156 research outputs found

    Table1_Identification of functional TF-miRNA-hub gene regulatory network associated with ovarian endometriosis.XLSX

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    Endometriosis (EMs), one of the most common gynecological diseases, seriously affects the health and wellness of women; however, the underlying pathogenesis remains unclear. This study focused on dysregulated genes and their predicted transcription factors (TFs) and miRNAs, which may provide ideas for further mechanistic research. The microarray expression dataset GSE58178, which included six ovarian endometriosis (OE) samples and six control samples, was downloaded from the Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs). Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to study the cellular and organism-level functions of DEGs. The protein-protein interaction (PPI) network was built and visualized using Cytoscape, and modules and hub genes were explored using various algorithms. Furthermore, we predicted miRNAs and TFs of hub genes using online databases, and constructed the TF-miRNA-hub gene network. There were 124 upregulated genes and 66 downregulated genes in EMs tissues. GO enrichment analysis showed that DEGs were concentrated in reproductive structure development and collagen-containing extracellular matrix, while KEGG pathway analysis showed that glycolysis/gluconeogenesis and central carbon metabolism in cancer require further exploration. Subsequently, HIF1A, LDHA, PGK1, TFRC, and CD9 were identified as hub genes, 22 miRNAs and 34 TFs were predicted to be upstream regulators of hub genes, and these molecules were pooled together. In addition, we found three key feedback loops in the network, MYC-miR-34a-5p-LDHA, YY1-miR-155-5p-HIF1A, and RELA-miR-93-5p-HIF1A, which may be closely related to OE development. Taken together, our study structured a TF-miRNA-hub gene network to decipher the molecular mechanism of OE, which may provide novel insights for clinical diagnosis and treatment.</p

    Table3_Identification of functional TF-miRNA-hub gene regulatory network associated with ovarian endometriosis.XLSX

    No full text
    Endometriosis (EMs), one of the most common gynecological diseases, seriously affects the health and wellness of women; however, the underlying pathogenesis remains unclear. This study focused on dysregulated genes and their predicted transcription factors (TFs) and miRNAs, which may provide ideas for further mechanistic research. The microarray expression dataset GSE58178, which included six ovarian endometriosis (OE) samples and six control samples, was downloaded from the Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs). Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to study the cellular and organism-level functions of DEGs. The protein-protein interaction (PPI) network was built and visualized using Cytoscape, and modules and hub genes were explored using various algorithms. Furthermore, we predicted miRNAs and TFs of hub genes using online databases, and constructed the TF-miRNA-hub gene network. There were 124 upregulated genes and 66 downregulated genes in EMs tissues. GO enrichment analysis showed that DEGs were concentrated in reproductive structure development and collagen-containing extracellular matrix, while KEGG pathway analysis showed that glycolysis/gluconeogenesis and central carbon metabolism in cancer require further exploration. Subsequently, HIF1A, LDHA, PGK1, TFRC, and CD9 were identified as hub genes, 22 miRNAs and 34 TFs were predicted to be upstream regulators of hub genes, and these molecules were pooled together. In addition, we found three key feedback loops in the network, MYC-miR-34a-5p-LDHA, YY1-miR-155-5p-HIF1A, and RELA-miR-93-5p-HIF1A, which may be closely related to OE development. Taken together, our study structured a TF-miRNA-hub gene network to decipher the molecular mechanism of OE, which may provide novel insights for clinical diagnosis and treatment.</p

    Table2_Identification of functional TF-miRNA-hub gene regulatory network associated with ovarian endometriosis.XLSX

