高温碳酸盐岩油藏酸压用酸液体系发展与应用现状

塔河油田碳酸盐岩缝洞型油藏储层改造存在高温条件下酸岩反应速度快、滤失量大的特点,常规酸液体系难以实现深度改造和提高酸蚀裂缝导流能力的目的.通过多年室内研究与现场试验,形成了以胶凝酸、变黏酸、转向酸、地面交联酸为主的多套酸液体系.通过高温流变实验,分析不同油藏类型酸压适合的酸液体系,指导单井酸压酸液选型和工艺优化,取得较好的现场应用效果.     

葡萄糖(半乳糖,乳糖)硬脂酸单酯的生物活性对比

为研究糖酯中糖基的种类对其生物活性的影响,本文从抗氧化和抑菌性两个方面对葡萄糖（半乳糖、乳糖）硬脂酸单酯进行生物活性研究。体外抗氧化实验结果表明,200μg/m L的各化合物对O-2·,·OH和DPPH·均具有清除能力,且各化合物的抗氧化能力无明显差异。抑菌实验结果表明,400μg/m L的葡萄糖（半乳糖,乳糖）硬脂酸单酯可有效抑制细菌（大肠杆菌,金黄色葡萄球菌,枯草芽孢杆菌和沙门氏杆菌）的生长,但对霉菌（根霉,毛霉,青霉和曲霉）无明显的抑制作用,且各化合物抑菌性无明显差异。      

响应面法优化酶解鸢乌贼制备抗氧化肽的工艺研究

利用响应面分析法对酶法水解鸢乌贼蛋白制备抗氧化肽的工艺条件进行优化。首先通过单因素实验最终确定木瓜蛋白酶为水解鸢乌贼蛋白制备抗氧化肽的最佳用酶,然后在单因素的基础上以加酶量、液料比、酶解时间为自变量,DPPH自由基清除率为响应值,建立二次回归设计模型,经修正后得到最佳酶解条件为:加酶量为0.66%(w/w),液料比为10.2(v/w),酶解时间为380 min,在此条件下DPPH自由基清除率为89.80%,与模型预测值相吻合。另外,氨基酸分析表明与鸢乌贼蛋白相比,优化后的酶解产物中必需氨基酸含量提高至原蛋白的2.2倍,蛋氨酸、色氨酸等抗氧化性氨基酸分别提高至7.2、25.6倍。      

除雾器在硫酸生产中的应用及故障分析

介绍了硫酸生产装置干燥塔、吸收塔和尾吸塔除雾器的应用情况和设计要点,分析了除雾器在硫酸生产过程中存在运行压差过大、发生腐蚀甚至短路、硫酸雾去除效率偏低等常见故障的原因,提出了根据不同工况选择除雾器类型、通过专业设计和加工制作控制除雾器的质量和性能、规范除雾器安装和系统运行操作过程等解决方案,为硫酸生产企业除雾器的检修和故障排除提供参考指导意见。     

硫辛酸清除自由基的反应动力学研究

利用脉冲辐解和激光光解瞬态吸收光谱装置,研究了硫辛酸清除活性氧自由基（ROS）的反应机理,获得涉及反应的瞬态吸收光谱和反应速率常数,测得硫辛酸清除OH,eaq,CO3^-,SO4^-,Br2^-的反应速率常数分别为7．4×10^9、1．3×10^10、9．8×10^8、2．3×10^9、2．0×10^9L·mol^-1·s^-1,并对可能的反应机理进行了探讨。结果表明,硫辛酸能有效地清除活性氧自由基,是个高效的抗氧化剂。     

玻璃包覆FeCoSiB微丝包覆层化学去除方法

以玻璃包覆FeCoSiB合金微丝为对象,研究了氢氟酸含量和反应温度对包覆层去除过程的影响,以及缓蚀剂对Fe-CoSiB芯丝的保护效果.结果表明:在反应温度为25℃的条件下,当所采用的HF质量分数从10%增加到40%时,玻璃包覆层去除速度从0.005μm·s^-1提高至0.076μm·s^-1;在HF质量分数为40%的条件下,当反应温度从10℃升高到45℃时,玻璃包覆层去除速度从0.033μm·s^-1提高到0.234μm·s^-1;反应温度为20~25℃时,用质量分数40%的氢氟酸溶液去除厚度范围为7.5~9.0μm高硼硅玻璃包覆层的最佳时间为150s;硫氰酸钠及硫氰酸钠+乌洛托品作为缓蚀剂均可显著抑制氢氟酸溶液对芯丝的腐蚀,硫氰酸钠+乌洛托品还可有效减少金属吸氢,有利于防止芯丝力学性能的劣化.

