A Credit Risk Contagion Intensity Model of Supply Chain Enterprises under Different Credit Modes

The rapid development of theoretical and practical innovations in corporate finance driven by supply chain finance has exacerbated the complexity of credit default risk contagion among supply chain enterprises. Financial risks in the supply chain greatly hinder its sustainable development; thus, strengthening financial risk management is necessary to ensure the sustainability of the supply chain. Based on the single-channel and dual-channel credit financing models of retailers in the supply chain, the purpose of this paper was to construct a model of the intensity of credit default risk contagion among supply chain enterprises under different credit financing models, and investigate the influencing factors of credit risk contagion among supply chain enterprises and its mechanism of action through a computational simulation system. The results were as follows: (1) there was a positive relationship between the production cost of suppliers and the contagion intensity of the supply chain credit default risk, and the contagion effect of the supply chain credit default risk increased significantly when both retailers defaulted on trade credit to suppliers; (2) the market retail price of the product was negatively related to the contagion intensity of the supply chain credit default risk, and the contagion intensity of the supply chain credit default risk increased significantly when both retailers defaulted on trade credit to the supplier; (3) the intensity of credit default risk contagion in the supply chain was positively correlated with both the commercial bank risk-free rate and the trade credit rate, and retailers’ repayment priority on trade credit debt was negatively correlated with suppliers’ wholesale prices and positively correlated with retailers’ order volumes, with retailers’ repayment priority positively affecting retailers’ bank credit rates and negatively affecting suppliers’ bank credit rates; and (4) retailers’ repayment priority on trade credit debt was negatively correlated with the intensity of supply chain credit default risk contagion, and the lower the retailer’s bank credit limit, the higher the trade credit limit, and the stronger the credit default contagion effect in the supply chain

Symmetry-Breaking Effect on the Electromagnetic Properties of Plasmonic Trimers Composed of Graphene Nanodisks

Plasmonic trimers composed of equal-sized graphene nanodisks are proposed in this paper. The symmetry-breaking effect on the electromagnetic properties of the nanostructure is numerically investigated by studying plasmon energy diagrams and optical scattering spectra in mid-infrared range with a gradient vertex angle. The degenerate plasmonic modes are lifted and new modes appear with increased vertex angle. The energy diagrams are consistent with scattering extinction spectra, about which the dipole moment distribution of the proposed structure is discussed to demonstrate the coupling strength of the collective plasmonic modes of the trimer. More specifically, the frequency tunability of the plasmonic trimer is pointed out by modifying the chemical potential of the graphene nanodisks without varying the geometric configuration. The proposed structure might find applications such as light-matter interaction, single molecule detection, and high-sensitivity chemical sensing

Table_3_Salvianolic Acid B Improves Mitochondrial Function in 3T3-L1 Adipocytes Through a Pathway Involving PPARγ Coactivator-1α (PGC-1α).XLSX

<p>Purpose: Mitochondrial dysfunction in adipose tissue has emerged as key to the development of obesity and diabetes. Salvianolic acid B (SalB) is a water-soluble ingredient derived from Salvia miltiorrhiza that has been shown to possess potential anti-obese and anti-diabetic activities. However, the cellular mechanism of SalB on mitochondrial function with respect to these metabolic disorders has not been elucidated. Therefore, we aim to investigate the effects of SalB on mitochondrial function in 3T3-L1 adipocytes and analyze the underlying molecular mechanism.</p><p>Methods: The effects of SalB on adipocyte differentiation, glucose uptake, and glycerol release were evaluated in 3T3-L1 adipocytes. Differentiated adipocytes were treated with SalB (50 μM) with or without PPARγ antagonist (GW9662, 20 μM) for 48 h, and mitochondrial oxygen consumption rate (OCR) as well as extracellular acidification rate (ECAR) were assessed using an XF Extracellular Flux Analyzer. The mitochondrial distribution of adipocytes was assessed using Mito Tracker Green (MTG) and observed under a fluorescent microscope. In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR. Finally, changes in the protein levels of peroxisome proliferators-activated receptor γ coactivator-1α (PGC-1α) were determined by western blotting and immunofluorescence analysis.</p><p>Results: Treatment with SalB increased glucose uptake and mitochondrial respiration, reduced glycerol release and promoted adipocyte differentiation by increasing mRNA expression of adipogenic transcription factors including PPARγ, C/EBPα, and PPARα. Furthermore, SalB enhanced adipocytes mitochondrial content, mitochondrial respiration and glycolysis capacity, which had been attenuated by GW9662 treatment through the increased expression of PGC-1α.</p><p>Conclusion: Our results provide novel insights into the role of PGC-1α and mitochondria as probable mediators of SalB activity in the regulation of adipocyte differentiation in 3T3-L1 adipocytes.</p

Table_2_Salvianolic Acid B Improves Mitochondrial Function in 3T3-L1 Adipocytes Through a Pathway Involving PPARγ Coactivator-1α (PGC-1α).XLSX

<p>Purpose: Mitochondrial dysfunction in adipose tissue has emerged as key to the development of obesity and diabetes. Salvianolic acid B (SalB) is a water-soluble ingredient derived from Salvia miltiorrhiza that has been shown to possess potential anti-obese and anti-diabetic activities. However, the cellular mechanism of SalB on mitochondrial function with respect to these metabolic disorders has not been elucidated. Therefore, we aim to investigate the effects of SalB on mitochondrial function in 3T3-L1 adipocytes and analyze the underlying molecular mechanism.</p><p>Methods: The effects of SalB on adipocyte differentiation, glucose uptake, and glycerol release were evaluated in 3T3-L1 adipocytes. Differentiated adipocytes were treated with SalB (50 μM) with or without PPARγ antagonist (GW9662, 20 μM) for 48 h, and mitochondrial oxygen consumption rate (OCR) as well as extracellular acidification rate (ECAR) were assessed using an XF Extracellular Flux Analyzer. The mitochondrial distribution of adipocytes was assessed using Mito Tracker Green (MTG) and observed under a fluorescent microscope. In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR. Finally, changes in the protein levels of peroxisome proliferators-activated receptor γ coactivator-1α (PGC-1α) were determined by western blotting and immunofluorescence analysis.</p><p>Results: Treatment with SalB increased glucose uptake and mitochondrial respiration, reduced glycerol release and promoted adipocyte differentiation by increasing mRNA expression of adipogenic transcription factors including PPARγ, C/EBPα, and PPARα. Furthermore, SalB enhanced adipocytes mitochondrial content, mitochondrial respiration and glycolysis capacity, which had been attenuated by GW9662 treatment through the increased expression of PGC-1α.</p><p>Conclusion: Our results provide novel insights into the role of PGC-1α and mitochondria as probable mediators of SalB activity in the regulation of adipocyte differentiation in 3T3-L1 adipocytes.</p