Our data suggest that the anti-apoptosis property of A549/Taxol cells originates from a defect in activation of the mitochondrial apoptotic pathway, and autophagy inhibitors can potentiate BZML-induced MC to overcome resistance to mitochondrial apoptosis.
Hydrocracking of 1-methylnaphthalene
to benzene (B), toluene (T),
and xylene (X) was performed over a series of bi-functional catalysts
(W/Beta) at 420 °C and 6 MPa. The reaction results and kinetic
study indicated that metal–acid balance (metal–acid
interaction and metal–acid ratio) and metal dispersion had
a great impact on the cracking, hydrogenation, and selective hydrogenation
activity, which directly determine the BTX yield. An inappropriate
metal–acid ratio would lead to producing plenty of intermediates
or by-products, and poor metal dispersion would result in low hydrogenation
activity. However, good metal dispersion usually accompanies the strong
metal–acid interaction, which reduces the sulfidation of metal.
In this work, a new tungsten precursor, W-complex, was used to prepare
the catalysts with good dispersion of metal oxides and high hydrogenation
activity. The external surface acidity of zeolite was modified to
regulate the metal–acid interaction by forming a layer of SiO2 on acid sites through chemical liquid deposition.
Purpose: We found in previous study that metformin could treat sepsis myocarditis in a mouse model. We employed the zebrafish model organism to investigate the effect of metformin on sepsis myocarditis. Methods and Results: Wild-type zebrafish was used to establish a sepsis myocarditis model and combined with image software analysis and cytokine detection, the protective dose of metformin was determined. The results showed that immersion with Escherichia coli could cause 75% mortality in zebrafish and make larvae appear as characteristics of severe sepsis myocarditis. Pretreatment with 10 mM metformin for 3 hours could effectively reduce heart congestion and swelling in zebrafish with sepsis myocarditis and increased the heart rate. It could reduce the mortality and prolong the survival time of zebrafish with sepsis myocarditis; Tg(mpx: EGFP) transgenic zebrafish were adopted to explore the number of neutrophils in zebrafish heart before and after metformin protection, and metformin could maintain the number of neutrophils in zebrafish heart; quantitative real-time reverse transcription–polymerase chain reaction showed that metformin could reduce the expression of pro-inflammatory factors, tumor necrosis factor-α and interleukin (IL)-6, and could promote the anti-inflammatory factor, transforming growth factor-β and IL-10 expression. Conclusion: We established a zebrafish sepsis myocarditis model and applied metformin in advance to provide a protective effect on the zebrafish heart.
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