硫酸法钛白废弃物硫酸亚铁的循环利用

提出一种将硫酸法钛白粉生产过程中废弃的硫酸亚铁回收,并与硫磺或硫铁矿混合掺烧,制备工业硫酸的工艺,解决硫酸法钛白生产过程中排放的固体废弃物—硫酸亚铁的处理难题,同时,产出的硫酸又可循环用于钛白粉生产,构建硫酸法钛白粉循环经济生产模式。该工艺已成功运用于国内多套钛白粉装置,使硫酸法钛白粉生产装置大型化得以实现。     

我国硫磷钛工业十年回顾及展望

2006—2016年是我国硫酸、磷肥、钛白粉工业快速发展的时期,2006—2016年硫酸产能年均增长率为9.2%,产量年均增长率为6.6%;磷肥产能年均增长率为4.0%,产量年均增长率为3.2%;钛白粉产能年均增长率为12.7%,产量年均增长率为11.7%。预计到2020年硫酸产量约为110 Mt,硫资源表观消费量约为39.5 Mt,磷肥产量有望保持在18.0 Mt,钛白粉产量约为3.1 Mt。回顾了近十年硫酸、磷肥、钛白粉技术进展,总结硫-磷-钛-铁循环经济产业链发展。今后硫磷钛行业必须加强技术进步和行业融合发展,协同解决废酸、废渣、废气彻底治理和资源、能源综合利用,实现可持续发展。     

工信部发布钛白粉行业清洁生产技术推广方案

8月16日国家工信部发布钛白粉行业清洁生产技术推广方案。其中应用技术有：沸腾氯化法钛白粉生产技术,钛矿连续酸解技术,利用联产硫酸与钛白粉生产过程产生的废热将硫酸法钛白粉副产的废酸浓缩,硫钛联产节能和废副处理（废酸浓缩渣或硫酸亚铁与硫精砂或硫磺混合制酸）技术,     

全钛渣原料硫酸法钛白粉生产工艺环境评价

硫酸法钛白粉生产过程副产的硫酸亚铁和废酸是制约硫酸法钛白粉生产工艺发展的重要因素之一。硫酸法钛白粉生产工艺所用原料有3种：全钛精矿、渣矿混合和全钛渣。对不同原料硫酸法钛白粉生产工艺的环境负荷进行了研究,结果表明：采用全钛渣为原料的硫酸法钛白粉生产工艺既能减少副产物对环境的影响,又能降低酸耗、能耗,是现阶段硫酸法钛白粉生产工艺中环境最优的。     

硫酸法钛白粉质量差的原因及解决办法

在硫酸法钛白粉生产过程中,钛白粉产品质量的控制关键在于物料净化、颗粒粒径及粒径分布和表面处理这三大环节。从这三大环节出发,分析了某厂钛白粉产品质量差的原因,主要是钛矿品位低、钛液净化工艺及设备落后、水解技术落后、晶型转化过程中转化剂分散不均匀、偏钛酸洗涤工艺不合理和各煅烧窑煅烧强度不一致等。针对这些原因,分别从工艺和设备上提出了一系列有利于提高硫酸法钛白粉产品质量的技术方案,并对生产装置加以改造。改选方案实施后,钛白粉产品质量大有提高,即钛白粉杂质含量降低,粒径变细且分布变窄,分散性能有了明显好转,遮盖力等指标有了明显提高。     

钛白粉废硫酸回收利用技术研究进展

介绍了硫酸法钛白粉副产废硫酸资源化利用技术进展。针对企业实际,可采用喷雾浓缩、真空多级蒸发浓缩回收利用硫酸资源,直接生产聚合硫酸铁、硫氧镁水泥。将钛白粉副产废硫酸与含钛原料一步反应可生成含有硫酸、硫酸铁和硫酸钛的自拟合纳米催化污水处理剂。该处理剂用于芬顿法印染污水处理,可减少硫酸、硫酸亚铁和双氧水消耗。     

联产法钛白粉清洁工艺通过鉴定

近日,中国石油和化学工业联合会、中国环境学会组织专家,对河南佰利联化学股份有限公司开发的硫铁钛联产法钛白粉清洁生产工艺进行了科技成果鉴定。中国工程院院士张懿等专家一致认为,该技术为中国硫酸法钛白粉产业破解环保困局、实现产业健康发展开辟了一条创新之路。鉴定组专家审议评定,佰利联公司是国内首家成功研发出硫铁钛联产法钛白粉清洁生产工艺的企业,该工艺技术成熟,具有独特的环保优越性和科技领先性,达到国际先进水平。据了解,该技术的成果特点,是将硫酸法钛白粉与硫黄制酸、铁系颜料生产、一水硫酸亚铁制备、氧化钪提取、钛石膏产品等装置进行联合生产,     

