562 research outputs found
Utilisation of Heat Released During the Production of Green Hydrogen Using Alkaline Electrolysis
No full textTo reduce greenhouse gas emissions and to limit global warming, fossil fuel based energy technologies need to be replaced by clean energy technologies. Renewable energy sources are dependent on weather conditions therefore security of energy supply is not ensured and the need for energy storage is growing. Hydrogen is considered a clean energy carrier that can be used for energy storage. Water electrolysis that uses renewable energy is a sustainable method for the production of green hydrogen. Water electrolysis is a process by which water is split into hydrogen and oxygen by using direct current to drive the reaction. During the production of green hydrogen heat is released to the environment. Little research has been conducted on the amount of heat released during green hydrogen production and on the temperature of the released heat. It is unclear if the released heat could be used. This research serves to answer the question "Is it possible to use the heat released during the production of green hydrogen using alkaline water electrolysis?". To answer this question a model has been developed in ASPEN Plus. This model represents an alkaline electrolyser, consisting of an electrochemical model, a thermal model and a cooling system. To validate the output of the model, the hydrogen production output has been compared with an alkaline electrolyser developed by the company Nel hydrogen. The thermal efficiency of the model has been calculated with and without using the waste heat. To use the waste heat the system first needs to be cooled. To determine which heat exchanger is best to use for recovering the heat of the alkaline electrolyser, three different designs have been implemented in the ASPEN model. The designs have been analyzed and the best option is implemented in the model. The amount of heat that can be recovered has been investigated as well as the options for the use of the recovered heat. The results are discussed and recommendations are made for follow-up research.Mechanical Engineering | Process and Energy Technolog
Observation of a flare signal from a fixed position in the Northern Hemisphere through muons with L3+C
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Role of alpha1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571
No full textBACKGROUND: Chronic myeloid leukemia is caused by a chromosomal translocation that results in an oncogenic fusion protein, Bcr-Abl. Bcr-Abl is a tyrosine kinase whose activity is inhibited by the antineoplastic drug STI571. This drug can cure mice given an injection of human leukemic cells, but treatment ultimately fails in animals that have large tumors when treatment is initiated. We created a mouse model to explore the mechanism of resistance in vivo. METHODS Nude mice were injected with KU812 Bcr-Abl(+) human leukemic cells. After 1 day (no evident tumors), 8 days, or 15 days (tumors >1 g), mice were treated with STI571 (160 mg/kg every 8 hours). Cells recovered from relapsing animals were used for in vitro experiments. Statistical tests were two-sided. RESULTS: Tumors regressed initially in all STI571-treated mice, but all mice treated 15 days after injection of tumor cells eventually relapsed. Relapsed animals did not respond to further STI571 treatment, and their Bcr-Abl kinase activity in vivo was not inhibited by STI571, despite high plasma concentrations of the drug. However, tumor cells from resistant animals were sensitive to STI571 in vitro, suggesting that a molecule in the plasma of relapsed animals may inactivate the drug. The plasma protein alpha1 acid glycoprotein (AGP) bound STI571 at physiologic concentrations in vitro and blocked the ability of STI571 to inhibit Bcr-Abl kinase activity in a dose-dependent manner. Plasma AGP concentrations were strongly associated with tumor load. Erythromycin competed with STI571 for AGP binding. When animals bearing large tumors were treated with STI571 alone or with a combination of STI571 and erythromycin, greater tumor reductions and better long-term tumor-free survival (10 of 12 versus one of 13 at day 180; P:<.001) were observed after the combination treatment. CONCLUSION: AGP in the plasma of relapsed animals binds to STI571, preventing this compound from inhibiting the Bcr/Abl tyrosine kinase. Molecules such as erythromycin that compete with STI571 for binding to AGP may enhance the therapeutic potential of this dru
Letter of intent: elastic scattering and exclusive diffraction dissociation with p-d colliding beams
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Early hemodynamic and renal effects of tumor necrosis factor alpha: role of thromboxane
No full textTNF alpha is an early mediator of endotoxemic shock. Its acute effect on renal hemodynamics is not known. In this study, the early hemodynamic and renal effects of TNF alpha were investigated in a rabbit model of shock, in which the measurement of the aortic blood flow before the bifurcation of the renal arteries allows one to differentiate between prerenal factors and hemodynamic renal response. Six groups of rabbits were studied, receiving either: (1) endotoxin, (2) endotoxin + thromboxane inhibitor Dazmegrel, (3) TNF alpha, (4) TNF alpha + Dazmegrel, (5) TNF alpha+indomethacin, or (6) placebo. Between 60 min and 3 hr after the injection, endotoxin induced a mean fall in arterial pressure of 32% (P < 0.01) and TNF alpha of 16% (P < 0.01). After endotoxin, the aortic blood flow decreased by 27% (P < 0.01) and after TNF alpha by 18% (P < 0.001). Both specific thromboxane inhibition and indomethacin abolished the TNF alpha central hemodynamic effect. The renal blood flow (-53%), the renal fraction of the aortic blood flow (-38%), and the glomerular filtration rate (-47%, P < 0.05) decreased 1 hr after endotoxin injection. In contrast, TNF alpha induced only a slight fall of the renal fraction of the aortic blood flow (-19%) after 2.5 hr. Glomerular filtration was not modified after TNF alpha injection most likely because of a 17% mean increase of filtration fraction in this group (P < 0.001). These data indicate that TNF alpha is implicated in the early hemodynamic changes of endotoxemic shock.(ABSTRACT TRUNCATED AT 250 WORDS
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