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Until the late 20th century, the idea of identifying wildfires in deep time was not generally accepted. One of the basic problems was the fact that charcoal-like wood fragments, so often found in sedimentary rocks and in coals, were termed fusain and, in addition, many researchers could not envision wildfires in peat-forming systems. The advent of Scanning Electron Microscopy and studies on modern charcoals and fossil fusains demonstrated beyond doubt that wildfire residues may be recognized in rocks dating back to at least 350 million years. Increasing numbers of studies on modern and fossil charcoal assemblages from the 1970s through the 1990s established the potential importance of wildfires in the fossil record, using Carboniferous examples in particular. Since the 1990s, extensive progress has been made in understanding modern wildfires and their byproducts. New techniques to study ancient charcoals have allowed considerable progress to be made to integrate modern and ancient fire studies, both before and after the evolution of mankind. Four important developments have made a reassessment of Carboniferous wildfires necessary: the recognition of the role of atmospheric oxygen in controlling the occurrence of wildfire; the development of new microscopical techniques allowing more detailed anatomical data to be obtained from charcoal; the integration of molecular studies with the evolution of fire traits; and new developments in or understanding of post-fire erosion/deposition systems. [ABSTRACT FROM AUTHOR]

Recent studies have suggested that the first arrival of humans in the Americas during the end of the last Ice Age is associated with marked anthropogenic influences on landscape; in particular, with the use of fire which, would have given even small populations the ability to have broad impacts on the landscape. Understanding the impact of these early people is complicated by the dramatic changes in climate occurring with the shift from glacial to interglacial conditions. Despite these difficulties, we here attempt to test the extent of anthropogenic influence using the California Channel Islands as a smaller, landscape-scale test bed. These islands are famous for the discovery of the 'Arlington Springs Man', which are some of the earliest human remains in the Americas. A unifying sedimentary charcoal record is presented from Arlington Canyon, Santa Rosa Island, based on over 20 detailed sedimentary sections from eight key localities. Radiocarbon dating was based on thin, fragile, long fragments of charcoal in order to avoid the 'inbuilt' age problem. Radiocarbon dating of 49 such fragments has allowed inferences regarding the fire and landscape history of the Canyon ca 19-11 ka BP. A significant period of charcoal deposition is identified approximately 14-12.5 ka BP and bears remarkable closeness to an estimated age range of the first human arrival on the islands.This article is part of the themed issue 'The interaction of fire and mankind'.

Tumour-specific CD8 T cell dysfunction is a differentiation state that is distinct from the functional effector or memory T cell states.sup.1-6. Here we identify the nuclear factor TOX as a crucial regulator of the differentiation of tumour-specific T (TST) cells. We show that TOX is highly expressed in dysfunctional TST cells from tumours and in exhausted T cells during chronic viral infection. Expression of TOX is driven by chronic T cell receptor stimulation and NFAT activation. Ectopic expression of TOX in effector T cells in vitro induced a transcriptional program associated with T cell exhaustion. Conversely, deletion of Tox in TST cells in tumours abrogated the exhaustion program: Tox-deleted TST cells did not upregulate genes for inhibitory receptors (such as Pdcd1, Entpd1, Havcr2, Cd244 and Tigit), the chromatin of which remained largely inaccessible, and retained high expression of transcription factors such as TCF-1. Despite their normal, 'non-exhausted' immunophenotype, Tox-deleted TST cells remained dysfunctional, which suggests that the regulation of expression of inhibitory receptors is uncoupled from the loss of effector function. Notably, although Tox-deleted CD8 T cells differentiated normally to effector and memory states in response to acute infection, Tox-deleted TST cells failed to persist in tumours. We hypothesize that the TOX-induced exhaustion program serves to prevent the overstimulation of T cells and activation-induced cell death in settings of chronic antigen stimulation such as cancer. The nuclear factor TOX is highly expressed in antigen-specific dysfunctional T cells in tumours and exhausted T cells during chronic viral infection and is a crucial regulator of the differentiation of tumour-specific T cells., Author(s): Andrew C. Scott [sup.1] [sup.2] , Friederike Dündar [sup.3] [sup.4] , Paul Zumbo [sup.3] [sup.4] , Smita S. Chandran [sup.5] [sup.6] , Christopher A. Klebanoff [sup.5] [sup.6] [sup.7] [sup.8] [...]