Establishing an S-scheme heterojunction is a promising method for increasing the photocatalytic activity of synthetic materials. In this study, nitrogen-doped g-C3N5/TiO2 S-scheme photocatalysts have ...been synthesized and examined for photocatalytic hydrogen production using thermal decomposition methods. Nitrogen-doped g-C3N5/TiO2 composites performed better than pure nitrogen-doped g-C3N5 and TiO2 alone. Using experiments and density functional theory (DFT) calculations, nitrogen (N) doping was identified as being introduced by replacing the carbon (C) atoms in the matrix of g-C3N5. In addition to its narrow band gap, N-doped g-C3N5 showed efficient carrier separation and charge transfer, resulting in the enhanced absorption of visible light and photocatalytic activity. DFT, XPS, optical property characteristics, and PL spectra confirmed these findings, which were attributed to the successful nitrogen doping, and the composite was proven to be a potential candidate for photocatalytic hydrogen generation under light irradiation. The quantity of H2 produced from the nitrogen-doped g-C3N5/TiO2 composite for 3 hours (3515.1 μmol g-1) was about three times that of N-doped g-C3N5. The H2 production percentage of the nitrogen-doped g-C3N5/TiO2 catalyst with Pt as the cocatalyst was improved by nearly ten times as compared to N-doped g-C3N5/TiO2 without a cocatalyst. Herein, we report the successful preparation of the N-doped g-C3N5/TiO2 S-scheme heterojunction and highlight a simple and efficient catalyst for energy storage requirements and environmental monitoring.
Establishing an S-scheme heterojunction is a promising method for increasing the photocatalytic activity of synthetic materials. In this study, nitrogen-doped g-C 3 N 5 /TiO 2 S-scheme photocatalysts ...have been synthesized and examined for photocatalytic hydrogen production using thermal decomposition methods. Nitrogen-doped g-C 3 N 5 /TiO 2 composites performed better than pure nitrogen-doped g-C 3 N 5 and TiO 2 alone. Using experiments and density functional theory (DFT) calculations, nitrogen (N) doping was identified as being introduced by replacing the carbon (C) atoms in the matrix of g-C 3 N 5 . In addition to its narrow band gap, N-doped g-C 3 N 5 showed efficient carrier separation and charge transfer, resulting in the enhanced absorption of visible light and photocatalytic activity. DFT, XPS, optical property characteristics, and PL spectra confirmed these findings, which were attributed to the successful nitrogen doping, and the composite was proven to be a potential candidate for photocatalytic hydrogen generation under light irradiation. The quantity of H 2 produced from the nitrogen-doped g-C 3 N 5 /TiO 2 composite for 3 hours (3515.1 μmol g −1 ) was about three times that of N-doped g-C 3 N 5 . The H 2 production percentage of the nitrogen-doped g-C 3 N 5 /TiO 2 catalyst with Pt as the cocatalyst was improved by nearly ten times as compared to N-doped g-C 3 N 5 /TiO 2 without a cocatalyst. Herein, we report the successful preparation of the N-doped g-C 3 N 5 /TiO 2 S-scheme heterojunction and highlight a simple and efficient catalyst for energy storage requirements and environmental monitoring.
Establishing an S-scheme heterojunction is a promising method for increasing the photocatalytic activity of synthetic materials. In this study, nitrogen-doped g-C
3
N
5
/TiO
2
S-scheme photocatalysts ...have been synthesized and examined for photocatalytic hydrogen production using thermal decomposition methods. Nitrogen-doped g-C
3
N
5
/TiO
2
composites performed better than pure nitrogen-doped g-C
3
N
5
and TiO
2
alone. Using experiments and density functional theory (DFT) calculations, nitrogen (N) doping was identified as being introduced by replacing the carbon (C) atoms in the matrix of g-C
3
N
5
. In addition to its narrow band gap, N-doped g-C
3
N
5
showed efficient carrier separation and charge transfer, resulting in the enhanced absorption of visible light and photocatalytic activity. DFT, XPS, optical property characteristics, and PL spectra confirmed these findings, which were attributed to the successful nitrogen doping, and the composite was proven to be a potential candidate for photocatalytic hydrogen generation under light irradiation. The quantity of H
2
produced from the nitrogen-doped g-C
3
N
5
/TiO
2
composite for 3 hours (3515.1 μmol g
−1
) was about three times that of N-doped g-C
3
N
5
. The H
2
production percentage of the nitrogen-doped g-C
3
N
5
/TiO
2
catalyst with Pt as the cocatalyst was improved by nearly ten times as compared to N-doped g-C
3
N
5
/TiO
2
without a cocatalyst. Herein, we report the successful preparation of the N-doped g-C
3
N
5
/TiO
2
S-scheme heterojunction and highlight a simple and efficient catalyst for energy storage requirements and environmental monitoring.
Explanation of the construction of the NCNT
x
S-scheme heterojunction photocatalyst.
