Financial risks to coal value chain from a cost-conscious shift to renewables in India

A realignment of the financial sector is necessary to both enable the energy system transformation and manage financial risks implied by a transition to net-zero emissions. These include transition risks stemming from policies that limit or price greenhouse gas emissions. The financial sector has turned to scenarios developed by the research community for information on how transitions may unfold. Emerging methodologies linking transition scenarios to risk assessment are in their early stages but are key to enable financial institutions (FIs) to carry out the task at hand. Commercial FIs are exposed to transition risks primarily through their portfolio holdings and how assets therein may fare in a transition. Understanding this counterparty risk is key for development and interpretation of climate-financial scenarios. FIs will need to consider how the firms in a portfolio—the counterparties—will react to the transition and their capacity to navigate the changes involved. Here we apply a transparent and flexible framework to explore transition risks to corporate firms from low-carbon transition scenarios. We show that considering firms' strategic responses to the changes in their operating environment is an important determinant of the resulting transition risk estimates. We provide an illustrative case study of the coal value chain in India to demonstrate how the framework can be applied to both risk assessment and business strategy setting

The cost of mitigation revisited

Estimates of economic implications of climate policy are important inputs into policy-making. Despite care to contextualize quantitative assessments of mitigation costs, one strong view outside academic climate economics is that achieving Paris Agreement goals implies sizable macroeconomic losses. Here, we argue that this notion results from unwarranted simplification or omission of the complexities of quantifying mitigation costs, which generates ambiguity in communication and interpretation. We synthesize key factors influencing mitigation cost estimates to guide interpretation of estimates, for example from the Intergovernmental Panel on Climate Change, and suggest ways to improve the underlying models. We propose alternatives for the scenario design framework, the framing of mitigation costs and the methods used to derive them, to better inform public debate and policy

Chagas disease: what is known and what is needed - A background article

Chagas disease began millions of years ago as an enzootic disease of wild animals and started to be transmitted to man accidentally in the form of an anthropozoonosis when man invaded wild ecotopes. Endemic Chagas disease became established as a zoonosis over the last 200-300 years through forest clearance for agriculture and livestock rearing and adaptation of triatomines to domestic environments and to man and domestic animals as a food source. It is estimated that 15 to 16 million people are infected with Trypanosoma cruzi in Latin America and 75 to 90 million people are exposed to infection. When T. cruzi is transmitted to man through the feces of triatomines, at bite sites or in mucosa, through blood transfusion or orally through contaminated food, it invades the bloodstream and lymphatic system and becomes established in the muscle and cardiac tissue, the digestive system and phagocytic cells. This causes inflammatory lesions and immune responses, particularly mediated by CD4+, CD8+, interleukin-2 (IL) and IL-4, with cell and neuron destruction and fibrosis, and leads to blockage of the cardiac conduction system, arrhythmia, cardiac insufficiency, aperistalsis, and dilatation of hollow viscera, particularly the esophagus and colon. T. cruzi may also be transmitted from mother to child across the placenta and through the birth canal, thus causing abortion, prematurity, and organic lesions in the fetus. In immunosuppressed individuals, T. cruzi infection may become reactivated such that it spreads as a severe disease causing diffuse myocarditis and lesions of the central nervous system. Chagas disease is characterized by an acute phase with or without symptoms, and with entry point signs (inoculation chagoma or Romaña's sign), fever, adenomegaly, hepatosplenomegaly, and evident parasitemia, and an indeterminate chronic phase (asymptomatic, with normal results from electrocardiogram and x-ray of the heart, esophagus, and colon) or with a cardiac, digestive or cardiac-digestive form. There is great regional variation in the morbidity due to Chagas disease, and severe cardiac or digestive forms may occur in 10 to 50% of the cases, or the indeterminate form in the other asymptomatic cases, but with positive serology. Several acute cases have been reported from Amazon region most of them by T. cruzi I, Z3, and a hybrid ZI/Z3. We conclude this article presenting the ten top Chagas disease needs for the near future

A role for extracellular amastigotes in the immunopathology of Chagas disease

In spite of the growing knowledge obtained about immune control of Trypanosoma cruzi infection, the mechanisms responsible for the variable clinico-pathological expression of Chagas disease remain unknown. In a twist from previous concepts, recent studies indicated that tissue parasitism is a pre-requisite for the development of chronic myocarditis. This fundamental concept, together with the realization that T. cruzi organisms consist of genetically heterogeneous clones, offers a new framework for studies of molecular pathogenesis. In the present article, we will discuss in general terms the possible implications of genetic variability of T. cruzi antigens and proteases to immunopathology. Peptide epitopes from a highly polymorphic subfamily of trans-sialidase (TS) antigens were recently identified as targets of killer T cell (CTL) responses, both in mice and humans. While some class I MHC restricted CTL recognize epitopes derived from amastigote-specific TS-related antigens (TSRA), others are targeted to peptide epitopes originating from trypomastigote-specific TSRA. A mechanistic hypothesis is proposed to explain how the functional activity and specificity of class I MHC restricted killer T cells may control the extent to which tissue are exposed to prematurely released amastigotes. Chronic immunopathology may be exacerbated due the progressive accumulation of amastigote-derived antigens and pro-inflammatory molecules (eg. GPI-mucins and kinin-releasing proteases) in dead macrophage bodies