Elsevier最新文献

Pesticide exposure is emerging as a risk factor for various human diseases. Breast cancer (BC) is a multifactorial disease with known genetic and non-genetic risk factors. Most BC cases are attibutable to non-genetic risk factors, with a history of adverse environmental exposures playing a significant role. Pesticide exposure can occur at higher levels in female populations participating in rural activities such as spraying of pesticides in the field, unprotected handling of pesticides at home, and washing of contaminated clothes. Exposure can also be significant in the drinking water of certain populations. Here, we reviewed the literature on women's exposure to pesticides and the risk of BC. We summarize the main links between pesticide exposure and BC and discuss the role of dose and exposure context, as well as potential mechanisms of toxicity. Overall, reports reviewed here have documented stronger associations between higher levels of exposure and BC risk, including documenting direct and acute pesticide exposure in certain female populations. However, discrepancies among studies regarding dose and mode of exposure may result in misunderstandings about the risks posed by pesticide exposure. Plausible mechanisms linking pesticides to breast cancer risk include their impacts as endocrine disruptors, as well as their roles as genotoxic agents, and modulators of the epigenome. Besides establishing links between pesticide exposure and breast cancer, the literature also highlights the critical need to understand the routes and doses of women's exposure to pesticides and the specific associations and mechanisms that are determinants of disease etiology and prognosis.

Phenacetin (PNCT) belongs to one of the earliest synthetic antipyretics. However, impact of PNCT on nitrifying microorganisms in wastewater treatment plants and its potential microbial mechanism was still unclear. In this study, PN could be initiated within six days by PNCT anaerobic soaking treatment (8 mg/L). In order to improve the stable performance of PN, 21 times of PNCT aerobic soaking treatment every three days was conducted and PN was stabilized for 191 days. After PN was damaged, ten times of PNCT aerobic soaking treatment every three days was conducted and PN was recovered after once soaking, maintained over 88 days. Ammonia oxidizing bacteria might change the dominant oligotype to gradually adjust to PNCT, and the increase of abundance and activity of Nitrosomonas promoted the initiation of PN. For nitrite-oxidizing bacteria (NOB), the increase of Candidatus Nitrotoga and Nitrospira destroyed PN, but PN could be recovered after once aerobic soaking illustrating NOB was not resistant to PNCT. KEGG and COG analysis suggested PNCT might disrupt rTCA cycle of Nitrospira, resulting in the decrease of relative abundance of Nitrospira. Moreover, PNCT did not lead to the sharp increase of absolute abundances of antibiotic resistance genes (ARGs), and the risk of ARGs transmission was negligible.

Invasive Aedes aegypti and Aedes albopictus mosquitoes transmit viruses such as dengue, chikungunya and Zika, posing a huge public health burden as well as having a less well understood economic impact. We present a comprehensive, global-scale synthesis of studies reporting these economic costs, spanning 166 countries and territories over 45 years. The minimum cumulative reported cost estimate expressed in 2022 US$ was 94.7 billion, although this figure reflects considerable underreporting and underestimation. The analysis suggests a 14-fold increase in costs, with an average annual expenditure of US$ 3.1 billion, and a maximum of US$ 20.3 billion in 2013. Damage and losses were an order of magnitude higher than investment in management, with only a modest portion allocated to prevention. Effective control measures are urgently needed to safeguard global health and well-being, and to reduce the economic burden on human societies. This study fills a critical gap by addressing the increasing economic costs of Aedes and Aedes-borne diseases and offers insights to inform evidence-based policy.

Anticoagulant rodenticides (ARs) are used globally to control rodent pests. Second-generation anticoagulant rodenticides (SGARs) persist in the liver and pose a significant risk of bioaccumulation and secondary poisoning in predators, including species that do not generally consume rodents. As such, there is a clear need to understand the consumption of ARs, particularly SGARs, by non-target consumers to determine the movement of these anticoagulants through ecosystems. We collected and analysed the livers from deceased common brushtail possums (Trichosurus vulpecula) and common ringtail possums (Pseudocheirus peregrinus), native Australian marsupials that constitute the main diet of the powerful owl (Ninox strenua), an Australian apex predator significantly exposed to SGAR poisoning. ARs were detected in 91 % of brushtail possums and 40 % of ringtail possums. Most of the detections were attributed to SGARs, while first-generation anticoagulant rodenticides (FGARs) were rarely detected. SGAR concentrations were likely lethal or toxic in 42 % of brushtail possums and 4 % of ringtail possums with no effect of age, sex, or weight detected in either species. There was also no effect of the landscape type possums were from, suggesting SGAR exposure is ubiquitous across landscapes. The rate of exposure detected in these possums provides insight into the pathway through which ARs are transferred to one of their key predators, the powerful owl. With SGARs entering food-webs through non-target species, the potential for bioaccumulation and broader secondary poisoning of predators is significantly greater and highlights an urgent need for routine rodenticide testing in non-target consumers that present as ill or found deceased. To limit their impact on ecosystem stability the use of SGARs should be significantly regulated by governing agencies.

