Anisotropic P‐wave attenuation measured from a multi‐azimuth surface seismic reflection survey

A system of aligned vertical fractures produces azimuthal variations in stacking velocity and amplitude variation with offset, characteristics often reported in seismic reflection data for hydrocarbon exploration. Studies of associated attenuation anisotropy have been mostly theoretical, laboratory or vertical seismic profiling based. We used an 11 common‐midpoint‐long portion of each of four marine surface‐seismic reflection profiles, intersecting each other at 45° within circa 100 m of a common location, to measure the azimuthal variation of effective attenuation, Q−1eff and stacking velocity, in a shallow interval, about 100 m thick, in which consistently orientated vertical fracturing was expected due to an underlying salt diapirism. We found qualitative and quantitative consistency between the azimuthal variation in the attenuation and stacking velocity, and published amplitude variation with offset results. The 135° azimuth line showed the least apparent attenuation (1000 Q−1eff= 16 ± 7) and the fastest stacking velocity, hence we infer it to be closest to the fracture trend: the orthogonal 45° line showed the most apparent attenuation (1000Q−1eff= 52 ± 15) and slowest stacking velocity. The variation of Q−1eff with azimuth φ is well fitted by 1000Q−1eff= 34 − 18cos[2(φ+40°)] giving a fracture direction of 140 ± 23° (±1SD, derived from ‘bootstrapping’ fits to all 114 combinations of individual common‐midpoint/azimuth measurements), compared to 134 ± 47° from published amplitude variation with offset data. The effects of short‐window spectral estimation and choices of spectral ratio bandwidth and offset ranges used in attenuation analysis, individually give uncertainties of up to ±13° in fracture direction. This magnitude of azimuthal variation can be produced by credible crack geometries (e.g., dry cracks, radius 6.5 m, aspect ratio 3 × 10−5, crack density 0.2) but we do not claim these to be the actual properties of the interval studied, because of the lack of well control (and its consequences for the choice of theoretical model and host rock physical properties) and the small number of azimuths available here

'Lifestyle', heart disease, and the British public: c.1950 to c.2000

This thesis looks at how and why 'lifestyle' (understood as diet, exercise and other health behaviours) became the primary focus of public health in post-war Britain. It uses Britain's biggest killer - heart disease - as a lens through which to view this paradigm, tracing lifestyle's development from its roots in risk-factor epidemiology, through health promotion campaigns, to its embedment in the practices of everyday life. Lifestyle’s origins in post-war social medicine and epidemiology are explored through two case studies. Firstly, the identification of physical inactivity as a risk factor, and how exercise was reinvented as a preventive health activity, consciously practiced to compensate for sedentary working lives. The second explores how research on sugar, a putative risk factor for heart disease, was unsuccessful, with its nutritional, rather than epidemiological, approach. Such epidemiological research was translated into the political and policy spheres via the consensus for prevention that developed in 1970s. This viewed lifestyle as a means of halting the rise of non-communicable diseases such as heart disease, and the concomitant burden that they placed on the welfare state. Lifestyle was conceived as a set of practices that individual citizens were encouraged to perform as a quid pro quo for the continuation of the NHS free at the point of delivery. This focus on personal responsibility continued into the 1980s, as a major campaign on heart disease tried to persuade a sceptical public to exercise and eat healthily. In doing so, it appealed to Thatcherite values of self-reliance and family values, suggesting a confluence between lifestyle public health, neoliberalism and social conservatism. However, an explicitly class-based analysis of public health also emerged concurrently. Health inequalities research, specifically the Whitehall studies, disrupted the lifestyle paradigm, highlighting the structural determinants of health and suggesting an alternative narrative for public health in Britain

Osteology of Klamelisaurus gobiensis (Dinosauria, Eusauropoda) and the evolutionary history of Middle–Late Jurassic Chinese sauropods

