The fold enrichment. (DOC)Table S7 The enriched Transcription factor target

The fold enrichment. (DOC)Table S7 The enriched Transcription factor target (TFT) families for the full set of imprinted genes in human according to the MSigDB database at significance level 0.01. M and P are the numbers of associated maternally and paternally expressed genes respectively. (DOC) Table S8 The enriched Transcription factor target (TFT) families for the full set of imprinted genes in mouse according to the MSigDB database at significance level 0.01. M and P are the numbers of associated maternally and paternally expressed genes respectively. (DOC) Figure S1 Heat map for the enriched transcription factor targets in the full set of imprinted genes in human (a) and mouse (b) at p-value of 0.01. Marked in red and blue in the top line are the maternally and paternally expressed genes, respectively. (TIFF)Author ContributionsConceived and designed the CY5-SE experiments: MH SI MP VH. Performed the experiments: MH. Analyzed the data: MH SI MP VH. Wrote the paper: MH MP VH.
Diseases caused by different Vibrio species have been observed in large populations throughout the world, particularly in Asia, the United States, and Africa [1?]. V. cholera and V. parahaemolyticus are the major etiological agents of vibriosis, which is associated with the ingestion of raw, undercooked, or contaminated seafood [1,2]. Grimontia 25033180 hollisae (previously named V. hollisae) has been frequently reported to cause diseases in humans, including severe gastroenteritis, hypovolemia, and septicemia following the consumption of shellfish or oysters [4?]. However, the Cy5 NHS Ester web mechanism of morbidity due to G. hollisae has not been thoroughly characterized. Although several specific laboratory examinations have detected G. hollisae, its incidence is likely highly underestimated because detection techniques are infrequently used throughout the world [7,8].The toxin thermostable direct hemolysin (TDH) is composed of 165 amino acid residues and exhibits biological activities that include hemolytic activity, cytotoxicity, and enterotoxicity [9]. The toxic effects of TDH have been identified in a variety of Vibrio species, including V. cholera non-O1, V. parahaemolyticus, V. mimicus, V. alginolyticus, and G. hollisae [10?4]. In addition, TDH production has been observed in bacteria with similar tdh gene sequences and pathogenicities [15,16]. The tdh gene is present in all strains of G. hollisae but not in all Vibrio species [10]. The physical characteristics of G. hollisae TDH (Gh-TDH) are not well known. Some studies have reported that Gh-TDH is detoxified by aggregation into fibrils after heating at 60?0uC; the protein can be reversibly refolded into the toxic 24786787 native form by rapid cooling after unfolding at higher temperatures [17]. The hemolytic activity of Gh-TDH is suppressed by the addition of Congo red [18]. In addition, the lipophilic effect of Gh-TDH has not been clearlyHepatotoxicity of Thermostable Direct Hemolysincharacterized. The toxic effects of TDH have been localized mainly in the intestinal portion of the gastrointestinal tract [19?21]. However, a relationship between the TDH and the liver has not been reported or analyzed. In addition to being absorbed by the intestine, TDH may also cause secondary injury to the liver via effects on the venous return of the portal system. In this study, we analyzed the hepatotoxicity of TDH in vivo and in vitro to provide insights into the acute injury and recovery stages of THD-induced hepatotoxicity in living animals.well) were.The fold enrichment. (DOC)Table S7 The enriched Transcription factor target (TFT) families for the full set of imprinted genes in human according to the MSigDB database at significance level 0.01. M and P are the numbers of associated maternally and paternally expressed genes respectively. (DOC) Table S8 The enriched Transcription factor target (TFT) families for the full set of imprinted genes in mouse according to the MSigDB database at significance level 0.01. M and P are the numbers of associated maternally and paternally expressed genes respectively. (DOC) Figure S1 Heat map for the enriched transcription factor targets in the full set of imprinted genes in human (a) and mouse (b) at p-value of 0.01. Marked in red and blue in the top line are the maternally and paternally expressed genes, respectively. (TIFF)Author ContributionsConceived and designed the experiments: MH SI MP VH. Performed the experiments: MH. Analyzed the data: MH SI MP VH. Wrote the paper: MH MP VH.
Diseases caused by different Vibrio species have been observed in large populations throughout the world, particularly in Asia, the United States, and Africa [1?]. V. cholera and V. parahaemolyticus are the major etiological agents of vibriosis, which is associated with the ingestion of raw, undercooked, or contaminated seafood [1,2]. Grimontia 25033180 hollisae (previously named V. hollisae) has been frequently reported to cause diseases in humans, including severe gastroenteritis, hypovolemia, and septicemia following the consumption of shellfish or oysters [4?]. However, the mechanism of morbidity due to G. hollisae has not been thoroughly characterized. Although several specific laboratory examinations have detected G. hollisae, its incidence is likely highly underestimated because detection techniques are infrequently used throughout the world [7,8].The toxin thermostable direct hemolysin (TDH) is composed of 165 amino acid residues and exhibits biological activities that include hemolytic activity, cytotoxicity, and enterotoxicity [9]. The toxic effects of TDH have been identified in a variety of Vibrio species, including V. cholera non-O1, V. parahaemolyticus, V. mimicus, V. alginolyticus, and G. hollisae [10?4]. In addition, TDH production has been observed in bacteria with similar tdh gene sequences and pathogenicities [15,16]. The tdh gene is present in all strains of G. hollisae but not in all Vibrio species [10]. The physical characteristics of G. hollisae TDH (Gh-TDH) are not well known. Some studies have reported that Gh-TDH is detoxified by aggregation into fibrils after heating at 60?0uC; the protein can be reversibly refolded into the toxic 24786787 native form by rapid cooling after unfolding at higher temperatures [17]. The hemolytic activity of Gh-TDH is suppressed by the addition of Congo red [18]. In addition, the lipophilic effect of Gh-TDH has not been clearlyHepatotoxicity of Thermostable Direct Hemolysincharacterized. The toxic effects of TDH have been localized mainly in the intestinal portion of the gastrointestinal tract [19?21]. However, a relationship between the TDH and the liver has not been reported or analyzed. In addition to being absorbed by the intestine, TDH may also cause secondary injury to the liver via effects on the venous return of the portal system. In this study, we analyzed the hepatotoxicity of TDH in vivo and in vitro to provide insights into the acute injury and recovery stages of THD-induced hepatotoxicity in living animals.well) were.

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