Sources of Military Change:Emulation, Politics, and Concept Development in UK Defence

Judging by its doctrinal publications, the UK Defence establishment stands poised to begin a process of unprecedented change. The language of ‘multi-domain’ thinking is prominent within this discourse and is identified as being a key vehicle via which UK Defence will deliver upon its programme of reform. This article seeks to offer an initial evaluation of these claims and to assess them in light of the burgeoning literatures on Western defence ‘transformation’ and military innovation that have emerged since the early 2000s. We argue that ‘multi-domain’ thinking reflects a form of ‘cosmetic’ emulation by the British Defence establishment and that its appearance within UK doctrine has been driven more by internal politics than by a clearly thought-through adoption of a new form of military practice.</p

Hox proteins drive cell segregation and non-autonomous apical remodelling during hindbrain segmentation

Hox genes encode a conserved family of homeodomain transcription factors regulating development along the major body axis. During embryogenesis, Hox proteins are expressed in segment-specific patterns and control numerous different segment-specific cell fates. It has been unclear, however, whether Hox proteins drive the epithelial cell segregation mechanism that is thought to initiate the segmentation process. Here, we investigate the role of vertebrate Hox proteins during the partitioning of the developing hindbrain into lineage-restricted units called rhombomeres. Loss-of-function mutants and ectopic expression assays reveal that Hoxb4 and its paralogue Hoxd4 are necessary and sufficient for cell segregation, and for the most caudal rhombomere boundary (r6/r7). Hox4 proteins regulate Eph/ephrins and other cell-surface proteins, and can function in a non-cell-autonomous manner to induce apical cell enlargement on both sides of their expression border. Similarly, other Hox proteins expressed at more rostral rhombomere interfaces can also regulate Eph/ephrins, induce apical remodelling and drive cell segregation in ectopic expression assays. However, Krox20, a key segmentation factor expressed in odd rhombomeres (r3 and r5), can largely override Hox proteins at the level of regulation of a cell surface target, Epha4. This study suggests that most, if not all, Hox proteins share a common potential to induce cell segregation but in some contexts this is masked or modulated by other transcription factors

Covers for S-acts and Condition (A) for a monoid S

A monoid S satisfies Condition (A) if every locally cyclic left S-act is cyclic. This condition first arose in Isbell's work on left perfect monoids, that is, monoids such that every left S-act has a projective cover. Isbell showed that S is left perfect if and only if every cyclic left S-act has a projective cover and Condition (A) holds. Fountain built on Isbell's work to show that S is left perfect if and only if it satisfies Condition (A) together with the descending chain condition on principal right ideals, MR. We note that a ring is left perfect (with an analogous definition) if and only if it satisfies MR. The appearance of Condition (A) in this context is, therefore, monoid specific. Condition (A) has a number of alternative characterisations, in particular, it is equivalent to the ascending chain condition on cyclic subacts of any left S-act. In spite of this, it remains somewhat esoteric. The first aim of this paper is to investigate the preservation of Condition (A) under basic semigroup-theoretic constructions. Recently, Khosravi, Ershad and Sedaghatjoo have shown that every left S-act has a strongly flat or Condition (P) cover if and only if every cyclic left S-act has such a cover and Condition (A) holds. Here we find a range of classes of S-acts such that every left S-act has a cover from if and only if every cyclic left S-act does and Condition (A) holds. In doing so we find a further characterisation of Condition (A) purely in terms of the existence of covers of a certain kind. Finally, we make some observations concerning left perfect monoids and investigate a class of monoids close to being left perfect, which we name lefta-perfect

Flexible and tenacious goal pursuit lead to improving well-being in an aging population: A ten-year cohort study

Background: Previous research has shown that tendencies to tenaciously pursue goals and flexibly adapt goals independently relate to well-being in adults in mid-to-late life, but research has not tested whether these tendencies interact. For example, tenacity may only predict well-being in combination with flexibility. This research tests whether these tendencies interact to predict changes in health-related outcomes. Methods: A large cohort of people (n=5,666), initially aged 55-56, completed measures of flexibility, tenacity, health-related outcomes (physical health, depression, hostility), as well as demographics. Participants provided follow-up data on all measures ten years later. Moderation analysis was used to test whether flexibility and tenacity interacted to predict changes in the health-related outcomes over the period. Results: The interaction between tenacity and flexibility significantly predicted changes in depression, hostility, and physical ill-health symptoms over ten years, such that highly flexible and tenacious individuals experienced the largest decreases in symptoms of depression, hostility, and physical ill-health. Conclusions: The interaction between flexibility and tenacity predicts greater well-being, such that one is most protective when an individual also scores highly on the other. The combination of flexibility and tenacity in the pursuit of personal goals may mean individuals can enjoy gains associated with goal pursuit without the detrimental effects of persevering in blocked goals

Microplastic burden in invasive signal crayfish (Pacifastacus leniusculus) increases along a stream urbanization gradient

