Cold-Chain-Food-Related COVID-19 Surveillance in Guangzhou between July 2020 and December 2022.

OBJECTIVE: To monitor severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA contamination in samples linked to imported cold-chain food and assess the situation from the implementation of a centralized supervision warehouse system in Guangzhou, Guangdong Province, China. METHODS: Swabs of workers and frozen-food-related samples were collected between July 2020 and December 2023 in Guangzhou, Guangdong Province. SARS-CoV-2 RNA was extracted and analyzed by a real-time quantitative polymerase chain reaction using the commercially available SARS-CoV-2 nucleic acid test kit. The risk level and food source were monitored simultaneously. RESULTS: A total of 283 positive cold-chain events were found in Guangzhou since the first cold-chain-related event of the coronavirus disease 2019 pandemic was identified in July 2020. Most positive samples were a low-to-medium risk, and the cycle threshold value was >30. No live virus was detected, and no staff came into direct contact with a live virus. In total, 87.63% of positive events were identified through sampling and testing at the centralized food warehouse. CONCLUSION: Cold-chain food has a relatively low risk of transmitting SARS-CoV-2. Centralized food storage can be used as an effective method to control this risk, and this measure can also be used for other food-related, contact-transmitted diseases.

Inhibition of chondrocyte apoptosis in a rat model of osteoarthritis by exosomes derived from miR­140­5p­overexpressing human dental pulp stem cells.

Osteoarthritis (OA) is a common joint disorder, and the restoration of the impaired cartilage remains a main concern for researchers and clinicians. MicroRNAs (miRNAs or miRs) play crucial roles in the pathogenesis of OA. The present study examined the therapeutic efficacy of exosomal­miR­140­5p for the treatment of OA using dental pulp stem cells (DPSCs). The findings indicated that the exosomal burden of miR­140­5p was substantially increased following the transfection of DPSCs with miR­140­5p mimic. The administration of DPSC­derived exosomes promoted chondrocyte­related mRNA expression, including aggrecan, Col2α1 and Sox9, in interleukin (IL)­1ß­treated human chondrocytes. This effect was substantially enhanced by miR­140­5p­enriched exosomes. The results further revealed that miR­140­5p­enriched exosomes induced a more significant reduction in IL­1ß­induced chondrocyte apoptosis than the DPSC­derived exosomes. Mechanistically, it was found that miR­140­enriched DPSC­derived exosomes exerted anti­apoptotic effects, probably by regulating the expression levels of apoptosis­related proteins. Furthermore, multiple administrations of miR­140­5p­enriched exosomes substantially improved knee joint conditions in a rat model of OA. Collectively, the data of the present study suggest that exosomes derived from genetically modified DPSCs may prove to be a potential strategy for the treatment of OA.

MeHg-induced autophagy via JNK/Vps34 complex pathway promotes autophagosome accumulation and neuronal cell death.

Methylmercury (MeHg), an environmental toxin, may specifically cause neurological disorders. Recent studies have reported that autophagy can be induced by metals and be involved in metal cytotoxicity. However, the role of autophagy in MeHg-induced neurotoxicity remains unknown. Here, we demonstrate that MeHg induces mTOR-independent autophagy through JNK/Vps34 complex pathway, which further promotes autophagosome accumulation and neuronal cell death. In addition to cell death, MeHg increased LC3-II expression in a concentration- and time-dependent manner in neuronal cells; furthermore, western blot analysis of LC3-II expression under baf A1-treated condition indicates that MeHg activates autophagy induction. However, we found lysosomal degradative function was impaired by MeHg. Under this condition, MeHg-activated autophagy induction would elicit autophagosome accumulation and cell death. Consistent with this inference, the autophagy inhibitor decreased the MeHg-induced autophagosome accumulation and neuronal cells death, whereas the autophagy inducers further augmented MeHg cytotoxicity. Then, the mechanism of autophagy induction is investigated. We show that MeHg-induced autophagy is mTOR-independent. Vacuolar protein sorting 34 (Vps34) complex is critical for mTOR-independent autophagy. MeHg induced the interaction between Beclin1 and Vps34 to form Vps34 complex. Importantly, knockdown of Vps34 inhibited autophagy induction by MeHg. Furthermore, we found that JNK, but not p38 or ERK, promoted the formation of Vps34 complex and autophagy induction. Finally, inhibition of JNK or downregulation of Vps34 decreased autophagosome accumulation and alleviated MeHg-induced neuronal cell death. The present study implies that inhibiting JNK/Vps34 complex autophagy induction pathway may be a novel therapeutic approach for the treatment of MeHg-induced neurotoxicity.