几种低粘度恒粘天然橡胶的性能研究

采用盐酸羟胺、硫酸羟胺、盐酸氨基脲和促进剂M作为恒粘剂分别制备了天然橡胶(NR)-HH,NR-HS,NR-SH和NR-MB低粘度恒粘NR,并研究NR的理化性质、贮存性能、硫化特性和物理性能。结果表明:与未采用恒粘剂的NR-CK相比,4种恒粘NR的塑性初值稍小,NR-MB的塑性保持率明显降低;NR-MB胶料的硫化速度大于NR-CK胶料,NR-HS,NR-HH和NR-SH胶料的硫化速度则小于NR-CK胶料;NR-HH,NR-HS和NR-SH硫化胶的拉伸强度和撕裂强度相当,均低于NR-CK硫化胶,而NR-MB硫化胶的拉伸强度和撕裂强则高于NR-CK硫化胶。几种恒粘剂均能有效降低NR的门尼粘度,改善其耐热空气老化性能,其中盐酸羟胺和硫酸羟胺对NR的恒粘效果较好。     

混炼外场条件对溶聚丁苯橡胶/天然橡胶胶料性能的影响

研究混炼外场条件对溶聚丁苯橡胶/天然橡胶胶料性能的影响。结果表明:随着转子转速增大,混炼胶的门尼粘度变化不大,FL先增大后减小,F_(max)增大,t_(10)缩短,t_(90)变化不大;硫化胶的邵尔A型硬度、拉伸强度和拉断伸长率增大,撕裂强度减小;胶料的Payne效应先增强后减弱。随着初始混炼温度升高,混炼胶的门尼粘度、FL和F_(max)增大,t_(10)和t_(90)缩短;硫化胶的300%定伸应力、拉伸强度、拉断伸长率和撕裂强度呈减小趋势;胶料的Payne效应明显增强。     

恒粘剂2-巯基苯并噻唑对天然橡胶性能的影响

采用恒粘剂2-巯基苯并噻唑(MT)制备恒粘天然橡胶(CVNR),研究其性能,并与传统的恒粘剂盐酸羟胺(HH)进行对比。结果表明:采用恒粘剂HH或MT均能制备出恒粘效果较好的NR。随着贮存时间的延长,MT-CVNR的重均相对分子质量(Mw)、塑性初值(P0)和门尼粘度基本恒定不变;HH-CVNR的Mw、P0和门尼粘度起初变化不大,但随着贮存时间的延长均有不同程度的增大,逐渐失去恒粘特征。与HH-CVNR硫化胶相比,MT-CVNR硫化胶的物理性能明显较好。     

炭黑和硫化程度对天然橡胶硫化胶疲劳性能的影响

研究了4种不同粒径的炭黑和不同硫化程度对天然橡胶(NR)硫化胶在25℃和100℃下耐疲劳性能的影响。结果表明,NR硫化胶的疲劳性能与炭黑粒径、硫化程度和疲劳温度有关,不同炭黑填充的NR硫化胶在100℃下的疲劳寿命均高于25℃下的疲劳寿命,100℃下疲劳破坏后胶料的交联密度增高,而25℃下疲劳破坏后则降低;100℃下以工艺正硫化时间(t_(90))制备的胶料疲劳寿命高,填充大粒径炭黑有利于延缓胶料的初始破坏,25℃下以理论正硫化时间(t_(100))制备的胶料疲劳寿命高,填充小粒径炭黑有利于延缓胶料的初始破坏。     

湿法混炼氧化石墨烯/天然橡胶复合材料的性能研究

采用湿法混炼工艺制备氧化石墨烯(GO)/天然橡胶(NR)复合材料,并对其性能进行研究。结果表明:加入GO的胶料门尼粘度增大,t_(10)和t_(90)延长,硫化胶的物理性能、导电性能和导热性能提高,储能模量增大,损耗因子减小;随着GO用量的增大,胶料的t_(10)和t_(90)先延长后缩短,硫化胶的定伸应力增大,拉伸强度和撕裂强度先增大后减小,导电性能变化不大,导热性能总体提高;当GO用量为2份时,复合材料的综合性能最佳,GO在复合材料中的分散性最好。     

