Theoretical and experimental investigation of an absorption refrigeration and pre-desalination system for marine engine exhaust gas heat recovery

Absorption-refrigeration-cycle-based exhaust gas heat recovery technology is effective in improving the thermal efficiency and fuel economy of marine diesel engines. However, the absorption refrigeration system is inflexible in the start–stop operation, and this cannot fulfil the fluctuating demand of refrigeration. This paper presents both the theoretical and experimental investigations of an absorption refrigeration and freezing pre-desalination-based marine engine exhaust gas heat recovery system. The energy storage subcycle is introduced to overcome the energy underutilisation and balance the excessive refrigerating output of the absorption refrigeration cycle. Seawater is utilised as the phase-change material and it is pre-desalinated in the energy storage subcycle. A mathematical model of the system is established and experimental investigation is conducted. Furthermore, the theoretical and experimental performances are compared, and an economic analysis of seawater desalination is performed to evaluate its economy. The results show that the total refrigeration output of the system ranges from 6.1 kW to 9.9 kW, and the system COP (Coefficient of Performance) can reach 16% under the experimental operating conditions. Additionally, the salinity of pre-desalinated seawater can be reduced to below 10 ppt. Moreover, the cost of RO (Reverse Osmosis) seawater desalination can be reduced by 26% through the pre-desalination process of seawater

Endothelium-derived Hyperpolarizing Factor (EDHF) Mediates Endothelium-dependent Vasodilator Effects of Aqueous Extracts from Eucommia ulmoides Oliv. Leaves in Rat Mesenteric Resistance Arteries

The vascular effects of an aqueous extract prepared from the leaves of Eucommia ulmoides Oliv. (ELE), a medicinal herb commonly used in antihypertensive herbal prescriptions in China, were investigated in rat mesenteric resistance arteries. The mesenteric vascular bed was perfused with Krebs solution and the perfusion pressure was measured with a pressure transducer. In preparations with an intact endothelium and precontracted with 7&#956;M methoxamine, perfusion of ELE (10&#65293;7&#65293;10&#65293;2mg/ml for 15min) caused a concentration-dependent vasodilatation, which was abolished by chemical removal of the endothelium. The ELE-induced vasodilatation was inhibited by neither indomethacin (INDO, a cyclooxygenase inhibitor) nor NG-nitro-L-arginine-methyl ester (L-NAME, a nitric oxide inhibitor). The ELE-induced vasodilatation was significantly inhibited by tetraethylammonium (TEA, a K+ channel blocker) and 18&#945;-glycyrrhetinic acid (18&#945;-GA, a gap-junction inhibitor), and abolished by high K+ -containing Krebs&#700; solution. Atropine (a muscarinic acetylcholine receptor antagonist) significantly inhibited the vasodilatation induced by ELE at high concentrations. These results suggest that the ELE-induced vasodilatation is endothelium-dependent but nitric oxide (NO)- and prostaglandin I2 (PGI2)-independent, and is mainly mediated by the endothelium-derived hyperpolarizing factor (EDHF) in the mesenteric resistance arteries. Furthermore, the ELE-induced EDHF-mediated response involves the activation of K+-channels and gap junctions.</p

Targeting P-Glycoprotein: Nelfinavir Reverses Adriamycin Resistance in K562/ADR Cells

Background/Aims: The emergence of multidrug resistance (MDR) caused by P-glycoprotein (P-gp) overexpression is a serious obstacle to the treatment of chronic myelocytic leukemia. In recent years, some clinical trials have shown that nelfinavir (NFV), a traditional anti-HIV drug, has anti-cancer effects. Some researchers have also shown NFV might be a potential P-gp inhibitor. This study is aimed at investigating whether nelfinavir can act as an MDR-reversal drug and to clarify its molecular mechanism as well. Methods: K562 and K562/ADR cell lines were applied in the study. Cytotoxicity was detected by CCK-8 reagents. Cell apoptosis was detected by flow cytometry and inverted fluorescence microscopy to detect the binding of apoptotic dyes to cells. Western blot was used to detect the expression of proteins. Drug-protein molecular docking simulation by using Sybyl-x 2.0 software. Results: Non-toxic concentrations of NFV (1.25–5 μM) could reverse Adriamycin (ADR), colchicine, paclitaxel, and imatinib resistance of K562/ADR cells, with reversal indexes of up to 10.8, 7.4, 57, and 9.3, respectively. NFV inhibited P-gp efflux function, as evidenced by the significant increase in the intracellular accumulation of ADR and Rho-123, without affecting P-gp protein and mRNA expression levels. Further ATP content detection and molecular docking simulations showed that NFV could decrease intracellular ATP content and has a high affinity with the active functional regions of P-gp, respectively. When co-administered with ADR, NFV increased intracellular reactive oxygen species as well as blocked the ERK/Akt signaling pathway, leading to cell apoptosis. Conclusion: NFV inhibited P-gp function, decreased intracellular ATP content, and promoted cell apoptosis in K562/ADR cells, thereby reversing MDR. These findings encourage further animal and clinical MDR studies with a combination therapy consisting of NFV and chemotherapeutic drugs

SIRT5 promotes IDH2 desuccinylation and G6PD deglutarylation to enhance cellular antioxidant defense

Abstract Excess in mitochondrial reactive oxygen species (ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 (IDH2) and glucose‐6‐phosphate dehydrogenase (G6PD), respectively, and thus activates both NADPH‐producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS. SIRT5 inactivation leads to the inhibition of IDH2 and G6PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress. Our study uncovers a SIRT5‐dependent mechanism that regulates cellular NADPH homeostasis and redox potential by promoting IDH2 desuccinylation and G6PD deglutarylation

Irradiation- Induced Extremes Create Hierarchical Face- /Body- Centered- Cubic Phases in Nanostructured High Entropy Alloys

A nanoscale hierarchical dual- phase structure is reported to form in a nanocrystalline NiFeCoCrCu high- entropy- alloy (HEA) film via ion irradiation. Under the extreme energy deposition and consequent thermal energy dissipation induced by energetic particles, a fundamentally new phenomenon is revealed, in which the original single- phase face- centered- cubic (FCC) structure partially transforms into alternating nanometer layers of a body- centered- cubic (BCC) structure. The orientation relationship follows the Nishiyama- Wasser- man relationship, that is, (011)BCC || (- 1¯1¯1)FCC and [100]BCC || [- 11¯0]FCC. Simulation results indicate that Cr, as a BCC stabilizing element, exhibits a tendency to segregate to the stacking faults (SFs). Furthermore, the high densities of SFs and twin boundaries in each nanocrystalline grain serve to accelerate the nucleation and growth of the BCC phase during irradiation. By adjusting the irradiation parameters, desired thicknesses of the FCC and BCC phases in the laminates can be achieved. This work demonstrates the controlled formation of an attractive dual- phase nanolaminate structure under ion irradiation and provides a strategy for designing new derivate structures of HEAs.A nanoscale hierarchical dual- phase structure is reported to form in a nanocrystalline NiFeCoCrCu high- entropy- alloy film via ion- irradiation- induced face- centered- cubic to body- centered- cubic phase transformation. Both kinetic and thermodynamic conditions for the phase transformation are explored. The results provide a new strategy for tailoring material structures on the nanometer or sub- nanometer scales.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162803/3/adma202002652_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162803/2/adma202002652.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162803/1/adma202002652-sup-0001-SuppMat.pd