心电图信号的频域分析

提出了一种简便有效的、由心电图（ECG）曲线提取QRS-T复合波的新方法，从而获得P波（当房颤未发生时）或f波（当房颤时）；利用功率谱、自相关、互相关等信号处理技术，对它进行了处理和分析，特别是，比较了未房颤时和发生房颤时的相关信息的显著差别。     

低温等离子体处理纤维素纤维的机理和性能研究

本文应用不同技术参数的低温等离子体对Lyocell纤维进行处理,借助SEM等手段对其表面特征和物理性能进行研究,通过化学热力学和化学动力学,对反应机理做了研究和分析,证明了通过这种新型手段对Lyocell纤维进行接枝和改性的可行性和优越性,并针对Lyocell纤维的一些相关性能进行了处理前和处理后的比较,结果表明低温等离子体处理后的Lyocell纤维在不降低物理机械性能的同时很大程度上减少了纤维的原纤化。     

Controlling micro‐ and nanofibrillar morphology of polymer blends in low‐speed melt spinning process. Part II: Influences of extrusion rate on morphological changes of a PLA/PVA blend through a capillary die

The effects of the extrusion rate on the morphological changes of poly(lactic acid) (PLA)/poly(vinyl alcohol) (PVA) blend through a capillary die were investigated. In this study, the extrusion rate or mass flow rate is altered from 0.5 g min^?1 to 2 g min^?1 with an increment of 0.5 g min^?1. The PLA/PVA blend with a composition of 30/70 (wt %) exhibits a particle matrix morphology with dispersed PLA droplets within the PVA matrix. It is found that, the spherical or ellipsoidal dispersed PLA droplets are elongated and coalesced into rod‐like or longer ellipsoidal droplets when they pass through the capillary die. When the extrusion rate increases, the coalescence between the large PLA droplets occurs more intense. However, the changes of the extrusion rate have no strong effect on the coalescence of small droplets having diameter less than about 150 nm. © 2016 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2016 , 133, 44257.     

Inhibition of hIAPP Amyloid Aggregation and Pancreatic β‐Cell Toxicity by OH‐Terminated PAMAM Dendrimer

Human islet amyloid polypeptide (hIAPP, or amylin) forms amyloid deposits in the islets of Langerhans, a phenomenon that is associated with type‐2 diabetes impacting millions of people worldwide. Accordingly, strategies against hIAPP aggregation are essential for the prevention and eventual treatment of the disease. Here, it is shown that generation‐3 OH‐terminated poly(amidoamine) dendrimer, a polymeric nanoparticle, can effectively halt the aggregation of hIAPP and shut down hIAPP toxicity in pancreatic MIN6 and NIT‐1 cells as well as in mouse islets. This finding is supported by high‐throughput dynamic light scattering experiment and thioflavin T assay, where the rapid evolution of hIAPP nucleation and elongation processes is halted by the addition of the dendrimer up to 8 h. Discrete molecular dynamics simulations further reveal that hIAPP residues bound strongly with the dendrimer near the c‐terminal portion of the peptide, where the amyloidogenic sequence (residues 22–29) locates. Furthermore, simulations of hIAPP dimerization reveal that binding with the dendrimer significantly reduces formation of interpeptide contacts and hydrogen bonds, thereby prohibiting peptide self‐association and amyloidosis. This study points to a promising nanomedicinal strategy for combating type‐2 diabetes and may have broader implications for targeting neurological disorders whose distinct hallmark is also amyloid fibrillation.     

Differential Domain Distribution of gnomAD- and Disease-Linked Connexin Missense Variants

