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Montmorillonite (MMT) is widely used as the catalyst in the commercial production of dimeric fatty acids (DAs). However, the dimerization activity of MMTs from different mineral sources is usually different, leading to unstable yield of DAs. In order to obtain a high and stable yield of DAs, the relationship between the dimerization activity and characteristics of MMT should be clarified. The characteristics of seven MMTs from different mineral sources, including the acidity (the type, strength, and amount of the acid sites), composition (interlayer cations, Si/Al ratio, water content, pH), and structure (basal spacing) are determined and correlated with their dimerization activity. Additionally, the relationship between dimerization activity and characteristics of MMT is quantified by nonlinear‐regression. It is found that the dimerization activity of MMT is mainly influenced by its Brønsted acidity and basal spacing. Stable DA yield of around 70% on MMT is obtained at the amount of weak Brønsted acid sites of more than 0.20 mmol g−1 and basal spacing of larger than 1.50 nm. Additionally, it is found that acid treatment is an effective method to adjust the Brønsted acidity and basal spacing of MMT. Practical Applications: The positive effect of Brønsted acid sites amount and basal spacing on the activity of MMT has practical value on the selection of highly efficient MMT catalyst for DA production. In addition, some MMT with poor activity can be activated by the acid treatment method mentioned in the paper. [ABSTRACT FROM AUTHOR]

At present, the utilization of grease has attracted more and more attention. This article presents a simple method that efficiently cleaves methyl oleate‐derived methyl 9,10‐epoxystearate (a) to give high yields of methyl 9‐oxononanoate (d) with nonanal (c) as co‐product. A WO3/MCM‐41 catalyst is prepared via direct mixed‐gel synthesis. The catalyst is tested in the oxidative cleavage of a to produce d which can be used as a polymer precursor or an important feedstock. The effects of WO3 loading, temperature, time, H2O2/a molar ratio, catalyst/a weight ratio, and t‐BuOH/a weight ratio on the a conversion and d yield are examined using single‐factor experiments. The optimal reaction conditions are determined by orthogonal experiments. The optimal WO3 loading, temperature, time, H2O2/a molar ratio, catalyst/a weight ratio, and t‐BuOH/a weight ratio are 35%, 80 °C, 20 min, 1.3, 0.04, and 0.5, respectively. Under these conditions, the a conversion and d yield reach 99.4 and 78.4%, respectively. In addition, the catalyst shows no significant decrease in activity after being reused three times. Moreover, the reaction mechanism is studied based on the product distribution over time. Practical Applications: Few studies on methyl 9,10‐epoxystearate used as the raw material to give methyl 9‐oxononanoate and nonanal are found. Because the ethylene oxide bond is more unstable than the carbon–carbon double bond, the oxidative cleavage of methyl 9,10‐epoxystearate is easier than cleavage of methyl oleate that allows the oxidative cleavage to be done under milder conditions. Methyl 9‐oxononanoate can be converted to a monomer of high‐value polymers and is also an important feedstock in the production of chemicals. The co‐product nonanal is a natural spice which can be used in the fragrance industry. The results show that the reaction time is short and methyl 9‐oxononanoate yield is high under mild reaction conditions. The method in this study can also be widely used in other oxidative cleavage reactions of epoxides. Methyl 9,10‐epoxystearate is used as the raw material to produce methyl 9‐oxononanoate with nonanal as co‐product using WO3/MCM‐41 as catalyst and H2O2 as oxidant. [ABSTRACT FROM AUTHOR]

Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (b FGF) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that b FGF administration can inhibit the endoplasmic reticulum ( ER) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro, b FGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert-Butyl hydroperoxide ( TBHP) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK1/2. Inhibition of these PI3K/Akt and ERK1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of b FGF. Taken together, our results indicate that the cardioprotective role of b FGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress-induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK1/2 signalling pathways. [ABSTRACT FROM AUTHOR]

Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (bFGF) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that bFGF administration can inhibit the endoplasmic reticulum (ER) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro, bFGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert-Butyl hydroperoxide (TBHP) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK1/2. Inhibition of these PI3K/Akt and ERK1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of bFGF. Taken together, our results indicate that the cardioprotective role of bFGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress-induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK1/2 signalling pathways., (© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)