Climate change will impact the carrot seed industry globally. One adaptation strategy to limit climatic impacts on the production of commercial carrot seeds is geographical shift. However, production must be shifted to climate-optimal places that are free from weeds such as wild carrots to avoid genetic contamination via hybridization. The process of gene flow between wild and cultivated carrots is critical to enable management of wild carrots in the face of climate change. This review systematically assesses the resilience of wild carrots to climate change and their impact on commercial carrot seed production globally with a focus on New Zealand as a major carrot seed producer. The literature was critically analyzed based on three specific components: i) resilience of wild carrots to climate change ii) genetic contamination between wild and cultivated carrots, and iii) management of wild carrots. The majority of the articles were published between 2013 and 2023 (64.71 %), and most of these studies were conducted in Europe (37.26 %) and North America (27.45 %). Country-wise analysis demonstrated that the majority of the studies were carried out in the United States (23.53 %) and the Netherlands (11.77 %). There was limited research conducted in other regions, especially in Oceania (1.96 %). Spatial distribution analysis revealed that the wild carrot was reported in around 100 countries. In New Zealand the North Island has a higher incidence of wild carrot invasion than the South Island. The findings indicated that the wild carrot is becoming more adaptable to climate change, compromising the genetic purity of cultivated carrots due to pollen flow from wild to cultivated carrots. Therefore, ongoing research will be helpful in developing sustainable weed management strategies and predicting potential geographical invasiveness. This study provides a guide for scientists, policymakers, industrialists, and farmers to control wild carrots and produce genetically pure commercial seeds amid climate change.

Ozone (O₃) is a major air pollutant that directly threatens the respiratory system, lung fatty acid metabolism disorder is an important molecular event in pulmonary inflammatory diseases. Liver kinase B1 (LKB1) and nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3) inflammasome not only regulate inflammation, but also have close relationship with fatty acid metabolism. However, the role and mechanism of LKB1 and NLRP3 inflammasome in lung fatty acid metabolism, which may contribute to ozone-induced lung inflammation, remain unclear, and effective strategy for preventing O₃-induced pulmonary inflammatory injury is lacking. To explore these, mice were exposed to 1.00 ppm O₃ (3 h/d, 5 days), and pulmonary inflammation was determined by airway hyperresponsiveness, histopathological examination, total cells and cytokines in bronchoalveolar lavage fluid (BALF). Targeted fatty acids metabolomics was used to detect medium and long fatty acid in lung tissue. Then, using LKB1-overexpressing adenovirus and NLRP3 knockout (NLRP3-/-) mice to explore the mechanism of O₃-induced lung fatty acid metabolism disorder. Results demonstrated that O₃ exposure caused pulmonary inflammatory injury and lung medium and long chain fatty acids metabolism disorder, especially decreased dihomo-γ-linolenic acid (DGLA). Meanwhile, LKB1 expression was decreased, and NLRP3 inflammasome was activated in lung of mice after O₃ exposure. Additionally, LKB1 overexpression alleviated O₃-induced lung inflammation and inhibited the activation of NLRP3 inflammasome. And we found that pulmonary fatty acid metabolism disorder was ameliorated of NLRP3 -/- mice compared with those in wide type mice after O₃ exposure. Furthermore, administrating DGLA intratracheally prior to O₃ exposure significantly attenuated O₃-induced pulmonary inflammatory injury. Taken together, these findings suggest that fatty acids metabolism disorder is involved in O₃-induced pulmonary inflammation, which is regulated by LKB1-mediated NLRP3 pathway, DGLA supplement could be a useful preventive strategy to ameliorate ozone-associated lung inflammatory injury.

