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Mercury is a potent neurotoxic substance and accounts for 250,000 intellectual disabilities annually. Worldwide, coastal fisheries contribute the majority of human exposure to mercury through fish consumption. Recent global mercury cycling and risk models attribute all the mercury loading to the ocean to atmospheric deposition. Nevertheless, new regional research has noted that the riverine mercury export to coastal oceans may also be significant to the oceanic burden of mercury. Here we construct an unprecedented high-spatial-resolution dataset estimating global river mercury and methylmercury exports. We find that rivers annually deliver 1,000 (minimum–maximum: 893–1,224) Mg mercury to coastal oceans, threefold greater than atmospheric deposition. Furthermore, high flow events, which are becoming more common with climate change, are responsible for a disproportionately large percentage of the export. Coastal oceans constitute 0.2% of the entire ocean volume but receive 27% of the external mercury input to the ocean. We estimate that the river mercury export could be responsible for a net annual export of 350 (interquartile range: 52–640) Mg mercury across the coastal–open-ocean boundary, although there is still high uncertainty around this estimate. Our results show that river export is the largest source of mercury to coastal oceans worldwide, and continued mercury risk modelling should incorporate the impact of rivers. Rivers transport about 1,000 Mg mercury annually to coastal oceans, which is threefold greater than the amount delivered by atmospheric deposition, according to a global analysis of mercury measurements in rivers.

Protecting the environment and enhancing food security are among the world’s greatest challenges. Fish consumption is widely considered to be the single significant dietary source of methylmercury. Nevertheless, by synthesizing data from the past six decades and using a variety of models, we find that rice could be a significant global dietary source of human methylmercury exposure, especially in South and Southeast Asia. In 2013, globalization caused 9.9% of human methylmercury exposure via the international rice trade and significantly aggravated rice-derived exposure in Africa (62%), Central Asia (98%) and Europe (42%). In 2016, 180 metric tons of mercury were generated in rice plants, 14-fold greater than that exported from oceans via global fisheries. We suggest that future research should consider both the joint ingestion of rice with fish and the food trade in methylmercury exposure assessments, and anthropogenic biovectors such as crops should be considered in the global mercury cycle. Fish consumption is considered to be the only significant dietary source of MeHg. Here the authors show that rice could also be a significant global dietary source, especially in South and Southeast Asia. International rice trade and joint ingestion of fish and rice could aggravate the MeHg exposure levels in many areas.

The mechanism of spiritual transformation in red tourism plays a key role in facilitating the inheritance of red culture. A survey of 385 tourists of Chinese nationality was conducted to explore the path of red tourism’s influence on tourists’ spiritual transformation. Based on the stimulus–organism–response theory, this paper explores tourists’ environmental perceptions of red tourism activities as special external stimuli, introduces a positive emotion factor, and constructs a path model of red tourism for tourists’ positive emotions based on educational function and cultural identity, which ultimately leads to their spiritual transformation. The results of the empirical tests using structural equation modelling indicated that environmental perceptions had a significantly positive effect on the stimulation of positive emotions, while positive emotions had an indirect effect on spiritual transformation. The research results enhance people’s understanding of the spiritual transformation brought by red tourism and provide management significance for red tourism planning.

Amifostine has been the only small molecule radio-protector approved by FDA for decades; however, the serious adverse effects limit its clinical use. To address the toxicity issues and maintain the good potency, a series of modified small polycysteine peptides had been prepared. Among them, compound 5 exhibited the highest radio-protective efficacy, the same as amifostine, but much better safety profile. To confirm the correlation between the radiation-protective efficacy and the DNA binding capability, each of the enantiomers of the polycysteine peptides had been prepared. As a result, the l -configuration compounds had obviously higher efficacy than the corresponding d -configuration enantiomers; among them, compound 5 showed the highest DNA binding capability and radiation-protective efficacy. To our knowledge, this is the first study that has proved their correlations using direct comparison. Further exploration of the mechanism revealed that the ionizing radiation (IR) triggered ferroptosis inhibition by compound 5 could be one of the pathways for the protection effect, which was different from amifostine. In summary, the preliminary result showed that compound 5 , a polycysteine as a new type of radio-protector, had been developed with good efficacy and safety profile. Further study of the compound for potential use is ongoing.

