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Annexin A2 gene interacting with viral matrix protein to promote bovine ephemeral fever virus release.Bovine ephemeral fever virus (BEFV) causes bovine ephemeral fever, which can produce considerable economic damage to the cattle industry. However, there is limited experimental evidence regarding the underlying mechanisms of BEFV. Annexin A2 (AnxA2) is a calcium and lipid-conjugated protein that binds phospholipids and the cytoskeleton in a Ca-dependent manner, and it participates in various cellular functions, including vesicular trafficking, organization of membrane domains, and virus proliferation. The role of the AnxA2 gene during virus infection has not yet been reported. In this study, we observed that AnxA2 gene expression was up-regulated in BHK-21 cells infected with the virus. Additionally, overexpression of the AnxA2 gene promoted the release of mature virus particles, whereas BEFV replication was remarkably inhibited after reducing AnxA2 gene expression by using the small interfering RNA (siRNA). For viral proteins, overexpression of the Matrix (M) gene promotes the release of mature virus particles. Moreover, the AnxA2 protein interaction with the M protein of BEFV was confirmed by GST pull-down and co-immunoprecipitation assays. Experimental results indicate that the C-terminal domain (268-334 aa) of AxnA2 contributes to this interaction. An additional mechanistic study showed that AnxA2 protein interacts with M protein and mediates the localization of the M protein at the plasma membrane. Furthermore, the absence of the AnxA2-V domain could attenuate the effect of AnxA2 on BEFV replication. These findings can contribute to elucidating the regulation of BEFV replication and may have implications for antiviral strategy development.
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#32232756 // Save this To Up
Investigation of plant species and their heavy metal accumulation in manganese mine tailings in Pingle Mn mine, China.Mine tailings are a characteristic of landscapes where mineral extraction has occurred and provide a prime opportunity for vegetation succession. In this study, soil heavy metal concentrations, plant composition and biodiversity, heavy metal accumulation, and their relationships were studied in the tailings of the Pingle Mn mine (abandoned for over 15 years) in South China. The total heavy metal concentrations ranged from 440 to 15,590 mg kg for Mn, 5.01 to 20.7 mg kg for Cd, 101 to 319 mg kg for Pb, 546 to 1693 mg kg for Zn, and 116 to 180 mg kg for Cu. According to soil contamination assessment by single contamination indexes and the Nemerow multifactor index, the tailing soil had a heavy pollution level. According to ecological risk assessment by monomial potential ecological risk factors and potential ecological risk indexes, the tailing soil presented a high ecological risk level, to which Cd was the key contributor. A total of 13 plant species from 2 families (Gramineae and Compositae) successfully colonized the tailings. Importance values based on relative height, relative coverage, relative abundance, and relative frequency indicated that Neyraudia reynaudiana K. and Paspalum orbiculare F. were the dominant species. The species were multi-metal-tolerant species, and most of them were shoot accumulators, as their translocation factor values were above 1. Plants exhibited the highest bioconcentration factor for Pb, and the average values for roots, stems, and leaves were 2.56, 1.45, and 1.70, respectively. There were positive relationships (P < 0.01) between soil Mn, Cd, Zn, and Cu and plant Pb; similar results were found for soil heavy metals and leaf/stem Mn. The species composition in the tailings of the Pingle Mn mine was reflective of long-term vegetation succession, and the results obtained in this study provide insight for selecting plant species and reconstruction practices for Mn wasteland restoration.
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Inferring Personalized and Race-Specific Causal Effects of Genomic Aberrations on Gleason Scores: A Deep Latent Variable Model.Extensive research has examined socioeconomic factors influencing prostate cancer (PCa) disparities. However, to what extent molecular and genetic mechanisms may also contribute to these inequalities still remains elusive. Although various , and population studies have originated to address this issue, they are often very costly and time-consuming by nature. In this work, we attempt to explore this problem by a preliminary study, where a joint deep latent variable model (DLVM) is proposed to quantify the personalized and race-specific effects that a genomic aberration may exert on the Gleason Score (GS) of each individual PCa patient. The core of the proposed model is a deep variational autoencoder (VAE) framework, which follows the causal structure of inference with proxies. Extensive experimental results on The Cancer Genome Atlas (TCGA) 270 European-American (EA) and 43 African-American (AA) PCa patients demonstrate that ERG fusions, somatic mutations in SPOP and ATM, and copy number alterations (CNAs) in ERG are the statistically significant genomic factors across all low-, intermediate-, and high-grade PCa that may explain the disparities between these two groups. Moreover, compared to a state-of-the-art deep inference method, our proposed method achieves much higher precision in causal effect inference in terms of the impact of a studied genomic aberration on GS. Further validation on an independent set and the assessment of the genomic-risk scores along with corresponding confidence intervals not only validate our results but also provide valuable insight to the observed racial disparity between these two groups regarding PCa metastasis. The pinpointed significant genomic factors may shed light on the molecular mechanism of cancer disparities in PCa and warrant further investigation.
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High omega arachidonic acid/docosahexaenoic acid ratio induces mitochondrial dysfunction and altered lipid metabolism in human hepatoma cells.Non-alcoholic fatty liver disease (NAFLD) is a common cause of liver disease worldwide and is a growing epidemic. A high ratio of omega-6 fatty acids to omega-3 fatty acids in the diet has been implicated in the development of NAFLD. However, the inflicted cellular pathology remains unknown. A high ratio may promote lipogenic pathways and contribute to reactive oxygen species (ROS)-mediated damage, perhaps leading to mitochondrial dysfunction. Therefore, these parameters were investigated to understand their contribution to NAFLD development.
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