Stratigraphy of Cretaceous to Lower Pliocene sediments in the northern part of Cyprus based on comparative 87Sr/86Sr isotopic, nannofossil and planktonic foraminiferal dating

New age data from Sr isotope analysis and both planktonic foraminifera and nannofossils are presented and discussed here for the Upper Eocene–Upper Miocene sedimentary rocks of the Değirmenlik (Kythrea) Group. New dating is also given of some Cretaceous and Pliocene sediments. In a revised stratigraphy the Değirmenlik (Kythrea) Group is divided into ten formations. Different Upper Miocene formations are developed to the north and south of a regionally important, E–W-trending syn-sedimentary fault. The samples were dated wherever possible by three independent methods, namely utilizing Sr isotopes, calcareous nannofossils and planktonic foraminifera. Some of the Sr isotopic dates are incompatible with the nannofossil and/or the planktonic foraminiferal dates. This is mainly due to reworking within gravity-deposited or current-affected sediments. When combined, the reliable age data allow an overall biostratigraphy and chronology to be erected. Several of the boundaries of previously defined formations are revised. Sr data that are incompatible with well-constrained biostratigraphical ages are commonly of Early Miocene age. This is attributed to a regional uplift event located to the east of Cyprus, specifically the collision of the Anatolian (Eurasian) and Arabian (African) plates during Early Miocene time. This study, therefore, demonstrates that analytically sound Sr isotopic ages can yield geologically misleading ages, particularly where extensive sediment reworking has occurred. Convincing ages are obtained when isotopic dating is combined with as many forms of biostratigraphical dating as possible, and this may also reveal previously unsuspected geological events (e.g. tectonic uplift or current activity)

Coupled CO2-leakage and in situ fluid-mineral reactions in a natural CO2 reservoir, Green River, Utah

Spectroscopic studies and atomistic simulations of (hydr)oxide surfaces, which show that some aqueous cations bind to two or four surface oxygen atoms, have increased interest in multi-dentate surface complexation models (SCMs) [1-3]. However, it remains unclear how the (fitted) values of intrinsic equilibrium constants K int/m (referenced to infinite dilution) for δ-dentate M surface-binding reactions (δ >1) depend on the choice of concentration scale. In existing SCM codes, a surface complex may be treated in scales of either: molarity/molality ([]); site coverage fraction (Θ); surface mole fraction (x); molecular surface density (Γ, in mol•m-2); or relative density Γ/Γo (o, where Γo = 2 •10-5 mol•m-2 is the reference adsorbed density [4]). Our aim was to investigate, for ‘denticities’ 1≤ δ ≤4, how to convert the K int,δ values fitted for a given titration data set (the same solid concentration cS, specific surface area As, and monolayer site density ΓC) between different concentration scales. For single-site monodentate surface binding reactions, K int/m expressed in all concentration scales ([], Θ, x, Γ, o) reduce to the same value K M int,1. For the binding with δ≤2, conversion factors from xKM int,δ to ΘKM int,δ are about δ. From []KM int,δ to any other scale, they involve (csAsΓx)δ-1 which is ca. 10-5 for δ = 2 or 10-15 for δ = 4 at typical cS = 1 g•dm-3, As = 10 m2g-1, and ΓC = 10-6 mol•m-2. Conversions of K/int from [], Θ and x scales into the Γ scale involve (ΓC)1-δ, which has a value ranging from 10/5 to 10/18 at 10-6 < ΓC < 10-5 mol•m-2. The K/int conversions from [], Θ and x to the o scale include (Γo/ΓC)δ-1 which vanishes if ΓC = Γo (then oKM int,δ = xKM int,δ). Our findings show that the use of published KM int,δ (δ ≥ 2) in SCMs may lead to erroneous results, if concentration scales are not precisely defined both in the original fitting and in the subsequent application. At trace ion concentrations, using formally monodentate surface species would be safe especially on ‘strong’ sites, for which the density is typically adjusted to reproduce multi-site isotherms. Our results from comparative fitting of KM/int,δ with SCM codes using different scales show the magnitudes of ‘denticity effects’; we discuss ways to correct for these effects in re-using, comparing or correlating values of KM/int,δ. In a further thermodynamic treatment, e.g. deriving the entropy effect of the adsorption reaction from KM/int,δ fitted for different temperatures, the constants must first be made dimensionless and independent of δ and ΓC by converting them into the (o) scale.http://dx.doi.org/10.1016/j.gca.2010.04.036University of Tennessee; Oak Ridge National Laborator

