Plastic recycling stripped naked – from circular product to circular industry with recycling cascade

This perspective combines various expertise to develop and analyse the concept of technology cascade for recycling waste plastics with the goal of displacing as much fossil crude oil as possible. It thereby presents archetype recycling technologies with their strengths and weaknesses. It then combines them in various cascades to process a representative plastic mix, and determines how much (fossil) naphtha could be displaced and at which energy consumption. The cascades rely on a limited number of parameters that are fully reported in supplementary information and that were used in a simple and transparent spreadsheet model. The calculated results bust several common myths in plastic recycling, e. g. by prioritizing here recycled volume over recycling efficiency, and prioritizing circular industry over circular products. It unravels the energy cost of solvent-based recycling processes, shows the key role of gasification and the possibility to displace up to 70 % of the fossil feedstock with recycled carbon, a recycling rate that compares well with that aluminium, steel or paper. It suggests that deeper naphtha displacement would require exorbitant amount of energy. It therefore argues for the need to complement recycling with the use of renewable carbon, e. g. based on biomass, to fully defossilise the plastic industry.</p

Clarifying European terminology in plastics recycling

The increasing activities in plastics recycling have led to a sprawl of terminology describing different technologies and technology categorizations. This creates not only linguistic confusion but also makes it difficult for regulators, investors, corporate leaders and other stakeholders to fully understand the relationship between different technologies, potentially leading to suboptimal decisions on policy, investment, or collaboration. To bring clarity to this topic, this manuscript provides an overview of (i) the different circular pathways for plastics, with a focus on recycling, (ii) the most common categorization of recycling technologies, (iii) what is considered ‘recycling’ by the European Commission and (iv) some alternative terms used in grey and academic literature to describe recycling technologies

Dark and visible matter with broken R-parity and the axion multiplet

A small breaking of R-parity reconciles thermal leptogenesis, gravitino dark matter and primordial nucleosynthesis. We find that the same breaking relaxes cosmological bounds on the axion multiplet. Naturally expected spectra become allowed and bounds from late particle decays become so weak that they are superseded by bounds from non-thermal axion production. In this sense, the strong CP problem serves as an additional motivation for broken R-parity.Comment: 13 pages + refs, 1 table, v2: refs added, minor changes in presentation, v3: refs added, added discussion of decays into Higgs and Higgsino, matches published versio

β3-Adrenoceptor-mediated relaxation of rat and human urinary bladder:roles of BKCa channels and Rho kinase

Previous studies suggest that the large-conductance Ca2+-activated K+ (BKCa) channel and Rho-kinase play major roles in the control of urinary bladder tone. Here, we investigated their involvement in beta-adrenoceptor (AR)-mediated relaxation of rat and human bladder. Concentration-response curves of isoprenaline and mirabegron-induced bladder relaxation were generated against passive tension and KCl- and carbachol-induced tone, in the absence or presence of the BKCa channel inhibitor iberiotoxin (100 nM) or the Rho-kinase inhibitor Y27,632 (1 mu M). Myosin light chain (MLC) phosphorylation was studied by Western blot. In rat, iberiotoxin only slightly altered isoprenaline- and mirabegron-induced relaxation against KCl-induced tone but attenuated relaxation by both agonists against carbachol-induced tone. Y27,632 enhanced isoprenaline- or mirabegron-induced relaxation only against carbachol-induced tone. In humans, iberiotoxin slightly enhanced relaxation by both agonists against carbachol-induced pre-contraction. Y27,632 did not change isoprenaline-induced relaxation but enhanced that by mirabegron. Under passive tension, MLC phosphorylation was markedly reduced by both beta-AR agonists, an effect insensitive to Y27,632. In the presence of carbachol, both beta-AR agonists increased MLC phosphorylation, an effect reduced by Y27,632 only in the presence of 1 mu M carbachol. These results indicate that the extent of BKCa channel and Rho-kinase involvement in relaxation induced by beta-AR agonists depends on pre contractile stimulus and species

