Investigation of sulfonated poly(ether ether ketone sulfone)/heteropolyacid composite membranes for high temperature fuel cell applications

The sulfonated poly(ether ether ketone sulfone) (SPEEKS)/heteropolyacid (HPA) composite membranes with different HPA content in SPEEKS copolymers matrix with different degree of sulfonation (DS) were investigated for high temperature proton exchange membrane fuel cells. Composite membranes were characterized by Fourier transfer infrared spectroscopy (FTIR) and scanning electron microscopy (SEM). FTIR band shifts suggested that the sulfonic acid groups on the copolymer backbone strongly interact with HPA particles. SEM pictures showed that the HPA particles were uniformly distributed throughout the SPEEKS membranes matrix and particle sizes decreased with the increment of copolymers' DS. The holes were not found in SPEEKS‐4/HPA30 (consisting of 70% SPEEKS copolymers with DS = 0.8 and 30% HPA) composite membrane after composite membranes were treated with boiling water for 24 h. Thermal stabilities of the composite membranes were better than those of pure sulfonated copolymers membranes. Although the composite membranes possessed lower water uptake, it exhibited higher proton conductivity for SPEEKS‐4/HPA30 especially at high temperature (above 100 °C). Its proton conductivity linearly increased from 0.068 S/cm at 25 °C to 0.095 S/cm at 120 °C, which was higher than 0.06 S/cm of Nafion 117. In contrast, proton conductivity of pure SPEEKS‐4 membrane only increased from 0.062 S/cm at 25 °C to 0.078 S/cm at 80 °C. At 120 °C, proton conductivity decreased to poor 0.073 S/cm. The result indicated that composite membranes exhibited high proton conductivity at high temperature. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 44: 1967–1978, 2006     

人工神经网络X射线荧光光谱法测定钢中酸溶铝

建立了一种人工神经网络-X射线荧光光谱法测定钢中酸溶铝的方法，用X射线荧光光谱法测定低合金钢中总铝值，应用所建立的ANN-BP网络模型，输入总铝含量直接预测出酸溶铝含量。同时使用改进的BP算法，避免了神经网络学习中可能产生的麻痹现象。该方法用于钢中酸溶铝的测定，结果满意。     

ISOLATION,CHARACTERIZATION AND EXPRESSION OF THE COMPLEMENTARY DNA FOR HUMAN TUMOR NECROSIS FACTOR (TNF-α)

A cDNA for human TNF-α (615bp) was isolated by means of polymerase chain reaction (PCR) using first strand cDNA from PMA-induced HL-60 cells as template. The result from sequencing the 615 bp cDNA fragment indicated that it corresponded to the entire sequence of mature human TNF coding region. Direct expression of mature human TNF was achieved using a plasmid pHT-1 constructed by ligation of the cDNA and a synthetic DNA. The IPTG-induced bacterial product (hTNF) showed cytotoxicity to mouse L-929 cells. The TNF activity was further identified by neutralization of a specific monoclonal antibody against human TNF-α. Approximately 80,000 units of activity were detected per ml of culture at A600=2.     

Sequential injection system with higher dimensional electrochemical sensor signals Part 1. Voltammetric e-tongue for the determination of oxidizable compounds

A sequential injection analysis (SIA) system was developed with the aim of obtaining an automatic and versatile way to prepare standards needed in the study of systems with higher dimensional sensor signals. To illustrate this, different analytical techniques were used in determinations of several analytes. Automated potentiometric calibrations of different potentiometric sensors, with and without interference, were carried out. Useful determinations of selectivity coefficients with two degrees of freedom were obtained. Simultaneous voltammetric determinations have also been done. Firstly, simultaneous determinations of lead and cadmium, using epoxy-graphite composite as the working electrode, have enabled a separate calibration for each metal to be obtained. Next, a voltammetric electronic tongue was designed and applied to the determination of oxidizable species. The use of artificial neural networks has solved the overlapped signal of ascorbic acid, 4-aminophenol and 4-acetamidophenol (paracetamol). A set of 63 data points was prepared automatically and has facilitated the training of an electronic tongue for these three analytes. Accurate predictions of test solutions, in the range of 12–410 μM for ascorbic acid, 17–530 μM for 4-aminophenol and 10–420 μM for paracetamol, have been achieved with RMSEs lower than 0.10 μM.     

