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Microplastic pollution has been recognised as a global threat in marine environments and a danger to prey, predators and humans. Yet, there have been few studies in the western Indian Ocean, specifically along the Kenyan coast, which makes it difficult to estimate the extent of such pollution in the region. This is the first study on microplastics (MPs) in the sediments within creeks and estuaries (Tudor, Port Reitz and Mida creeks) on the Kenyan coast. In January/February and September 2018 sediment samples were collected for MPs analysis. The concentration of MPs differed between the sampling seasons and was distinctively higher in the second sampling season across particle sizes, suggesting that there were more MPs from larger terrestrial discharges due to increased runoff. The concentrations of total MPs, and the occurrence of different sizes, shapes and colours, were established under a microscope. The overall mean concentration was highest for the large size category of MPs (500–4 999 µm) at 9.1 (SE 0.8) particles cm−2, with Tudor Creek being more polluted with MPs than Port Reitz and Mida creeks. We recommend formulation of policies on proper plastic waste management and disposal to protect nearshore ecosystems which are rich in marine biodiversity. [ABSTRACT FROM AUTHOR]

In this letter, we report recent work on atomistic modeling of diffusion migration events of the fission gas product xenon in UO2 nuclear fuel. Under nonequilibrium conditions, Xe atoms can occupy the octahedral interstitial site, in contrast to the thermodynamically most stable uranium substitutional site. A transient migration mechanism involving Xe and two oxygen atoms is identified using basin constrained molecular dynamics employing a Buckingham type interatomic potential. This mechanism is then validated using density functional theory calculations using the nudged elastic band method. An overall reduction in the migration barrier of 1.6-2.7 eV is obtained compared to vacancy-mediated diffusion on the uranium sublattice. [ABSTRACT FROM AUTHOR]

Management of recreational fisheries cannot be based on biological and stock assessment data alone but needs to include appropriate social aspects (including knowledge, attitudes and behaviour) of anglers within the fishery. The primary purpose of this study was to evaluate and complement existing recreational fisheries research, through the analysis of demographic and psychographic angler attributes collected from two independent, shore-based snapshot monitoring surveys conducted on the KwaZulu-Natal (KZN) coastline of South Africa, in 1994–1996 and 2009–2010. Results show significant changes between the two survey events in the demographics of anglers (including ethnic composition, age distribution, years of fishing experience and employment status) participating in the KZN shore-based linefishery. Traditional management regulations (minimum size limits, daily bag limits and closed seasons), though appearing to have support, have had limited effectiveness, based on the increased levels of admitted non-compliance and poor knowledge of regulations for target species. Anglers in both surveys believed that catches had declined over the years, with overfishing being the most common reason given. The results are discussed in the context of changing management practices in the KZN recreational shore-based linefishery. The implications of changes in fisheries management policies and responsibilities along the KZN coast are highlighted. [ABSTRACT FROM PUBLISHER]

Background/Objectives:Obese subjects have increased number of enlarged fat cells that are reduced in size but not in number in post-obesity. We performed DNA methylation profiling in fat cells with the aim of identifying differentially methylated DNA sites (DMS) linked to adipose hyperplasia (many small fat cells) in post-obesity.Subjects/Methods:Genome-wide DNA methylation was analyzed in abdominal subcutaneous fat cells from 16 women examined 2 years after gastric bypass surgery at a post-obese state (body mass index (BMI) 26±2 kg m-2, mean±s.d.) and from 14 never-obese women (BMI 25±2 kg m-2). Gene expression was analyzed in subcutaneous adipose tissue from nine women in each group. In a secondary analysis, we examined DNA methylation and expression of adipogenesis genes in 15 and 11 obese women, respectively.Results:The average degree of DNA methylation of all analyzed CpG sites was lower in fat cells from post-obese as compared with never-obese women (P=0.014). A total of 8504 CpG sites were differentially methylated in fat cells from post-obese versus never-obese women (false discovery rate 1%). DMS were under-represented in CpG islands and surrounding shores. The 8504 DMS mapped to 3717 unique genes; these genes were over-represented in cell differentiation pathways. Notably, 27% of the genes linked to adipogenesis (that is, 35 of 130) displayed DMS (adjusted P=10−8) in post-obese versus never-obese women. Next, we explored DNA methylation and expression of genes linked to adipogenesis in more detail in adipose tissue samples. DMS annotated to adipogenesis genes were not accompanied by differential gene expression in post-obese compared with never-obese women. In contrast, adipogenesis genes displayed differential DNA methylation accompanied by altered expression in obese women.Conclusions:Global CpG hypomethylation and over-representation of DMS in adipogenesis genes in fat cells may contribute to adipose hyperplasia in post-obese women. [ABSTRACT FROM AUTHOR]