钛白粉生产工艺技术进展

介绍了硫酸法、氯化法生产钛白粉的工艺流程、反应原理、原材料消耗，以及该种方法的优、缺点。同时介绍了钛白粉的新的生产工艺——盐酸法，介绍了该法的工艺流程，指出该工艺可生产纳米、锐钛型和金红石型钛白粉。该工艺特征是盐酸循环使用，副产物只有氧化铁渣。     

新型螺旋卸料沉降-过滤离心机在钛白行业的应用

随着钛白粉行业的快速发展,硫酸法生产工艺对分离设备的要求也越来越高。为满足市场需求,公司研发了新型LWLC450×1250螺旋卸料沉降-过滤离心机,并将其应用在硫酸法钛白粉生产中。结果表明：离心机分离出的液相含钛总质量浓度大于160 g/L,固体含钛质量分数小于0.41%,大大提高了钛液的质量和收率,同时能有效节能降耗,改善工作环境,是钛白粉行业理想的分离设备。     

硫—磷—钛产业链循环经济模式的评述

以硫酸法钛白为主体,评述了硫—磷—钛的循环经济模式,硫酸法钛白配套硫酸及磷化工,前者在硫铁矿制酸系统中可以消耗钛白废酸浓缩时产生的一水硫酸亚铁渣,后者可消耗多余的浓缩废酸,解决硫酸法钛白废副综合利用难题,并能获取一定的经济效益。针对目前有硫酸和磷化工的企业推荐了一个硫—磷—钛的佳配方案,并提供了相关工程经验和技术简述。     

辉光放电电解降解水体中阳离子桃红FG的机理

用辉光放电电解（GDE）技术对模拟染料废水阳离子桃红FG的降解过程进行了研究。通过发射光谱法测定了GDE产生的活性粒子,用紫外光谱和总有机碳（TOC）分析仪研究了不同放电时间下的脱色率和去除率,用电导率仪和酸度计测定了降解过程中溶液的电导率和pH的变化,同时用离子色谱对降解中间产物进行了分析。结合各种分析结果,探讨了GDE降解阳离子桃红FG的机理。结果表明,在最佳电压600 V时,溶液中产生HO·、O·、H·等高活性粒子;放电120 min时,200 ml 20 mg/L阳离子桃红FG的脱色率和TOC去除率分别可达99.0%和72.6%;降解液pH先减小后增大,电导率存在先增大后减小的趋势;离子色谱测试表明,降解过程中产生多种有机小分子酸。羟基自由基（HO·）对阳离子桃红FG的降解起关键作用,GDE降解阳离子桃红FG的机理为：HO·作用下助色基团键断裂,产生酚类等中间产物,然后继续被降解为醌和小分子有机酸,最终矿化为Cl^-、NO₃^-、CO₂和H₂O。     

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.     

正反向同时引发ATRP制备凹凸棒土/聚苯乙烯杂化粒子

通过脱醇法在凹凸棒土（ATP）表面接枝γ-氨丙基三乙氧基硅烷（APTES）实现氨基化（ATP-APTES）,再经酰胺化反应接枝α-溴代异丁酰溴,从而在ATP表面固载ATRP引发基团（ATP-Br）;最后以2,2-偶氮二异丁腈（AIBN）和ATP-Br为双组分引发体系进行正反向同时引发原子转移自由基聚合（SR&NI ATRP）制备ATP接枝聚苯乙烯杂化粒子（ATP@PS）。结果表明AIBN结合ATP-Br引发体系进行SR&NI ATRP具有活性/可控聚合的特征,随催化剂用量增大,体系过早偏离一级动力学行为。聚合温度在80℃,投料比为单体/催化剂/AIBN/ATP-Br=200/0.3/0.05/0.5的条件下,接枝聚合物和游离聚合物分子量差异随转化率（c）增大逐渐增加,转化率为31.1%时,两者分子量分布（PDI）均保持在1.54以下,ATP-Br表面ATRP引发基团的引发效率为6.3%。杂化粒子在PS基体中分散得到明显改善。     

Anti-Inflammatory Therapeutic Approaches to Prevent or Delay Post-Traumatic Osteoarthritis (PTOA) of the Knee Joint with a Focus on Sustained Delivery Approaches

Inflammation plays a central role in the pathogenesis of knee PTOA after knee trauma. While a comprehensive therapy capable of preventing or delaying post-traumatic osteoarthritis (PTOA) progression after knee joint injury does not yet clinically exist, current literature suggests that certain aspects of early post-traumatic pathology of the knee joint may be prevented or delayed by anti-inflammatory therapeutic interventions. We discuss multifaceted therapeutic approaches that may be capable of effectively reducing the continuous cycle of inflammation and concomitant processes that lead to cartilage degradation as well as those that can simultaneously promote intrinsic repair processes. Within this context, we focus on early disease prevention, the optimal timeframe of treatment and possible long-lasting sustained delivery local modes of treatments that could prevent knee joint-associated PTOA symptoms. Specifically, we identify anti-inflammatory candidates that are not only anti-inflammatory but also anti-degenerative, anti-apoptotic and pro-regenerative.     