Twenty-one human genes encode connexins, a family of homologous proteins making gap junction (GJ) channels, which mediate direct intercellular communication to synchronize tissue/organ activities. Genetic variants in more than half of the connexin genes are associated with dozens of different Mendelian inherited diseases. With rapid advances in DNA sequencing technology, more variants are being identified not only in families and individuals with diseases but also in people in the general population without any apparent linkage to Mendelian inherited diseases. Nevertheless, it remains challenging to classify the pathogenicity of a newly identified connexin variant. Here, we analyzed the disease- and Genome Aggregation Database (gnomAD, as a proxy of the general population)-linked variants in the coding region of the four disease-linked α connexin genes. We found that the most abundant and position-sensitive missense variants showed distinct domain distribution preference between disease- and gnomAD-linked variants. Plotting missense variants on topological and structural models revealed that disease-linked missense variants are highly enriched on the structurally stable/resolved domains, especially the pore-lining domains, while the gnomAD-linked missense variants are highly enriched in the structurally unstable/unresolved domains, especially the carboxyl terminus. In addition, disease-linked variants tend to be on highly conserved residues and those positions show evolutionary co-variation, while the gnomAD-linked missense variants are likely on less conserved residue positions and on positions without co-variation. Collectively, the revealed distribution patterns of disease- and gnomAD-linked missense variants further our understanding of the GJ structure–biological function relationship, which is valuable for classifying the pathogenicity of newly identified connexin variants.     

Use of modified sample entropy measurement to classify ventricular tachycardia and fibrillation

A study of ventricular fibrillation (VF) and ventricular tachycardia (VT) was undertaken using modified sample entropy analysis. Sample entropy (SampEn) is believed to provide the quantitative information about the complexity of experimental data that is corrupted by noise, short in data length. However, the similarity definition of vectors is based on a Heaviside function, of which the boundary is discontinuous and hard, which may cause the problems in the validity and accuracy of SampEn. To deal with the encountered problems, a modified sample entropy (mSampEn) based on fuzzy membership function was proposed. Its performances on characterizing VF and VT signals, as well as several simulated time series, demonstrate that mSampEn can more efficiently measure the complexity of time series. It is shown that, as a criteria for discriminating between VF and VT, mSampEn provides a significantly (p < 0.0001) higher (99%) accuracy rate than the standard one.     

Lyocell纤维——减少原纤化的替代方法

除了用树脂整理来减少Ｌｙｏｃｅｌｌ纤维原纤化之外，还存在其他可能，本文对 可能性进行了研究。反应性染料由于结构和浓度因素而影响原纤维化性能，甚至连无色的反应性物质也能对此造成影响，这很容易由Ｌｙｏｃｅｌｌ纤维的湿态抗原纤维所证实。对抗皱与洗旧性也进行了评价。     

Simvastatin Attenuates the Oxidative Stress,Endothelial Thrombogenicity and the Inducibility of Atrial Fibrillation in a Rat Model of Ischemic Heart Failure

Increased atrial oxidative stress has an important role in inducing and maintaining atrial fibrillation (AF), and the activation of the small GTPase Rac1 contributes to the oxidative stress. We investigated the relationship of Rac1, atrial endothelial thromboprotective markers and AF inducibility and if simvastatin has a potential beneficial effect on a myocardial infarction (MI)-induced heart failure (HF) rat model. Rats were randomized into three groups (shams, MI group and simvastatin treatment group) and underwent echocardiography, AF induction studies and left atrial (LA) fibrosis analysis. Atrial Rac 1, sodium calcium exchanger (I_NCX), sarcoplasmic reticulum calcium ATPase (SERCA), endothelial nitric oxide synthase (eNOS) and induced nitric oxide synthase (iNOS) were measured. AF inducibility, AF duration and LA fibrosis were significantly higher in the MI group (p < 0.001 vs. sham), which were significantly reduced by simvastatin (p < 0.05 vs. MI). The reduced expressions of atrial eNOS, SERCA, thrombomodulin, tissue factor pathway inhibitor and tissue plasminogen activator in the MI group were significantly improved by simvastatin. Furthermore, the increased expression of atrial iNOS, I_NCX and Rac1 activity were significantly decreased by the simvastatin. Oxidative stress, endothelial dysfunction and thrombogenicity are associated with the promotion of AF in a rat model of ischemic HF. These were associated with increased Rac1 activity, and simvastatin treatment prevents these changes.     

聚丙烯基原位成纤复合材料研究进展

以聚对苯二甲酸乙二酯(PET)、尼龙(PA)66、PA6、超高分子量聚乙烯(UHMWPE)、聚苯硫醚(PPS)、聚萘二甲酸乙二酯(PEN)等热塑性树脂为成纤聚合物,综述了利用这些成纤聚合物制备聚丙烯(PP)基原位成纤复合材料的方法、技术及复合材料的结构特征、力学性能.提出了优化PP基原位成纤复合材料综合力学性能的思路.