We employ a combination of first-principles calculations and optical characterization experiments to explain the mechanism by which Ga3+ doping prevents the trapping of free carriers due to shallow traps in RE3Al5O12 garnet scintillators (where RE represents a 3+ rare-earth cation). Specifically, we confirm that Ga3+ doping does not reduce the defect concentration (defect engineering), but rather leads to shifts in the valence and conduction bands such that the energy level of shallow defects is no longer in the forbidden gap where electrons can be trapped (band-gap engineering). [ABSTRACT FROM AUTHOR]

There is an increasing interest in the use of donor-derived cfDNA (dd-cfDNA) in transplantation for non-invasive diagnosis of allograft injury. We hereby describe a non-commercial routine procedure for dd-cfDNA detection and quantification using digital droplet PCR and target-specific preamplification of a SNP-panel of 35 SNP-assays. The method is based on the difference in genotype between recipients and donors. After establishing our protocol, it has been used in a prospective study following recipients for 12 months after heart transplantation (HTx), and we here briefly describe our protocol. A total of 728 samples from 67 HTx patients have been retrieved and analyzed. The recipients were genotyped preoperatively with respect to the SNP-panel. Upon transplantation, the donor genotype was interrogated with respect to the homozygous alleles found in the recipient. After HTx, blood samples were collected in cell free DNA collection tubes and delivered within the same day to the hospital laboratory. Plasma was separated by centrifugation at 2000g and 16000g, respectively. Isolated plasma was stored at -80C or used immediately for cfDNA extraction. Quality controls were performed by the 4200 Tape Station. The same primers were used for preamplification and downstream PCR. Non-template controls were included in all preamplification steps. The amount of dd-cfDNA was calculated as a fraction of the total cfDNA. The variation of extracted cfDNA yield was 10-130 ng/ml plasma. The 50-800 bp sized cfDNA constitutes 90% of the extracted samples, indicating a low background. An average of 2-5 informative SNPS assays for each transplant recipient were used for dd-cfDNA quantification with a detection rate down to 0.01% dd-cfDNA. Elevation of dd-cfDNA was seen not only in conjunction with cellular rejection but also during infection and in episodes of heart failure Samples from HTx recipients demonstrated low levels of dd-cfDNA in consecutive samples during optimal treatment in non-eventful cases. Elevation of dd-cfDNA was seen not only during rejection but also in other conditions. This non-invasive method is relatively cheap, enables large sample yields by preamplification, has a fast turn-around time (48 hours) and is thus useful for clinical monitoring of HTx patients. However, it needs to be carefully related to clinical events. [ABSTRACT FROM AUTHOR]

The clinical course of patients after heart transplantation (HTx) is complex and consists of multiple possibly hazardous events affecting both the recipient and the graft. We established a non-commercial, university-hospital based routine procedure to investigate patients after HTx that allowed us to measure not only the hitherto used donor fraction of but also total values of donor-derived cell-free DNA (dd-cfDNA) and recipient-derived cell-free DNA (rd-cfDNA). We then tested this approach in a prospective trial. We used the method described by our group, that is, SNP-panel based digital droplet PCR in 67 prospective patients on 728 paired blood samples and endomyocardial biopsies during one year after HTx. We had full access to the patients' clinical course. The course of cfDNA was expressed separately for both dd-cfDNA, rd-cfDNA as well as the well-known donor fraction. Rejection could be detected by a rise in both dd-cfDNA and donor fraction. The proposed level of.2% donor fraction as a threshold for stable graft function could be confirmed. Amongst the unexpected findings, a transient but marked elevation of rd-cfDNA in the middle follow-up period was the most consistent. This could only sometimes be explained clinically (e.g., by infection or bleeding) and led to several false-positive values of donor fraction when rd-cfDNA levels returned to basic, despite constant low levels of dd-cfDNA. Other interesting findings included chronic rejection (high levels of dd-cfDNA and donor fraction), cardiac CMV-infection (increased levels of dd-cfDNA with moderate rise in rd-cfDNA, thus mimicking rejection with high donor fraction), false-negative rejection (low levels of dd-cfDNA but a positive biopsy), chronic kidney failure (rd-cfDNA levels showing partial positive covariance with creatinine-levels), right heart failure (markedly elevated dd-cfDNA) and medication issues (high levels of dd-cfDNA and a history of poor adherence, but negative biopsy). The full statistical analysis will be available later. The course of cfDNA after HTx is more complex than it has been presented so far. Our study illustrates clear advantages of separately monitoring dd-cfDNA and rd-cfDNA as opposed to only donor fraction as it is the standard so far. It also stresses the importance of close contact between the laboratory and clinicians involved in patient care. [ABSTRACT FROM AUTHOR]

