Concert recording 2022-03-31

[Track 1]. Concerto no. 7 in E minor. I. Allegro / François Devienne -- [Track 2]. Diary of an Allen. II. Drifting ; III. No rotary phone / Margaret Brouwer -- [Track 3]. Suite antique. Prelude ; Ostinato ; Aria ; Waltz ; Chanson ; Rondeau / John Rutter -- [Track 4]. Polka. L\u27oiseau du bois (The wooden bird) / Charles Le Thiere

Ginsenoside Compound K Induces Ros-Mediated Apoptosis and Autophagic Inhibition in Human Neuroblastoma Cells In Vitro and In Vivo

Autophagy can result in cellular adaptation, as well as cell survival or cell death. Modulation of autophagy is increasingly regarded as a promising cancer therapeutic approach. Ginsenoside compound K (CK), an active metabolite of ginsenosides isolated from Panax ginseng C.A. Meyer, has been identified to inhibit growth of cancer cell lines. However, the molecular mechanisms of CK effects on autophagy and neuroblastoma cell death have not yet been investigated. In the present study, CK inhibited neuroblastoma cell proliferation in vitro and in vivo. Treatment by CK also induced the accumulation of sub-G1 population, and caspase-dependent apoptosis in neuroblastoma cells. In addition, CK promotes autophagosome accumulation by inducing early-stage autophagy but inhibits autophagic flux by blocking of autophagosome and lysosome fusion, the step of late-stage autophagy. This effect of CK appears to be mediated through the induction of intracellular reactive oxygen species (ROS) and mitochondria membrane potential loss. Moreover, chloroquine, an autophagy flux inhibitor, further promoted CK-induced apoptosis, mitochondrial ROS induction, and mitochondria damage. Interestingly, those promoted phenomena were rescued by co-treatment with a ROS scavenging agent and an autophagy inducer. Taken together, our findings suggest that ginsenoside CK induced ROS-mediated apoptosis and autophagic flux inhibition, and the combination of CK with chloroquine, a pharmacological inhibitor of autophagy, may be a novel therapeutic potential for the treatment of neuroblastoma

Concert recording 2021-11-18

[Track 1]. Prelude, op. 43, no. 1 / Reinhold Glière -- [Track 2]. Etude in D minor, op. 109, no. 13, The storm / Friedrich Burgmüller -- [Track 3]. Liebestraum no. 3 / Franz Liszt -- [Track 4]. Sonata no. 13 in E-flat major, op. 27, no. 1. III. Adagio con espressione, Presto / Ludwig van Beethoven -- [Track 5]. Moment Musicaux in B minor op. 16, no. 3 ; Prelude in C-sharp minor, op. 3, no. 2 / Sergei Rachmaninov -- [Track 6]. Album Leaf / Claude Debussy ; Autumn leaves / Joseph Kosma, Johnny Mercer, Jacques Prevert ; arranged by Morgan Brown ; Jazz exercise no. 2 / Oscar Peterson -- [Track 7]. Fantasia in C minor, K. 475 / Wolfgang Amadeus Mozart -- [Track 8]. 6 Romanian Folk Dances. I. Stick Dance. II. Sash Dance. III. In One Spot. IV. Horn Dance. V. Romanian Polka. VI. Fast Dance / Béla Bartók

Therapeutic potential of ginseng leaf extract in inhibiting mast cell-mediated allergic inflammation and atopic dermatitis-like skin inflammation in DNCB-treated mice

Ginseng leaves are known to contain high concentrations of bioactive compounds, such as ginsenosides, and have potential as a treatment for various conditions, including fungal infections, cancer, obesity, oxidative stress, and age-related diseases. This study assessed the impact of ginseng leaf extract (GLE) on mast cell-mediated allergic inflammation and atopic dermatitis (AD) in DNCB-treated mice. GLE reduced skin thickness and lymph node nodules and suppressed the expression and secretion of histamine and pro-inflammatory cytokines. It also significantly lowered the production of inflammatory response mediators including ROS, leukotriene C4 (LTC4), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). GLE inhibited the phosphorylation of MAPKs (ERK, P38, JNK) and the activation of NF-κB, which are both linked to inflammatory cytokine expression. We demonstrated that GLE’s inhibitory effect on mast cell-mediated allergic inflammation is due to the blockade of the NF-κB and inflammasome pathways. Our findings suggest that GLE can be an effective therapeutic agent for mast-cell mediated and allergic inflammatory conditions

Concert recording 2021-11-07a

[Track 1]. La maniere de Shumann /Jean-Michel Defaye -- [Track 2]. Sang till lotta / Jan Sandstrom -- [Track 3]. Concertino in B♭ / Ernst Sachse -- [Track 4]. Nearer my God to thee for 9 celli / James Stevens -- [Track 5]. Ave Maria / Franz Biebl -- [Track 6]. Soundtrack for trombone / Brian Sadler

Ginsenoside CK Inhibits the Early Stage of Adipogenesis via the AMPK, MAPK, and AKT Signaling Pathways

