Consumer-based actions to reduce plastic pollution in rivers: a multi-criteria decision analysis approach

The use and management of single use plastics is a major area of concern for the public, regulatory and business worlds. Focusing on the most commonly occurring consumer plastic items present in European freshwater environments, we identified and evaluated consumer-based actions with respect to their direct or indirect potential to reduce macroplastic pollution in freshwater environments. As the main end users of these items, concerned consumers are faced with a bewildering array of choices to reduce their plastics footprint, notably through recycling or using reusable items. Using a Multi-Criteria Decision Analysis approach, we explored the effectiveness of 27 plastic reduction actions with respect to their feasibility, economic impacts, environmental impacts, unintended social/environmental impacts, potential scale of change and evidence of impact. The top ranked consumer-based actions were identified as: using wooden or reusable cutlery; switching to reusable water bottles; using wooden or reusable stirrers; using plastic free cotton-buds; and using refill detergent/ shampoo bottles. We examined the feasibility of top-ranked actions using a SWOT analysis (Strengths, Weaknesses, Opportunities and Threats) to explore the complexities inherent in their implementation for consumers, businesses, and government to reduce the presence of plastic in the environment

Macroplastic pollution in freshwater environments: focusing public and policy action

Understanding and managing plastic pollution is an increasingly important environmental priority for policy makers, businesses and scientists. Awareness of the potential damage to the world’s oceans has grown but there is less attention given to freshwater ecosystems. Yet, rivers are the dominant source of plastic pollution to the marine environment, as well as a potential sink, accumulating plastic from multiple sources. Actions to reduce the presence of macroplastics in rivers is fundamental to conserving both freshwater and marine environments, but there is limited understanding of potential pollution sources, vectors and storage. Importantly, there are only a handful of studies examining the typologies of freshwater macroplastic pollution, often using different categories and collection methods. This impedes setting priorities for scientific investigation and mitigation measures. The present study identifies the most prevalent macroplastic items in freshwater environments in Europe, with a focus on consumer plastic items, i.e. those that could potentially be reduced by targeted actions by the public, as well as industrial and government intervention. Our analysis addresses the differences between reported macroplastics in freshwater and marine environments as well as those estimated from litter rates. Our results identify a macroplastic “top ten”, i.e. those dominant plastic typologies that require a more focused effort to reformulate their use and management, as well as setting a common baseline for a more consistent data gathering and reporting approach

An in-service dynamic model of a diesel railcar from operational modal analysis and finite-element model updating

Builders of passenger rail vehicles need methods for predicting vibrational behaviour so that they can meet ride quality specifications. Conventional finite-element (FE) models used for stress analysis may not be accurate enough for this because of imponderables such as the stiffness of spot-welded joints. One solution is to adjust FE models based on vibration measurements. This model updating is now possible using commercially available software. Usually, the updating is based on vibration tests carried out under laboratory conditions, which may produce different results from normal operation. In this paper, two simple FE models of a railcar are updated using vibration data obtained from a newly designed railcar under in-service conditions. Measurements were made on a railcar loaded to represent crush-loaded conditions and running down track, with the only excitation that naturally occurring due to track roughness, engine excitation, aerodynamic loading etc. Unlike standard laboratory vibration testing, this input excitation could not be measured, so advanced forms of output-only analysis were required. By using these data as input to a commercial updating package, the simple FE models have been updated and the effectiveness of the technique assessed

Gene-mutation assays in lambda-lacZ transgenic mice : comparison of lacZ with endogenous genes in splenocytes and small intestinal epithelium

Comparison of results derived from transgenic animal gene-mutation assays with those from mutation analyses in endogenous genes is an important step in the validation of the former. We have used λlacZ transgenic mice to study alkylation-induced mutagenesis in vivo in (a) lacZ and hprt in spleen cells, and (b) lacZ and Dlb-1 in small intestine from λlacZ(+/0)/Dlb-1(a/b) mice. Induction of mutations by ethyl- and methylnitrosourea (ENU, MNU) and ethyl methanesulphonate (EMS) was investigated at 7 weeks after a single i.p. dose of each of these chemicals. In the small intestine, treatment with various dosages of ENU (10-150 mg/kg) resulted in a linear dose-response in both lacZ and Dlb-1. MNU (30 mg/kg) was also mutagenic in lacZ and Dlb-1, while EMS (250 mg/kg) did not significantly induce mutations in either gene. In spleen, ENU gave a linear dose-related response in both lacZ and hprt, MNU induced mutations in both lacZ and hprt, and EMS was only positive for lacZ. No differences in response were observed between single and split-dose treatment with ENU (1x50 or 5x10 mg/kg with a 1- or 7-day interval), both in spleen and small intestine, except for lacZ in small intestine, where the single high dose gave a significantly higher induction than the split dose with the 7-day interval. The overall results suggest that mutagenic effects of fractionated doses are generally additive. In most cases, the induction factor (ratio treated over controls) for mutations in lacZ was lower than that for hprt and Dlb-1, presumably due to a higher background in lacZ and/or a lower mutability of lacZ. The general concordance between the data for lacZ and the endogenous genes indicates that λlacZ transgenic mice are a suitable model to study induction of gene mutations in vivo. Chemicals/CAS: Alkylating Agents; Ethyl Methanesulfonate, 62-50-0; Ethylnitrosourea, 759-73-9; Genetic Markers; Hypoxanthine Phosphoribosyltransferase, EC 2.4.2.8; Methylnitrosourea, 684-93-5; Mutagen

