Scheduling problems with two competing agents

We consider the scheduling problems arising when two agents, each with a set of nonpreemptive jobs, compete to perform their respective jobs on a common processing resource. Each agent wants to minimize a certain objective function, which depends on the completion times of its jobs only. The objective functions we consider in this paper are maximum of regular functions (associated with each job), number of late jobs, and total weighted completion times. We obtain different scenarios, depending on the objective function of each agent, and on the structure of the processing system (single machine or shop). For each scenario, we address the complexity of various problems, namely, finding the optimal solution for one agent with a constraint on the other agent's cost function, finding single nondominated schedules (i.e., such that a better schedule for one of the two agents necessarily results in a worse schedule for the other agent), and generating all nondominated schedules

The ansa subclavia: a review of the literature

The ansa subclavia, subclavian loop, Vieussens’ ansa or Vieussens’ loop is a nerve cord that connects the middle cervical and inferior cervical sympathetic ganglia, forming a loop around the subclavian artery. The structure of the ansa subclavia is evolutionarily conserved from rats, guinea pigs, the porcine species and dogs to humans. A common application in physiological studies is to electrically stimulate the ansa subclavia in animal models as a robust protocol to modulate stimulatory cardiac sympathetic input. Despite a large number of physiological studies utilizing the ansa subclavia, only very brief descriptions have been devoted to it in standard anatomy texts. An extensive search found only one report in the English language literature concerning the anatomy of the ansa subclavia. The aim of this report, therefore, was to provide a comprehensive review of the clinical anatomy of the ansa subclavia and to discuss its potential physiological functions

Generalized iterated wreath products of cyclic groups and rooted trees correspondence

Consider the generalized iterated wreath product $\mathbb{Z}_{r_1}\wr \mathbb{Z}_{r_2}\wr \ldots \wr \mathbb{Z}_{r_k}$ where $r_i \in \mathbb{N}$. We prove that the irreducible representations for this class of groups are indexed by a certain type of rooted trees. This provides a Bratteli diagram for the generalized iterated wreath product, a simple recursion formula for the number of irreducible representations, and a strategy to calculate the dimension of each irreducible representation. We calculate explicitly fast Fourier transforms (FFT) for this class of groups, giving literature's fastest FFT upper bound estimate.Comment: 15 pages, to appear in Advances in the Mathematical Science

Business process modelling and visualisation to support e-government decision making: Business/IS alignment

© 2017 Springer-Verlag. The final publication is available at Springer via https://doi.org/10.1007/978-3-319-57487-5_4.Alignment between business and information systems plays a vital role in the formation of dependent relationships between different departments in a government organization and the process of alignment can be improved by developing an information system (IS) according to the stakeholders’ expectations. However, establishing strong alignment in the context of the eGovernment environment can be difficult. It is widely accepted that business processes in the government environment plays a pivotal role in capturing the details of IS requirements. This paper presents a method of business process modelling through UML which can help to visualise and capture the IS requirements for the system development. A series of UML models have been developed and discussed. A case study on patient visits to a healthcare clinic in the context of eGovernment has been used to validate the models

Semaphorin 3F signaling actively retains neutrophils at sites of inflammation

Neutrophilic inflammation is central to disease pathogenesis, for example, in chronic obstructive pulmonary disease, yet the mechanisms that retain neutrophils within tissues remain poorly understood. With emerging evidence that axon guidance factors can regulate myeloid recruitment and that neutrophils can regulate expression of a class 3 semaphorin, SEMA3F, we investigated the role of SEMA3F in inflammatory cell retention within inflamed tissues. We observed that neutrophils upregulate SEMA3F in response to proinflammatory mediators and following neutrophil recruitment to the inflamed lung. In both zebrafish tail injury and murine acute lung injury models of neutrophilic inflammation, overexpression of SEMA3F delayed inflammation resolution with slower neutrophil migratory speeds and retention of neutrophils within the tissues. Conversely, constitutive loss of sema3f accelerated egress of neutrophils from the tail injury site in fish, whereas neutrophil-specific deletion of Sema3f in mice resulted in more rapid neutrophil transit through the airways, and significantly reduced time to resolution of the neutrophilic response. Study of filamentous-actin (F-actin) subsequently showed that SEMA3F-mediated retention is associated with F-actin disassembly. In conclusion, SEMA3F signaling actively regulates neutrophil retention within the injured tissues with consequences for neutrophil clearance and inflammation resolution