Obesity is considered a health hazard in part due to the associated multiple diseases. As rates of obesity continue to increase, a new strategy for its prevention and treatment is required. Compound-K, an active ingredient in ginseng, possesses antioxidant, anti-inflammatory, and anti-cancer properties. Although ginseng has used as various therapeutics, its potential ability to alleviate metabolic diseases by regulating adipocyte differentiation is still unknown. In this study, we found that CK treatment significantly inhibited lipid droplet and adipogenesis by downregulating the mRNA expression of C/ebpα, Ppar-γ, Fabp4, Srebp1, and adiponectin as well as protein levels of C/EBPα, PPAR-γ, and FABP4. CK also decreased the production of reactive oxygen species (ROS), while it increased endogeneous antioxidant enzymes such as catalase, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) 3 and SOD2. We observed that CK treatment suppressed the expression of cyclin-dependent kinase 1 (CDK1) and cyclin B1 during the mitotic clonal expansion (MCE) of adipocyte differentiation, and it arrested adipocytes at the G2/M stage due to the increased expression of p21 and p27. CK decreased the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 and protein kinase B (AKT) in early-stage adipogenesis. In addition, the inhibition of adipogenesis by CK significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). Interestingly, AMPK pharmacological inhibition with Dorsomorphin limited the effect of CK on suppressing PPAR-γ expression in differentiated 3T3-L1 cells. Our results suggest that CK exerts anti-adipogenic effects in 3T3-L1 cells through the activation of AMPK and inhibition of ERK/p38 and AKT signaling pathways

Ginsenoside Rk1 Induces Apoptosis in Neuroblastoma Cells Through Loss of Mitochondrial Membrane Potential and Activation of Caspases

Neuroblastoma (NB) is the most common childhood cancer, with a very poor prognosis. More than 60% of children with NB die within five years; therefore, a more effective therapy for NB is required. Although ginsenoside has been shown to significantly inhibit the growth of various cancers, the effect of ginsenoside Rk1 on neuroblastoma has not been known yet. Hence, we examined the anticancer effects of highly pure Rk1 on neuroblastoma cell lines. The apoptotic effects of Rk1 on neuroblastoma cells were examined using cell viability assay, flow cytometry and cell staining assay, and the change in gene expression levels were analysed using RT-PCR, western blots, and immunohistochemistry. The metastatic effect of Rk1 was monitored by wound healing assay, invasion and migration with Matrigels. Rk1 inhibited neuroblastoma cell viability dose-dependently. Rk1-induced apoptosis was investigated through nuclear condensation and mitochondrial membrane potential loss, and it showed that Rk1 can induce cell cycle arrest at the G0/G1 phase but also inhibit the metastatic ability of neuroblastoma cells. Moreover, Rk1 (30 mg/kg) injections markedly inhibited xenograft tumor growth. These findings demonstrate that Rk1 might be valuable in the development of anti-cancer agents for neuroblastoma treatment

Thermal design and transient analysis of nitrogen Brayton cycle coupled with sodium-cooled fast reactor

Sodium-cooled fast reactors (SFRs) are one of the most promising reactor types for near-term deployment among Generation IV nuclear systems. Although the steam Rankine cycle has been generally adopted as a power conversion system (PCS) of an SFR, the potential chemical reaction between sodium and water has been known to be a major safety issue and economic disadvantage. To this end, a nitrogen Brayton cycle has been considered as an alternative PCS option for SFRs because of the chemical stability of nitrogen with liquid sodium. In this study, based on the thermal design of the nitrogen Brayton cycle PCS coupled with an SFR (hereinafter abbreviated as “N2-PCS”), an off-design performance curve or map of the main components in N2-PCS are derived. Quasi-steady-state analyses and transient behaviors of N2-PCS are discussed based on data obtained from the results of system code simulation. To obtain the main component design parameters and off-design performance curve/map, one-dimensional codes of printed circuit heat exchangers and the design codes of axial-type turbomachinery are developed. The design results and derived performance curve/map are applied to a commercial system code (Flomaster) for transient analysis. The outlet temperature of the compressor obtained from a quasi-steady-state simulation is discovered to be higher than the target conditions because of the discrepancy between the results calculated using the system code based on the perfect gas model and the compressor design based on the real gas model. By applying the effect of the gas model difference on the compressor to a cooler component located at the compressor outlet, the temperature differences between the simulation results and target conditions are reduced. A simple power-swing transient scenario is applied to the N2-PCS system code. Finally, it is noteworthy that the transient results provide perspectives on the performance of N2-PCS during power swing.1

Ginsenoside Compound K Induces Adult Hippocampal Proliferation and Survival of Newly Generated Cells in Young and Elderly Mice

Cognitive impairment can be associated with reduced adult hippocampal neurogenesis, and it may contribute to age-associated neurodegenerative diseases such as Alzheimer’s (AD). Compound K (CK) is produced from the protopanaxadiol (PPD)-type ginsenosides Rb1, Rb2, and Rc by intestinal microbial conversion. Although CK has been reported as an inducing effector for neuroprotection and improved cognition in hippocampus, its effect on adult neurogenesis has not been explored yet. Here, we investigated the effect of CK on hippocampal neurogenesis in both young (2 months) and elderly (24 months) mice. CK treatment increased the number of cells co-labeled with 5-ethynyl-2′-deoxyuridine (EdU) and proliferating cell nuclear antigen (PCNA); also, Ki67, specific markers for progenitor cells, was more expressed, thus enhancing the generation of new cells and progenitor cells in the dentate gyrus of both young and elderly mice. Moreover, CK treatment increased the number of cells co-labeled with EdU and NeuN, a specific marker for mature neuron in the dentate gyrus, suggesting that newly generated cells survived and differentiated into mature neurons at both ages. These findings demonstrate that CK increases adult hippocampal neurogenesis, which may be beneficial against neurodegenerative disorders such as AD