Improved bounds for speed scaling in devices obeying the cube-root rule

Speed scaling is a power management technology that involves dynamically changing the speed of a processor. This technology gives rise to dual-objective scheduling problems, where the operating system both wants to conserve energy and optimize some Quality of Service (QoS) measure of the resulting schedule. In the most investigated speed scaling problem in the literature, the QoS constraint is deadline feasibility, and the objective is to minimize the energy used. The standard assumption is that the processor power is of the form s^a where s is the processor speed, and a>1 is some constant; a˜3 for CMOS based processors. In this paper we introduce and analyze a natural class of speed scaling algorithms, that we call qOA. The algorithm qOA sets the speed of the processor to be q times the speed that the optimal offline algorithm would run the jobs in the current state. When a=3, we show that qOA is 6.7-competitive, improving upon the previous best guarantee of 27 achieved by the algorithm Optimal Available (OA). We also give almost matching upper and lower bounds for qOA for general a. Finally, we give the first non-trivial lower bound, namely e^(a-1) / a, on the competitive ratio of a general deterministic online algorithm for this problem

A genomic prediction model for racecourse starts in the Thoroughbred horse

Durability traits in Thoroughbred horses are heritable, economically valuable and may affect horse welfare. The aims of this study were to test the hypotheses that (i) durability traits are heritable and (ii) genetic data may be used to predict a horse's potential to have a racecourse start. Heritability for the phenotype ‘number of 2‐ and 3‐year‐old starts’ was estimated to be urn:x-wiley:02689146:media:age12798:age12798-math-0001 = 0.11 ± 0.02 (n = 4499). A genome‐wide association study identified SNP contributions to the trait. The neurotrimin (NTM), opioid‐binding protein/cell adhesion molecule like (OPCML) and prolylcarboxypeptidase (PRCP) genes were identified as candidate genes associated with the trait. NTM functions in brain development and has been shown to have been selected during the domestication of the horse. PRCP is an established expression quantitative trait locus involved in the interaction between voluntary exercise and body composition in mice. We hypothesise that variation at these loci contributes to the motivation of the horse to exercise, which may influence its response to the demands of the training and racing environment. A random forest with mixed effects (RFME) model identified a set of SNPs that contributed to 24.7% of the heritable variation in the trait. In an independent validation set (n = 528 horses), the cohort with high genetic potential for a racecourse start had significantly fewer unraced horses (16% unraced) than did low (27% unraced) potential horses and had more favourable race outcomes among those that raced. Therefore, the information from SNPs included in the model may be used to predict horses with a greater chance of a racecourse start

Middle Convolution and Harnad Duality

We interpret the additive middle convolution operation in terms of the Harnad duality, and as an application, generalize the operation to have a multi-parameter and act on irregular singular systems.Comment: 50 pages; v2: Submitted version once revised according to referees' comment

The Australian Early Years Learning Framework: learning what?

Early childhood education and care have assumed importance in many government policy agendas. This attention is often accompanied by calls for greater accountability regarding the anticipated learning outcomes for young children. In Australia, the expected learning outcomes for children aged birth to five years are outlined in the recently published Early Years Learning Framework (EYLF). In this article, the author examines the relationship between the EYLF’s outcomes and subject area or content knowledge. The article draws from post-structural and social constructionist understandings of knowledge as unfinished, contestable and contextual. The author concludes that it is not content knowledge itself that is problematic, but it is the way the child and teacher are often positioned in relation to that knowledge that constrains the potential for effective teaching and learning in the early years. The author suggests that revisiting traditional assumptions about content knowledge extends and develops many of the ideas about teaching and learning that are identified in the EYLF, and opens up new identity positions for both children and early childhood educators

Open-label, phase 2 study of blinatumomab after frontline R-chemotherapy in adults with newly diagnosed, high-risk DLBCL

This open-label, multicenter, single-arm, phase 2 study assessed the safety and efficacy of blinatumomab consolidation therapy in adult patients with newly diagnosed, high-risk diffuse large B-cell lymphoma (DLBCL; International Prognostic Index 3–5 and/or double-/triple-hit or double MYC/BCL-2 expressors) who achieved complete response (CR), partial response (PR), or stable disease (SD) following run-in with 6 cycles of R-chemotherapy (NCT03023878). Of the 47 patients enrolled, 28 received blinatumomab. Five patients (17.9%) experienced grade 4 treatment-emergent adverse events of interest (neutropenia, n = 4; infection, n = 1). Two deaths reported at the end of the study were unrelated to treatment with blinatumomab (disease progression, n = 1; infection, n = 1). 3/4 patients with PR and 4/4 patients with SD after R-chemotherapy achieved CR following blinatumomab. Consolidation with blinatumomab in patients with newly diagnosed, high-risk DLBCL who did not progress under R-chemotherapy was better tolerated than in previous studies where blinatumomab was used for treatment of patients with lymphoma

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele