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Risk of a feedback loop between climatic warming and human mobility.

ABSTRACT: Human behaviours alter-and are altered by-climate. Might the impacts of warming on human behaviours amplify anthropogenic contributions to climate change? Here, we show that warmer temperatures substantially increase transportation use in the USA. To do so, we combine meteorological data with data on vehicle miles travelled (VMT) and public transit trips (PTT) between 2002 and 2018. Moving from freezing temperatures up to 30°C increases VMT by over 10% and amplifies use of public transit by nearly 15%. Temperatures beyond 30°C exert little influence on either outcome. We then examine climate model projections to highlight the possible transportation impacts of future climatic changes. We project that warming over the coming century may add over one trillion cumulative VMT and six billion PTT in the USA alone, presenting the risk of a novel feedback loop in the human-environmental system.

SUBMITTER: Obradovich N

PROVIDER: S-EPMC6769312 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Risk of a feedback loop between climatic warming and human mobility.

Obradovich Nick N Rahwan Iyad I

Journal of the Royal Society, Interface 20190911 158

Human behaviours alter-and are altered by-climate. Might the impacts of warming on human behaviours amplify anthropogenic contributions to climate change? Here, we show that warmer temperatures substantially increase transportation use in the USA. To do so, we combine meteorological data with data on vehicle miles travelled (VMT) and public transit trips (PTT) between 2002 and 2018. Moving from freezing temperatures up to 30°C increases VMT by over 10% and amplifies use of public transit by near ...[more]

PMID: 31506044

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Project description:BackgroundFibrosis is defined as an excessive accumulation of extracellular matrix (ECM) components. Many organs are subjected to fibrosis including the lung, liver, heart, skin, kidney, and muscle. Muscle fibrosis occurs in response to trauma, aging, or dystrophies and impairs muscle function. Fibrosis represents a hurdle for the treatment of human muscular dystrophies. While data on the mechanisms of fibrosis have mostly been investigated in mice, dystrophic mouse models often do not recapitulate fibrosis as observed in human patients. Consequently, the cellular and molecular mechanisms that lead to fibrosis in human muscle still need to be identified.MethodsCombining mass cytometry, transcriptome profiling, in vitro co-culture experiments, and in vivo transplantation in immunodeficient mice, we investigated the role and nature of nonmyogenic cells (fibroadipogenic progenitors, FAPs) from human fibrotic muscles of healthy individuals (FibMCT ) and individuals with oculopharyngeal muscular dystrophy (OPMD; FibMOP ), as compared with nonmyogenic cells from human nonfibrotic muscle (MCT ).ResultsWe found that the proliferation rate of FAPs from fibrotic muscle is 3-4 times higher than those of FAPs from nonfibrotic muscle (population doubling per day: MCT 0.2 ± 0.1, FibMCT 0.7 ± 0.1, and FibMOP 0.8 ± 0.3). When cocultured with muscle cells, FAPs from fibrotic muscle impair the fusion index unlike MCT FAPs (myoblasts alone 57.3 ± 11.1%, coculture with MCT 43.1 ± 8.9%, with FibMCT 31.7 ± 8.2%, and with FibMOP 36.06 ± 10.29%). We also observed an increased proliferation of FAPs from fibrotic muscles in these co-cultures in differentiation conditions (FibMCT +17.4%, P < 0.01 and FibMOP +15.1%, P < 0.01). This effect is likely linked to the increased activation of the canonical TGFβ-SMAD pathway in FAPs from fibrotic muscles evidenced by pSMAD3 immunostaining (P < 0.05). In addition to the profibrogenic TGFβ pathway, we identified endothelin as a new actor implicated in the altered cross-talk between muscle cells and fibrotic FAPs, confirmed by an improvement of the fusion index in the presence of bosentan, an endothelin receptor antagonist (from 33.8 ± 10.9% to 52.9 ± 10.1%, P < 0.05).ConclusionsOur data demonstrate the key role of FAPs and their cross-talk with muscle cells through a paracrine signalling pathway in fibrosis of human skeletal muscle and identify endothelin as a new druggable target to counteract human muscle fibrosis.

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Risk of a feedback loop between climatic warming and human mobility.

Publications

Risk of a feedback loop between climatic warming and human mobility.

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