• Applied Chemistry for Engineering
• /
• v.10 no.3
• /
• pp.388-393
• /
• 1999

Polyurethane foams are polymeric material with repeating groups of urethane and urea. When these are heated with ethylene glycol and K acetate catalyst at $200^{\circ}C$, the transesterification of them leads to soluble products. The mechanisms of the reaction were investigated from the molecular weight and the component distributions of the products by GPC and IR analysis. The degradation of the urethane groups was faster than that of urea groups in transesterification reaction. K acetate catalyst accelerated the rate of the transesterification because it had a high ionization tendency. Each reaction, using K or Sr acetate as a catalyst, progressed in the same reaction path but yielded different compositions in products because of the difference of the reaction rate.

• Molecules and Cells
• /
• v.38 no.10
• /
• pp.843-850
• /
• 2015

The1hepatic cell death induced by acetaminophen (APAP) is closely related to cellular adenosine triphosphate (ATP) depletion, which is mainly caused by mitochondrial dysfunction. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a key sensor of low energy status. AMPK regulates metabolic homeostasis by stimulating catabolic metabolism and suppressing anabolic pathways to increase cellular energy levels. We found that the decrease in active phosphorylation of AMPK in response to APAP correlates with decreased ATP levels, in vivo. Therefore, we hypothesized that the enhanced production of ATP via AMPK stimulation can lead to amelioration of APAP-induced liver failure. A769662, an allosteric activator of AMPK, produced a strong synergistic effect on AMPK Thr172 phosphorylation with APAP in primary hepatocytes and liver tissue. Interestingly, activation of AMPK by A769662 ameliorated the APAP-induced hepatotoxicity in C57BL/6N mice treated with APAP at a dose of 400 mg/kg intraperitoneally. However, mice treated with APAP alone developed massive centrilobular necrosis, and APAP increased their serum alanine aminotransferase and aspartate aminotransferase levels. Furthermore, A769662 administration prevented the loss of intracellular ATP without interfering with the APAP-mediated reduction of mitochondrial dysfunction. In contrast, inhibition of glycolysis by 2-deoxy-glucose eliminated the beneficial effects of A769662 on APAP-mediated liver injury. In conclusion, A769662 can effectively protect mice against APAP-induced liver injury through ATP synthesis by anaerobic glycolysis. Furthermore, stimulation of AMPK may have potential therapeutic application for APAP overdose.

• Korean Journal of Soil Science and Fertilizer
• /
• v.10 no.2
• /
• pp.85-92
• /
• 1977

The six soybean cultivars (Lee, Hill, Harosoy, Clark-63 Chippewa and R56-49) different in phosphorus sensitivity were cultured with $NH_4-N$, $NO_3-N$ or urea-N under water culture condition. Free sugars and organic chrematogram. Three peaks (unknown x, y and sucrose) were appeared as considerable main peaks. The X compound appeared as trace in the nitrate fed plant while unexpectedly high in ammonium or urea fed plant. The Y compound tend to decrase in urea fed plant. Sucrose was trace in ammonium fed plant but it was greater in urea onethan in nitrate one. The X was assumed a four carbon sugar acid derived from erythrose or a ring compound derived from purine or pyrimidine. While Y was assumed a hexose derived from glycolysis path. Since Y/x ratio is a good index of phosphorus sensitivity (inve rserelation) these compounds appears keycompounds to elucidate phosphorus sensitivity and ammonium toxicity.

• Asian-Australasian Journal of Animal Sciences
• /
• v.32 no.11
• /
• pp.1789-1800
• /
• 2019

Objective: Although alveolar macrophages play a key role in the respiratory immunity of livestock, studies on the mechanism of differentiation and survival of alveolar macrophages are lacking. Therefore, we undertook to investigate changes in the lipid metabolism and survival rate, using 3D4/31 macrophages and Dudleya brittonii which has been used as a traditional asthma treatment. Methods: 3D4/31 macrophages were used as the in vitro porcine alveolar macrophages model. The cells were activated by exposure to phorbol 12-myristate 13-acetate (PMA). Dudleya brittonii extraction was performed with distilled water. For evaluating the cell survival rate, we performed the water-soluble tetrazolium salt cell viability assay and growth curve analysis. To confirm cell death, cell cycle and intracellular reactive oxygen species (ROS) levels were measured using flow cytometric analysis by applying fluorescence dye dichlorofluorescein diacetate and propidium iodide. Furthermore, we also evaluated cellular lipid accumulation with oil red O staining, and fatty acid synthesis related genes expression levels using quantitative polymerase chain reaction (qPCR) with SYBR green dye. Glycolysis, fatty acid oxidation, and tricarboxylic acid (TCA) cycle related gene expression levels were measured using qPCR after exposure to Dudleya brittonii extract (DB) for 12 h. Results: The ROS production and cell death were induced by PMA treatment, and exposure to DB reduced the PMA induced downregulation of cell survival. The PMA and DB treatments upregulated the lipid accumulation, with corresponding increase in the acetyl-CoA carboxylase alpha, fatty acid synthase mRNA expressions. DB-PMA co-treatment reduced the glycolysis genes expression, but increased the expressions of fatty acid oxidation and TCA cycle genes. Conclusion: This study provides new insights and directions for further research relating to the immunity of porcine respiratory system, by employing a model based on alveolar macrophages and natural materials.

