原位螯合制备含镁聚磷酸铵的工艺研究

采用一步投料法,将磷铵、尿素和硫酸镁充分混合后粉碎,再加入反应器中原位螯合制备含镁元素的水溶性聚磷酸铵（APP）肥料。研究镁添加量、尿素/磷铵物质的量比、反应温度、反应器搅拌转速对产品聚合度及聚合度分布的影响。结果表明：当镁添加量＜5%（质量分数）时,可以促进磷铵与尿素的聚合反应,提高产品聚合度;增加尿素比例、提高反应温度,可显著提高产品聚合度;随着反应器搅拌转速增加,含镁APP产品聚合度增加,而纯APP产品聚合度降低。各实验因素对APP聚合度的影响由大到小顺序为尿素/磷铵物质的量比、反应温度、搅拌转速、镁添加量。     

不同钙离子浓度体外条件下磷酸化对肌联蛋白降解的影响

以羊背最长肌中肌联蛋白为原料,添加蛋白激酶A和碱性磷酸酶体外孵育使肌联蛋白发生磷酸化和去磷酸化反应。反应后添加μ-钙蛋白酶,在钙离子浓度分别为0.05 mmol/L和2 mmol/L条件下,4 ℃孵育2 d。测定孵育体系pH值、肌联蛋白磷酸化水平及其降解程度。结果表明：不同处理组孵育体系pH值差异不显著（P＞0.05）;蛋白激酶A组肌联蛋白磷酸化水平显著高于对照组,对照组肌联蛋白磷酸化水平显著高于碱性磷酸酶组（P＜0.05）;当钙离子浓度为0.05 mmol/L时,蛋白激酶A组和对照组未检测到分子质量为1 200 kDa的降解条带,而碱性磷酸酶组在孵育12 h检测到该条带;当钙离子浓度为2 mmol/L时,蛋白激酶A组和对照组均在孵育12 h检测到1 200 kDa降解条带,而碱性磷酸酶组在孵育0.5 h时检测到该条带。结论：蛋白激酶A和碱性磷酸酶能够促进肌联蛋白发生磷酸化和去磷酸化反应;随着钙离子浓度增加,肌联蛋白降解速率加快;并且在相同钙离子浓度下,肌联蛋白在碱性磷酸酶组降解较快,表明去磷酸化可以促进肌联蛋白的降解。     

凝结芽孢杆菌中耐热木酮糖激酶基因的克隆表达及生信分析

该研究以凝结芽孢杆菌（Bacillus coagulans）IPE22为研究对象,通过聚合酶链式反应（PCR）扩增获得木酮糖激酶基因Bc-XK,将其与载体pET-30a连接后,在大肠杆菌（Escherichia coli）BL21(DE3)中进行诱导表达。然后采用镍柱亲和层析纯化重组酶Bc-XK,对基因Bc-XK及其编码的蛋白质进行生信分析。结果表明,纯化后重组酶Bc-XK的酶比活力为（20.56±3.31） U/mg,热稳定性好,在60 ℃保持活力180 min以上,具有很好的工业应用潜力。Bc-XK基因含有一个1 536 bp的开放阅读框,共编码511个氨基酸,其编码的蛋白质为亲水蛋白,等电点（PI）为5.46,分子质量为56.15 kDa,二级结构中α-螺旋、无规卷曲和延伸链含量丰富,3个催化位点分别为天冬氨酸-8、苏氨酸-11、天冬氨酸-239,高度保守。     

饲养方式对苏尼特羊肌内脂肪沉积途径AMPK-ACC-CPT1通路和肉品品质的影响

以放牧和舍饲两种饲养条件下12 月龄苏尼特羊股二头肌为实验材料,利用酶联免疫吸附测定法和实时荧光定量聚合酶链式反应法对肌内脂肪沉积动态平衡中脂肪酸β氧化一磷酸腺苷激活蛋白激酶（AMP-activated protein kinase,AMPK）-乙酰辅酶A羧化酶（acetyl-CoA carboxylase,ACC）-肉毒碱脂酰转移酶1（carnitine palmitoyltransferase,CPT1）通路所涉及的相关酶活力和质量浓度、相关基因mRNA表达量及肉品品质等指标进行测定,研究不同饲养方式对AMPK-ACC-CPT1信号通路相关指标、肌内脂肪含量及肉品品质产生的影响。结果表明：放牧饲养组羊股二头肌AMPK质量浓度、AMPK活力、CPT1质量浓度、AMPK mRNA表达量、亮度、黄度和剪切力显著大于舍饲饲养组（P＜0.05）;放牧饲养组羊股二头肌ACC活力、ACC mRNA表达量、肌内脂肪含量显著低于舍饲饲养组（P＜0.05）。由此可见,放牧饲养可以一定程度上激活AMPK-ACC-CPT1通路,从而减少肌内脂肪沉积,增加羊肉亮度和黄度,降低嫩度,进而影响肉品品质。     

三聚氰胺聚磷酸盐-双季戊四醇发泡体系在水性钢构防火涂料中的应用

使用三聚氰胺聚磷酸盐(MPP)-双季戊四醇(DPER)发泡体系(M-D体系)取代聚磷酸铵(APP)-三聚氰胺(MEL)-季戊四醇(PER)体系(A-M-P体系)制备了水性钢构防火涂料。讨论了MPP/DPER质量比、基料用量、基料配比对涂层初期耐火性及耐浸出性能的影响,对比了M-D体系水性防火涂料与A-M-P体系水性及溶剂型防火涂料的耐浸出性及浸泡后耐火性能可持续性。结果表明:M-D体系展现出与聚合物较好的相容性和较强的疏水性,由其所制备的涂层具有较好的抗溶失性,长期浸泡后涂层仍具备优异的耐火性能可持续性,适宜在户外或较为潮湿的地下结构和隧道等有长期耐水需求的钢结构保护场合中使用。     

