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Background: The genetic diversity of malaria parasites traces the origin and spread of new variants and can be used to evaluate the effectiveness of malaria control measures. Therefore, this study aims to improve the understanding of the molecular epidemiology of Plasmodium vivax malaria at the China-Myanmar border by genotyping the PvMSP-3α and PvMSP-3β genes., Methods: Blood samples were collected from P. vivax malaria patients along the China-Myanmar border. The PvMSP-3α and PvMSP-3β genes were amplified by polymerase chain reaction (PCR) and the genetic polymorphism and haplotype of the two genes were analyzed., Results: A total of 422 blood samples were used for this study, of which 224 were analyzed at PvMSP-3α and 126 at PvMSP-3β. Samples mainly were from young adults aged 18-45 years, although local patients were significantly younger than migrant laborers crossing the border at Tengchong (P < 0.0001). Molecular evolutionary analysis revealed that PvMSP-3α and PvMSP-3β underwent diversifying natural selection, and intragenic recombination contributed to the diversity of the isolates. Based on the length of the genes, we identified three types of PvMSP-3α [1.9-2.0 kb (Type-A), 1.4-1.5 kb (Type-B), and 1.1-1.3 kb (Type-C)] and two types of PvMSP-3β [1.7-2.2 kb (Type-A) and 1.4-1.5 kb (Type-B)]. Migrant laborers returning to China through Tengchong bore P. vivax infections displaying significantly higher genetic diversity than local residents., Conclusions: Both PvMSP-3 paralogs were subjected to diversifying selection in each sample population. Clustering of alleles supports ephemeral endemic differentiation of alleles, but the broader phylogeny suggests that alleles transit the globe, perhaps accelerated by movements of migrants such as those transiting Tengchong., Competing Interests: Declaration of Competing Interest The research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Deoxynivalenol (DON) is a mycotoxin produced by multipleFusariumspecies that often contaminates cereals and threatens human and animal health. A wide range of cytotoxic effects, such as the induction of DNA damage, an increase in mitochondrial permeability and the inhibition of macromolecule synthesis, have been reported. However, the effects of DON on cell migration-a fundamental process in living cells critical for normal development, immune responses, and disease processes-and the mechanism underlying these effects are still unclear. Here, we showed that DONsignificantly inhibited the migration of MRC-5, CCD-18Co, HCT116 and WM793 cells at 50 ng/ml, 50 ng/ml, 400 ng/ml and 250 ng/ml, respectively, which maintained cell viability at 90%. Further analysis showed that DON inhibited the expression of tumour endothelial marker 8 (TEM8), a key gene in cell migration. Furthermore, we showed that DON inhibited the expression of TEM8 through increasing the level of H3K27me3 in the TEM8 promoter. Finally, overexpression of TEM8 or treating by H3K27me3-specific inhibitor GSK126 attenuated the inhibitory effect of DON on cell migration. In summary, low doses of DON at approximately dietary exposure significantly inhibited cell migration by downregulating the expression of TEM8 in a manner mediated by H3K27me3, which may generate increasing concerns for the risk of DON exposure., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Aflatoxin B 1 (AFB 1 ), a member of the aflatoxin family, is a common contaminant in foods and feeds, and AFB 1 exposure is associated with various clinical conditions. Thus far, research on the toxicity of AFB 1 has mainly focused on its induction of liver cancer, but little research has been reported on renal toxicity, especially with regards to the underlying molecular mechanisms. In this study, we found that AFB 1 treatment significantly induced kidney damage and reduced kidney weight. The human kidney cell line HEK293T was used to further study the molecular mechanism of the toxicity of AFB 1 to kidney cells. We found that AFB 1 significantly and dose-dependently induced S phase arrest and upregulated p21 mRNA and protein expression. Upstream of p21, three negative regulators, PLK1, MYC, and PLD1, were significantly downregulated under AFB 1 treatment . Consistently, p21 was upregulated, and PLK1, MYC and PLD1 were downregulated in mouse kidney after AFB 1 treatment. Interestingly, AFB 1 also decreased the physical interaction between PLK1 and MYC and weakened the stability of the MYC protein. Importantly, overexpression of PLK1, MYC and PLD1 significantly blocked the upregulation of p21 and attenuated the S phase arrest caused by AFB 1 . In summary, AFB 1 markedly induces kidney damage and strongly induces S phase arrest by upregulating the expression of p21 via PLK1, PLD1 and MYC, which represents a noval mechanism of the renal toxicity of AFB 1 ., (Copyright © 2019 Elsevier Inc. All rights reserved.)