Spit-systems – an overlooked target in hydrocarbon exploration: the Holocene to Recent Skagen Odde, Denmark

Well-constrained depositional models are essential for successful exploration and field development. The Skagen spitsystem offers a unique possibility for the establishment of a depositional model constrained by excellent outcrops, well-defined palaeogeography, good age control and detailed observations on hydrodynamics and morphology of the prograding part of the spit-system. The model offers a supplementary interpretation of shallow marine sandstones to the existing delta and linear shoreface models. The sand-dominated Skagen spit-system is c. 22 km long, 4 km wide and up to 35 m thick, with a sand volume of c. 2.2 km3. If filled with oil, this system would contain 0.6 km3 corresponding to 3.8 x 109 barrels assuming a porosity of 30% and an oil saturation of 90%. This is comparable in size with the largest Danish oil field (the Dan field), in the North Sea. Reservoir models for isolated linear ‘offshore’ sandstone bodies have been controversial for many years. Their size and internal indications of palaeocurrent directions are similar to those of the spit-system model, and this model may therefore be applicable for some of these bodies

The Rødryggen-1 and Brorson Halvø-1 fully cored boreholes (Upper Jurassic – Lower Cretaceous), Wollaston Forland, North-East Greenland – an introduction

Two fully cored boreholes, the Rødryggen-1 and the Brorson Halvø-1, were drilled in Wollaston Forland, North-East Greenland, in 2009 and 2010, respectively. The objective was to test the stratigraphic development of the Upper Jurassic – Lower Cretaceous mud-dominated succession in two different settings within the same fault block of a developing half-graben: centrally (Rødryggen-1 borehole) and near the uplifted crest of the rotating fault block (Brorson Halvø-1 borehole). The drilled deposits are equivalent to the principal petroleum source-rock sequence of the petroliferous basins of North-West Europe, Siberia, and basins off eastern Canada and provide a new record of an important phase of marine deoxygenation in the proto-North Atlantic region

Organic geochemistry of an Upper Jurassic – Lower Cretaceous mudstone succession in a narrow graben setting, Wollaston Forland Basin, North-East Greenland

The Oxfordian–Ryazanian was a period of widespread deposition of marine organic-rich mudstones in basins formed during the early phases of the rifting that heralded the formation of the present-day North Atlantic. Occasionally, uninterrupted deposition prevailed for 20 million years or more. Today, mudstones of this time interval are found on the shelves bordering the North Atlantic and adjacent areas from Siberia to the Netherlands. Here, we report data on two fully cored boreholes from Wollaston Forland (North-East Greenland, approx. 74° N), which represent an uninterrupted succession from the upper Kimmeridgian to the Hauterivian. The boreholes record basin development at two different positions within an evolving halfgraben, located at the margin of the main rift, and thus partially detached from it. Although the overall depositional environment remained an oxygen-restricted deep-shelf setting, rifting-related changes can be followed through the succession. The Kimmeridgian was a period of eustatic highstand and records the incipient rifting with a transgressive trend straddling the transition to the lower Volgian by a gradual change from deposits with high levels of total organic carbon (TOC) and kerogen rich in allochthonous organic matter to deposits with lower TOC and a higher proportion of autochthonous organic matter. This is followed by a slight regressive trend with lower TOC and increased proportions of allochthonous organic matter until rifting culminated in the middle Volgian–Ryazanian, indicated by increasing autochthonous organic matter and higher TOC, which prevailed until basin ventilation occurred towards the end of the Ryazanian. The properties of the reactive kerogen fraction remained rather stable irrespective of TOC, underlining the effect of terrigenous matter input for TOC. These variations are also captured by biological markers and stable carbon isotopes. The deposits are very similar to equivalent successions elsewhere in the proto-North Atlantic region, albeit the proportion of terrigenous kerogen is greater

Cell type-specific anti-cancer properties of valproic acid: independent effects on HDAC activity and Erk1/2 phosphorylation