     

Pharmaceutical Development of Nanostructured Vesicular Hydrogel Formulations of Rifampicin for Wound Healing

Chronic wounds exhibit elevated levels of inflammatory cytokines, resulting in the release of proteolytic enzymes which delay wound-healing processes. In recent years, rifampicin has gained significant attention in the treatment of chronic wounds due to an interesting combination of antibacterial and anti-inflammatory effects. Unfortunately, rifampicin is sensitive to hydrolysis and oxidation. As a result, no topical drug product for wound-healing applications has been approved. To address this medical need two nanostructured hydrogel formulations of rifampicin were developed. The liposomal vesicles were embedded into hydroxypropyl methylcellulose (HPMC) gel or a combination of hyaluronic acid and marine collagen. To protect rifampicin from degradation in aqueous environments, a freeze-drying method was developed. Before freeze-drying, two well-defined hydrogel preparations were obtained. After freeze-drying, the visual appearance, chemical stability, residual moisture content, and redispersion time of both preparations were within acceptable limits. However, the morphological characterization revealed an increase in the vesicle size for collagen–hyaluronic acid hydrogel. This was confirmed by subsequent release studies. Interactions of marine collagen with phosphatidylcholine were held responsible for this effect. The HPMC hydrogel formulation remained stable over 6 months of storage. Moving forward, this product fulfills all criteria to be evaluated in preclinical and clinical studies.     

Usnic Acid-Mediated Exchange of Protons for Divalent Metal Cations across Lipid Membranes: Relevance to Mitochondrial Uncoupling

Usnic acid (UA), a unique lichen metabolite, is a protonophoric uncoupler of oxidative phosphorylation, widely known as a weight-loss dietary supplement. In contrast to conventional proton-shuttling mitochondrial uncouplers, UA was found to carry protons across lipid membranes via the induction of an electrogenic proton exchange for calcium or magnesium cations. Here, we evaluated the ability of various divalent metal cations to stimulate a proton transport through both planar and vesicular bilayer lipid membranes by measuring the transmembrane electrical current and fluorescence-detected pH gradient dissipation in pyranine-loaded liposomes, respectively. Thus, we obtained the following selectivity series of calcium, magnesium, zinc, manganese and copper cations: Zn²⁺ > Mn²⁺ > Mg²⁺ > Ca²⁺ >> Cu²⁺. Remarkably, Cu²⁺ appeared to suppress the UA-mediated proton transport in both lipid membrane systems. The data on the divalent metal cation/proton exchange were supported by circular dichroism spectroscopy of UA in the presence of the corresponding cations.     

The Reactions of N,N′-Diphenyldithiomalondiamide with Arylmethylidene Meldrum’s Acids

The Michael addition reaction between dithiomalondianilide (N,N′-diphenyldithiomalondiamide) and arylmethylidene Meldrum’s acids, accompanied by subsequent heterocyclization, was investigated along with factors affecting the mixture composition of the obtained products. The plausible mechanism includes the formation of stable Michael adducts which, under the studied conditions, undergo further transformations to yield corresponding N-methylmorpholinium 4-aryl-6-oxo-3-(N-phenylthio-carbamoyl)-1,4,5,6-tetrahydropyridin-2-thiolates and their oxidation derivatives, 4,5-dihydro-3H-[1,2]dithiolo[3,4-b]pyridin-6(7H)-ones. The structure of one such product, N-methylmorpholinium 2,2-dimethyl-5-(1-(2-nitrophenyl)-3-(phenylamino)-2-(N-phenylthiocarbamoyl)-3-thioxopropyl)-4-oxo-4H-1,3-dioxin-6-olate, was confirmed via X-ray crystallography.     

Upregulation of Nrf2 Signalling and the Inhibition of Erastin-Induced Ferroptosis by Ferulic Acid in MIN6 Cells

Ferroptosis is a regulated cell death process characterised by the iron-dependent accumulation of oxidised polyunsaturated fatty acid-containing phospholipids. Its initiation is complicated and involves reactive oxygen species (ROS) and a loss of the activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4). These play critical roles in the development of ferroptotic cell damage by lipid peroxidation. Antioxidant therapy is a promising therapeutic strategy to prevent or even reverse the progression of ferroptosis. This study was designed to demonstrate the protective effect of ferulic acid (FA) against oxidative stress and erastin-mediated ferroptosis in murine MIN6 cells. Cells were treated with FA or its metabolite ferulic acid 4-O-sulfate disodium salt (FAS) and 20 μM of erastin. Cell viability was determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay, iron levels were measured by inductively coupled plasma mass spectrometry (ICP-MS), ROS levels were determined by a dihydrodichlorofluorescein (H2DCF) cell-permeant probe, and glutathione and lipid peroxidation were assayed with commercially available kits. The phenolic acids enhanced cell viability in erastin-treated MIN6 cells in a dose-dependent manner. Furthermore, MIN6 cells exposed to erastin alone showed elevated levels of iron and ROS, glutathione (GSH) depletion, and lipid peroxidation (p < 0.05) compared to cells that were protected by co-treatment with FA or FAS. The treatment of MIN6 cells with FA or FAS following exposure to erastin increased the nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2) protein levels. Consequently, levels of its downstream antioxidant proteins, HO-1, NQO1, GCLC, and GPX4, increased. FA and FAS greatly decreased erastin-induced ferroptosis in the presence of the Nrf2 inhibitor, ML385, through the regulation of Nrf2 response genes. In conclusion, these results show that FA and FAS protect MIN6 cells from erastin-induced ferroptosis by the Nrf2 antioxidant protective mechanism.