β-Catenin activation synergizes with PTEN loss to cause bladder cancer formation

Although deregulation of the Wnt signalling pathway has been implicated in urothelial cell carcinoma (UCC), the functional significance is unknown. To test its importance, we have targeted expression of an activated form of beta-catenin to the urothelium of transgenic mice using Cre-Lox technology (UroIICRE(+) beta-catenin(exon3/+)). Expression of this activated form of beta-catenin led to the formation of localized hyperproliferative lesions by 3 months, which did not progress to malignancy. These lesions were characterized by a marked increase of the phosphatase and tensin homologue (PTEN) tumour suppressor protein. This appears to be a direct consequence of activating Wnt signalling in the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult bladder led rapidly to coincident beta-catenin and PTEN expression. This PTEN expression blocked proliferation. Next, we combined PTEN deficiency with beta-catenin activation and found that this caused papillary UCC. These tumours had increased pAKT signalling and were dependent on mammalian target of rapamycin (mTOR). Importantly, in human UCC, there was a significant correlation between high levels of beta-catenin and pAKT (and low levels of PTEN). Taken together these data show that deregulated Wnt signalling has a critical role in promoting UCC, and suggests that human UCC that have high levels of Wnt and PI3 kinase signalling may be responsive to mTOR inhibition

Cdx2 determines the fate of postnatal intestinal endoderm

Knock out of intestinal Cdx2 produces different effects depending upon the developmental stage at which this occurs. Early in development it produces histologically ordered stomach mucosa in the midgut. Conditional inactivation of Cdx2 in adult intestinal epithelium, as well as specifically in the Lgr5-positive stem cells, of adult mice allows long-term survival of the animals but fails to produce this phenotype. Instead, the endodermal cells exhibit cell-autonomous expression of gastric genes in an intestinal setting that is not accompanied by mesodermal expression of Barx1, which is necessary for gastric morphogenesis. Cdx2-negative endodermal cells also fail to express Sox2, a marker of gastric morphogenesis. Maturation of the stem cell niche thus appears to be associated with loss of ability to express positional information cues that are required for normal stomach development. Cdx2-negative intestinal crypts produce subsurface cystic vesicles, whereas untargeted crypts hypertrophy to later replace the surface epithelium. These observations are supported by studies involving inactivation of Cdx2 in intestinal crypts cultured in vitro. This abolishes their ability to form long-term growing intestinal organoids that differentiate into intestinal phenotypes. We conclude that expression of Cdx2 is essential for differentiation of gut stem cells into any of the intestinal cell types, but they maintain a degree of cell-autonomous plasticity that allows them to switch on a variety of gastric genes.

Hepatoprotective activity of Schouwia thebica Webb

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Lrig1 controls intestinal stem-cell homeostasis by negative regulation of ErbB signalling

Maintenance of adult tissues is carried out by stem cells and is sustained throughout life in a highly ordered manner. Homeostasis within the stem-cell compartment is governed by positive- and negative-feedback regulation of instructive extrinsic and intrinsic signals. ErbB signalling is a prerequisite for maintenance of the intestinal epithelium following injury and tumour formation. As ErbB-family ligands and receptors are highly expressed within the stem-cell niche, we hypothesize that strong endogenous regulators must control the pathway in the stem-cell compartment. Here we show that Lrig1, a negative-feedback regulator of the ErbB receptor family, is highly expressed by intestinal stem cells and controls the size of the intestinal stem-cell niche by regulating the amplitude of growth-factor signalling. Intestinal stem-cell maintenance has so far been attributed to a combination of Wnt and Notch activation and Bmpr inhibition. Our findings reveal ErbB activation as a strong inductive signal for stem-cell proliferation. This has implications for our understanding of ErbB signalling in tissue development and maintenance and the progression of malignant disease