The thermal and magnetic properties of uranium dioxide, a prime nuclear fuel and thoroughly studied actinide material, remain a long standing puzzle, a result of strong coupling between magnetism and lattice vibrations. The magnetic state of this cubic material is characterized by a 3-k non-collinear antiferromagnetic structure and multidomain Jahn-Teller distortions, likely related to its anisotropic thermal properties. Here we show that single crystals of uranium dioxide subjected to strong magnetic fields along threefold axes in the magnetic state exhibit the abrupt appearance of positive linear magnetostriction, leading to a trigonal distortion. Upon reversal of the field the linear term also reverses sign, a hallmark of piezomagnetism. A switching phenomenon occurs at ±18 T, which persists during subsequent field reversals, demonstrating a robust magneto-elastic memory that makes uranium dioxide the hardest piezomagnet known. A model including a strong magnetic anisotropy, elastic, Zeeman, Heisenberg exchange, and magnetoelastic contributions to the total energy is proposed.The nuclear fuel uranium dioxide is of intrinsic interest due to its industrial applications but it also exhibits intriguing electronic and magnetic properties. Here, the authors demonstrate how its complex magnetic structure and interactions give rise to a strong piezomagnetic effect.

The development of embedded atom method (EAM) many-body potentials for actinide oxides and associated mixed oxide (MOX) systems has motivated the development of a complementary parameter set for gas-actinide and gas-oxygen interactions. A comprehensive set of density functional theory (DFT) calculations were used to study Xe and Kr incorporation at a number of sites in CeO2, ThO2, UO2 and PuO2. These structures were used to fit a potential, which was used to generate molecular dynamics (MD) configurations incorporating Xe and Kr at 300 K, 1500 K, 3000 K and 5000 K. Subsequent matching to the forces predicted by DFT for these MD configurations was used to refine the potential set. This fitting approach ensured weighted fitting to configurations that are thermodynamically significant over a broad temperature range, while avoiding computationally expensive DFT-MD calculations. The resultant gas potentials were validated against DFT trapping energies and are suitable for simulating combinations of Xe and Kr in solid solutions of CeO2, ThO2, UO2 and PuO2, providing a powerful tool for the atomistic simulation of conventional nuclear reactor fuel UO2 as well as advanced MOX fuels.

Molecular dynamics simulations have been conducted to study the effects of dislocations and grain boundaries on He diffusion in [Formula: see text]. Calculations were carried out for the {1 0 0}, {1 1 0} and {1 1 1} [Formula: see text] edge dislocations, the screw [Formula: see text] dislocation and Σ5, Σ13, Σ19 and Σ25 tilt grain boundaries. He diffusivity as a function of distance from the dislocation core and grain boundaries was investigated for the temperature range 2300-3000 K. An enhancement in diffusivity was predicted within 20 Å of the dislocations or grain boundaries. Further investigation showed that He diffusion in the edge dislocations follows anisotropic behaviour along the dislocation core, suggesting that pipe diffusion occurs. An Arrhenius plot of He diffusivity against the inverse of temperature was also presented and the activation energy calculated for each structure, as a function of distance from the dislocation or grain boundary.

Using ab initio molecular dynamics simulations and nudged elastic band calculations we examine the finite temperature stability, transition pathways, and migration mechanisms of large oxygen clusters in UO(2+x). Here we specifically consider the recently proposed split quad-interstitial and cuboctahedral oxygen clusters. It is shown that isolated cuboctahedral clusters may transform into more stable configurations that are closely linked to the split quad-interstitial. The split quad-interstitial is stable with respect to single interstitials occupying the empty octahedral holes of the UO(2) lattice. In order to better understand discrepancies between theory and experiments, the simulated atomic pair distribution functions for the split quad-interstitial structures are analyzed with respect to the distribution function for U(4)O(9) previously obtained from neutron diffraction data. Our nudged elastic band calculations suggest that the split quad-interstitial may migrate by translating one of its constituent di-interstitial clusters via a barrier that is lower than the corresponding barrier for individual interstitials, but higher than the barrier for the most stable di-interstitial cluster.