Glycogen synthase 2 is a novel target gene of peroxisome proliferator-activated receptors

Glycogen synthase 2 (Gys-2) is the ratelimiting enzyme in the storage of glycogen in liver and adipose tissue, yet little is known about regulation of Gys-2 transcription. The peroxisome proliferator-activated receptors (PPARs) are transcription factors involved in the regulation of lipid and glucose metabolism and might be hypothesized to govern glycogen synthesis as well. Here, we show that Gys-2 is a direct target gene of PPARα, PPARβ/δ and PPARγ. Expression of Gys-2 is significantly reduced in adipose tissue of PPARα-/-, PPARβ/δ-/- and PPARγ+/- mice. Furthermore, synthetic PPARβ/δ, and γ agonists markedly up-regulate Gys-2 mRNA and protein expression in mouse 3T3-L1 adipocytes. In liver, PPARα deletion leads to decreased glycogen levels in the refed state, which is paralleled by decreased expression of Gys-2 in fasted and refed state. Two putative PPAR response elements (PPREs) were identified in the mouse Gys-2 gene: one in the upstream promoter (DR-1prom) and one in intron 1 (DR-1int). It is shown that DR-1int is the response element for PPARs, while DR-1prom is the response element for Hepatic Nuclear Factor 4 alpha (HNF4α). In adipose tissue, which does not express HNF4α, DR-1prom is occupied by PPARβ/δ and PPARγ, yet binding does not translate into transcriptional activation of Gys-2. Overall, we conclude that mouse Gys-2 is a novel PPAR target gene and that transactivation by PPARs and HNF4α is mediated by two distinct response elements

IL-10 Mediates Rosiglitazone-Induced Kidney Protection in Cisplatin Nephrotoxicity

Cisplatin, a major anti-neoplastic drug, is known to be nephrotoxic and inflammation-inducing. A peroxisome proliferator-activated receptor gamma agonist, regulating lipid metabolism, has known to have anti-inflammatory effect, but the protection mechanisms in various kidney injuries are not fully understood. The purpose of this study was to examine the reno-protective effect of rosiglitazone on cisplatin nephrotoxicity in mice focusing on inflammation and apoptosis. Male BALB/c mice were pretreated with rosiglitazone (10 mg/kg) or vehicle through daily intraperitoneal injection for 3 days and then were given a single injection of cisplatin (20 mg/kg). Cisplatin induced a significant rise in blood urea nitrogen and creatinine levels, and tubular cell damage with marked tissue inflammation. Tissue cytokines and chemokines measured by a cytometric bead array showed increased TNF-α, IL-6, MCP-1, and IFN-γ levels, while IL-10, an anti-inflammatory cytokine, was significantly decreased by cisplatin treatment. However, rosiglitazone pretreatment substantially reversed the depressed IL-10 level with simultaneous suppression of proinflammatory cytokines and chemokines. This tissue cytokine and chemokine milieu was associated with marked attenuation of kidney injury elicited by cisplatin. These findings suggest that the rosiglitazone-mediated renoprotective effect in cisplatin nephrotoxicity of mice is partially mediated by upregulation of anti-inflammatory IL-10 production

The transcription factor osterix (SP7) regulates BMP6‐induced human osteoblast differentiation