The Fanconi Anemia Core Complex Is Dispensable during Somatic Hypermutation and Class Switch Recombination

To generate high affinity antibodies during an immune response, B cells undergo somatic hypermutation (SHM) of their immunoglobulin genes. Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C transversions. In contrast to A/T mutations which depend on PCNA ubiquitination, it remains unclear how G/C transversions are regulated during SHM. Several lines of evidence indicate a mechanistic link between the Fanconi Anemia (FA) pathway and TLS. To investigate the contribution of the FA pathway in SHM we analyzed FancG-deficient B cells. B cells deficient for FancG, an essential member of the FA core complex, were hypersensitive to treatment with cross-linking agents. However, the frequencies and nucleotide exchange spectra of SHM remained comparable between wild-type and FancG-deficient B cells. These data indicate that the FA pathway is not involved in regulating the outcome of SHM in mammals. In addition, the FA pathway appears dispensable for class switch recombination

Differential roles for the oxygen sensing enzymes PHD1 and PHD3 in the regulation of neutrophil metabolism and function

Background Neutrophils are essential in the early innate immune response to pathogens. Harnessing their antimicrobial powers, without driving excessive and damaging inflammatory responses, represents an attractive therapeutic possibility. The neutrophil population is increasingly recognised to be more diverse and malleable than was previously appreciated. Hypoxic signalling pathways are known to regulate important neutrophil behaviours and, as such, are potential therapeutic targets for regulating neutrophil antimicrobial and inflammatory responses. Methods We used a combination of in vivo and ex vivo models, utilising neutrophil and myeloid specific PHD1 or PHD3 deficient mouse lines to investigate the roles of oxygen sensing prolyl hydroxylase enzymes in the regulation of neutrophilic inflammation and immunity. Mass spectrometry and Seahorse metabolic flux assays were used to analyse the role of metabolic shifts in driving the downstream phenotypes. Results We found that PHD1 deficiency drives alterations in neutrophil metabolism and recruitment, in an oxygen dependent fashion. Despite this, PHD1 deficiency did not significantly alter ex vivo neutrophil phenotypes or in vivo outcomes in mouse models of inflammation. Conversely, PHD3 deficiency was found to enhance neutrophil antibacterial properties without excessive inflammatory responses. This was not linked to changes in the abundance of core metabolites but was associated with increased oxygen consumption and increased mitochondrial reactive oxygen species (mROS) production. Conclusions PHD3 deficiency drives a favourable neutrophil phenotype in infection and, as such, is an important potential therapeutic target

Loss of heterozygosity (LOH), malignancy grade and clonality in microdissected prostate cancer

The aim of the present study was to find out whether increasing malignancy of prostate carcinoma correlates with an overall increase of loss of heterozygosity (LOH), and whether LOH typing of microdissected tumour areas can help to distinguish between multifocal or clonal tumour development. In 47 carcinomas analysed at 25 chromosomal loci, the overall LOH rate was found to be significantly lower in grade 1 areas (2.2%) compared with grade 2 (9.4%) and grade 3 areas (8.3%, P = 0.007). A similar tendency was found for the mean fractional allele loss (FAL, 0.043 for grade 1, 0.2 for grade 2 and 0.23 for grade 3, P = 0.0004). Of 20 tumours (65%) with LOH in several microdissected areas, 13 had identical losses at 1–4 loci within two or three areas, suggesting clonal development of these areas. Markers near RB, DCC, BBC1, TP53 and at D13S325 (13q21–22) showed higher loss rates in grades 2 and 3 (between 25% and 44.4%) compared with grade 1 (0–6.6%). Tumour-suppressor genes (TSGs) near these loci might, thus, be important for tumour progression. TP53 mutations were detected in 27%, but BBC1 mutations in only 7%, of samples with LOH. Evaluation of all 25 loci in every tumour made evident that each prostate cancer has its own pattern of allelic losses. © 1999 Cancer Research Campaig