraints when executing model change operations.

Distribution feeder voltage support and power factor control by distributed multiple inverters

The potential of distributed reactive power control to improve the voltage profile of radial distribution feeders has been reported in literature by few authors. However, the multiple inverters injecting or absorbing reactive power across a distribution feeder may introduce control interactions and/or voltage instability. Such controller interactions can be alleviated if the inverters are allowed to operate on voltage droop. First, the paper demonstrates that a linear shallow droop line can maintain the steady state voltage profile close to reference, up to a certain level of loading. Then, impacts of the shallow droop line control on line losses and line power factors are examined. Finally, a piecewise linear droop line which can achieve reduced line losses and close to unity power factor at the feeder source is proposed.

Interactive processes link the multiple symptoms of fatigue in sport competition

Muscle physiologists often describe fatigue simply as a decline of muscle force and infer this causes an athlete to slow down. In contrast, exercise scientists describe fatigue during sport competition more holistically as an exercise-induced impairment of performance. The aim of this review is to reconcile the different views by evaluating the many performance symptoms/measures and mechanisms of fatigue. We describe how fatigue is assessed with muscle, exercise or competition performance measures. Muscle performance (single muscle test measures) declines due to peripheral fatigue (reduced muscle cell force) and/or central fatigue (reduced motor drive from the CNS). Peak muscle force seldom falls by >30% during sport but is often exacerbated during electrical stimulation and laboratory exercise tasks. Exercise performance (whole-body exercise test measures) reveals impaired physical/technical abilities and subjective fatigue sensations. Exercise intensity is initially sustained by recruitment of new motor units and help from synergistic muscles before it declines. Technique/motor skill execution deviates as exercise proceeds to maintain outcomes before they deteriorate, e.g. reduced accuracy or velocity. The sensation of fatigue incorporates an elevated rating of perceived exertion (RPE) during submaximal tasks, due to a combination of peripheral and higher CNS inputs. Competition performance (sport symptoms) is affected more by decision-making and psychological aspects, since there are opponents and a greater importance on the result. Laboratory based decision making is generally faster or unimpaired. Motivation, self-efficacy and anxiety can change during exercise to modify RPE and, hence, alter physical performance. Symptoms of fatigue during racing, team-game or racquet sports are largely anecdotal, but sometimes assessed with time-motion analysis. Fatigue during brief all-out racing is described biomechanically as a decline of peak velocity, along with altered kinematic components. Longer sport events involve pacing strategies, central and peripheral fatigue contributions and elevated RPE. During match play, the work rate can decline late in a match (or tournament) and/or transiently after intense exercise bursts. Repeated sprint ability, agility and leg strength become slightly impaired. Technique outcomes, such as velocity and accuracy for throwing, passing, hitting and kicking, can deteriorate. Physical and subjective changes are both less severe in real rather than simulated sport activities. Little objective evidence exists to support exercise-induced mental lapses during sport. A model depicting mind-body interactions during sport competition shows that the RPE centre-motor cortex-working muscle sequence drives overall performance levels and, hence, fatigue symptoms. The sporting outputs from this sequence can be modulated by interactions with muscle afferent and circulatory feedback, psychological and decision-making inputs. Importantly, compensatory processes exist at many levels to protect against performance decrements. Small changes of putative fatigue factors can also be protective. We show that individual fatigue factors including diminished carbohydrate availability, elevated serotonin, hypoxia, acidosis, hyperkalaemia, hyperthermia, dehydration and reactive oxygen species, each contribute to several fatigue symptoms. Thus, multiple symptoms of fatigue can occur simultaneously and the underlying mechanisms overlap and interact. Based on this understanding, we reinforce the proposal that fatigue is best described globally as an exercise-induced decline of performance as this is inclusive of all viewpoints.