In the presence of ouabain (1 mM), acetylcholine and KCl (5 mM) evoked endothelium-independent relaxations in rat hepatic arteries. Treatment with capsaicin (10 microM), scopolamine (1 microM) or CGRP(8 - 37) (3 microM) prevented these relaxations. Acetylcholine-induced relaxations in intact arterial segments in the presence of indomethacin (10 microM) and N(G)-nitro-L-arginine (0.3 mM) were only partially inhibited by ouabain plus BaCl(2) (30 microM). However, ouabain plus BaCl(2) almost abolished such relaxations in capsaicin-pre-treated preparations. In arteries without endothelium, the neurosecretagogue alpha-latrotoxin (1 nM) induced complete relaxations, which were abolished by CGRP(8 - 37) or pre-treatment with capsaicin. alpha-Latrotoxin also induced a smooth muscle hyperpolarization (12+/-2 mV), which was abolished by CGRP(8 - 37). The ability of ouabain to disclose a CGRP-mediated neurogenic relaxation must be considered when this agent is used as a pharmacological tool. The results further suggest that CGRP is a nerve-derived hyperpolarizing factor in the rat hepatic artery.

1. In the rat hepatic artery, the SK(Ca) inhibitors UCL 1684 (300 nM) completely blocked, and scyllatoxin (1 microM) and d-tubocurarine (100 microM) partially inhibited EDHF relaxations when each of them was combined with charybdotoxin (300 nM). 2. The IK(Ca) inhibitors clotrimazole (3 microM) and 2-chlorophenyl-bisphenyl-methanol (3 microM) strongly depressed EDHF relaxations when each of them was combined with apamin (300 nM). The cytochrome P450 mono-oxygenase inhibitor ketoconazole (10 microM) had no effect in the presence of apamin. 3. Ciclazindol (10 microM), which abolishes EDHF relaxations in the presence of apamin, almost completely prevented the calcium ionophore (A23187) stimulated (86)Rb(+) influx via the Gardos channel (IK(Ca)) in human erythrocytes. 4. The Na(+)/K(+) ATPase inhibitor ouabain (500 microM) and the K(IR) blocker Ba(2+) (30 microM) neither alone nor in combination inhibited EDHF relaxations. Ba(2+) was also without effect in the presence of either apamin or charybdotoxin. 5. In contrast to EDHF, an increase in extracellular [K(+)] from 4.6 mM to 9.6, 14.6 and 19.6 mM inconsistently relaxed arteries. In K(+)-free physiological salt solution, re-admission of K(+) always caused complete and sustained relaxations which were abolished by ouabain but unaffected by Ba(2+). 6. The present study provides pharmacological evidence for the involvement of SK(Ca) and IK(Ca) in the action of EDHF in the rat hepatic artery. Our results are not consistent with the idea that EDHF is K(+) activating Na(+)/K(+) ATPase and K(IR) in this blood vessel.

The endogenous cannabinoid receptor agonist anandamide is a powerful vasodilator of isolated vascular preparations, but its mechanism of action is unclear. Here we show that the vasodilator response to anandamide in isolated arteries is capsaicin-sensitive and accompanied by release of calcitonin-gene-related peptide (CGRP). The selective CGRP-receptor antagonist 8-37 CGRP, but not the cannabinoid CB1 receptor blocker SR141716A, inhibited the vasodilator effect of anandamide. Other endogenous (2-arachidonylglycerol, palmitylethanolamide) and synthetic (HU 210, WIN 55,212-2, CP 55,940) CB1 and CB2 receptor agonists could not mimic the action of anandamide. The selective 'vanilloid receptor' antagonist capsazepine inhibited anandamide-induced vasodilation and release of CGRP. In patch-clamp experiments on cells expressing the cloned vanilloid receptor (VR1), anandamide induced a capsazepine-sensitive current in whole cells and isolated membrane patches. Our results indicate that anandamide induces vasodilation by activating vanilloid receptors on perivascular sensory nerves and causing release of CGRP. The vanilloid receptor may thus be another molecular target for endogenous anandamide, besides cannabinoid receptors, in the nervous and cardiovascular systems.