Microcalorimetric investigation of influence of cancerogenic and anticancerogenic compounds on nuclear chromatin of tumor cells

The influence of mitoxantron (M) and benz(a)pyrene (BP) on chromatin DNA in composition of spleen and liver tissues and cells of BALB/c mice were studied using a high-sensitive differential scanning microcalorimeter. It was established that BP can cause a) the specific breaks in inactive chromatin DNA chain and unfolding of the whole domain (a loop of chromatin) which should lead to uncontrolled genome activation; b) the breaks in the DNA double-helix creating short duplexes.M at low doses, interacting with naked linker DNA of tumor restores the chromatin structure, at high doses or at repeated injections,M causes the disturbance of chromatin structure.     

水体透射光谱结合主成分分析(PCA )改进化学需氧量(COD)含量估算研究

化学需氧量（Chemical Oxygen Demand,COD）是水体有机污染的一项重要指标,化学需氧量越高,表示水污染程度越严重。 为了解决传统的COD测量方法耗时较长,不利于快速、实时地获取水体中COD的信息等问题。本文提出了基于透射光谱测量结合主成分分析(Principal Component Analysis, PCA)改进水体COD含量估算模型。具体的,采集100组COD水体光谱信息,分别使用3种不同的高光谱数据预处理方法对光谱数据进行预处理,分析不同预处理方法对模型精度的影响,并基于不同的预处理方法分别建立高斯过程回归模型(Gaussian Process Regression, GPR)和BP神经网络模型,分析不同预处理方法对模型精度的影响;并对各模型结合PCA数据降维方法进行模型的改进,通过比较模型的精度选择最优模型进行水体COD含量的检测。结果显示,相比于原始光谱数据建立的GPR模型和BP神经网络模型,数据预处理后的模型精度明显提升;且结合PCA对预处理后的数据进一步降维处理后,模型精度得到了进一步的提升。其中,基于标准正态变量变换特征结合PCA改进BP神经网络模型基于PCA改进的BP神经网络模型R^2高达0.9940,均方根误差RMSE为0.022540。证明了基于PCA改进的BP神经网络数据降维方法对预处理后的光谱数据进行降维处理,有利于去除光谱中的冗余信息,提取特征信息,可以实现高光谱检测方法可以实现COD含量估算模型的优化,从而为传统COD测量方法存在的问题提出了一种新的解决思路。     

A Note on ＂Global Exponential Convergence Analysis of Hopfield Neural Networks with Continuously Distributed Delays＂

In this note, we would like to point out that （i） of Corollary 1 given by Zhang et al. （cf Commun. Theor. Phys. 39 （2003） 381） is incorrect in general.     

Novel Iron Oxide Nanoparticles Induce Ferroptosis in a Panel of Cancer Cell Lines

The use of nanomaterials rationally engineered to treat cancer is a burgeoning field that has reported great medical achievements. Iron-based polymeric nano-formulations with precisely tuned physicochemical properties are an expanding and versatile therapeutic strategy for tumor treatment. Recently, a peculiar type of regulated necrosis named ferroptosis has gained increased attention as a target for cancer therapy. Here, we show for the first time that novel iron oxide nanoparticles coated with gallic acid and polyacrylic acid (IONP–GA/PAA) possess intrinsic cytotoxic activity on various cancer cell lines. Indeed, IONP–GA/PAA treatment efficiently induces ferroptosis in glioblastoma, neuroblastoma, and fibrosarcoma cells. IONP–GA/PAA-induced ferroptosis was blocked by the canonical ferroptosis inhibitors, including deferoxamine and ciclopirox olamine (iron chelators), and ferrostatin-1, the lipophilic radical trap. These ferroptosis inhibitors also prevented the lipid hydroperoxide generation promoted by the nanoparticles. Altogether, we report on novel ferroptosis-inducing iron encapsulated nanoparticles with potent anti-cancer properties, which has promising potential for further in vivo validation.     