Role of CYP27A in cholesterol and bile acid metabolism Dubrac, Sandrine; Lear, Steven R.; Ananthanarayanan, Meena ...
Journal of lipid research,
January 2005, 2005, 2005-Jan, 2005-01-00, 20050101, 2005-01-01, Letnik:
46, Številka:
1
Journal Article
Recenzirano
Odprti dostop
The CYP27A gene encodes a mitochondrial cytochrome P450 enzyme, sterol 27-hydroxylase, that is expressed in many different tissues and plays an important role in cholesterol and bile acid metabolism. ...In humans, CYP27A deficiency leads to cerebrotendinous xanthomatosis. To gain insight into the roles of CYP27A in the regulation of cholesterol and bile acid metabolism, cyp27A gene knockout heterozygous, homozygous, and wild-type littermate mice were studied. In contrast to homozygotes, heterozygotes had increased body weight and were mildly hypercholesterolemic, with increased numbers of lipoprotein particles in the low density lipoprotein size range. Cyp7A expression was not increased in heterozygotes but was in homozygotes, suggesting that parts of the homozygous phenotype are secondary to increased cyp7A expression and activity. Homozygotes exhibited pronounced hepatomegaly and dysregulation in hepatic cholesterol, bile acid, and fatty acid metabolism. Hepatic cholesterol synthesis and synthesis of bile acid intermediates were increased; however, side chain cleavage was impaired, leading to decreased bile salt concentrations in gallbladder bile. Expression of Na-taurocholate cotransporting polypeptide, the major sinusoidal bile salt transporter, was increased, and that of bile salt export pump, the major canalicular bile salt transporter, was decreased. Gender played a modifying role in the homozygous response to cyp27A deficiency, with females being generally more severely affected.
Thus, both cyp27A genotype and gender affected the regulation of hepatic bile acid, cholesterol, and fatty acid metabolism.
Water borne polyurethane dispersions synthesized using poly caprolactone–isophorone diisocyanate combination and caprolactone–metatetramethyl xylene diisocyanate combination. Thermal stability of the ...polyurethane dispersions was studied using thermogravimetric technique. The activation energy of decomposition of these polyurethane dispersions was determined by applying classical kinetic models and isoconversional method. Though the classical kinetic models assume constant activation energy for any reaction, the activation energy determined is in good agreement with that obtained via isoconversional analysis. However, the advantage of isoconversional analysis is highlighted compared to classical kinetic models based on the mechanism delineating capacity of isoconversional analysis. The present work compares the thermal stability of the aqueous polyurethane dispersion formed from poly caprolactone–isophorone diisocyanate with caprolactone–metatetramethyl xylene diisocyanate.
ATP-binding cassette, subfamily B member 11 (ABCB11) is an efflux transporter for bile acids on the liver canalicular membrane. The expression of this transporter is reduced in cholestasis; however, ...the mechanisms contributing to this reduction are unclear. In this study, we sought to determine whether miR-199a-5p contributes to the depletion of ABCB11/Abcb11 in cholestasis in mice. In a microRNA (miRNA) screen of mouse liver after common bile duct ligation (CBDL), we found that miR-199a-5p was significantly upregulated by approximately fourfold. In silico analysis predicted that miR-199a-5p would target the 3′-untranslated region (3′-UTR) of ABCB11/Abcb11 mRNA. The expression of ABCB11-3′-UTR luciferase construct in Huh-7 cells was markedly inhibited by cotransfection of a miRNA-199a-5p mimic, which was reversed by an miRNA-199a-5p mimic inhibitor. We also show treatment of mice after CBDL with the potent nuclear receptor FXR agonist obeticholic acid (OCA) significantly increased Abcb11 mRNA and protein and decreased miR-199a-5p expression. Computational mapping revealed a well-conserved FXR-binding site (FXRE) in the promoter of the gene encoding miR-199a-5, termed miR199a-2. Electromobility shift, chromatin immunoprecipitation, and miR199a-2 promoter-luciferase assays confirmed that this binding site was functional. Finally, CBDL in mice led to depletion of nuclear repressor NcoR1 binding at the miR199a-2 promoter, which facilitates transcription of miR199a-2. In CBDL mice treated with OCA, NcoR1 recruitment to the miR199a-2 FXRE was maintained at levels found in sham-operated mice. In conclusion, we demonstrate that miR-199a-5p is involved in regulating ABCB11/Abcb11 expression, is aberrantly upregulated in obstructive cholestasis, and is downregulated by the FXR agonist OCA.
