Paris Agreement climate proposals need a boost to keep warming well below 2 °C.

The Paris climate agreement aims at holding global warming to well below 2 degrees Celsius and to "pursue efforts" to limit it to 1.5 degrees Celsius. To accomplish this, countries have submitted Intended Nationally Determined Contributions (INDCs) outlining their post-2020 climate action. Here we assess the effect of current INDCs on reducing aggregate greenhouse gas emissions, its implications for achieving the temperature objective of the Paris climate agreement, and potential options for overachievement. The INDCs collectively lower greenhouse gas emissions compared to where current policies stand, but still imply a median warming of 2.6-3.1 degrees Celsius by 2100. More can be achieved, because the agreement stipulates that targets for reducing greenhouse gas emissions are strengthened over time, both in ambition and scope. Substantial enhancement or over-delivery on current INDCs by additional national, sub-national and non-state actions is required to maintain a reasonable chance of meeting the target of keeping warming well below 2 degrees Celsius.

Building equity in: strategies for integrating equity into modelling for a 1.5°C world.

Emission pathways consistent with limiting temperature increase to 1.5°C raise pressing questions from an equity perspective. These pathways would limit impacts and benefit vulnerable communities but also present trade-offs that could increase inequality. Meanwhile, rapid mitigation could exacerbate political debates in which equity has played a central role. In this paper, we first develop a set of elements we suggest are essential for evaluating the equity implications of policy actions consistent with 1.5°C. These elements include (i) assess climate impacts, adaptation, loss and damage; (ii) be sensitive to context; (iii) compare costs of mitigation and adaptation policy action; (iv) incorporate human development and poverty; (v) integrate inequality dynamics; and (vi) be clear about normative assumptions and responsive to users. We then assess the ability of current modelling practices to address each element, focusing on global integrated assessment models augmented by national modelling and scenarios. We find current practices face serious limitations across all six dimensions although the severity of these varies. Finally, based on our assessment we identify strategies that may be best suited for enabling us to generate insights into each of the six elements in the context of assessing pathways for a 1.5°C world.This article is part of the theme issue 'The Paris Agreement: understanding the physical and social challenges for a warming world of 1.5°C above pre-industrial levels'.

Corrigendum to "Towards a theory of just transition: A neo-Gramscian understanding of how to shift development pathways to zero poverty and zero carbon" [Energy Res. Soc. Sci. 70 (2020) 101789].

[This corrects the article DOI: 10.1016/j.erss.2020.101789.].

Towards a theory of just transition: A neo-Gramscian understanding of how to shift development pathways to zero poverty and zero carbon.

As a global community, we need to understand better how a just transition can shift development paths to achieve net zero emissions and eliminate poverty. Our past development trajectories have led to high emissions, persistent inequality and a world that is fragmented across multiple contradictions. How can countries shift to development pathways that deliver zero poverty and zero carbon? In developing a theory of just transition, the article begins by reviewing a range of theoretical approaches from different traditions, building in particular on neo-Gramscian approaches. It applies and modifies core components of Gramsci's approach, building a neo-Gramscian theory of just transitions around concepts of ideology, hegemony, change agents and fundamental conditions. The theory suggests how coalitions of change agents can come together behind a just transition. The coalition needs to gain broader support, establish a new cultural hegemony in support of just transitions and be able to transform the fundamental conditions of the 21st century. The article briefly considers how this better understanding can be applied to the practice of shifting development pathways. The penultimate section reflects on limitations, including that a fuller development of a theory of just transition will require application for detailed concrete examples and a community effort. Together, we might address the multiple challenges of our present conditions to transition to development that enables human flourishing and a healthy planet.

The adenosine deaminase inhibitor erythro-9-[2-hydroxyl-3-nonyl]-adenine decreases intestinal permeability and protects against experimental sepsis: a prospective, randomised laboratory investigation.

INTRODUCTION: The treatment of septic conditions in critically ill patients is still one of medicine's major challenges. Cyclic nucleotides, adenosine and its receptors play a pivotal role in the regulation of inflammatory responses and in limiting inflammatory tissue destruction. The aim of this study was to verify the hypothesis that adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibition by erythro-9-[2-hydroxyl-3-nonyl]-adenine could be beneficial in experimental endotoxicosis/sepsis. METHOD: We used two established animal models for endotoxicosis and sepsis. Twenty-four male Wistar rats that had been given intravenous endotoxin (Escherichia coli lipopolysaccharide) were treated with either erythro-9-[2-hydroxyl-3-nonyl]-adenine infusion or 0.9% saline during a study length of 120 minutes. Sepsis in 84 female C57BL/6 mice was induced by caecal ligation and puncture. Animals were treated with repeated erythro-9-[2-hydroxyl-3-nonyl]-adenine injections after 0, 12 and 24 hours or 4, 12 and 24 hours for delayed treatment. RESULTS: In endotoxaemic rats, intestinal production of hypoxanthine increased from 9.8 +/- 90.2 micromol/l at baseline to 411.4 +/- 124.6 micromol/l and uric acid formation increased from 1.5 +/- 2.3 mmol/l to 13.1 +/- 2.7 mmol/l after 120 minutes. In endotoxaemic animals treated with erythro-9-[2-hydroxyl-3-nonyl]-adenine, we found no elevation of adenosine metabolites. The lactulose/L-rhamnose ratio (14.3 versus 4.2 in control animals; p = 2.5 x 10(-7)) reflects a highly permeable small intestine and through the application of erythro-9-[2-hydroxyl-3-nonyl]-adenine, intestinal permeability could be re-established. The lipopolysaccharide animals had decreased L-rhamnose/3-O-methyl-D-glucose urine excretion ratios. Erythro-9-[2-hydroxyl-3-nonyl]-adenine reduced this effect. The mucosa damage score of the septic animals was higher compared with control and therapy animals (p < 0.05). Septic shock induction by caecal ligation and puncture resulted in a 160-hour survival rate of about 25%. In contrast, direct adenosine deaminase-1 inhibition resulted in a survival rate of about 75% (p = 0.0018). A protective effect was still present when erythro-9-[2-hydroxyl-3-nonyl]-adenine treatment was delayed for four hours (55%, p = 0.029). CONCLUSIONS: We present further evidence of the beneficial effects achieved by administering erythro-9-[2-hydroxyl-3-nonyl]-adenine, an adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibitor, in an endotoxicosis and sepsis animal model. This suggests a potential therapeutic option in the treatment of septic conditions.

Delayed anticoagulation-related intracranial haemorrhage after minor head injury.

Treatment with anticoagulants and antiplatelet agents are well-known risk factors for an unfavourable outcome after traumatic brain injury (TBI). Guidelines for decision making in patients who sustained mild head injury do not apply to anticoagulated patients and therefore, in these cases diagnostic and therapeutic procedures have to be tailored patient-specific. A 69-year-old patient was referred to our hospital after sustaining mild head injury. Due to anticoagulation therapy, a cranial computed tomography was carried out and was without pathologic findings. After negative workup for TBI, the patient was admitted to the ward solely because of intermittent cardiac arrhythmia. The next day, the patient developed a hemiparesis and repeated brain imaging showed a large posttraumatic intracranial haematoma which had to be evacuated surgically. In the further clinical course, the patient recovered completely and a cardiac pacemaker was implanted. Emergency physicians have to be highly alert with anticoagulated patients after head injury, even if the trauma was mild and initial diagnostic procedures demonstrate no acute pathology. Delayed traumatic intracranial haemorrhage may have fatal consequences for patients and while the threshold for admission to a hospital ward should be low, adequate observation at home has to be ensured if patients are discharged.