Milk from cows fed a diet with a high forage:concentrate ratio improves inflammatory state,oxidative stress,and mitochondrial function in rats

Excessive energy intake may evoke complex biochemical processes characterized by inflammation, oxidative stress, and impairment of mitochondrial function that represent the main factors underlying noncommunicable diseases. Because cow milk is widely used for human nutrition and in food industry processing, the nutritional quality of milk is of special interest with respect to human health. In our study, we analyzed milk produced by dairy cows fed a diet characterized by a high forage:concentrate ratio (high forage milk, HFM). In view of the low n-6:n-3 ratio and high content of conjugated linoleic acid of HFM, we studied the effects of this milk on lipid metabolism, inflammation, mitochondrial function, and oxidative stress in a rat model. To this end, we supplemented for 4 wk the diet of male Wistar rats with HFM and with an isocaloric amount (82 kJ, 22 mL/d) of milk obtained from cows fed a diet with low forage:concentrate ratio, and analyzed the metabolic parameters of the animals. Our results indicate that HFM may positively affect lipid metabolism, leptin:adiponectin ratio, inflammation, mitochondrial function, and oxidative stress, providing the first evidence of the beneficial effects of HFM on rat metabolism.     

由乙腈一步法制备乙酸丁酯的研究

以丁醇和制备丙烯腈的副产物乙腈为原料 ,采用一步法合成了乙酸丁酯。通过正交实验得到了影响反应的 4种因素。确定了最佳的工艺条件为 :催化剂的量为样品质量的 40 % ;n(CH3CN)∶ n(C4 H9OH) =1∶ 1 .0 5 ;反应温度为 1 0 5℃ ;反应时间为 8h。在此反应条件下 ,乙酸丁酯的收率为 88.8% ,纯度可达 99.5 %。并用气相色谱及红外光谱对产品的纯度进行了表征     

用环境友好催化剂合成丙酸异丁酯的研究

报道了以固载杂多酸盐TiSiW12O40/TiO2为环境友好催化剂，对以丙酸和异丁醇为原料合成丙酸异丁酯的反应条件进行了研究。实验表明：TiSiW12O40/TiO2是合成丙酸异丁酯的良好催化剂，最佳反应条件为：n（醇）：n(酸）=1.2:1，催化剂用量为反应物料总质量的2.0%。反应时间1.0h，反应温度106-125℃，上述条件下，丙酸异丁酯的收率可达79.1%。     

Some factors affecting the electrical properties of carbon-black-loaded butyl rubber during vulcanization

Butyl rubber mixtures loaded with 70 phr general purpose furnace black (GPF) and tetramethyl thiuram disulphide (TMTD)/S as vulcanizing system were prepared. The kinetics of their electrical conductivity development during the vulcanization process were followed by using an especially devised system. It was found that the increase in the electrical conductivity during vulcanization obeys an exponential growth function with time constant τ, which markedly decreases with increasing vulcanization temperature as well as with the efficiency of the vulcanizing system. After completion of the vulcanization process, about 80 min, the samples obtained possess reasonable stability and reproducibility of electrical conductivity.     

溶液中微量甲基异丁基酮的分析方法

研究了微量甲异丁基酮在氟氧铌酸（H2NbOF5)及氟钽酸（H2TaF7)溶液中存在的形式，找到利用碘仿-硫代硫酸钠联合滴定的方法，来标定微量甲基异丁基酮在H2NbOF5及H2TaF7溶液中的含量，本方法在钽铌冶炼过程中操作简便易行且结果重现性好。     

聚氨酯/聚(甲基丙烯酸甲酯-甲基丙烯酸丁酯)互穿聚合物网络聚合物的阻尼性能

采用本体聚合法合成出一系列阻尼性能良好的聚氨酯/聚(甲基丙烯酸甲酯-甲基丙烯酸丁酯)(PU/P(MMA-BMA))互穿聚合物网络(IPN)聚合物,通过动态力学分析方法表征了PU/P(MMA-BMA)IPN聚合物的阻尼性能。探讨了加入催化剂、高温后处理、交联剂用量及PU与P(MMA-BMA)的质量比对PU/P(MMA-BMA)IPN聚合物阻尼性能的影响。实验结果表明,经高温后处理后,以二月桂酸二丁基锡为催化剂、交联剂二乙烯基苯用量(占MMA和BMA的摩尔分数)为1.5%、PU与P(MMA-BMA)的质量比接近1或小于1时,PU/P(MMA-BMA)IPN聚合物具有良好的阻尼性能。     

丁酸异戊酯催化合成研究进展

综述了采用FeCl3·6H2O、十二水合硫酸铁铵、硫酸铝、硫酸钛、杂多酸(盐)、对甲苯磺酸、氨基磺酸、强酸性阳离子交换树脂DOOX和脂肪酶等催化合成丁酸异戊酯的方法     

Resveratrol Butyrate Esters Inhibit BPA-Induced Liver Damage in Male Offspring Rats by Modulating Antioxidant Capacity and Gut Microbiota

Resveratrol can affect the physiology or biochemistry of offspring in the maternal–fetal animal model. However, it exhibits low bioavailability in humans and animals. Fifteen-week SD pregnant female rats were orally administered bisphenol A (BPA) and/or resveratrol butyrate ester (RBE), and the male offspring rats (n = 4–8 per group) were evaluated. The results show that RBE treatment (BPA + R30) compared with the BPA group can reduce the damage caused by BPA (p < 0.05). RBE enhanced the expression of selected genes and induced extramedullary hematopoiesis and mononuclear cell infiltration. RBE increased the abundance of S24-7 and Adlercreutzia in the intestines of the male offspring rats, as well as the concentrations of short-chain fatty acids (SCFAs) in the feces. RBE also increased the antioxidant capacity of the liver by inducing Nrf2, promoting the expression of HO-1, SOD, and CAT. It also increased the concentration of intestinal SCFAs, enhancing the barrier formed by intestinal cells, thereby preventing BPA-induced metabolic disruption in the male offspring rats, and reduced liver inflammation. This study identified a potential mechanism underlying the protective effects of RBE against the liver damage caused by BPA exposure during the peri-pregnancy period, and the influence of the gut microbiota on the gut–liver axis in the offspring.     

Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7

Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with congenital fiber type disproportion and muscle weakness. The molecular mechanisms underlying muscle dysfunction in this disease remain unclear. Here, we observed that this mutation causes an abnormally high Ca²⁺-sensitivity of myofilaments in vitro and in muscle fibers. To determine the critical conformational changes that myosin, actin, and tropomyosin undergo during the ATPase cycle and the alterations in these changes caused by R90P replacement in Tpm3.12, we used polarized fluorimetry. It was shown that the R90P mutation inhibits the ability of tropomyosin to shift towards the outer domains of actin, which is accompanied by the almost complete depression of troponin’s ability to switch actin monomers off and to reduce the amount of the myosin heads weakly bound to F-actin at a low Ca²⁺. These changes in the behavior of tropomyosin and the troponin–tropomyosin complex, as well as in the balance of strongly and weakly bound myosin heads in the ATPase cycle may underlie the occurrence of both abnormally high Ca²⁺-sensitivity and muscle weakness. BDM, an inhibitor of myosin ATPase activity, and W7, a troponin C antagonist, restore the ability of tropomyosin for Ca²⁺-dependent movement and the ability of the troponin–tropomyosin complex to switch actin monomers off, demonstrating a weakening of the damaging effect of the R90P mutation on muscle contractility.