Maintenance of hepatocyte homeostasis plays an important role in mediating the pathogenesis of many diseases. A growing body of literature has established a critical role played by tumor necrosis ...factor-α (TNFα) in maintaining hepatocyte homeostasis; however, the transcriptional mechanisms underlying constitutive
expression are unknown. Whole liver fractions and primary hepatocytes from adult control C57BL/6 mice and the murine hepatocyte cell line AML12 were assessed for constitutive
expression. Impacts of glycogen synthase kinase-3 β (GSK3β) and nuclear factor κB (NF-κB) inhibition on constitutive
expression were assessed in AML12 cells. Finally, AML12 cell proliferation following GSK3β and NF-κB inhibition was evaluated. Constitutive
gene expression is present in whole liver, primary hepatocytes, and cultured AML12 hepatocytes. Cytokine-induced
gene expression is regulated by NF-κB activation. Pharmacological inhibition of GSK3β resulted in a time- and dose-dependent inhibition of
gene expression. GSK3β inhibition decreased nuclear levels of the NF-κB subunits p65 and p50. We determined that NF-κB transcription factor subunit p65 binds to consensus sequence elements present in the murine TNFα promoter and inhibition of GSK3β decreases binding and subsequent
expression. Finally, AML12 cell growth was significantly reduced following GSK3β and NF-κB inhibition. These results demonstrate that GSK3β and NF-κB are essential for mediating
expression and constitutive hepatocyte cell growth. These findings add to a growing body of literature on TNFα mediated hepatocyte homeostasis and identify novel molecular mechanisms involved in mediating response to various disease states in the liver.
Maintenance of hepatocyte homeostasis plays an important role in controlling the pathogenesis of many diseases. Our findings add to a growing body of literature on tumor necrosis factor-α (TNFα)-mediated hepatocyte homeostasis and identify novel molecular mechanisms involved in regulating this response.
The developmental immaturity of the innate immune system helps explains the increased risk of infection in the neonatal period. Importantly, innate immune signaling pathways such as p65/NFκB and ...c-Jun/AP1 are responsible for the prevention of hepatocyte apoptosis in adult animals, yet whether developmental immaturity of these pathways increases the risk of hepatic injury in the neonatal period is unknown.
Using a murine model of endotoxemia (LPS 5 mg/kg IP x 1) in neonatal (P3) and adult mice, we evaluated histologic evidence of hepatic injury and apoptosis, presence of p65/NFκB and c-Jun/AP1 activation and associated transcriptional regulation of apoptotic genes.
We demonstrate that in contrast to adults, endotoxemic neonatal (P3) mice exhibit a significant increase in hepatic apoptosis. This is associated with absent hepatic p65/NFκB signaling and impaired expression of anti-apoptotic target genes. Hepatic c-Jun/AP1 activity was attenuated in endotoxemic P3 mice, with resulting upregulation of pro-apoptotic factors.
These results demonstrate that developmental absence of innate immune p65/NFκB and c-Jun/AP1 signaling, and target gene expression is associated with apoptotic injury in neonatal mice. More work is needed to determine if this contributes to long-term hepatic dysfunction, and whether immunomodulatory approaches can prevent this injury.
Various aspects of developmental immaturity of the innate immune system may help explain the increased risk of infection in the neonatal period. In adult models of inflammation and infection, innate immune signaling pathways such as p65/NFκB and c-Jun/AP1 are responsible for a protective, pro-inflammatory transcriptome and regulation of apoptosis. We demonstrate that in contrast to adults, endotoxemic neonatal (P3) mice exhibit a significant increase in hepatic apoptosis associated with absent hepatic p65/NFκB signaling and c-Jun/AP1 activity. We believe that these results may explain in part hepatic dysfunction with neonatal sepsis, and that there may be unrecognized developmental and long-term hepatic implications of early life exposure to systemic inflammatory stress.
Elevated serum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the setting of systemic inflammatory response syndrome and contribute to distal organ hypoperfusion and pulmonary ...hypertension. Thus, understanding the cellular source and transcriptional regulation of systemic inflammatory stress-induced ET-1 expression may reveal therapeutic targets. Using a murine model of LPS-induced septic shock, we demonstrate that the hepatic macrophage is the primary source of elevated circulating ET-1, rather than the endothelium as previously proposed. Using pharmacologic inhibitors, ET-1 promoter luciferase assays, and by silencing and overexpressing NF-κB inhibitory protein IκB expression, we demonstrate that LPS-induced ET-1 expression occurs via an NF-κB-dependent pathway. Finally, the specific role of the cRel/p65 inhibitory protein IκBβ was evaluated. Although cytoplasmic IκBβ inhibits activity of cRel-containing NF-κB dimers, nuclear IκBβ stabilizes NF-κB/DNA binding and enhances gene expression. Using targeted pharmacologic therapies to specifically prevent IκBβ/NF-κB signaling, as well as mice genetically modified to overexpress IκBβ, we show that nuclear IκBβ is both necessary and sufficient to drive LPS-induced ET-1 expression. Together, these results mechanistically link the innate immune response mediated by IκBβ/NF-κB to ET-1 expression and potentially reveal therapeutic targets for patients with Gram-negative septic shock.
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