Phosphorylation of ERK-Dependent NF-κB Triggers NLRP3 Inflammasome Mediated by Vimentin in EV71-Infected Glioblastoma Cells

Enterovirus 71 (EV71) is a dominant pathogenic agent that may cause severe central nervous system (CNS) diseases among infants and young children in the Asia-pacific. The inflammasome is closely implicated in EV71-induced CNS injuries through a series of signaling pathways. However, the activation pathway of NLRP3 inflammasome involved in EV71-mediated CNS injuries remains poorly defined. In the studies, EV71 infection, ERK1/2 phosphorylation, and activation of NLRP3 are abolished in glioblastoma cells with low vimentin expression by CRISPR/Cas9-mediated knockdown. PD098059, an inhibitor of p-ERK, remarkably blocks the vimentin-mediated ERK1/2 phosphorylation in EV71-infected cells. Nuclear translocation of NF-κB p65 is dependent on p-ERK in a time-dependent manner. Moreover, NLRP3 activation and caspase-1 production are limited in EV71-infected cells upon the caffeic acid phenethyl ester (CAPE) administration, an inhibitor of NF-κB, which contributes to the inflammasome regulation. In conclusion, these results suggest that EV71-mediated NLRP3 inflammasome could be activated via the VIM-ERK-NF-κB pathway, and the treatment of the dephosphorylation of ERK and NF-κB inhibitors is beneficial to host defense in EV71-infected CNS.     

Human Serum Amyloid a Impaired Structural Stability of High-Density Lipoproteins (HDL) and Apolipoprotein (Apo) A-I and Exacerbated Glycation Susceptibility of ApoA-I and HDL

Human serum amyloid A (SAA) is an exchangeable apolipoprotein (apo) in high-density lipoprotein (HDL) that influences HDL quality and functionality, particularly in the acute phase of inflammation. On the other hand, the structural and functional correlations of HDL containing SAA and apoA-I have not been reported. The current study was designed to compare the change in HDL quality with increasing SAA content in the lipid-free and lipid-bound states in reconstituted HDL (rHDL). The expressed recombinant human SAA1 (13 kDa) was purified to at least 98% and characterized in the lipid-free and lipid-bound states with apoA-I. The dimyristoyl phosphatidylcholine (DMPC) binding ability of apoA-I was impaired severely by the addition of SAA, while SAA alone could not bind with DMPC. The recombinant human SAA1 was incorporated into the rHDL (molar ratio 95:5:1, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC): cholesterol: apoA-I) with various apoA-I:SAA molar ratios from 1:0 to 1:0.5, 1:1 and 1:2. With increasing SAA1 content, the rHDL particle size was reduced from 98 Å to 93 Å, and the α-helicity of apoA-I:SAA was decreased from 73% to 40% for (1:0) and (1:2), respectively. The wavelength maximum fluorescence (WMF) of tryptophan in rHDL was red-shifted from 339 nm to 345 nm for (1:0) and (1:2) of apoA-I:SAA, respectively, indicating that the addition of SAA to rHDL destabilized the secondary structure of apoA-I. Upon denaturation by urea treatment from 0 M to 8 M, SAA showed only a 3 nm red-shift in WMF, while apoA-I showed a 16 nm red-shift in WMF, indicating that SAA is resistant to denaturation and apoA-I had higher conformational flexibility than SAA. The glycation reaction of apoA-I in the presence of fructose was accelerated up to 1.8-fold by adding SAA in a dose-dependent manner than that of apoA-I alone. In conclusion, the incorporation of SAA in rHDL impaired the structural stability of apoA-I and exacerbated glycation of HDL and apoA-I.