Nanoplastic pollution typically exhibits more biotoxicity to marine organisms than microplastic pollution. Limited research exists on the toxic effects of small-sized nanoplastics on marine fish, especially regarding their post-exposure resilience. In this study, red drum (Sciaenops ocellatus) were exposed to small-sized polystyrene nanoplastics (30 nm, PS-NPs) for 7 days for the exposure experiments, followed by 14 days of recovery experiments. Histologically, hepatic lipid droplets and branchial epithelial liftings were the primary lesions induced by PS-NPs during both exposure and recovery periods. The inhibition of total superoxide dismutase activity and the accumulation of malondialdehyde content throughout the exposure and recovery periods. Transcriptional and metabolic regulation revealed that PS-NPs induced lipid metabolism disorders and DNA damage during the initial 1-2 days of exposure periods, followed by immune responses and neurotoxicity in the later stages (4-7 days). During the early recovery stages (2-7 days), lipid metabolism and cell cycle were activated, while in the later recovery stage (14 days), the emphasis shifted to lipid metabolism and energy metabolism. Persistent histological lesions, changes in antioxidant capacity, and fluctuations in gene and metabolite expression were observed even after 14 days of recovery periods, highlighting the severe biotoxicity of small-sized PS-NPs to marine fish. In summary, small-sized PS-NPs have severe biotoxicity, causing tissue lesions, oxidative damage, lipid metabolism disorders, DNA damage, immune responses, and neurotoxicity in red drum. This study offers valuable insights into the toxic effects and resilience of small-sized nanoplastics on marine fish.

Introduction: Subjective well-being, an important index for measuring mental health, is presently declining among junior high school students. Envy, one of their common emotions, is inextricably linked to subjective well-being. Based on the Dual Envy Theory, our research explores the bidirectional relationship between benign-malicious envy and subjective well-being. The mediating role of self-esteem, as well as the related gender differences, is examined.

Methods: Chinese middle school students (n = 1566, boys 50.3%, age = 13.96 ± 0.88 years old) were assessed at two time points over a 3-month interval. Structural equation modeling was used to examine the longitudinal relationships among the variables.

Results: (1) Cross-lagged analysis showed a positive bidirectional relationship between benign envy and subjective well-being and a negative bidirectional relationship between malicious envy and subjective well-being in the total sample. However, the path from T1 subjective well-being to T2 malicious envy in boys was not significant. (2) Self-esteem mediated the relationship between both benign and malicious envy and subjective well-being among both boys and girls. A Wald chi-square test showed that T2 self-esteem was a stronger predictor of T2 benign envy in boys than in girls.

Conclusion: The results reveal a virtuous cycle of benign envy and subjective well-being, and a vicious cycle of malicious envy and subjective well-being, while emphasizing the role of self-esteem in this process. Gender differences were also noted. These findings have important implications for improving the subjective well-being of secondary school students and exploring the positive effects of envy.

Objectives: To date, there are no standardized treatment algorithms or recommendations for patients with infective endocarditis (IE) and concomitant spondylodiscitis (SD). Therefore, our aim was to analyze whether the sequence of surgical treatment of IE and SD has an impact on postoperative outcome and to identify risk factors for survival and postoperative recurrence.

Methods: Patients with IE underwent surgery in 4 German university hospitals between 1994 and 2022. Univariable and multivariable analyses were performed to identify possible predictors of 30-day/1-year mortality and recurrence of IE and/or SD.

Results: From the total IE cohort (n = 3991), 150 patients (4.4%) had concomitant SD. Primary surgery for IE was performed in 76.6%, and primary surgery for SD in 23.3%. The median age was 70.0 [64.0-75.6] years and patients were mostly male (79.5%). The most common pathogens detected were enterococci and Staphylococcus aureus followed by streptococci, and Coagulase Negative Staphylococci (CoNS). If SD was operated on first, 30-day mortality was significantly higher than if IE was operated on first (25.7% vs 11.4%; p = 0.037) and we observed a tendency for a higher 1-year mortality. If IE was treated first, we observed a higher recurrence rate within one year (12.2% vs 0%; p = 0.023). Multivariable analysis showed that primary surgery for SD was an independent predictor of 30-day mortality.

Conclusions: Primary surgical treatment for SD was an independent risk factor for 30-day mortality. When IE was treated surgically first, recurrence rate of IE and/or SD was higher.