Projecting heat-related cardiovascular mortality burden attributable to human-induced climate change in China.

BACKGROUND: Cardiovascular disease (CVD) has been found to be particularly vulnerable to climate change and temperature variability. This study aimed to assess the extent to which human-induced climate change contributes to future heat-related CVD burdens. METHODS: Daily data on CVD mortality and temperature were collected in 161 Chinese communities from 2007 to 2013. The association between heat and CVD mortality was established using a two-stage time-series design. Under the natural forcing, human-induced, and combined scenarios, we then separately projected excess cause-/age-/region-/education-specific mortality from future high temperature in 2010-2100, assuming no adaptation and population changes. FINDINGS: Under shared socioeconomic pathway with natural forcing scenario (SSP2-4.5-nat), heat-related attributable fraction of CVD deaths decreased slightly from 3.3% [95% empirical confidence interval (eCI): 0.3, 5.8] in the 2010s to 2.8% (95% eCI: 0.1, 5.2) in the 2090s, with relative change of -0.4% (95% eCI: -0.8, 0.0). However, for combined natural and human-induced forcings, this estimate would surge to 8.9% (95% eCI: 1.5, 15.7), 14.4% (95% eCI: 1.5, 25.3), 21.3% (95% eCI: -0.6, 39.4), and 28.7% (95% eCI: -3.3, 48.0) in the 2090s under SSP1-2.6, SSP2-4.5, SSP3-7.0, and SSP5-8.5 scenarios, respectively. When excluding the natural forcing, the number of human-induced heat-related CVD deaths would increase from approximately eight thousand (accounting for 31% of total heat-related CVD deaths) in the 2010s to 33,052 (68%), 63,283 (80%), 101,091 (87%), and 141,948 (90%) in the 2090s under SSP1-2.6, SSP2-4.5, SSP3-7.0, and SSP5-8.5 scenarios, respectively. Individuals with stroke, females, the elderly, people living in rural areas, and those with lower education level would exhibit heightened susceptibility to future high temperature. In addition, Southern and Eastern regions of China were expected to experience a faster increase in heat-related attributable fraction of CVD deaths. INTERPRETATION: Human activities would significantly amplify the future burden of heat-related CVD. Our study findings suggested that active adaptation and mitigation measures towards future warming could yield substantial health benefits for the patients with CVD. FUNDING: National Natural Science Foundation of China.

Fungal oxysterol-binding protein-related proteins promote pathogen virulence and activate plant immunity.

Oxysterol-binding protein-related proteins (ORPs) are a conserved class of lipid transfer proteins that are closely involved in multiple cellular processes in eukaryotes, but their roles in plant-pathogen interactions are mostly unknown. We show that transient expression of ORPs of Magnaporthe oryzae (MoORPs) in Nicotiana benthamina plants triggered oxidative bursts and cell death; treatment of tobacco Bright Yellow-2 suspension cells with recombinant MoORPs elicited the production of reactive oxygen species. Despite ORPs being normally described as intracellular proteins, we detected MoORPs in fungal culture filtrates and intercellular fluids from barley plants infected with the fungus. More importantly, infiltration of Arabidopsis plants with recombinant Arabidopsis or fungal ORPs activated oxidative bursts, callose deposition, and PR1 gene expression, and enhanced plant disease resistance, implying that ORPs may function as endogenous and exogenous danger signals triggering plant innate immunity. Extracellular application of fungal ORPs exerted an opposite impact on salicylic acid and jasmonic acid/ethylene signaling pathways. Brassinosteroid Insensitive 1-associated Kinase 1 was dispensable for the ORP-activated defense. Besides, simultaneous knockout of MoORP1 and MoORP3 abolished fungal colony radial growth and conidiation, whereas double knockout of MoORP1 and MoORP2 compromised fungal virulence on barley and rice plants. These observations collectively highlight the multifaceted role of MoORPs in the modulation of plant innate immunity and promotion of fungal development and virulence in M. oryzae.