Vitamin D Deficiency and Exogenous Vitamin D Excess Similarly Increase Diffuse Atherosclerotic Calcification in Apolipoprotein E Knockout Mice

Background: Observational data associate lower levels of serum vitamin D with coronary artery calcification, cardiovascular events and mortality. However, there is little interventional evidence demonstrating that moderate vitamin D deficiency plays a causative role in cardiovascular disease. This study examined the cardiovascular effects of dietary vitamin D deficiency and of vitamin D receptor agonist (paricalcitol) administration in apolipoprotein E knockout mice. Methods: Mice were fed atherogenic diets with normal vitamin D content (1.5IU/kg) or without vitamin D. Paricalcitol, or matched vehicle, was administered 3× weekly by intraperitoneal injection. Following 20 weeks of these interventions cardiovascular phenotype was characterized by histological assessment of aortic sinus atheroma, soluble markers, blood pressure and echocardiography. To place the cardiovascular assessments in the context of intervention effects on bone, structural changes at the tibia were assessed by microtomography. Results: Vitamin D deficient diet induced significant reductions in plasma vitamin D (p<0.001), trabecular bone volume (p<0.01) and bone mineral density (p<0.005). These changes were accompanied by an increase in calcification density (number of calcifications per mm2) of von Kossa-stained aortic sinus atheroma (461 versus 200, p<0.01). Paricalcitol administration suppressed parathyroid hormone (p<0.001), elevated plasma calcium phosphate product (p<0.005) and induced an increase in calcification density (472 versus 200, p<0.005) similar to that seen with vitamin D deficiency. Atheroma burden, blood pressure, metabolic profile and measures of left ventricular hypertrophy were unaffected by the interventions. Conclusion: Vitamin D deficiency, as well as excess, increases atherosclerotic calcification. This phenotype is induced before other measures of cardiovascular pathology associated clinically with vitamin D deficiency. Thus, maintenance of an optimal range of vitamin D signalling may be important for prevention of atherosclerotic calcification

Sr-Nd isotope geochemistry of the early Precambrian sub-alkaline mafic igneous rocks from the southern Bastar craton, Central India

Sr–Nd isotope data are reported for the early Precambrian sub-alkaline mafic igneous rocks of the southern Bastar craton, central India. These mafic rocks are mostly dykes but there are a few volcanic exposures. Field relationships together with the petrological and geochemical characteristics of these mafic dykes divide them into two groups; Meso-Neoarchaean sub-alkaline mafic dykes (BD1) and Paleoproterozoic (1.88 Ga) sub-alkaline mafic dykes (BD2). The mafic volcanics are Neoarchaean in age and have very close geochemical relationships with the BD1 type. The two groups have distinctly different concentrations of high-field strength (HFSE) and rare earth elements (REE). The BD2 dykes have higher concentrations of HFSE and REE than the BD1 dykes and associated volcanics and both groups have very distinctive petrogenetic histories. These rocks display a limited range of initial 143Nd/144Nd but a wide range of apparent initial 87Sr/86Sr. Initial 143Nd/144Nd values in the BD1 dykes and associated volcanics vary between 0.509149 and 0.509466 and in the BD2 dykes the variation is between 0.510303 and 0.510511. All samples have positive &#949;Nd values the BD1 dykes and associated volcanics have &#949;Nd values between +0.3 and +6.5 and the BD2 dykes between +1.9 to +6.0. Trace element and Nd isotope data do not suggest severe crustal contamination during the emplacement of the studied rocks. The positive &#949;Nd values suggest their derivation from a depleted mantle source. Overlapping positive &#949;Nd values suggest that a similar mantle source tapped by variable melt fractions at different times was responsible for the genesis of BD1 (and associated volcanics) and BD2 mafic dykes. The Rb–Sr system is susceptible to alteration and resetting during post-magmatic alteration and metamorphism. Many of the samples studied have anomalous apparent initial 87Sr/86Sr suggesting post-magmatic changes of the Rb–Sr system which severely restricts the use of Rb–Sr for petrogenetic interpretation

