Could thermal fluctuations seed cosmic structure?

We examine the possibility that thermal, rather than quantum, fluctuations are responsible for seeding the structure of our universe. We find that while the thermalization condition leads to nearly Gaussian statistics, a Harrisson-Zeldovich spectrum for the primordial fluctuations can only be achieved in very special circumstances. These depend on whether the universe gets hotter or colder in time, while the modes are leaving the horizon. In the latter case we find a no-go theorem which can only be avoided if the fundamental degrees of freedom are not particle-like, such as in string gases near the Hagedorn phase transition. The former case is less forbidding, and we suggest two potentially successful ``warming universe'' scenarios. One makes use of the Phoenix universe, the other of ``phantom'' matter.Comment: minor corrections made, references added, matches the version accepted to PR

Localization dynamics in a binary two-dimensional cellular automaton: the Diffusion Rule

We study a two-dimensional cellular automaton (CA), called Diffusion Rule (DR), which exhibits diffusion-like dynamics of propagating patterns. In computational experiments we discover a wide range of mobile and stationary localizations (gliders, oscillators, glider guns, puffer trains, etc), analyze spatio-temporal dynamics of collisions between localizations, and discuss possible applications in unconventional computing.Comment: Accepted to Journal of Cellular Automat

Cerebral malaria: Gamma-interferon redux

There are two theories that seek to explain the pathogenesis of cerebral malaria, the mechanical obstruction hypothesis and the immunopathology hypothesis. Evidence consistent with both ideas has accumulated from studies of the human disease and experimental models. Thus, some combination of these concepts seems necessary to explain the very complex pattern of changes seen in cerebral malaria. The interactions between malaria parasites, erythrocytes, the cerebral microvascular endothelium, brain parenchymal cells, platelets and microparticles need to be considered. One factor that seems able to knit together much of this complexity is the cytokine interferon-gamma (IFN-?). In this review we consider findings from the clinical disease, in vitro models and the murine counterpart of human cerebral malaria in order to evaluate the roles played by IFN-? in the pathogenesis of this often fatal and debilitating condition. © 2014 Hunt, Ball, Hansen, Khaw, Guo, Bakmiwewa, Mitchell, Combes and Grau

Partisan Views of the Economy

In this paper it is argued that political parties may have incentives to adopt a partisan view on the working of the economic system. Our approach is based on a dynamical spatial voting model in which political parties are policy oriented. This model revolves around two interrelated issues x and y. The policy maker sets x directly. There exist two views on the relationship between x and y. Model uncertainty confronts policy makers with the problem of the selection of a model to base their actions on. We show that if voters have imperfect information about the working of the economic system that model selection contains a strategic element. Policy makers are inclined to adopt a view on the working of the economic system which fits in with their preferences. There is no inherent logic that places monetarists to the right of New Economists. They have different models of economic mechanism, but they need not have different political values. A conservative can be a Keynesian and a liberal a monetarist. These combinations are in fact surprisingly rare. James Tobin, 1974,The New Economics One Decade Older, p. 62. I am greatly indebted to Peter Broer, Ben Heydra, Jos Jansen and Wilko Letterie for many helpful suggestions. Furthermore, I would like to thank an anonymous referee for his comments

Magnetic Field Amplification in Galaxy Clusters and its Simulation

We review the present theoretical and numerical understanding of magnetic field amplification in cosmic large-scale structure, on length scales of galaxy clusters and beyond. Structure formation drives compression and turbulence, which amplify tiny magnetic seed fields to the microGauss values that are observed in the intracluster medium. This process is intimately connected to the properties of turbulence and the microphysics of the intra-cluster medium. Additional roles are played by merger induced shocks that sweep through the intra-cluster medium and motions induced by sloshing cool cores. The accurate simulation of magnetic field amplification in clusters still poses a serious challenge for simulations of cosmological structure formation. We review the current literature on cosmological simulations that include magnetic fields and outline theoretical as well as numerical challenges.Comment: 60 pages, 19 Figure

'Who Wrote 2 Thessalonians:A Fresh Look at an Old Problem'

In light of the New Perspective on Paul, recognition of apocalyptic as a central category in Pauline theology, and the crumbling consensus concerning seven authentic epistles of Paul, it is time to reconsider the arguments for the authenticity of his letters. Here the specific question of the authorship of 2 Thessalonians is re-examined. It is noted that many of the standard arguments for or against the authenticity of 2 Thessalonians are either irrelevant or inconclusive. This discussion seeks to reveal the slender evidential basis of certain ‘classic’ arguments against the authenticity of the letter, and also to present some fresh reasons why the epistle should be regarded as written by Paul. The implications of including 2 Thessalonians among the authentic Pauline writings are then examined. In particular, it is suggested that the development in Paul’s thinking as reflected in 2 Thessalonians reveals that his theological formulations developed in response to situations in his fledgling communities. In this regard, Paul’s theological positions emerged through a negotiated response to pressing pastoral situations

