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We study whether climate transition risk is reflected in the credit default swap (CDS) spreads of European firms. Using information on the vulnerability of a firm's value to the transition to a low-carbon economy, we construct a climate transition risk (CTR) factor, and report how this factor shifts the term structure of the CDS spreads of more but not of less vulnerable firms. Considering the CTR factor, we find that different climate transition policies have asymmetric and significant economic impacts on the credit risk of more vulnerable firms, and negligible effects on less vulnerable firms.

Energy transition requires huge amounts of critical metals —called energy transition metals (ETMs)— to deploy clean energy technologies. The growing demand for ETMs and uncertainties regarding the path to net-zero emissions could cause ETM price oscillations, with potential effects on the prices of other commodities. We explore whether upward and downward movements in ETM prices have a neutral effect on the level and volatility of energy and non-energy commodity prices. By characterizing the conditional dependence between ETM and commodity prices, we document that, except for natural gas, extreme ETM price changes have a non-neutral effect on commodity prices, although this effect vanishes for non-extreme price movements. The implications of this evidence for investors operating in commodity markets are evaluated in terms of commodity risk-adjusted returns, commodity tail risk, and liquidity needs for trading in commodity futures contracts.

De-risking green investments is crucial to unlocking climate finance and to spurring investors’ interest in allocating resources to activities consistent with a resilient low-carbon economy. We explore the extent to which green bonds could de-risk investments in low-carbon assets by considering different market circumstances. We characterize joint dependence between green bonds and low-carbon assets and consider a de-risking metric based on expected shortfall. Our analysis for the Chinese, European and US markets for 2016 to 2020 indicates that green-bond and low-carbon stock returns move in opposite directions or independently, and a fall in green-bond returns below the 5% quantile increases the expected value of low-carbon stocks by 8.6% and 15.1% in the Chinese and European markets, respectively, but has a negligible effect on the US market. We also document that green bonds have sizeable diversification benefits when they are included in low-carbon investment portfolios.

The original version of this article unfortunately contained a mistake. Paul Clement and Steven De Vleeschouwer were not listed among the authors.

Iron deficiency (ID) is common in patients with heart failure (HF) and is associated with poor outcomes, yet its role in the pathophysiology of HF is not well-defined. We sought to determine the consequences of HF neurohormonal activation in iron homeostasis and mitochondrial function in cardiac cells. HF was induced in C57BL/6 mice by using isoproterenol osmotic pumps and embryonic rat heart-derived H9c2 cells were subsequently challenged with Angiotensin II and/or Norepinephrine. The expression of several genes and proteins related to intracellular iron metabolism were assessed by Real time-PCR and immunoblotting, respectively. The intracellular iron levels were also determined. Mitochondrial function was analyzed by studying the mitochondrial membrane potential, the accumulation of radical oxygen species (ROS) and the adenosine triphosphate (ATP) production. Hearts from isoproterenol-stimulated mice showed a decreased in both mRNA and protein levels of iron regulatory proteins, transferrin receptor 1, ferroportin 1 and hepcidin compared to control mice. Furthermore, mitoferrin 2 and mitochondrial ferritin were also downregulated in the hearts from HF mice. Similar data regarding these key iron regulatory molecules were found in the H9c2 cells challenged with neurohormonal stimuli. Accordingly, a depletion of intracellular iron levels was found in the stimulated cells compared to non-stimulated cells, as well as in the hearts from the isoproterenol-induced HF mice. Finally, neurohormonal activation impaired mitochondrial function as indicated by the accumulation of ROS, the impaired mitochondrial membrane potential and the decrease in the ATP levels in the cardiac cells. HF characteristic neurohormonal activation induced changes in the regulation of key molecules involved in iron homeostasis, reduced intracellular iron levels and impaired mitochondrial function. The current results suggest that iron could be involved in the pathophysiology of HF.