新型促进剂STU对天然橡胶性能的影响

研究新型促进剂STU对天然橡胶(NR)硫化特性和物理性能的影响。结果表明:在较低的硫化温度下,添加促进剂STU可以缩短NR胶料的t90;当促进剂STU/促进剂CZ摩尔比为1∶1时,可达到最佳的硫化促进效果;添加促进剂STU可以提高NR硫化胶的拉伸性能。     

恒粘剂OPRHAZ对天然橡胶性能的影响

研究恒粘剂OPRHAZ对天然橡胶（NR）性能的影响，并与塑解剂A86进行对比。结果表明：恒粘剂OPRHAZ通过与NR的化学反应来降低NR的门尼粘度，不减小NR相对分子质量，降低NR凝胶含量，提高NR胶料物理性能。恒粘剂OPRHAZ在稳定NR停放过程中的门尼粘度、提高NR胶料的物理性能方面比传统塑解剂A86更具有优势。     

助交联剂HVA-2对天然橡胶性能的影响

研究助交联剂HVA-2在硫黄硫化体系下对天然橡胶(NR)性能的影响。结果表明:加入助交联剂HVA-2后,NR胶料的t_(10)延长,F_(max)增大,硫化胶的拉伸强度、拉断伸长率和撕裂强度增大,剪切储能模量和损耗因子减小;随着老化时间的延长,硫化胶的交联密度增大;当助交联剂HVA-2用量为1份时,NR硫化胶的耐热氧老化和耐疲劳性能最好。     

排胶温度对全钢载重子午线轮胎胎面胶性能的影响

试验研究排胶温度对全钢载重子午线轮胎胎面胶性能的影响。结果表明:混炼胶的排胶温度升高后,胶料的F_L和F_(max)减小,t_(s2)和t_(10)延长,t_(90)略有延长,总体来说对胶料的硫化特性影响不大;硫化胶的邵尔A型硬度、定伸应力和撕裂强度明显提高,阿克隆磨耗量显著减小,压缩生热略有上升,拉断伸长率降低,综合物理性能提高。     

液体聚丁二烯替代芳烃油在全钢载重子午线轮胎胎圈护胶中的应用研究

研究液体橡胶液体聚丁二烯(LPBD)替代芳烃油对全钢载重子午线轮胎胎圈护胶(顺丁橡胶/天然橡胶并用胶)的硫化特性、加工性能、物理性能、生热性能和动态力学性能的影响。结果表明:LPBD等量替代芳烃油后,胶料的t_(10)略有延长,t_(90)略有缩短,LPBD的增塑作用小于芳烃油;硫化胶的硬度、拉伸性能和抗撕裂性能提高,压缩温升降低,LPBD Activ-1000硫化胶的动态力学性能较好,LPBD Activ-50硫化胶与芳烃油硫化胶的动态力学性能相近。     

关于科研开发效率的思考

作者从认识论和方法论的角度出发，对提高科研开发效率提出如下看法：１．当代的经济竞争，实质是科技产业化能力的竞争。２．研究开发应是从投入到产出的完整系统。３．产业部门的研究开发要面向市场。４．只有充分利用专利保护，才能在国际竞争中赢得主动。５．要保持竞争优势，须把信息工作提到新水平。     

Synergistic Interactions of Cannabidiol with Chemotherapeutic Drugs in MCF7 Cells: Mode of Interaction and Proteomics Analysis of Mechanisms

Cannabidiol (CBD), a nonpsychoactive phytocannabinoid, has recently emerged as a potential cytotoxic agent in addition to its ameliorative activity in chemotherapy-associated side effects. In this work, the potential interactions of CBD with docetaxel (DOC), doxorubicin (DOX), paclitaxel (PTX), vinorelbine (VIN), and 7-ethyl-10-hydroxycamptothecin (SN−38) were explored in MCF7 breast adenocarcinoma cells using different synergy quantification models. The apoptotic profiles of MCF7 cells after the treatments were assessed via flow cytometry. The molecular mechanisms of CBD and the most promising combinations were investigated via label-free quantification proteomics. A strong synergy was observed across all synergy models at different molar ratios of CBD in combination with SN−38 and VIN. Intriguingly, synergy was observed for CBD with all chemotherapeutic drugs at a molar ratio of 636:1 in almost all synergy models. However, discording synergy trends warranted the validation of the selected combinations against different models. Enhanced apoptosis was observed for all synergistic CBD combinations compared to monotherapies or negative controls. A shotgun proteomics study highlighted 121 dysregulated proteins in CBD-treated MCF7 cells compared to the negative controls. We reported the inhibition of topoisomerase II β and α, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation. We observed 91 significantly dysregulated proteins in MCF7 cells treated with the synergistic combination of CBD with SN−38 (CSN−38), compared to the monotherapies. Regulation of telomerase, cell cycle, topoisomerase I, EGFR1, protein metabolism, TP53 regulation of DNA repair, death receptor signalling, and RHO GTPase signalling pathways contributed to the proteome-wide synergistic molecular mechanisms of CSN−38. In conclusion, we identified significant synergistic interactions between CBD and the five important chemotherapeutic drugs and the key molecular pathways of CBD and its synergistic combination with SN−38 in MCF7 cells. Further in vivo and clinical studies are warranted to evaluate the implementation of CBD-based synergistic adjuvant therapies for breast cancer.     

