Stability analysis of the simplest Takagi-Sugeno fuzzy control system using circle criterion

A frequency-domain-based sufficient condition is derived to guarantee the globally asymptotic stability of the simplest Takagi-Sugeno (T-S) fuzzy control system by using the circle criterion. The analysis is performed in the frequency domain, and hence the condition is of great significance when the frequency-response method, which is widely used in the linear control theory and practice, is employed to synthesize the simplest T-S fuzzy controller. Besides, this sufficient condition is featured by a graphical interpretation, which makes the condition straightforward to be used. Comparisons are drawn between the performance of the simplest T-S fuzzy controller and that of the linear compensator. Two numerical examples are presented to demonstrate how this sufficient condition can be applied to both stable and unstable plants.     

The PREPL A protein, a new member of the prolyl oligopeptidase family, lacking catalytic activity

The PREPL (previously called KIAA0436) gene encodes a putative serine peptidase from the prolyl oligopeptidase family. A chromosomal deletion involving the PREPL gene leads to a severe syndrome with multiple symptoms. Homology with oligopeptidase B suggested that the enzyme cleaves after an arginine or lysine residue. Several PREPL splice variants have been identified, and a 638-residue variant (PREPL A) was expressed in Escherichia coli and purified. Its secondary structure was similar to that of oligopeptidase B, but differential-scanning calorimetry indicated a higher conformational stability. Dimerization may account for the enhanced stability. Unexpectedly, the PREPL A protein did not cleave peptide substrates containing a P1 basic residue, but did slowly hydrolyse an activated ester substrate, and reacted with diisopropyl fluorophosphate. These results indicated that the catalytic serine is a reactive residue. However, the negligible hydrolytic activity suggests that the function of PREPL A is different from that of the other members of the prolyl oligopeptidase family.     

Predation on eggs of Schneider’s dwarf caiman,Paleosuchus trigonatus (Schneider, 1807), by armadillos and other predators

Nests of Schneider’s dwarf caiman, Paleosuchus trigonatus, were located in the forests around three streams that drain into the Xingu River, Brazilian Amazonia, in October 2014. Camera traps were installed at the edge of four nests to document predators and female parental care. At two nests, females unsuccessfully defended their nests against one or more giant armadillos, Priodontes maximus, and nine-banded armadillos, Dasypus novemcinctus. Both armadillo species responded to the attack by fleeing and returning on the opposite side of the nest by going around the tree under which the nest was located. Giant armadillos have never before been recorded consuming caiman eggs and their diet has been described as consisting mostly of ants and termites. Another species of armadillo, Cabassous unicinctus, was also registered digging into a nest and probably consuming eggs, though it is generally considered to be primarily insectivorous. A tayra (Eira barbara), lizard (Tupinambis teguixin) and coati (Nasua nasua) were also registered taking eggs from nests during the day, but we obtained no registers of nest defence by caimans during the day. The three nests were attacked after 60 days of incubation, when the eggs were well developed.     

Profilin1 biology and its mutation,actin(g) in disease

Profilins were discovered in the 1970s and were extensively studied for their significant physiological roles. Profilin1 is the most prominent isoform and has drawn special attention due to its role in the cytoskeleton, cell signaling, and its link to conditions such as cancer and vascular hypertrophy. Recently, multiple mutations in the profilin1 gene were linked to amyotrophic lateral sclerosis (ALS). In this review, we will discuss the physiological and pathological roles of profilin1. We will further highlight the cytoskeletal function and dysfunction caused by profilin1 dysregulation. Finally, we will discuss the implications of mutant profilin1 in various diseases with an emphasis on its contribution to the pathogenesis of ALS.     

Genome-wide association study identifies a new melanoma susceptibility locus at 1q21.3

We performed a genome-wide association study of melanoma in a discovery cohort of 2,168 Australian individuals with melanoma and 4,387 control individuals. In this discovery phase, we confirm several previously characterized melanoma-associated loci at MC1R, ASIP and MTAP-CDKN2A. We selected variants at nine loci for replication in three independent case-control studies (Europe: 2,804 subjects with melanoma, 7,618 control subjects; United States 1: 1,804 subjects with melanoma, 1,026 control subjects; United States 2: 585 subjects with melanoma, 6,500 control subjects). The combined meta-analysis of all case-control studies identified a new susceptibility locus at 1q21.3 (rs7412746, P = 9.0 × 10(-11), OR in combined replication cohorts of 0.89 (95% CI 0.85-0.95)). We also show evidence suggesting that melanoma associates with 1q42.12 (rs3219090, P = 9.3 × 10(-8)). The associated variants at the 1q21.3 locus span a region with ten genes, and plausible candidate genes for melanoma susceptibility include ARNT and SETDB1. Variants at the 1q21.3 locus do not seem to be associated with human pigmentation or measures of nevus density.     