Seismic and geochemical evidence for large-scale mantle upwelling beneath the eastern Atlantic and western and central Europe

Seismic tomography and the isotope geochemistry of Cenozoic volcanic rocks suggest the existence of a large, sheet-like region of upwelling in the upper mantle which extends from the eastern Atlantic Ocean to central Europe and the western Mediterranean. A belt of extension and rifting in the latter two areas appears to lie above the intersection of the centre of the upwelling region with the base of the lithosphere. Lead, strontium and neodymium isotope data for all three regions converge on a restricted composition, inferred to be that of the upwelling mantle

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all &gt;0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

Effects of fluoxetine on functional outcomes after acute stroke (FOCUS): a pragmatic, double-blind, randomised, controlled trial

Background Results of small trials indicate that fluoxetine might improve functional outcomes after stroke. The FOCUS trial aimed to provide a precise estimate of these effects. Methods FOCUS was a pragmatic, multicentre, parallel group, double-blind, randomised, placebo-controlled trial done at 103 hospitals in the UK. Patients were eligible if they were aged 18 years or older, had a clinical stroke diagnosis, were enrolled and randomly assigned between 2 days and 15 days after onset, and had focal neurological deficits. Patients were randomly allocated fluoxetine 20 mg or matching placebo orally once daily for 6 months via a web-based system by use of a minimisation algorithm. The primary outcome was functional status, measured with the modified Rankin Scale (mRS), at 6 months. Patients, carers, health-care staff, and the trial team were masked to treatment allocation. Functional status was assessed at 6 months and 12 months after randomisation. Patients were analysed according to their treatment allocation. This trial is registered with the ISRCTN registry, number ISRCTN83290762. Findings Between Sept 10, 2012, and March 31, 2017, 3127 patients were recruited. 1564 patients were allocated fluoxetine and 1563 allocated placebo. mRS data at 6 months were available for 1553 (99·3%) patients in each treatment group. The distribution across mRS categories at 6 months was similar in the fluoxetine and placebo groups (common odds ratio adjusted for minimisation variables 0·951 [95% CI 0·839–1·079]; p=0·439). Patients allocated fluoxetine were less likely than those allocated placebo to develop new depression by 6 months (210 [13·43%] patients vs 269 [17·21%]; difference 3·78% [95% CI 1·26–6·30]; p=0·0033), but they had more bone fractures (45 [2·88%] vs 23 [1·47%]; difference 1·41% [95% CI 0·38–2·43]; p=0·0070). There were no significant differences in any other event at 6 or 12 months. Interpretation Fluoxetine 20 mg given daily for 6 months after acute stroke does not seem to improve functional outcomes. Although the treatment reduced the occurrence of depression, it increased the frequency of bone fractures. These results do not support the routine use of fluoxetine either for the prevention of post-stroke depression or to promote recovery of function. Funding UK Stroke Association and NIHR Health Technology Assessment Programme

Fluid flow and diagenesis in carbonate dominated Foreland Fold and Thrust Belts: petrographic inferences from field studies of late-diagenetic fabrics from Albania, Belgium, Canada, Mexico and Pakistan

Five different Foreland Fold and Thrust Belt (FFTB) systems have been studied with the aim of reconstructing the fluid flow history through time and to deduce the primary processes affecting reservoir units. By placing the diagenetic history into its kinematic framework, a database is generated allowing to predict diagenetic processes in FFTBs. Particular attention is paid to the late diagenetic processes since petrographical and geochemical data indicate that several of these processes reflect nonequilibrium conditions with respect to their host rocks. Some of these systems involve channeled fluid flow where the system is, to some extent, water dominated (e.g. hydrothermal karstification, MVT mineralisation, zebra dolomitization and cooling of formation water). Other processes are less fluid prone, but here cooling of entire thrust sheets by thrusting and recrystallisation of dolomite by layer parallel shortening during tectonic compression are processes proposed to explain the diagenetic alteration of some reservoirs