Detection and exposure assessment of pesticide residues in leek in He’nan Province

ObjectiveTo evaluate the health risk of pesticide exposure from leek， the pesticide residue in leek from Henan market was investigated.MethodsThe residues of 16 pesticides in leek sold on Henan market in 2020 were detected and analyzed. According to health guidance values such as food consumption data of the World Health Organization， acute reference dose formulated by Joint Meeting on Pesticide Residues and adaptable daily intake in “National food safety standard-Maximum residue limits for pesticides in food”， the acute and chronic exposure risks of pesticide residues in leek were evaluated by point assessment method， and the cumulative exposure was evaluated by hazard index method.ResultsThere were many types of pesticide residues in leek samples and 93.81% （424/452） of the samples were positive. 7 of the 14 pesticides exceeded their MRLs， and the violation rate of all samples was 16.15%. The detection of multiple pesticides was relatively serious， and 56.42% of the samples contained more than two pesticide residues. In the acute exposure assessment， the acute risks of carbofuran， procymidone and phorate exceeded the acceptable level. In the chronic exposure assessment， the chronic risk of omethoate exceeded the acceptable level. And insecticide pesticides had cumulative poisoning risk.ConclusionThe situation of pesticide residues in leek in Henan province was relatively prominent. To ensure the safety of agricultural products， it was recommended that the routine monitoring and use of pesticide， especially high-risk pesticides such as omethoate， carbofuran， procymidone and phorate should be strengthened

Genomic and transcriptomic analyses reveal distinct biological functions for cold shock proteins (<i>Vpa</i>CspA and <i>Vpa</i>CspD) in <i>Vibrio parahaemolyticus</i> CHN25 during low-temperature survival

Abstract Background Vibrio parahaemolyticus causes serious seafood-borne gastroenteritis and death in humans. Raw seafood is often subjected to post-harvest processing and low-temperature storage. To date, very little information is available regarding the biological functions of cold shock proteins (CSPs) in the low-temperature survival of the bacterium. In this study, we determined the complete genome sequence of V. parahaemolyticus CHN25 (serotype: O5:KUT). The two main CSP-encoding genes (VpacspA and VpacspD) were deleted from the bacterial genome, and comparative transcriptomic analysis between the mutant and wild-type strains was performed to dissect the possible molecular mechanisms that underlie low-temperature adaptation by V. parahaemolyticus. Results The 5,443,401-bp V. parahaemolyticus CHN25 genome (45.2% G + C) consisted of two circular chromosomes and three plasmids with 4,724 predicted protein-encoding genes. One dual-gene and two single-gene deletion mutants were generated for VpacspA and VpacspD by homologous recombination. The growth of the ΔVpacspA mutant was strongly inhibited at 10 °C, whereas the VpacspD gene deletion strongly stimulated bacterial growth at this low temperature compared with the wild-type strain. The complementary phenotypes were observed in the reverse mutants (ΔVpacspA-com, and ΔVpacspD-com). The transcriptome data revealed that 12.4% of the expressed genes in V. parahaemolyticus CHN25 were significantly altered in the ΔVpacspA mutant when it was grown at 10 °C. These included genes that were involved in amino acid degradation, secretion systems, sulphur metabolism and glycerophospholipid metabolism along with ATP-binding cassette transporters. However, a low temperature elicited significant expression changes for 10.0% of the genes in the ΔVpacspD mutant, including those involved in the phosphotransferase system and in the metabolism of nitrogen and amino acids. The major metabolic pathways that were altered by the dual-gene deletion mutant (ΔVpacspAD) radically differed from those that were altered by single-gene mutants. Comparison of the transcriptome profiles further revealed numerous differentially expressed genes that were shared among the three mutants and regulators that were specifically, coordinately or antagonistically modulated by VpaCspA and VpaCspD. Our data also revealed several possible molecular coping strategies for low-temperature adaptation by the bacterium. Conclusions This study is the first to describe the complete genome sequence of V. parahaemolyticus (serotype: O5:KUT). The gene deletions, complementary insertions, and comparative transcriptomics demonstrate that VpaCspA is a primary CSP in the bacterium, while VpaCspD functions as a growth inhibitor at 10 °C. These results have improved our understanding of the genetic basis for low-temperature survival by the most common seafood-borne pathogen worldwide

Experimental preparation of eight-partite linear and two-diamond shape cluster states for photonic qumodes

The preparation of multipartite entangled states is the prerequisite for exploring quantum information networks and quantum computation. In this letter, we present the first experimental demonstration of eight-partite spatially separated CV entangled states. The initial resource quantum states are eight squeezed states of light, through the linearly optical transformation of which two types of the eight-partite cluster entangled states are prepared, respectively. The generated eight entangled photonic qumodes are spatially separated, which provide valuable quantum resources to implement more complicated quantum information task.Comment: 14 pages, 7 figure

Comprehensive investigation and regulatory function of lncRNAs engaged in western honey bee larval immune response to Ascosphaera apis invasion