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.     

苯酚/丙酮市场供需现状与展望

分析了世界和我国苯酚／丙酮供需现状及消费结构,对未来供需进行了预测,提出了发展我国苯酚／丙酮装置的具体建议。     

Nitric Oxide-Dependent Mechanisms Underlying MK-801- or Scopolamine-Induced Memory Dysfunction in Animals: Mechanistic Studies

MK-801, an NMDA receptor antagonist, and scopolamine, a cholinergic receptor blocker, are widely used as tool compounds to induce learning and memory deficits in animal models to study schizophrenia or Alzheimer-type dementia (AD), respectively. Memory impairments are observed after either acute or chronic administration of either compound. The present experiments were performed to study the nitric oxide (NO)-related mechanisms underlying memory dysfunction induced by acute or chronic (14 days) administration of MK-801 (0.3 mg/kg, i.p.) or scopolamine (1 mg/kg, i.p.). The levels of L-arginine and its derivatives, L-citrulline, L-glutamate, L-glutamine and L-ornithine, were measured. The expression of constitutive nitric oxide synthases (cNOS), dimethylaminohydrolase (DDAH1) and protein arginine N-methyltransferases (PMRTs) 1 and 5 was evaluated, and the impact of the studied tool compounds on cGMP production and NMDA receptors was measured. The studies were performed in both the cortex and hippocampus of mice. S-nitrosylation of selected proteins, such as GLT-1, APP and tau, was also investigated. Our results indicate that the availability of L-arginine decreased after chronic administration of MK-801 or scopolamine, as both the amino acid itself as well as its level in proportion to its derivatives (SDMA and NMMA) were decreased. Additionally, among all three methylamines, SDMA was the most abundant in the brain (~70%). Administration of either compound impaired eNOS-derived NO production, increasing the monomer levels, and had no significant impact on nNOS. Both compounds elevated DDAH1 expression, and slight decreases in PMRT1 and PMRT5 in the cortex after scopolamine (acute) and MK-801 (chronic) administration were observed in the PFC, respectively. Administration of MK-801 induced a decrease in the cGMP level in the hippocampus, accompanied by decreased NMDA expression, while increased cGMP production and decreased NMDA receptor expression were observed after scopolamine administration. Chronic MK-801 and scopolamine administration affected S-nitrosylation of GLT-1 transport protein. Our results indicate that the analyzed tool compounds used in pharmacological models of schizophrenia or AD induce changes in NO-related pathways in the brain structures involved in cognition. To some extent, the changes resemble those observed in human samples.     

Dextran sulfate sodium inhibits alanine synthesis in caco-2 cells

To understand and characterize the pathogenic mechanisms of inflammatory bowel disease, dextran sulfate sodium (DSS) has been used to induce acute and chronic colitis in animal models by causing intestinal epithelium damage. The mechanism of action of DSS in producing this outcome is not well understood. In an effort to understand how DSS might impact epithelial cell metabolism, we studied the intestinal epithelial cell line Caco-2 incubated with 1% DSS over 56 hours using (1)H NMR spectroscopy. We observed no difference in cell viability as compared to control cultures, and an approximately 1.5-fold increase in IL-6 production upon incubation with 1% DSS. The effect on Caco-2 cell metabolism as measured through changes in the concentration of metabolites in the cell supernatant included a three-fold decrease in the concentration of alanine. Given that the concentrations of other amino acids in the cell culture supernatant were not different between treated and control cultures over 56 hours suggest that DSS inhibits alanine synthesis, specifically alanine aminotransferase, without affecting other key metabolic pathways. The importance of alanine aminotransferase in inflammatory bowel disease is discussed.     

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。     

Glutamate and GABA in Microglia-Neuron Cross-Talk in Alzheimer’s Disease

The physiological balance between excitation and inhibition in the brain is significantly affected in Alzheimer’s disease (AD). Several neuroactive compounds and their signaling pathways through various types of receptors are crucial in brain homeostasis, among them glutamate and γ-aminobutyric acid (GABA). Activation of microglial receptors regulates the immunological response of these cells, which in AD could be neuroprotective or neurotoxic. The novel research approaches revealed the complexity of microglial function, including the interplay with other cells during neuroinflammation and in the AD brain. The purpose of this review is to describe the role of several proteins and multiple receptors on microglia and neurons, and their involvement in a communication network between cells that could lead to different metabolic loops and cell death/survival. Our review is focused on the role of glutamatergic, GABAergic signaling in microglia–neuronal cross-talk in AD and neuroinflammation. Moreover, the significance of AD-related neurotoxic proteins in glutamate/GABA-mediated dialogue between microglia and neurons was analyzed in search of novel targets in neuroprotection, and advanced pharmacological approaches.