<p>Abstract</p> <p>Background</p> <p>The anti-epileptic drug valproic acid (VPA) has attracted attention as an anti-cancer agent.</p> <p>Methods</p> <p>The present study investigated effects of VPA exposure on histone deacetylase (HDAC) inhibition, cell growth, cell speed, and the degree of Erk1/2 phosphorylation in 10 cell lines (BT4C, BT4Cn, U87MG, N2a, PC12-E2, CSML0, CSML100, HeLa, L929, Swiss 3T3).</p> <p>Results</p> <p>VPA induced significant histone deacetylase (HDAC) inhibition in most of the cell lines, but the degree of inhibition was highly cell type-specific. Moreover, cell growth, motility and the degree of Erk1/2 phosphorylation were inhibited, activated, or unaffected by VPA in a cell type-specific manner. Importantly, no relationship was found between the effects of VPA on HDAC inhibition and changes in the degree of Erk1/2 phosphorylation, cell growth, or motility. In contrast, VPA-induced modulation of the MAPK pathway downstream of Ras but upstream of MEK (i.e., at the level of Raf) was important for changes in cell speed.</p> <p>Conclusions</p> <p>These results suggest that VPA can modulate the degree of Erk1/2 phosphorylation in a manner unrelated to HDAC inhibition and emphasize that changes in the degree of Erk1/2 phosphorylation are also important for the anti-cancer properties of VPA.</p

Cost effectiveness of potential ART adherence monitoring interventions in sub-saharan Africa

Background Interventions based around objective measurement of adherence to antiretroviral drugs for HIV have potential to improve adherence and to enable differentiation of care such that clinical visits are reduced in those with high adherence. It would be useful to understand the approximate upper limit of cost that could be considered for such interventions of a given effectiveness in order to be cost effective. Such information can guide whether to implement an intervention in the light of a trial showing a certain effectiveness and cost. Methods An individual-based model, calibrated to Zimbabwe, which incorporates effects of adherence and resistance to antiretroviral therapy, was used to model the potential impact of adherence monitoring-based interventions on viral suppression, death rates, disability adjusted life years and costs. Potential component effects of the intervention were: enhanced average adherence when on ART, reduced risk of ART discontinuation, and reduced risk of resistance acquisition. We considered a situation in which viral load monitoring is not available and one in which it is. In the former case, it was assumed that care would be differentiated based on the adherence level, with fewer clinic visits in those demonstrated to have high adherence. In the latter case, care was assumed to be primarily differentiated according to viral load level. The maximum intervention cost required to be cost effective was calculated based on a cost effectiveness threshold of $500 per DALY averted. Findings In the absence of viral load monitoring, an adherence monitoring-based intervention which results in a durable 6$50 per person-year on ART, mainly driven by the cost savings of differentiation of care. In the presence of viral load monitoring availability, an intervention with a similar effect on viral load suppression was cost-effective when costing $23-$32 per year, depending on whether the adherence intervention is used to reduce the level of need for viral load measurement. Conclusion The cost thresholds identified suggest that there is clear scope for adherence monitoringbased interventions to provide net population health gain, with potential cost-effective use in situations where viral load monitoring is or is not available. Our results guide the implementation of future adherence monitoring interventions found in randomized trials to have health benefit

Mortality prediction in chronic obstructive pulmonary disease comparing the GOLD 2015 and GOLD 2019 staging: a pooled analysis of individual patient data

In 2019, The Global Initiative for Chronic Obstructive Lung Disease (GOLD) modified the grading system for patients with COPD, creating 16 subgroups (1A–4D). As part of the COPD Cohorts Collaborative International Assessment (3CIA) initiative, we aim to compare the mortality prediction of the 2015 and 2019 COPD GOLD staging systems. We studied 17 139 COPD patients from the 3CIA study, selecting those with complete data. Patients were classified by the 2015 and 2019 GOLD ABCD systems, and we compared the predictive ability for 5-year mortality of both classifications. In total, 17 139 patients with COPD were enrolled in 22 cohorts from 11 countries between 2003 and 2017; 8823 of them had complete data and were analysed. Mean±sd age was 63.9±9.8 years and 62.9% were male. GOLD 2019 classified the patients in milder degrees of COPD. For both classifications, group D had higher mortality. 5-year mortality did not differ between groups B and C in GOLD 2015; in GOLD 2019, mortality was greater for group B than C. Patients classified as group A and B had better sensitivity and positive predictive value with the GOLD 2019 classification than GOLD 2015. GOLD 2015 had better sensitivity for group C and D than GOLD 2019. The area under the curve values for 5-year mortality were only 0.67 (95% CI 0.66–0.68) for GOLD 2015 and 0.65 (95% CI 0.63–0.66) for GOLD 2019

The Nature of Knowledge in Composition and Literary Understanding: The Question of Specificity

↵PETER SMAGORINSKY is Assistant Professor, College of Education, University of Oklahoma, 820 Van Vleet Oval, Norman, OK 73019-0. He specializes in classroom literacy.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema

<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p