玉米肽-麦芽糊精糖基化产物与α-生育酚共组装纳米粒子的制备及其性质

通过美拉德反应制备玉米肽-麦芽糊精糖基化产物,再通过反溶剂法制备糖基化产物与α-生育酚共组装纳米粒子,系统地研究了制备参数对于复合粒子的影响。结果表明,糖基化产物浓度、玉米肽与α-生育酚质量比、pH对于复合粒子的粒度与ζ电位有重要的影响。采用动态光散射、ζ电位观察发现,通过调节制备参数,荷载α-生育酚的玉米肽-麦芽糊精糖基化产物可以形成平均粒度为80～100 nm的纳米粒子,其表面电荷分布在-23～-32 mV之间。与玉米肽、玉米肽/麦芽糊精混合物相比,玉米肽-麦芽糊精糖基化产物对于α-生育酚具有更高的荷载效率以及更好的pH稳定性。     

Participation of Amyloid and Tau Protein in Post-Ischemic Neurodegeneration of the Hippocampus of a Nature Identical to Alzheimer’s Disease

Recent evidence suggests that amyloid and tau protein are of vital importance in post-ischemic death of CA1 pyramidal neurons of the hippocampus. In this review, we summarize protein alterations associated with Alzheimer’s disease and their gene expression (amyloid protein precursor and tau protein) after cerebral ischemia, as well as their roles in post-ischemic hippocampus neurodegeneration. In recent years, multiple studies aimed to elucidate the post-ischemic processes in the development of hippocampus neurodegeneration. Their findings have revealed the dysregulation of genes for amyloid protein precursor, β-secretase, presenilin 1 and 2, tau protein, autophagy, mitophagy, and apoptosis identical in nature to Alzheimer’s disease. Herein, we present the latest data showing that amyloid and tau protein associated with Alzheimer’s disease and their genes play a key role in post-ischemic neurodegeneration of the hippocampus with subsequent development of dementia. Therefore, understanding the underlying process for the development of post-ischemic CA1 area neurodegeneration in the hippocampus in conjunction with Alzheimer’s disease-related proteins and genes will provide the most important therapeutic development goals to date.     

表面张力对自由落体液滴形变的影响

液滴运动过程中的形状变化对液滴的蒸发、燃烧等过程有重要影响,表面张力是影响其形状变化的因素之一。为研究表面张力对液滴形变的影响规律,采用低浓度的表面活性剂(十二烷基苯磺酸钠SDBS)配制表面张力为30~72mN·m^-1的水溶液。利用不同外径的针管得到3~5mm粒径的液滴。高速摄像机(PhantomV211,1000pps,800×600pixel)对这些液滴在自由落体过程中的形变规律进行了可视化实验研究,得到了关于Eötvös数(Eo)的半经验关系式。实验结果表明,液滴在自由落体过程中会形成周期性振动形变,振动周期和振幅随表面张力增大而减小。进一步研究发现,初始时液滴形成并断裂所引起的瞬态冲量使液滴内部动量传递进而表现出周期性振动形变。     

Interphases in the Adhesive Bonding of Fluoropolymers

Strong and durable adhesive bonds may be made between polytetrafluoroethylene (PTFE) and either cyanoacrylate (CA) or epoxy adhesives, if the PTFE surface is modified by the use of a “primer” such as triphenylphosphine (TPP) or diaminodiphenylmethane (DDM). The primer mixes with the PTFE surface, and the modified surface is then capable of forming an interphase, tens to hundreds of nanometers thick, where interpenetration of the adhesive and adherend occurs. Using CA adhesives, PTFE/CA/PTFE block compression shear bond strength (ASTM D4501-85) of over 10 MPa can be achieved, with failure occurring cohesively. Initial work with epoxy adhesives indicates that the use of DDM primer gives adhesive bonds comparable in strength with those produced by modification of the fluoropolymer surface by sodium naphthalenide.     