Anthropogenic activities have led to widespread contamination with mercury (Hg), a potent neurotoxin that bioaccumulates through food webs. Recent models estimated that, presently, 200 to 600 t of Hg is sequestered annually in deep-sea sediments, approximately doubling since industrialization. However, most studies did not extend to the hadal zone (6,000- to 11,000-m depth), the deepest ocean realm. Here, we report on measurements of Hg and related parameters in sediment cores from four trench regions (1,560 to 10,840 m), showing that the world’s deepest ocean realm is accumulating Hg at remarkably high rates (depth-integrated minimum–maximum: 24 to 220 μg · m−2 · y−1) greater than the global deep-sea average by a factor of up to 400, with most Hg in these trenches being derived from the surface ocean. Furthermore, vertical profiles of Hg concentrations in trench cores show notable increasing trends from pre-1900 [average 51 ± 14 (1σ) ng · g−1] to post-1950 (81 ± 32 ng · g−1). This increase cannot be explained by changes in the delivery rate of organic carbon alone but also need increasing Hg delivery from anthropogenic sources. This evidence, along with recent findings on the high abundance of methylmercury in hadal biota [R. Sun et al., Nat. Commun. 11, 3389 (2020); J. D. Blum et al., Proc. Natl. Acad. Sci. U. S. A. 117, 29292–29298 (2020)], leads us to propose that hadal trenches are a large marine sink for Hg and may play an important role in the regulation of the global biogeochemical cycle of Hg.

Environmental stress has emerged as a critical driver of population displacement, yet its interaction with migration intentions remains underexplored. This study investigates how environmental vulnerability shapes individuals’ intentions to migrate, drawing on the push–pull theory of migration. Data were collected from residents of high-risk environmental zones in China and analyzed using a dual-stage approach. The findings reveal that environmental stress and perceived economic opportunities significantly influence migration intentions, with perceived risk mediating the effect of environmental stress. Moreover, policy awareness moderates the relationship between perceived economic opportunity and migration intention. The results highlight environmental stress as the most influential factor, underscoring the importance of proactive policies to reduce involuntary migration and strengthen community resilience. This study contributes to migration research by integrating environmental, economic, and policy perspectives, offering valuable insights for both scholars and policymakers.

The SARS-CoV-2 papain-like protease (PL pro ) is a cysteine protease that cleaves viral polyproteins and antagonizes the host immune response during viral replication. Jun12682 and PF-07957472 are the first-in-class PL pro inhibitors showing potent in vivo antiviral efficacy in mouse models. In this study, we characterize naturally occurring mutations at residues located at the drug-binding site of Jun12682 . The results reveal several PL pro mutants showing significant drug resistance while maintaining comparable enzymatic activity as the wild-type PL pro . The physiological relevance of the identified drug-resistant mutants, including E167G and Q269H, is validated through independent serial viral passage experiments. Molecular dynamics simulations and perturbative free energy calculations show that drug-resistant PL pro mutants weaken hydrogen bonding and π-π stacking interactions. Collectively, this study identifies E167, Y268, and Q269 as drug-resistant hotspots for PL pro inhibitors that bind to the BL2 loop and groove region, which are valuable in informing the design of the next-generation PL pro inhibitors. This study identifies E167, Y268, and Q269 as drug-resistant hotspots for SARS-CoV papain-like protease inhibitors that bind to the BL2 loop and groove region, which are valuable in informing the design of the next-generation PLpro inhibitors.