• Journal of the Korean Applied Science and Technology
• /
• v.35 no.4
• /
• pp.1433-1441
• /
• 2018

The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid which causes the release of a proton and the formation of the acid salt sodium lactate. Through this explanation, when the rate of lactate production is high enough to exceed cellular proton buffering capacity, cellular pH is decreased. This biochemical process has been termed lactic acidosis. This belief has been an interpretation that lactate production causes acidosis and fatigue during intense exercise. However, this review provides clear evidence that there is no biochemical support for lactate production causing acidosis and fatigue. Metabolic acidosis is caused by an increased reliance on nonmitochondrial ATP turnover. Lactate production is essential for muscle to produce cytosolic $NAD^+$ to support continued ATP regeneration from glycolysis. In addition, Lactate production consumes protons. Although lactate accumulation can be a good indirect indicator for decreased cellular and blood pH, that is not direct causing acidosis.

• The Plant Pathology Journal
• /
• v.37 no.1
• /
• pp.36-46
• /
• 2021

Acidovorax citrulli (Ac) is the causal agent of bacterial fruit blotch (BFB) in watermelon, a disease that poses a serious threat to watermelon production. Because of the lack of resistant cultivars against BFB, virulence factors or mechanisms need to be elucidated to control the disease. Glycerol-3-phosphate dehydrogenase is the enzyme involved in glycerol production from glucose during glycolysis. In this study, we report the functions of a putative glycerol-3-phosphate dehydrogenase in Ac (GlpdAc) using comparative proteomic analysis and phenotypic observation. A glpdAc knockout mutant, AcΔglpdAc(EV), lost virulence against watermelon in two pathogenicity tests. The putative 3D structure and amino acid sequence of GlpdAc showed high similarity with glycerol-3-phosphate dehydrogenases from other bacteria. Comparative proteomic analysis revealed that many proteins related to various metabolic pathways, including carbohydrate metabolism, were affected by GlpdAc. Although AcΔglpdAc(EV) could not use glucose as a sole carbon source, it showed growth in the presence of glycerol, indicating that GlpdAc is involved in glycolysis. AcΔglpdAc(EV) also displayed higher cell-to-cell aggregation than the wild-type bacteria, and tolerance to osmotic stress and ciprofloxacin was reduced and enhanced in the mutant, respectively. These results indicate that GlpdAc is involved in glycerol metabolism and other mechanisms, including virulence, demonstrating that the protein has pleiotropic effects. Our study expands the understanding of the functions of proteins associated with virulence in Ac.

• Food Science of Animal Resources
• /
• v.42 no.3
• /
• pp.389-397
• /
• 2022

Carcass vascular rinsing and chilling involves infusing a chilled isotonic solution (98.5% water and a blend of mono- and di-saccharides and phosphates) into the vasculature immediately upon exsanguination. Primary purposes of carcass vascular rinsing are to (1) effectively remove residual blood from the carcass; (2) lower internal muscle temperature rapidly; and (3) optimize pH decline by effective delivery of glycolytic substrates in the rinse solution. Previous studies have revealed that the beef carcass vascular rinsing early postmortem positively affects meat quality, product shelflife, and food safety. Thus, the objective of this review is to provide a more comprehensive understanding of the physical and biochemical mechanisms associated with beef carcass vascular rinsing, focusing on the relationship between quality attributes (CIE L^*, a^*, b^*; chemical states of myoglobin; oxygen consumption and sarcomere length) and muscle metabolic response to various substrate solutions (Rinse & Chill^®, fructose, sodium phosphate, and dipotassium phosphate) that stimulate or inhibit the rate of glycolysis early postmortem. In addition, this review discusses the absence of metabolite residues (phosphorus, sodium, and glucose) related to the application of the chilled isotonic solution. This review primarily focuses on beef and as such extending the understanding of the mechanisms and meat quality effects discussed to other species associated with vascular rinsing, in particular pork, may be limited.