Improvement Effects of Myelophil on Symptoms of Chronic Fatigue Syndrome in a Reserpine-Induced Mouse Model

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is associated with various symptoms, such as depression, pain, and fatigue. To date, the pathological mechanisms and therapeutics remain uncertain. The purpose of this study was to investigate the effect of myelophil (MYP), composed of Astragali Radix and Salviae miltiorrhizae Radix, on depression, pain, and fatigue behaviors and its underlying mechanisms. Reserpine (2 mg/kg for 10 days, intraperitoneally) induced depression, pain, and fatigue behaviors in mice. MYP treatment (100 mg/kg for 10 days, intragastrically) significantly improved depression behaviors, mechanical and thermal hypersensitivity, and fatigue behavior. MYP treatment regulated the expression of c-Fos, 5-HT1A/B receptors, and transforming growth factor β (TGF-β) in the brain, especially in the motor cortex, hippocampus, and nucleus of the solitary tract. MYP treatment decreased ionized calcium binding adapter molecule 1 (Iba1) expression in the hippocampus and increased tyrosine hydroxylase (TH) expression and the levels of dopamine and serotonin in the striatum. MYP treatment altered inflammatory and anti-oxidative-related mRNA expression in the spleen and liver. In conclusion, MYP was effective in recovering major symptoms of ME/CFS and was associated with the regulation of dopaminergic and serotonergic pathways and TGF-β expression in the brain, as well as anti-inflammatory and anti-oxidant mechanisms in internal organs.     

小胶质细胞对阿尔兹海默病发生发展的影响作用

阿尔兹海默病(老年性痴呆,AD)是由β淀粉样蛋白(Aβ)和微管相关蛋白(Tau)聚集形成的具有毒性作用的寡聚物而引起的老年人主要以记忆力下降和脑部形成老年斑、神经纤维缠绕为特征的神经退行性疾病. 小胶质细胞作为中枢神经系统中的固有免疫细胞,是脑内免疫监视的关键成分,发挥内源性免疫防御作用. 正常生理状态的小胶质细胞能有效吞噬和清除毒性Aβ寡聚体,阻止AD发生. 在AD病理过程中,过度激活的小胶质细胞通过补体依赖途径过度吞噬突触,导致突触丧失,同时大量释放炎症因子,促进Tau相关病理变化,对神经元造成直接损伤,导致认知功能下降. 由此可见,小胶质细胞在AD发生发展过程中起着双刃剑的作用,探明小胶质细胞的极化状态及其在AD疾病机理中的作用将为攻克AD的药物研发提供突破性思路.     

Molecular Pathogenesis of Neuromyelitis Optica

Neuromyelitis optica (NMO) is a rare autoimmune disorder, distinct from multiple sclerosis, causing inflammatory lesions in the optic nerves and spinal cord. An autoantibody (NMO IgG) against aquaporin-4 (AQP4), a water channel expressed on astrocytes is thought to be causative. Peripheral production of the antibody is triggered by an unknown process in genetically susceptible individuals. Anti-AQP4 antibody enters the central nervous system (CNS) when the blood brain barrier is made permeable and has high affinity for orthogonal array particles of AQP4. Like other autoimmune diseases, Th17 cells and their effector cytokines (such as interleukin 6) have been implicated in pathogenesis. AQP4 expressing peripheral organs are not affected by NMO IgG, but the antibody causes extensive astrocytic loss in specific regions of the CNS through complement mediated cytotoxicity. Demyelination occurs during the inflammatory process and is probably secondary to oligodendrocyte apoptosis subsequent to loss of trophic support from astrocytes. Ultimately, extensive axonal injury leads to severe disability. Despite rapid advances in the understanding of NMO pathogenesis, unanswered questions remain, particularly with regards to disease mechanisms in NMO IgG seronegative cases. Increasing knowledge of the molecular pathology is leading to improved treatment strategies.