Bile acids are acknowledged as signaling molecules involved in metabolic syndrome. The Takeda G protein-coupled receptor 5 (TGR5) functions as a significant bile acid receptor. The accumulated evidence suggests that TGR5 involves lipid homeostasis, glucose metabolism, and inflammation regulation. In line with this, recent preclinical studies also demonstrate that TGR5 plays a significant role in the generation and progression of metabolic syndrome, encompassing type 2 diabetes mellitus, obesity, atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). In this review, we discuss the role of TGR5 in metabolic syndrome, illustrating the underlying mechanisms and therapeutic targets.

Human activities have emitted substantial mercury into the atmosphere, significantly impacting ecosystems and human health worldwide. Currently, consistent methodologies to evaluate long-term mercury emissions across countries and industries are scant, hindering efforts to prioritize emission controls. Here, we develop a high-spatiotemporal-resolution dataset to comprehensively analyze global anthropogenic mercury emission patterns. We show that global emissions increased 330% during 1960–2021, with declines in developed Global North countries since the 1990s and China since the 2010s completely offset by rapid growth in Global South countries (excluding China). Consequently, global emissions have continued to rise slightly since the 2013 Minamata Convention. In 2021, Global South countries produced two-thirds of global emissions, despite comprising only one-fifth of the global economy. We predict that, although large uncertainties exist, continued emission growth in Global South countries under a business-as-usual scenario could increase 10%-50% global mercury emissions by 2030. Our findings demonstrate that global control of anthropogenic mercury emissions has reached a critical juncture, highlighting the urgent need to target reductions in Global South countries to prevent worsening health and environmental impacts. Global mercury emissions increased 330% from 1960–2021, with declines in the Global North and China offset by rapid growth in the Global South, which now produces two-thirds of emissions. Without urgent action, emissions could rise 10%–50% by 2030.

Gypenosides (GP), extracted from the traditional Chinese herb Gynostemma pentaphyllum (Thunb.) Makino, have been used to treat metabolic disorders, including lipid metabolism disorders and diabetes. Although recent studies have confirmed their beneficial effects in nonalcoholic fatty liver disease (NAFLD), the underlying therapeutic mechanism remains unclear. In this study, we explored the protective mechanism of GP against NAFLD in mice and provided new insights into the prevention and treatment of NAFLD. Male C57BL6/J mice were divided into three experimental groups: normal diet, high-fat diet (HFD), and GP groups. The mice were fed an HFD for 16 weeks to establish an NAFLD model and then treated with GP for 22 weeks. The transcriptome and proteome of the mice livers were profiled using RNA sequencing and high-resolution mass spectrometry, respectively. The results showed that GP decreased serum lipid levels, liver index, and liver fat accumulation in mice. Principal component and heatmap analyses indicated that GP significantly modulated the changes in the expression of genes associated with HFD-induced NAFLD. The 164 differentially expressed genes recovered using GP were enriched in fatty acid and steroid metabolism pathways. Further results showed that GP reduced fatty acid synthesis by downregulating the expression of Srebf1 , Fasn , Acss2 , Acly , Acaca , Fads1 , and Elovl6 ; modulated glycerolipid metabolism by inducing the expression of Mgll ; promoted fatty acid transportation and degradation by inducing the expression of Slc27a1 , Cpt1a , and Ehhadh ; and reduced hepatic cholesterol synthesis by downregulating the expression of Tm7sf2 , Ebp , Sc5d , Lss , Fdft1 , Cyp51 , Nsdhl , Pmvk , Mvd , Fdps , and Dhcr7 . The proteomic data further indicated that GP decreased the protein expression levels of ACACA, ACLY, ACSS2, TM7SF2, EBP, FDFT1, NSDHL, PMVK, MVD, FDPS, and DHCR7 and increased those of MGLL, SLC27A1, and EHHADH. In conclusion, GP can regulate the key genes involved in hepatic lipid metabolism in NAFLD mice, providing initial evidence for the mechanisms underlying the therapeutic effect of GP in NAFLD.