    No full text
    Endometriosis (EMs), one of the most common gynecological diseases, seriously affects the health and wellness of women; however, the underlying pathogenesis remains unclear. This study focused on dysregulated genes and their predicted transcription factors (TFs) and miRNAs, which may provide ideas for further mechanistic research. The microarray expression dataset GSE58178, which included six ovarian endometriosis (OE) samples and six control samples, was downloaded from the Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs). Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to study the cellular and organism-level functions of DEGs. The protein-protein interaction (PPI) network was built and visualized using Cytoscape, and modules and hub genes were explored using various algorithms. Furthermore, we predicted miRNAs and TFs of hub genes using online databases, and constructed the TF-miRNA-hub gene network. There were 124 upregulated genes and 66 downregulated genes in EMs tissues. GO enrichment analysis showed that DEGs were concentrated in reproductive structure development and collagen-containing extracellular matrix, while KEGG pathway analysis showed that glycolysis/gluconeogenesis and central carbon metabolism in cancer require further exploration. Subsequently, HIF1A, LDHA, PGK1, TFRC, and CD9 were identified as hub genes, 22 miRNAs and 34 TFs were predicted to be upstream regulators of hub genes, and these molecules were pooled together. In addition, we found three key feedback loops in the network, MYC-miR-34a-5p-LDHA, YY1-miR-155-5p-HIF1A, and RELA-miR-93-5p-HIF1A, which may be closely related to OE development. Taken together, our study structured a TF-miRNA-hub gene network to decipher the molecular mechanism of OE, which may provide novel insights for clinical diagnosis and treatment.</p

    Chemisorption of Perfluorooctanoic Acid on Powdered Activated Carbon Initiated by Persulfate in Aqueous Solution

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    Perfluorooctanoic acid (PFOA) is a perfluorocarboxylic acid that is difficult to treat by most conventional methods. As a result, it is often removed from solution by adsorption on powdered activated carbon (PAC), followed by incineration of the spent carbon. To provide a new approach for treatment, PFOA was exposed to sulfate radicals (SO<sub>4</sub><sup>–•</sup>) produced by thermolysis of persulfate (S<sub>2</sub>O<sub>8</sub><sup>2–</sup>) in the presence of PAC. Under acidic conditions, thermal activation of persulfate resulted in transformation of PFOA to shorter-chain-length perfluorinated compounds, as previously reported. However, when thermolysis of persulfate occurred under circumneutral pH conditions in the presence of PAC, a new removal pathway for PFOA was observed. Under these conditions, the removal of PFOA was attributable to chemisorption, a process in which PAC catalyzed persulfate decomposition and reacted with the transformation products to produce covalently bound PFOA. At PAC concentrations between 200 and 1000 mg/L and an initial PFOA concentration of 0.5 μM, covalent bonding resulted in removal of 10–40% of the PFOA. Under these conditions, the process resulted in removal of more than half of a more hydrophilic perfluoroalkyl acid (i.e., perfluorobutanoic acid, PFBA), which was greater than the amount of PFBA removed by physical adsorption on PAC. Although the high reaction temperatures (i.e., 80 °C) and relatively high doses of PAC used in this study may be impractical for drinking water treatment, this process may be applied to the treatment of these recalcitrant compounds in industrial wastewater, reverse osmosis concentrate, and other waters that contain high concentrations of PFOA and other perfluorocarboxylic acids

    Direct Catalytic Asymmetric 1,6-Conjugate Addition of Amides to <i>p</i>‑Quinone Methides

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    Amide pronucleophiles were successfully incorporated into a 1,6-conjugate addition reaction manifold using <i>p</i>-quinone methides (<i>p</i>-QMs) as electrophiles. Four different types of functionalities were tolerated as α-substituents of the amides, allowing for expeditious access to a range of enantiomerically enriched diarylmethine products. The 7-azaindoline unit is critically important for in situ catalytic enolization of the amide pronucleophile, engaging in 1,6-conjugate addition to <i>p</i>-QMs with readily available catalyst components

    Leucine supplementation ameliorates early life “programming” of obesity in rats

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       The advanced cessation of lactation elevates the risk of programmed obesity and obesity-related metabolic disorders in adulthood. The study used multi-omics analysis to investigate the mechanism behind this phenomenon and the effects of leucine supplementation on ameliorating programmed obesity development. Wistar/SD rat offspring were subjected to early weaning (EW) at d 17 (EWWIS and EWSD groups) or normal weaning at d 21 (CWIS and CSD groups). Half rats from the EWSD group were selected to create a new group with two-month leucine supplementation at d 150. The results showed that EW impaired lipid metabolic gene expressions and increased insulin, neuropeptide Y, and feed intake, inducing obesity in adulthood. Six lipid metabolism-related genes (Acot1, Acot2, Acot4, Scd, Abcg8, and Cyp8b1) were influenced by EW during the whole experimental period. Additionally, adult early-weaned rats exhibited cholesterol and fatty acid β-oxidation disorders, liver taurine reduction, cholestasis, and insulin and leptin resistance. Leucine supplementation partly alleviated these metabolic disorders and increased liver L-carnitine, retarding programmed obesity development. This study provides new insights into the mechanism of programmed obesity development and the potential benefits of leucine supplementation, which may offer suggestions for life planning and programmed obesity prevention.</p

