Accumulating evidence indicates exposure to pesticides during the crucial neurodevelopmental period increases susceptibility to many diseases, including the neurodevelopmental disorder known as autism spectrum disorder (ASD). In the last few years, it has been hypothesized that gut microbiota dysbiosis is strongly implicated in the aetiopathogenesis of ASD. Recently, new studies have suggested that the gut microbiota may be involved in the neurological and behavioural defects caused by pesticides, including ASD symptoms. This review highlights the available evidence from recent animal and human studies on the relationship between pesticides that have the potential to disturb intestinal microbiota homeostasis, and ASD symptoms. The mechanisms through which gut microbiota dysbiosis may trigger ASD-like behaviours induced by pesticides exposure during the neurodevelopmental period via the altered production of bacterial metabolites (short chain fatty acids, lipids, retinol, and amino acid) are also described. According to recent research, gut microbiota dysbiosis may be a major contributor to the symptoms of ASD associated with pesticides exposure. However, to determine the detailed mechanism of action of gut microbiota on pesticide-induced ASD behaviours, actual population exposure scenarios from epidemiological studies should be used as the basis for the appropriate exposure pattern and dosage to be used in animal studies.

Background: With the rapid spread of the mpox epidemic, cases have emerged in multiple countries, mainly among men who have sex with men. Because of the connectedness of today’s world, countries have to be prepared to face risks in advance. Therefore, this study aimed to investigate awareness of mpox-related knowledge among men who have sex with men in China. Methods: With the assistance of the social organizations of men who have sex with men, a cross-sectional survey of men who have sex with men in China was conducted through an online questionnaire between July 1 and July 18, 2022. A nationwide sample of Chinese men who have sex with men (N = 3,257) was recruited. Results: Only 36.9% of participants had mpox-related knowledge. Awareness of mpox-related knowledge among respondents was positively associated with those in older age groups (33 to 42 years and 51 years or older) (adjusted odds ratio [AOR] = 1.31; 95% confidence interval [CI]: 1.03–1.67, AOR = 1.61; 95% CI: 1.16–2.24; respectively), married (AOR = 1.55; 95% CI: 1.09–2.19), and those with a graduate degree or above (AOR = 2.14; 95% CI: 1.11–4.13), while negatively associated with those living in the western parts of China (AOR = 0.74; 95% CI: 0.60–0.92), and those who were unsure of their history of Human Immunodeficiency Virus (HIV) status (AOR = 0.44; 95% CI: 0.30–0.63). Conclusion: Mpox-related knowledge is fairly low among men who have sex with men in China. China needs to spread knowledge to the public through multiple channels, especially in key populations (men who have sex with men, HIV-infected, etc.), and take preventive measures to effectively avoid outbreaks of mpox.

Dibutyl phthalate (DBP) and Benzo(a)pyrene (BaP) are ubiquitous contaminants in environment and foodstuffs, which increase the chance of their combined exposure to humans in daily life. However, the combined effects of DBP and BaP on liver and the underlying mechanisms are still unclear. In this study, we explored the combined effects of DBP and BaP on liver and the potential mechanisms in a rat model. We found that DBP and BaP co-exposure activated the MyD88/NF-κB pathway through increasing TLR4 acetylation (TLR4ac) level, leading to the imbalance of pro-inflammatory factors (CXCL-13, IL-6 and TNF-α) and anti-inflammatory factors (IL-10), ultimately resulting in liver tissue damage and functional changes. Sporoderm-broken spores of Ganoderma lucidum (SSGL) had strong alleviating effects on liver injury induced by DBP and BaP co-exposure. Our study found that SSGL suppressed TLR4ac-regulated MyD88/NF-κB signaling to reduce the release of pro-inflammatory factors, and promote the secretion of IL-10, thus alleviating liver injury caused by DBP and BaP co-exposure. In conclusion, SSGL contributed to liver protection against DBP and BaP-induced liver injury in rats via suppressing the TLR4ac-regulated MyD88/NF-κB signaling.