Perivascular macrophages create an intravascular niche for CD8 + T cell localisation prior to the onset of fatal experimental cerebral malaria

Objectives: The immunologic events that build up to the fatal neurological stage of experimental cerebral malaria (ECM) are incompletely understood. Here, we dissect immune cell behaviour occurring in the central nervous system (CNS) when Plasmodium berghei ANKA (PbA)-infected mice show only minor clinical signs. Methods: A 2-photon intravital microscopy (2P-IVM) brain imaging model was used to study the spatiotemporal context of early immunological events in situ during ECM. Results: Early in the disease course, antigen-specific CD8+ T cells came in contact and arrested on the endothelium of post-capillary venules. CD8+ T cells typically adhered adjacent to, or were in the near vicinity of, perivascular macrophages (PVMs) that line post-capillary venules. Closer examination revealed that CD8+ T cells crawled along the inner vessel wall towards PVMs that lay on the abluminal side of large post-capillary venules. 'Activity hotspots' in large post-capillary venules were characterised by T-cell localisation, activated morphology and clustering of PVM, increased abutting of post-capillary venules by PVM and augmented monocyte accumulation. In the later stages of infection, when mice exhibited neurological signs, intravascular CD8+ T cells increased in number and changed their behaviour, actively crawling along the endothelium and displaying frequent, short-term interactions with the inner vessel wall at hotspots. Conclusion: Our study suggests an active interaction between PVM and CD8+ T cells occurs across the blood-brain barrier (BBB) in early ECM, which may be the initiating event in the inflammatory cascade leading to BBB alteration and neuropathology

No evidence that protein truncating variants in BRIP1 are associated with breast cancer risk: implications for gene panel testing.

BACKGROUND: BRCA1 interacting protein C-terminal helicase 1 (BRIP1) is one of the Fanconi Anaemia Complementation (FANC) group family of DNA repair proteins. Biallelic mutations in BRIP1 are responsible for FANC group J, and previous studies have also suggested that rare protein truncating variants in BRIP1 are associated with an increased risk of breast cancer. These studies have led to inclusion of BRIP1 on targeted sequencing panels for breast cancer risk prediction. METHODS: We evaluated a truncating variant, p.Arg798Ter (rs137852986), and 10 missense variants of BRIP1, in 48 144 cases and 43 607 controls of European origin, drawn from 41 studies participating in the Breast Cancer Association Consortium (BCAC). Additionally, we sequenced the coding regions of BRIP1 in 13 213 cases and 5242 controls from the UK, 1313 cases and 1123 controls from three population-based studies as part of the Breast Cancer Family Registry, and 1853 familial cases and 2001 controls from Australia. RESULTS: The rare truncating allele of rs137852986 was observed in 23 cases and 18 controls in Europeans in BCAC (OR 1.09, 95% CI 0.58 to 2.03, p=0.79). Truncating variants were found in the sequencing studies in 34 cases (0.21%) and 19 controls (0.23%) (combined OR 0.90, 95% CI 0.48 to 1.70, p=0.75). CONCLUSIONS: These results suggest that truncating variants in BRIP1, and in particular p.Arg798Ter, are not associated with a substantial increase in breast cancer risk. Such observations have important implications for the reporting of results from breast cancer screening panels.The COGS project is funded through a European Commission's Seventh Framework Programme grant (agreement number 223175 - HEALTH-F2-2009-223175). BCAC is funded by Cancer Research UK [C1287/A10118, C1287/A12014] and by the European Community´s Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 16 CA148065 and 1U19 CA148112 - the GAME-ON initiative), the Department of Defense (W81XWH-10-1- 0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. This study made use of data generated by the Wellcome Trust Case Control consortium. Funding for the project was provided by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Project established by the National Cancer Institute and National Human Genome Research Institute.This is the author accepted manuscript. The final version is available from BMJ Group at http://dx.doi.org/10.1136/jmedgenet-2015-103529

Majority Adder Implementation by Competing Patterns in Life-Like Rule B2/S2345

In this paper we present a two-dimensional chaotic cellular automaton, the Life rule B2/S2345, able to simulate the action of an adder with majority gates, stimulated by gliders collisions transformed as competing patterns. Values of Boolean variables are encoded into two types of patterns --- symmetric (FALSE) and asymmetric (TRUE) patterns -- which compete for the `empty' space when propagate in the channels. We construct basic logical gates and elementary arithmetical circuits by simulating logical signals with gliders reaction propagating geometrically restricted by stationary non-destructible still life. Therefore an implementation of universal logical gates and a majority binary adder is constructe