    Parabola-Like Shaped pH-Rate Profile for Phenols Oxidation by Aqueous Permanganate

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    Oxidation of phenols by permanganate in the pH range of 5.0–9.0 generally exhibits a parabola-like shape with the maximum reaction rate obtained at pH close to phenols' p<i>K</i><sub>a</sub>. However, a monotonic increase or decrease is observed if phenols' p<i>K</i><sub>a</sub> is beyond the pH range of 5.0–9.0. A proton transfer mechanism is proposed in which the undissociated phenol is directly oxidized by permanganate to generate products while a phenolate–permanganate adduct, intermediate, is formed between dissociated phenol and permanganate ion and this is the rate-limiting step for phenolates oxidation by permanganate. The intermediate combines with H<sup>+</sup> and then decomposes to products. Rate equations derived based on the steady-state approximation can well simulate the experimentally derived pH-rate profiles. Linear free energy relationships (LFERs) were established among the parameters obtained from the modeling, Hammett constants, and oxygen natural charges in phenols and phenolates. LFERs reveal that chlorine substituents have opposite influence on the susceptibility of phenols and phenolates to permanganate oxidation and phenolates are not necessarily more easily oxidized than their neutral counterparts. The chlorine substituents regulate the reaction rate of chlorophenolates with permanganate mainly by influencing the natural charges of the oxygen atoms of dissociated phenols while they influence the oxidation of undissociated chlorophenols by permanganate primarily by forming intramolecular hydrogen bonding with the phenolic group

    Optimal H<sub>2</sub> Input Load Disturbance Rejection Controller Design for Nonminimum Phase Systems Based on Algebraic Theory

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    This work discusses the issue of input load disturbance rejection (ILDR) for open-loop nonminimum phase (NMP) plants. A novel analytical solution is proposed on the basis of the internal model control (IMC) theory. Differing from other methods, the proposed design is conducted to optimize the ILDR criterion. Optimization of the input disturbance response of the controller is performed under the constraints on robustness. When the input load disturbance is taken into consideration, the proposed controller performs better disturbance rejection capability in terms of 2-norm than most explored IMC-based controllers derived from the conventional criterion. Typical NMP processes are systematically analyzed. Numerical examples are given to illustrate the effectiveness of the novel solution. The quantitative performance specifications and robust stability can be obtained by monotonously tuning the single parameter. Results show that the proposed solution makes the proposed method yield the expected dynamic responses

    Direct Catalytic Asymmetric Mannich-Type Reaction en Route to α‑Hydroxy-β-amino Acid Derivatives

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    A direct catalytic Mannich-type reaction of α‑oxygen-functionalized amides was achieved. The use of 7-azaindoline amide was crucial to facilitate direct enolization and subsequent stereoselective addition to imines in a cooperative catalytic system comprising a soft Lewis acid and Brønsted base. The operationally simple room-temperature protocol furnished a <i>syn</i>-Mannich adduct with high stereoselectivity. Divergent functional group transformation of the amide moiety of the product allowed for expeditious access to enantioenriched <i>syn</i>-configured α-hydroxy-β-amino carboxylic acid derivatives, highlighting the synthetic utility of the present catalysis

    Assessment of neuronal cytotoxicity of SPIONs.

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    <p>Based on their miRNA target profile, 5883 mRNAs were predicted to be regulated in cells following treatment with SPIONs. Approximately 31% of the mRNA candidates were significantly regulated by nanomaterial treatment. This gene set was enriched for gene ontology (GO) functions (A). We also sorted the mRNAs into KEGG pathways through DAVID. The “Amyotrophic Lateral Sclerosis (ALS) pathway” (C) was of the most highly affected KEGG pathway with p <10<sup>−7</sup>(B).</p
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