Microplastics are a globally pervasive pollutant with the potential to directly impact species and accumulate in ecosystems. However, there remains a relative paucity of research addressing their accumulation in freshwater ecosystems and a near absence of work in crayfish, despite their high ecological and economic importance. This study investigated the presence of microplastics in the invasive signal crayfish Pacifastacus leniusculus along a stream urbanization gradient. The results demonstrate a ubiquitous presence of microplastics in crayfish digestive tracts at all sites and provide the first evidence of microplastic accumulation in tail tissue. Evidence of a positive linear trend was demonstrated between microplastic concentration in crayfish and upstream urban area size in generalized linear models. Evidence for a positive effect of the upstream urban area and a negative effect of crayfish length on microplastic concentrations in crayfish was demonstrated in multiple generalized linear regression models. Our results extend the current understanding of microplastics presence in freshwater ecosystems and demonstrate their presence in crayfish in the wild for the first time

Anaplastic Lymphoma Kinase Spares Organ Growth during Nutrient Restriction in Drosophila

SummaryDeveloping animals survive periods of starvation by protecting the growth of critical organs at the expense of other tissues. Here, we use Drosophila to explore the as yet unknown mechanisms regulating this privileged tissue growth. As in mammals, we observe in Drosophila that the CNS is more highly spared than other tissues during nutrient restriction (NR). We demonstrate that anaplastic lymphoma kinase (Alk) efficiently protects neural progenitor (neuroblast) growth against reductions in amino acids and insulin-like peptides during NR via two mechanisms. First, Alk suppresses the growth requirement for amino acid sensing via Slimfast/Rheb/TOR complex 1. And second, Alk, rather than insulin-like receptor, primarily activates PI3-kinase. Alk maintains PI3-kinase signaling during NR as its ligand, Jelly belly (Jeb), is constitutively expressed from a glial cell niche surrounding neuroblasts. Together, these findings identify a brain-sparing mechanism that shares some regulatory features with the starvation-resistant growth programs of mammalian tumors.PaperCli

Individual variation in cognitive performance: developmental and evolutionary perspectives.

notes: PMCID: PMC3427550types: Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; ReviewAnimal cognition experiments frequently reveal striking individual variation but rarely consider its causes and largely ignore its potential consequences. Studies often focus on a subset of high-performing subjects, sometimes viewing evidence from a single individual as sufficient to demonstrate the cognitive capacity of a species. We argue that the emphasis on demonstrating species-level cognitive capacities detracts from the value of individual variation in understanding cognitive development and evolution. We consider developmental and evolutionary interpretations of individual variation and use meta-analyses of data from published studies to examine predictors of individual performance. We show that reliance on small sample sizes precludes robust conclusions about individual abilities as well as inter- and intraspecific differences. We advocate standardization of experimental protocols and pooling of data between laboratories to improve statistical rigour. Our analyses show that cognitive performance is influenced by age, sex, rearing conditions and previous experience. These effects limit the validity of comparative analyses unless developmental histories are taken into account, and complicate attempts to understand how cognitive traits are expressed and selected under natural conditions. Further understanding of cognitive evolution requires efforts to elucidate the heritability of cognitive traits and establish whether elevated cognitive performance confers fitness advantages in nature

Diet suppresses tumour initiation by maintaining quiescence of mutation-bearing neural stem cells

Glioblastoma is thought to originate from neural stem cells (NSCs) of the subventricular zone that acquire genetic alterations. In the adult brain, NSCs are largely quiescent, suggesting that deregulation of quiescence maintenance may be a pre-requisite for tumour initiation. Although inactivation of the tumour suppressor p53 is a frequent event in gliomagenesis, whether, or how, it affects quiescent NSCs (qNSCs) remains unclear. Here we show that p53 maintains quiescence by inducing fatty acid oxidation (FAO) and that acute p53 deletion in qNSCs results in their premature activation to a proliferative state. Mechanistically, this occurs through direct transcriptional induction of PPARGC1a, which in turn activates PPARα to upregulate FAO genes. Strikingly, dietary supplementation with fish oil containing omega-3 fatty acids, natural PPARα ligands, fully restores quiescence of p53-deficient NSCs and delays tumour initiation in a glioblastoma mouse model. Thus, diet can silence glioblastoma driver mutations, with important implications for cancer prevention

Diet suppresses glioblastoma initiation in mice by maintaining quiescence of mutation-bearing neural stem cells

Glioblastoma is thought to originate from neural stem cells (NSCs) of the subventricular zone that acquire genetic alterations. In the adult brain, NSCs are largely quiescent, suggesting that deregulation of quiescence maintenance may be a prerequisite for tumor initiation. Although inactivation of the tumor suppressor p53 is a frequent event in gliomagenesis, whether or how it affects quiescent NSCs (qNSCs) remains unclear. Here, we show that p53 maintains quiescence by inducing fatty-acid oxidation (FAO) and that acute p53 deletion in qNSCs results in their premature activation to a proliferative state. Mechanistically, this occurs through direct transcriptional induction of PPARGC1a, which in turn activates PPARα to upregulate FAO genes. Dietary supplementation with fish oil containing omega-3 fatty acids, natural PPARα ligands, fully restores quiescence of p53-deficient NSCs and delays tumor initiation in a glioblastoma mouse model. Thus, diet can silence glioblastoma driver mutations, with important implications for cancer prevention