Ascosphaera apis is a fungal pathogen that exclusively infects bee larvae, causing chalkbrood disease, which results in severe damage for beekeeping industry. Long non-coding RNAs (lncRNAs) are versatile regulators in various biological processes such as immune defense and host-pathogen interaction. However, expression pattern and regulatory role of lncRNAs involved in immune response of bee host to A. apis invasion is still very limited. Here, the gut tissues of Apis mellifera ligustica 4-, 5-, and 6-day-old larvae inoculated by A. apis spores (AmT1, AmT2, and AmT3 groups) and corresponding un-inoculated larval guts (AmCK1, AmCK2, and AmCK3 groups) were prepared and subjected to deep sequencing, followed by identification of lncRNAs, analysis of differentially expressed lncRNAs (DElncRNAs), and investigation of competing endogenous RNA (ceRNA) network. In total, 3,746 A. m. ligustica lncRNAs were identified, including 78 sense lncRNAs, 891 antisense lncRNAs, 1,893 intergenic lncRNAs, 346 bidirectional lncRNAs, and 210 intronic lncRNAs. In the 4-, 5-, and 6- comparison groups, 357, 236, and 505 DElncRNAs were discovered. Additionally, 217, 129, and 272 DElncRNAs were respectively predicted to regulate neighboring genes via cis-acting manner, and these targets were associated with a series of GO terms and KEGG pathways of great importance, such as response to stimulus and Jak-STAT signaling pathway. Moreover, 197, 95, and 356 DElncRNAs were observed to target 10, eight, and 21 DEmiRNAs and further target 147, 79, and 315 DEmRNAs, forming complex regulatory networks. Further investigation suggested that these targets were engaged in several key cellular and humoral immune pathways, such as phagosome and MAPK signaling pathway. Ultimately, the expression trends of nine randomly selected DElncRNAs were verified by RT-qPCR, confirming the authenticity and reliability of our transcriptome data. Findings in this current work not only provide candidate DElncRNAs for functional study, but also lay a foundation for unclosing the mechanism underlying DElncRNA-regulated larval immune responses to A. apis invasion

Paradoxical Role of Prion Protein Aggregates in Redox-Iron Induced Toxicity

Imbalance of iron homeostasis has been reported in sporadic Creutzfeldt-Jakob-disease (sCJD) affected human and scrapie infected animal brains, but the contribution of this phenotype to disease associated neurotoxicity is unclear.Using cell models of familial prion disorders, we demonstrate that exposure of cells expressing normal prion protein (PrP(C)) or mutant PrP forms to a source of redox-iron induces aggregation of PrP(C) and specific mutant PrP forms. Initially this response is cytoprotective, but becomes increasingly toxic with time due to accumulation of PrP-ferritin aggregates. Mutant PrP forms that do not aggregate are not cytoprotective, and cells show signs of acute toxicity. Intracellular PrP-ferritin aggregates induce the expression of LC3-II, indicating stimulation of autophagy in these cells. Similar observations are noted in sCJD and scrapie infected hamster brains, lending credence to these results. Furthermore, phagocytosis of PrP-ferritin aggregates by astrocytes is cytoprotective, while culture in astrocyte conditioned medium (CM) shows no measurable effect. Exposure to H(2)O(2), on the other hand, does not cause aggregation of PrP, and cells show acute toxicity that is alleviated by CM.These observations suggest that aggregation of PrP in response to redox-iron is cytoprotective. However, subsequent co-aggregation of PrP with ferritin induces intracellular toxicity unless the aggregates are degraded by autophagosomes or phagocytosed by adjacent scavenger cells. H(2)O(2), on the other hand, does not cause aggregation of PrP, and induces toxicity through extra-cellular free radicals. Together with previous observations demonstrating imbalance of iron homeostasis in prion disease affected brains, these observations provide insight into the mechanism of neurotoxicity by redox-iron, and the role of PrP in this process

Dramatic reduction of surface recombination by in-situ surface passivation of silicon nanowires

Nanowires have unique optical properties [1-4] and are considered as important building blocks for energy harvesting applications such as solar cells. [2, 5-8] However, due to their large surface-to-volume ratios, the recombination of charge carriers through surface states reduces the carrier diffusion lengths in nanowires a few orders of magnitude,[9] often resulting in the low efficiency (a few percent or less) of nanowire-based solar cells. [7, 8, 10, 11] Reducing the recombination by surface passivation is crucial for the realization of high performance nanosized optoelectronic devices, but remains largely unexplored. [7, 12-14] Here we show that a thin layer of amorphous silicon (a-Si) coated on a single-crystalline silicon nanowire (sc-SiNW), forming a core-shell structure in-situ in the vapor-liquid-solid (VLS) process, reduces the surface recombination nearly two orders of magnitude. Under illumination of modulated light, we measure a greater than 90-fold improvement in the photosensitivity of individual core-shell nanowires, compared to regular nanowires without shell. Simulations of the optical absorption of the nanowires indicate that the strong absorption of the a-Si shell contributes to this effect, but we conclude that the effect is mainly due to the enhanced carrier lifetime by surface passivation