The transcription factor Osterix (Sp7) is essential for osteoblastogenesis and bone formation in mice. Genome wide association studies have demonstrated that Osterix is associated with bone mineral density in humans; however, the molecular significance of Osterix in human osteoblast differentiation is poorly described. In this study we have characterized the role of Osterix in human mesenchymal progenitor cell (hMSC) differentiation. We first analyzed temporal microarray data of primary hMSC treated with bone morphogenetic protein‐6 (BMP6) using clustering to identify genes that are associated with Osterix expression. Osterix clusters with a set of osteoblast‐associated extracellular matrix (ECM) genes, including bone sialoprotein (BSP) and a novel set of proteoglycans, osteomodulin (OMD), osteoglycin, and asporin. Maximum expression of these genes is dependent upon both the concentration and duration of BMP6 exposure. Next we overexpressed and repressed Osterix in primary hMSC using retrovirus. The enforced expression of Osterix had relatively minor effects on osteoblastic gene expression independent of exogenous BMP6. However, in the presence of BMP6, Osterix overexpression enhanced expression of the aforementioned ECM genes. Additionally, Osterix overexpression enhanced BMP6 induced osteoblast mineralization, while inhibiting hMSC proliferation. Conversely, Osterix knockdown maintained hMSC in an immature state by decreasing expression of these ECM genes and decreasing mineralization and hMSC proliferation. Overexpression of the Osterix regulated gene OMD with retrovirus promoted mineralization of hMSC. These results suggest that Osterix is necessary, but not sufficient for hMSC osteoblast differentiation. Osterix regulates the expression of a set of ECM proteins which are involved in terminal osteoblast differentiation. J. Cell. Physiol. 227: 2677–2685, 2012. © 2011 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90208/1/jcp_23010_sm_SupplData.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/90208/2/23010_ftp.pd

Activation of Human Stearoyl-Coenzyme A Desaturase 1 Contributes to the Lipogenic Effect of PXR in HepG2 Cells

The pregnane X receptor (PXR) was previously known as a xenobiotic receptor. Several recent studies suggested that PXR also played an important role in lipid homeostasis but the underlying mechanism remains to be clearly defined. In this study, we found that rifampicin, an agonist of human PXR, induced lipid accumulation in HepG2 cells. Lipid analysis showed the total cholesterol level increased. However, the free cholesterol and triglyceride levels were not changed. Treatment of HepG2 cells with rifampicin induced the expression of the free fatty acid transporter CD36 and ABCG1, as well as several lipogenic enzymes, including stearoyl-CoA desaturase-1 (SCD1), long chain free fatty acid elongase (FAE), and lecithin-cholesterol acyltransferase (LCAT), while the expression of acyl:cholesterol acetyltransferase(ACAT1) was not affected. Moreover, in PXR over-expressing HepG2 cells (HepG2-PXR), the SCD1 expression was significantly higher than in HepG2-Vector cells, even in the absence of rifampicin. Down-regulation of PXR by shRNA abolished the rifampicin-induced SCD1 gene expression in HepG2 cells. Promoter analysis showed that the human SCD1 gene promoter is activated by PXR and a novel DR-7 type PXR response element (PXRE) response element was located at -338 bp of the SCD1 gene promoter. Taken together, these results indicated that PXR activation promoted lipid synthesis in HepG2 cells and SCD1 is a novel PXR target gene. © 2013 Zhang et al

Simultaneous non-negative matrix factorization for multiple large scale gene expression datasets in toxicology

Non-negative matrix factorization is a useful tool for reducing the dimension of large datasets. This work considers simultaneous non-negative matrix factorization of multiple sources of data. In particular, we perform the first study that involves more than two datasets. We discuss the algorithmic issues required to convert the approach into a practical computational tool and apply the technique to new gene expression data quantifying the molecular changes in four tissue types due to different dosages of an experimental panPPAR agonist in mouse. This study is of interest in toxicology because, whilst PPARs form potential therapeutic targets for diabetes, it is known that they can induce serious side-effects. Our results show that the practical simultaneous non-negative matrix factorization developed here can add value to the data analysis. In particular, we find that factorizing the data as a single object allows us to distinguish between the four tissue types, but does not correctly reproduce the known dosage level groups. Applying our new approach, which treats the four tissue types as providing distinct, but related, datasets, we find that the dosage level groups are respected. The new algorithm then provides separate gene list orderings that can be studied for each tissue type, and compared with the ordering arising from the single factorization. We find that many of our conclusions can be corroborated with known biological behaviour, and others offer new insights into the toxicological effects. Overall, the algorithm shows promise for early detection of toxicity in the drug discovery process