Genome-wide association study identifies susceptibility loci for open angle glaucoma at TMCO1 and CDKN2B-AS1

We report a genome-wide association study for open-angle glaucoma (OAG) blindness using a discovery cohort of 590 individuals with severe visual field loss (cases) and 3,956 controls. We identified associated loci at TMCO1 (rs4656461[G] odds ratio (OR) = 1.68, P = 6.1 × 10(-10)) and CDKN2B-AS1 (rs4977756[A] OR = 1.50, P = 4.7 × 10(-9)). We replicated these associations in an independent cohort of cases with advanced OAG (rs4656461 P = 0.010; rs4977756 P = 0.042) and two additional cohorts of less severe OAG (rs4656461 combined discovery and replication P = 6.00 × 10(-14), OR = 1.51, 95% CI 1.35-1.68; rs4977756 combined P = 1.35 × 10(-14), OR = 1.39, 95% CI 1.28-1.51). We show retinal expression of genes at both loci in human ocular tissues. We also show that CDKN2A and CDKN2B are upregulated in the retina of a rat model of glaucoma.     

腾冲嗜酸两性菌硫氧化还原酶分子结构中铁原子结合位点的新特征

前期研究表明, 铁原子对于嗜酸两性菌中硫氧化还原酶(SOR)的活性至关重要. 本研究表明, 2,2′-联吡啶、1,2-二羟基苯-3,5-二磺酸钠、8-羟基喹啉等特异性铁离子螯合剂强烈抑制腾冲嗜酸两性菌SOR酶活性, 进一步表明铁原子是SOR酶活必需. 对目前基因组数据库中的SOR基因或者SOR类似基因进行序列比对, 发现了一个潜在的铁原子结合模体(H⁸⁶-X₃- H⁹⁰-X_n-E¹¹⁴-X_n-E¹²⁹). 据此, 本研究采用定点突变技术, 将氨基酸残基H⁸⁶, H⁹⁰和E¹²⁹分别突变为苯丙氨酸或者丙氨酸, 圆二色光谱测定发现突变体(H⁸⁶F, H⁹⁰F和E¹²⁹A)的二级结构没有明显改变, 但是这3个突变体全部丧失了酶活性. 突变体蛋白中铁原子含量测定结果表明, 3个突变体全部或者部分丢失了铁原子, 而之前研究中获得的3个半胱氨酸突变体(完全丧失了酶活)铁原子含量没有变化. 根据本研究并结合前期实验结果可知, SOR分子中模体C³¹-X_n-C¹⁰¹-X₂-C¹⁰⁴是底物硫分子活化区域; 而模体H⁸⁶-X₃-H⁹⁰-X₂₃-E¹¹⁴-X_¹⁴-(E/D)¹²⁹是SOR分子中铁原子的结合区域, 与铁原子结合形成一个非卟啉铁中心, 是SOR的氧化还原中心; 这两个区域均是SOR酶活性的必需部分.     

修正表面张力系数的包膜气泡动力学模型

基于包膜造影剂气泡的实际应用, 在传统的三层模型基础上提出了一个修正的动力学模型来描绘包膜气泡的动力学行为. 通过衔接三层模型中包膜的两个边界条件, 得到一个两层模型并简化了方程的结构. 为了使动力平衡更加准确, 在建立边界条件时考虑了包膜质量, 并将包膜层厚度与气泡半径的关系具体化. 更为重要的是, 我们对绝大多数文献中的表面张力系数不变的假设进行了修正, 认为其随半径变化呈非线性变化, 且通过数值计算对表面张力系数修正带来的变化进行了讨论. 此外, 我们应用本文模型对实验得到的Optison及Sonozoid微气泡的动力学曲线进行了拟合, 并与其他经典模型的拟合结果进行了比较, 结论证明了本文模型具有很好的适用性.     

东方龙虱鞘翅:形态学及力学性能研究

研究了东方龙虱鞘翅的拓扑结构及其鞘翅生物材料的力学性能. SEM观测表明鞘翅横向截面和纵向截面结构相同, 是一种具 “桥墩” 状连接的空腔轻质结构, 由致密的黑色外表皮层和其下数十层几丁质纤维层平行、螺旋交织构成的内表皮层组成; 纳米压痕仪测得新鲜鞘翅外侧区域的硬度和弹性模量分别为0.31和6.13 GPa; 拉伸实验得到新鲜鞘翅横向和纵向的强度极限分别为169.2和194.5 MPa; 干燥鞘翅对应的强度极限为85.38和90.91 MPa, 新鲜鞘翅的强度是干燥鞘翅值的2倍; 结果表明甲虫鞘翅是一种力学性能呈现拓扑分布规律的轻质生物复合材料, 该研究为航空航天材料的轻质结构的设计提供了生物学的参考.     

耦合诱导的金纳米棒禁戒等离激元模式激发

用时域有限差分方法（finite-difference time-domain,FDTD）模拟了有不同局域等离激元共振频率和不同体积的外来金纳米颗粒以及外来介质纳米颗粒与金纳米棒的耦合,研究了正入射条件下与各种颗粒耦合对诱发金棒上纵向等离激元的禁戒模式的不同影响,发现外来颗粒上足够多的电荷积聚造成的电场对称性破缺是诱发禁戒模式的原因.这一发现对理解金属纳米颗粒的近场光学实验探测有重要意义.