Per- and polyfluoroalkyl substances (PFAS) are ubiquitous global environmental contaminants, environmentally persistent, mobile, can bioaccumulate and are toxic. Increasing emphasis is placed on the immobilisation and removal of PFAS from contaminated environmental matrices such as: potable water, surface water, groundwater, wastewater, sediments and soils (Dauchy et al., 2017; Cao et al., 2019; Hepburn et al., 2019). To achieve this, development of PFAS sorbents is increasingly undertaken (Du et al., 2014). Sorption studies are used to observe the interaction of sorbent and sorbate, but have two key limitations when undertaking sorption experiments for PFAS (1) the experimental protocol and (2) analytical techniques. The current batch sorption methods approached recommended by OECD Guideline 106 (OECD, 2000) are problematic, firstly, due to large sample numbers and PFAS specific laboratory difficulties, including near ubiquitous background PFAS contamination. Secondly, PFAS analytical techniques currently require solid-phase extraction (SPE) to be employed, which is slow and expensive, prior to instrumental analysis with liquid chromatography-mass spectrometry (LC-MS). A suitable alternative approach is needed to mitigate the drawbacks of current methodologies whilst catering for the high sample throughput required by benchtop trials characterising the sorption behaviour of PFAS - sorbent pairings.•A suitable method for PFAS measurement, overcoming shortcomings of current batch sorption methodologies is presented•The method can be applied to a wide range of sorbents and sorption environment conditions associated with PFAS immobilisation or removal in the environment•The presented method is novel through its high sample throughput, simple approach and minimisation of cross contamination sources.

In recent times, there has been increased focus on a holistic approach to soil remediation with consideration of social, economic and environmental factors. Consequently, there is a demand from practitioners and regulators alike for suitable ways to measure ancillary outcomes, for example, effects on soil quality. Here we show that biochar, when applied to land to remediate lead (Pb)-contaminated soils, can lead to environmental improvements not realized by adding mined or manufactured phosphates. Here, we study a Pb-contaminated soil amended with two phosphate fertilizers (slow- and fast-release) and with biochars produced from poultry litter and from biosolids at three temperatures (300 °C, 400 °C and 500 °C). The results show that, unlike the fast-release P fertilizer, biochars did not result in an increase in the amount of leachable P that could be released into the environment. Biochars prepared at 500 °C presented a higher value of the integrative geometric mean of soil enzyme activity, compared to the P fertilizers. Overall, our research shows that biochars, particularly those prepared at the higher temperature tested, are a suitable alternative to P fertilizers as an integrative remediation strategy in Pb-contaminated soils, enabling soil biological restoration.

Primary central nervous system lymphoma (PCNSL) is a rare type of non-Hodgkin lymphoma with an aggressive clinical course. To investigate the potential of immune-checkpoint therapy, we retrospectively studied the tumor microenvironment (TME) using high-plex immunohistochemistry in 22 PCNSL and compared to 7 secondary CNS lymphomas (SCNSL) and 7 "other" CNSL lymphomas with the presence of the Epstein-Barr virus and/or compromised immunity. The TME in PCNSL was predominantly composed of CD8+ cytotoxic T cells and CD163+ phagocytes. Despite molecular differences between PCNSL and SCNSL, the cellular composition and the functional spectrum of cytotoxic T cells were similar. But cytotoxic T cell activation was significantly influenced by pre-biopsy corticosteroids intake, tumor expression of PD-L1 and the presence of EBV. The presence of low numbers of CD8+ T cells and geographic-type necrosis each predicted inferior outcome in PCNSL. Both M1-like (CD68 + CD163low) and M2-like (CD68 + CD163high) phagocytes were identified, and an increased ratio of M1-like/M2-like phagocytes was associated with a better survival. PD-L1 was expressed in lymphoma cells in 28% of cases, while PD1 was expressed in only 0.4% of all CD8+ T cells. TIM-3, a marker for T cell exhaustion, was significantly more expressed in CD8posPD-1pos T cells compared to CD8posPD-1neg T cells, and a similar increased expression was observed in M2-like pro-tumoral phagocytes. In conclusion, the clinical impact of TME composition supports the use of immune-checkpoint therapies in PCNSL. Based on observed differences in immune-checkpoint expression, combinations that boost cytotoxic T cell activation (by blocking TIM-3 or TGFBR1) prior to the administration of PD-L1 inhibition could be of interest.