14 research outputs found

    General GAN-generated image detection by data augmentation in fingerprint domain

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    In this work, we investigate improving the generalizability of GAN-generated image detectors by performing data augmentation in the fingerprint domain. Specifically, we first separate the fingerprints and contents of the GAN-generated images using an autoencoder based GAN fingerprint extractor, followed by random perturbations of the fingerprints. Then the original fingerprints are substituted with the perturbed fingerprints and added to the original contents, to produce images that are visually invariant but with distinct fingerprints. The perturbed images can successfully imitate images generated by different GANs to improve the generalization of the detectors, which is demonstrated by the spectra visualization. To our knowledge, we are the first to conduct data augmentation in the fingerprint domain. Our work explores a novel prospect that is distinct from previous works on spatial and frequency domain augmentation. Extensive cross-GAN experiments demonstrate the effectiveness of our method compared to the state-of-the-art methods in detecting fake images generated by unknown GANs

    Cancer-associated fibroblast-secreted IGFBP7 promotes gastric cancer by enhancing tumor associated macrophage infiltration via FGF2/FGFR1/PI3K/AKT axis

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    Abstract We previously reported that IGFBP7 plays a role in maintaining mRNA stability of oncogenic lncRNA UBE2CP3 by RNA-RNA interaction in gastric cancer (GC). Clinical cohort studies had implied an oncogenic role of IGFBP7 in GC. However, the molecular mechanism of IGFBP7 in GC progression remains unknown. In this study, clinical analysis based on two independent cohorts showed that IGFBP7 was positively associated with poor prognosis and macrophage infiltration in GC. Loss-of-function studies confirmed the oncogenic properties of IGFBP7 in regulating GC cell proliferation and invasion. Mechanismly, IGFBP7 was highly expressed in cancer-associated fibroblasts (CAF) and mesenchymal cells, and was induced by epithelial-to-mesenchymal transition (EMT) signaling, since its expression was increased by TGF-beta treatment and reduced by overexpression of OVOL2 in GC. RNA sequencing, qRT-PCR, ELISA assay showed that IGFBP7 positively regulated FGF2 expression and secretion in GC. Transcriptome analysis revealed that FGFR1 was downregulated in M1 polarization but upregulated in M2 polarization. Exogenous recombinant IGFBP7 treatment in macrophages and GC cells further identified that IGFBP7 promotes tumor associated macrophage (TAM) polarization via FGF2/FGFR1/PI3K/AKT axis. Our finding here represented the first evidence that IGFBP7 promotes GC by enhancing TAM/M2 macrophage polarization through FGF2/FGFR1/PI3K/AKT axis

    Whole genome analyses reveal novel genes associated with chicken adaptation to tropical and frigid environments

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    Introduction: Investigating the genetic footprints of historical temperature selection can get insights to the local adaptation and feasible influences of climate change on long-term population dynamics. Object: Chicken is a significative species to study genetic adaptation on account of its similar domestication track related to human activity with the most diversified varieties. Yet, few studies have demonstrated the genetic signatures of its adaptation to naturally tropical and frigid environments. Method: Here, we generated whole genome resequencing of 119 domesticated chickens in China including the following breeds which are in order of breeding environmental temperature from more tropical to more frigid: Wenchang chicken (WCC), green-shell chicken (GSC), Tibetan chicken (TBC), and Lindian chicken (LDC). Results: Our results showed WCC branched off earlier than LDC with an evident genetic admixture between WCC and LDC, suggesting their closer genetic relationship. Further comparative genomic analyses solute carrier family 33 member 1 (SLC33A1) and thyroid stimulating hormone receptor (TSHR) genes exhibited stronger signatures for positive selection in the genome of the more tropical WCC. Furthermore, genotype data from about 3,000 African local ecotypes confirmed that allele frequencies of single nucleotide polymorphisms (SNPs) in these 2 genes appeared strongly associated with tropical environment adaptation. In addition, the NADH:ubiquinone oxidoreductase subunit S4 (NDUFS4) gene exhibited a strong signature for positive selection in the LDC genome, and SNPs with marked allele frequency differences indicated a significant relationship with frigid environment adaptation. Conclusion: Our findings partially clarify how selection footprints from environmental temperature stress can lead to advantageous genomic adaptions to tropical and frigid environments in poultry and provide a valuable resource for selective breeding of chickens

    Salt-sensitive ileal microbiota plays a role in atrial natriuretic peptide deficiency-induced cardiac injury

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    Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP(−/−) mice to analyze the role of the salt-sensitive ileal microbiome on cardiac injury. ANP(−/−) mice showed an increase in blood pressure (BP), the heart weight/body weight (HW/BW) ratio, and cardiac hypertrophy compared with wild-type (WT) mice. ANP deficiency did not impact the histological structure but reduced occludin expression in the ileum. Antibiotics significantly relieved BP and cardiac hypertrophy in ANP(−/−) mice. A high-salt diet (HSD) increased BP, the HW/BW ratio, and cardiac hypertrophy/fibrosis in WT and ANP(−/−) mice, and an HSD treatment in ANP(−/−) mice exacerbated these cardiac parameters. The HSD markedly decreased muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of WT and ANP(−/−) mice. Furthermore, the HSD increased the level of TLR4 and IL-1β in ANP(−/−) mice ileum compared with WT mice. Antibiotics reduced the HW/BW ratio, cardiac hypertrophy/fibrosis, and the level of TLR4 and IL-1β in the ileum, and rescued the muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of HSD-ANP(−/−) mice. Importantly, ANP deficiency induced the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum on the NSD diet, which was only observed in HSD-induced WT mice but not in WT mice on the NSD. Besides, the HSD significantly enhanced the sum of the percentage of the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum of ANP(−/−) mice. Ileal microbiota transfer (IMT) from ANP(−/−) mice to healthy C57BL/6J mice drove Lactobacillus johnsonii and Lactobacillus reuteri colonization in the ileum, which manifested an increase in BP, the HW/BW ratio, cardiac hypertrophy, and ileal pathology compared with IMT from WT mice. The HSD in C57BL/6J mice with IMT from ANP(−/−) mice drove the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum and further exacerbated the cardiac and ileal pathology. Our results suggest that salt-sensitive ileal microbiota is probably related to ANP deficiency-induced cardiac injury
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