Fossil-rich deposits from the Middle and Late Jurassic of China have yielded a diverse array of sauropod dinosaurs, including numerous species referred to Mamenchisaurus and Omeisaurus. Despite an abundance of fossils and a proliferation of taxa, the anatomy of Middle–Late Jurassic Chinese sauropods remains poorly documented. Here, we comprehensively redescribe and illustrate Klamelisaurus gobiensis from the Middle–Late Jurassic Shishugou Formation of northwest China. Phylogenetic analyses conducted under parsimony and time-calibrated Bayesian optimality criteria consistently recover Klamelisaurus as a member of a predominantly Chinese radiation of exceptionally long-necked eusauropods that includes Mamenchisaurus spp., Chuanjiesaurus, Qijianglong and Wamweracaudia. In most analyses, this lineage also includes Euhelopus, reviving a ‘traditional’ Euhelopodidae and calling into question the macronarian affinities of Euhelopus. Klamelisaurus shares several features with Euhelopus that are unique to a subset of East Asian taxa or rare among sauropods, including a convex ventral margin of the prezygodiapophyseal lamina in middle–posterior cervical vertebrae, a ventrally bifurcated postzygodiapophyseal lamina in posterior cervical vertebrae, and development of a rugose projection extending anteriorly from the epipophysis into the spinodiapophyseal fossa in most cervical vertebrae. Anatomical comparisons of the cervical vertebrae of Klamelisaurus to several other sauropodomorphs and insights from myological studies of extant archosaurs strongly suggest that this latter structure, often considered part of an epipophyseal-prezygapophyseal lamina, is an epaxial muscle scar that is distinct from pneumatic structures of the lateral surface of the neural spine. The phylogenetic and comparative anatomical data presented here provide a foundation for future revision of the taxonomy and systematics of sauropods from the Junggar and Sichuan basins

Post impact evaluation of an E-learning cross-infection control CD-ROM provided to all general dental practitioners in England

Aim To carry out a post-impact evaluation of a cross-infection control CD-ROM, developed for NHS dental teams as a continuing professional development e-learning tool. The program was commissioned by the Department of Health and developed by a project team through the UK Committee of Postgraduate Dental Deans. The Dental Practice Boardhad originally sent one copy of the CD-ROM to each dental practice in England in 2004. Method A quantitative statistical analysis of the results of 326 online respondents to the learning package and a survey of 118 dental practitioners drawn from the Dental Practice Board database. Results Practitioners felt the CD-ROM in this instance was well designed and appropriate for their needs. It is inclusive and accessible to a wide range of dental professionals including nurses and hygienists. Conclusions This form of continuing professional development is popular with dental practitioners, although it should not be the only form of continuing professional development available. However, whilst the project was generally regarded as successful, there were problems with the distribution of the CD-ROM. This suggests that anonline resource should be made available in the future

Activating protein phosphatase 2A (PP2A) enhances tristetraprolin (TTP) anti-inflammatory function in A549 lung epithelial cells

© 2016. Chronic respiratory diseases are driven by inflammation, but some clinical conditions (severe asthma, COPD) are refractory to conventional anti-inflammatory therapies. Thus, novel anti-inflammatory strategies are necessary. The mRNA destabilizing protein, tristetraprolin (TTP), is an anti-inflammatory molecule that functions to induce mRNA decay of cytokines that drive pathogenesis of respiratory disorders. TTP is regulated by phosphorylation and protein phosphatase 2A (PP2A) is responsible for dephosphorylating (and hence activating) TTP, amongst other targets. PP2A is activated by small molecules, FTY720 and AAL(S), and in this study we examine whether these compounds repress cytokine production in a cellular model of airway inflammation using A549 lung epithelial cells stimulated with tumor necrosis factor α (TNFα) in vitro. PP2A activators significantly increase TNFα-induced PP2A activity and inhibit mRNA expression and protein secretion of interleukin 8 (IL-8) and IL-6; two key pro-inflammatory cytokines implicated in respiratory disease and TTP targets. The effect of PP2A activators is not via an increase in TNFα-induced TTP mRNA expression; instead we demonstrate a link between PP2A activation and TTP anti-inflammatory function by showing that specific knockdown of TTP with siRNA reversed the repression of TNFα-induced IL-8 and IL-6 mRNA expression and protein secretion by FTY720. Therefore we propose that PP2A activators affect the dynamic equilibrium regulating TTP; shifting the equilibrium from phosphorylated (inactive) towards unphosphorylated (active) but unstable TTP. PP2A activators boost the anti-inflammatory function of TTP and have implications for future pharmacotherapeutic strategies to combat inflammation in respiratory disease

Parity Doubling and the S Parameter Below the Conformal Window

We describe a lattice simulation of the masses and decay constants of the lowest-lying vector and axial resonances, and the electroweak S parameter, in an SU(3) gauge theory with $N_f = 2$ and 6 fermions in the fundamental representation. The spectrum becomes more parity doubled and the S parameter per electroweak doublet decreases when $N_f$ is increased from 2 to 6, motivating study of these trends as $N_f$ is increased further, toward the critical value for transition from confinement to infrared conformality.Comment: 4 pages, 5 figures; to be submitted to PR

Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease

© 2019 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology Inc. Objective: Chronic obstructive pulmonary disease (COPD) is a progressive disease that causes significant mortality and morbidity worldwide and is primarily caused by the inhalation of cigarette smoke (CS). Lack of effective treatments for COPD means there is an urgent need to identify new therapeutic strategies for the underlying mechanisms of pathogenesis. Tristetraprolin (TTP) encoded by the Zfp36 gene is an anti-inflammatory protein that induces mRNA decay, especially of transcripts encoding inflammatory cytokines, including those implicated in COPD. Methods: Here, we identify a novel protective role for TTP in CS-induced experimental COPD using Zfp36aa/aa mice, a genetically modified mouse strain in which endogenous TTP cannot be phosphorylated, rendering it constitutively active as an mRNA-destabilising factor. TTP wild-type (Zfp36+/+) and Zfp36aa/aa active C57BL/6J mice were exposed to CS for four days or eight weeks, and the impact on acute inflammatory responses or chronic features of COPD, respectively, was assessed. Results: After four days of CS exposure, Zfp36aa/aa mice had reduced numbers of airway neutrophils and lymphocytes and mRNA expression levels of cytokines compared to wild-type controls. After eight weeks, Zfp36aa/aa mice had reduced pulmonary inflammation, airway remodelling and emphysema-like alveolar enlargement, and lung function was improved. We then used pharmacological treatments in vivo (protein phosphatase 2A activator, AAL(S), and the proteasome inhibitor, bortezomib) to promote the activation and stabilisation of TTP and show that hallmark features of CS-induced experimental COPD were ameliorated. Conclusion: Collectively, our study provides the first evidence for the therapeutic potential of inducing TTP as a treatment for COPD

Use of re-randomized data in meta-analysis

BACKGROUND: Outcomes collected in randomized clinical trials are observations of random variables that should be independent and identically distributed. However, in some trials, the patients are randomized more than once thus violating both of these assumptions. The probability of an event is not always the same when a patient is re-randomized; there is probably a non-zero covariance coming from observations on the same patient. This is of particular importance to the meta-analysts. METHODS: We developed a method to estimate the relative error in the risk differences with and without re-randomization of the patients. The relative error can be estimated by an expression depending on the percentage of the patients who were re-randomized, multipliers (how many times more likely it is to repeat an event) for the probability of reoccurrences, and the ratio of the total events reported and the initial number of patients entering the trial. RESULTS: We illustrate our methods using two randomized trials testing growth factors in febrile neutropenia. We showed that under some circumstances the relative error of taking into account re-randomized patients was sufficiently small to allow using the results in the meta-analysis. Our findings indicate that if the study in question is of similar size to other studies included in the meta-analysis, the error introduced by re-randomization will only minimally affect meta-analytic summary point estimate. We also show that in our model the risk ratio remains constant during the re-randomization, and therefore, if a meta-analyst is concerned about the effect of re-randomization on the meta-analysis, one way to sidestep the issue and still obtain reliable results is to use risk ratio as the measure of interest. CONCLUSION: Our method should be helpful in the understanding of the results of clinical trials and particularly helpful to the meta-analysts to assess if re-randomized patient data can be used in their analyses

Experimental demonstration of an ultra-low latency control plane for optical packet switching in data center networks

Optical interconnection networks have the potential to reduce latency and power consumption while increasing the bisection bandwidth of data center networks compared to electrical network architectures. Optical circuit-switched networking has been proposed but it is reconfigurable in milliseconds. Although switches operating on nanosecond timescales have been demonstrated, centrally scheduling such switching architectures is considered to be of high complexity, incurring significant delay penalties on the total switching latency. In this paper we present a high-speed control plane design based on a central switch scheduler for nanosecond optical switching which significantly reduces the end-to-end latency in the network compared to using the best electronic switches. We discuss the implementation of our control plane on field-programmable gate array (FPGA) boards and quantify its delay components. We focus on the output-port allocation circuit design which limits the scheduling delay and the end-to-end latency. Using our FPGA-implemented control plane, for a 32 × 32 switch, we experimentally demonstrate rack-scale optical packet switching with a minimum end-to-end head-to-tail latency of 71.0 ns, outperforming current state-of-the-art electronic switches. The effect of asynchronous control plane operation on the switch performance is evaluated experimentally. Finally, a new parallel allocation circuit design is presented decreasing the scheduling delay by 42.7% and the minimum end-to-end latency to 54.6 ns. More importantly, it enables scaling to a switch double the size (64 × 64) with a minimum end-to-end latency less than 71.0 ns. In a developed cycle-accurate network emulator we demonstrate nanosecond switching up to 60% of port capacity and average end-to-end latency less than 10 μs at full capacity while maintaining zero packet loss across all traffic loads