单宁酸通过抑制TRAF6向细胞质膜的招募抑制Akt信号通路

目的：表皮生长因子受体（epidermal growth factor receptor,EGFR）/蛋白激酶B（protein kinase B, PKB,也称Akt）信号通路在大多数人类实体肿瘤中过度激活、表达失调,促进肿瘤细胞增殖。植物单宁属于植物 多酚类物质,能够抑制肿瘤细胞的增殖。然而,单宁酸通过何种机制调控肿瘤细胞中过度激活的Akt信号通路仍不 清楚。方法：本实验选用人胶质瘤U87细胞作为模型,研究单宁酸抑制人胶质瘤U87细胞EGFR/Akt信号通路的分子 机制。结果：单宁酸抑制人胶质瘤U87细胞Akt的磷酸化以及受Akt信号通路调控的相关蛋白4EBP-1和核糖体S6蛋 白的磷酸化。进一步研究发现,单宁酸抑制肿瘤坏死因子受体相关因子6（tumor necrosis receptor-associated factor 6,TRAF6）向细胞质膜的招募,导致与TRAF6相互作用的Akt蛋白减少,进而抑制人胶质瘤细胞中Akt的磷酸化 激活。利用EGFR组成型激活突变体EGFR vIII研究单宁酸对TRAF6向细胞质膜招募的影响发现：一方面单宁酸对 EGFR的抑制作用需要EGFR胞外区第2～7外显子区域的存在;另一方面单宁酸对EGFR磷酸化的抑制是导致TRAF6 向细胞质膜招募减少的原因。结论：EGFR是单宁酸发挥其抗肿瘤作用的受体蛋白,单宁酸通过抑制EGFR的磷酸 化改变TRAF6向细胞质膜的招募进而介导了单宁酸对肿瘤细胞中Akt磷酸化的抑制,从而控制蛋白质的翻译,为食 品来源单宁酸的抗肿瘤研究提供理论依据。     

In situ synthesized and dispersed melamine polyphosphate flame retardant epoxy resin composites

The dispersion of flame retardants in polymer matrix has significant impact on the final properties of the final materials. Homogenous dispersion for additive type flame retardant powder in polymer melt or solution with high viscosity is a challenge all the time. In the present research, melamine polyphosphate (MPP) is employed to flame-retard the epoxy resin (EP). Different from direct addition of MPP powder in viscous EP glue like conventional means, MPP is firstly synthesized by melamine and polyphosphoric acid in a good solvent for EP. Keeping fine and even dispersion of the produced MPP particles, EP prepolymer is added into the MPP containing solution. By this way, perfect dispersion of the flame retardant can be achieved both in the glue and the cured resin. A series of tests such as the particle size analysis, flammability evaluation, and mechanical properties tests are conducted to compare the MPP flame retardant EP obtained by this method and the conventional one. It shows that the in situ synthesis and compounding method can endow the MPP incorporated EP glue system with better homogeneity and stability, hence leading to higher flame retardancy and obviously improved mechanical performance of the final composite. © 2018 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2019 , 136, 47194.     

Improvement of Flame Retardant Properties of Polyurethane Composites Using Microencapsulation Technology

One kind of microencapsulated flame retardant containing melamine polyphosphate(MPP) and hydrophobic resin layer as core and shell material was synthesized by in situ polymerization technology. The structures and properties of microencapsulated MPP were characterized by Fourier transform infrared spectroscopy, scanning electron microscopy and water contact angle. Thermal behaviors of the composites containing microencapsulated MPP were analyzed by thermogravimetric analysis. Flame retardant tests indicated that the microencapsulated MPP with the polymer resin led to an improvement of the hydrophobicity. Results revealed that the flame retardancy of the composites was improved at the same fillers loading through the microencapsulation technology, which the char yields reached (~26.9wt%) and flame retardance grade (LOI-38%) with optimized MPP addition (~40%) to polymer matrix.     

Structure-Based Design,Synthesis, and Biological Evaluation of Imidazo[4,5-b]Pyridin-2-one-Based p38 MAP Kinase Inhibitors: Part 2

We identified novel potent inhibitors of p38 mitogen-activated protein (MAP) kinase using a structure-based design strategy, beginning with lead compound, 3-(butan-2-yl)-6-(2,4-difluoroanilino)-1,3-dihydro-2H-imidazo[4,5-b]pyridin-2-one ( 1 ). To enhance the inhibitory activity of 1 against production of tumor necrosis factor-α (TNF-α) in human whole blood (hWB) cell assays, we designed and synthesized hybrid compounds in which the imidazo[4,5-b]pyridin-2-one core was successfully linked with the p-methylbenzamide fragment. Among the compounds evaluated, 3-(3-tert-butyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-b]pyridin-6-yl)-4-methyl-N-(1-methyl-1H-pyrazol-3-yl)benzamide ( 25 ) exhibited potent p38 inhibition, superior suppression of TNF-α production in hWB cells, and also significant in vivo efficacy in a rat model of collagen-induced arthritis (CIA). In this paper, we report the discovery of potent, selective, and orally bioavailable imidazo[4,5-b]pyridin-2-one-based p38 MAP kinase inhibitors.