• Journal of Periodontal and Implant Science
• /
• v.52 no.4
• /
• pp.282-297
• /
• 2022

Purpose: To explore differences in the subgingival microbiome according to the presence of periodontitis and/or type 2 diabetes mellitus (T2D), a metagenomic sequencing analysis of the subgingival microbiome was performed. Methods: Twelve participants were divided into 4 groups based on their health conditions (periodontitis, T2D, T2D complicated with periodontitis, and generally healthy). Subgingival plaque was collected for metagenomic sequencing, and gingival crevicular fluids were collected to analyze the concentrations of short-chain fatty acids. Results: The shifts in the subgingival flora from the healthy to periodontitis states were less prominent in T2D subjects than in subjects without T2D. The pentose and glucuronate interconversion, fructose and mannose metabolism, and galactose metabolism pathways were enriched in the periodontitis state, while the phosphotransferase system, lipopolysaccharide (LPS) and peptidoglycan biosynthesis, bacterial secretion system, sulfur metabolism, and glycolysis pathways were enriched in the T2D state. Multiple genes whose expression was upregulated from the red and orange complex bacterial genomes were associated with bacterial biofilm formation and pathogenicity. The concentrations of propionic acid and butyric acid were significantly higher in subjects with periodontitis, with or without T2D, than in healthy subjects. Conclusions: T2D patients are more susceptible to the presence of periodontal pathogens and have a higher risk of developing periodontitis. The pentose and glucuronate interconversion, fructose and mannose metabolism, galactose metabolism, and glycolysis pathways may represent the potential microbial functional association between periodontitis and T2D, and butyric acid may play an important role in the interaction between these 2 diseases. The enrichment of the LPS and peptidoglycan biosynthesis, bacterial secretion system, and sulfur metabolism pathways may cause T2D patients to be more susceptible to periodontitis.

• BMB Reports
• /
• v.54 no.11
• /
• pp.563-568
• /
• 2021

Cancer cells predominantly generate energy via glycolysis, even in the presence of oxygen, to support abnormal cell proliferation. Suppression of PDHA1 by PDK1 prevents the conversion of cytoplasmic pyruvate into Acetyl-CoA. Several PDK inhibitors have been identified, but their clinical applications have not been successful for unclear reasons. In this study, endogenous PDHA1 in A549 cells was silenced by the CRISPR/Cas9 system, and PDHA1^WT and PDHA1^3SD were transduced. Since PDHA1^3SD cannot be phosphorylated by PDKs, it was used to evaluate the specific activity of PDK inhibitors. This study highlights that PDHA1^WT and PDHA1^3SD A549 cells can be used as a cell-based PDK inhibitor-distinction system to examine the relationship between PDH activity and cell death by established PDK inhibitors. Leelamine, huzhangoside A and otobaphenol induced PDH activity-dependent apoptosis, whereas AZD7545, VER-246608 and DCA effectively enhanced PDHA1 activity but little toxic to cancer cells. Furthermore, the activity of phosphomimetic PDHA1 revealed the complexity of its regulation, which requires further in-depth investigation.

• Journal of Ginseng Research
• /
• v.47 no.6
• /
• pp.784-794
• /
• 2023

Background: ginsenoside Rg5 is a rare ginsenoside with known hypoglycemic effects in diabetic mice. This study aimed to explore the effects of ginsenoside Rg5 on skin wound-healing in the Lepr^db/db mutant (db/db) mice (C57BL/KsJ background) model and the underlying mechanisms. Methods: Seven-week-old male C57BL/6J, SLC7A11-knockout (KO), the littermate wild-type (WT), and db/db mice were used for in vivo and ex vivo studies. Results: Ginsenoside Rg5 provided through oral gavage in db/db mice significantly alleviated the abundance of apoptotic cells in the wound areas and facilitated skin wound healing. 50 μM ginsenoside Rg5 treatment nearly doubled the efferocytotic capability of bone marrow-derived dendritic cells (BMDCs) from db/db mice. It also reduced NF-κB p65 and SLC7A11 expression in the wounded areas of db/db mice dose-dependently. Ginsenoside Rg5 physically interacted with SLC7A11 and suppressed the cystine uptake and glutamate secretion of BMDCs from db/db and SLC7A11-WT mice but not in BMDCs from SLC7A11-KO mice. In BMDCs and conventional type 1 dendritic cells (cDC1s), ginsenoside Rg5 reduced their glycose storage and enhanced anaerobic glycolysis. Glycogen phosphorylase inhibitor CP-91149 almost abolished the effect of ginsenoside Rg5 on promoting efferocytosis. Conclusion: ginsenoside Rg5 can suppress the expression of SLC7A11 and inhibit its activity via physical binding. These effects collectively alleviate the negative regulations of SLC7A11 on anaerobic glycolysis, which fuels the efferocytosis of dendritic cells. Therefore, ginsenoside Rg5 has a potential adjuvant therapeutic reagent to support patients with wound-healing problems, such as diabetic foot ulcers.