Bivariate C1 cubic spline space over a nonuniform type-2 triangulation and its subspaces with boundary conditions

AbstractIn this paper, we discuss the algebraic structure of bivariate C1 cubic spline spaces over nonuniform type-2 triangulation and its subspaces with boundary conditions. The dimensions of these spaces are determined and their local support bases are constructed

Generation and Role of Oscillatory Contractions in Mouse Airway Smooth Muscle

Background/Aims: Tetraethylammonium chloride (TEA) induces oscillatory contractions in mouse airway smooth muscle (ASM); however, the generation and maintenance of oscillatory contractions and their role in ASM are unclear. Methods: In this study, oscillations of ASM contraction and intracellular Ca2+ were measured using force measuring and Ca2+ imaging technique, respectively. TEA, nifedipine, niflumic acid, acetylcholine chloride, lithium chloride, KB-R7943, ouabain, 2-Aminoethoxydiphenyl borate, thapsigargin, tetrodotoxin, and ryanodine were used to assess the mechanism of oscillatory contractions. Results: TEA induced depolarization, resulting in activation of L-type voltage-dependent Ca2+ channels (LVDCCs) and voltage-dependent Na+ (VNa) channels. The former mediated Ca2+ influx to trigger a contraction and the latter mediated Na+ entry to enhance the contraction via activating LVDCCs. Meanwhile, increased Ca2+-activated Cl- channels, inducing depolarization that resulted in contraction through LVDCCs. In addition, the contraction was enhanced by intracellular Ca2+ release from Ca2+ stores mediated by inositol (1,4,5)-trisphosphate receptors (IP3Rs). These pathways together produce the contractile phase of the oscillatory contractions. Furthermore, the increased Ca2+ activated the Na+-Ca2+ exchanger (NCX), which transferred Ca2+ out of and Na+ into the cells. The former induced relaxation and the latter activated Na+/K+-ATPase that induced hypopolarization to inactivate LVDCCs causing further relaxation. This can also explain the relaxant phase of the oscillatory contractions. Moreover, the depolarization induced by VNa channels and NCX might be greater than the hypopolarization caused by Na+/K+-ATPase alone, inducing LVDCC activation and resulting in further contraction. Conclusions: These data indicate that the TEA-induced oscillatory contractions were cooperatively produced by LVDCCs, VNa channels, Ca2+-activated Cl- channels, NCX, Na+/K+ ATPase, IP3Rs-mediated Ca2+ release, and extracellular Ca2+

Semen cassiae Extract Inhibits Contraction of Airway Smooth Muscle

β2-adrenoceptor agonists are commonly used as bronchodilators to treat obstructive lung diseases such as asthma and chronic obstructive pulmonary disease (COPD), however, they induce severe side effects. Therefore, developing new bronchodilators is essential. Herbal plants were extracted and the extracts’ effect on airway smooth muscle (ASM) precontraction was assessed. The ethyl alcohol extract of semen cassiae (EESC) was extracted from Semen cassia. The effects of EESC on the ACh- and 80 mM K+-induced sustained precontraction in mouse and human ASM were evaluated. Ca2+ permeant ion channel currents and intracellular Ca2+ concentration were measured. HPLC analysis was employed to determine which compound was responsible for the EESC-induced relaxation. The EESC reversibly inhibited the ACh- and 80 mM K+-induced precontraction. The sustained precontraction depends on Ca2+ influx, and it was mediated by voltage-dependent L-type Ca2+ channels (LVDCCs), store-operated channels (SOCs), TRPC3/STIM/Orai channels. These channels were inhibited by aurantio-obtusin, one component of EESC. When aurantio-obtusin removed, EESC’s action disappeared. In addition, aurantio-obtusin inhibited the precontraction of mouse and human ASM and intracellular Ca2+ increases. These results indicate that Semen cassia-contained aurantio-obtusin inhibits sustained precontraction of ASM via inhibiting Ca2+-permeant ion channels, thereby, which could be used to develop new bronchodilators

Improved Whale Optimization Algorithm for Solving Constrained Optimization Problems

In view of the shortcomings of the whale optimization algorithm (WOA), such as slow convergence speed, low accuracy, and easy to fall into local optimum, an improved whale optimization algorithm (IWOA) is proposed. First, the standard WOA is improved from the three aspects of initial population, convergence factor, and mutation operation. At the same time, Gaussian mutation is introduced. Then the nonfixed penalty function method is used to transform the constrained problem into an unconstrained problem. Finally, 13 benchmark problems were used to test the feasibility and effectiveness of the proposed method. Numerical results show that the proposed IWOA has obvious advantages such as stronger global search ability, better stability, faster convergence speed, and higher convergence accuracy; it can be used to effectively solve complex constrained optimization problems

Application of the Improved Differential Evolution Algorithm in Portfolio

Aiming at the NP hard problem of portfolio optimization, an improved differential evolution algorithm is proposed. In this algorithm, the mutation operator and crossover operator are set up adaptively, and then according to the characteristics of the mutation itself, two kinds of mutation operators with global search ability and local search ability are improved .The improved algorithm can improve the convergence speed and ensure the precision of the algorithm. Through five stocks of the same type and 20 different types of stocks for empirical analysis, the results show that the proposed algorithm has a certain guiding role in solving the problem of portfolio optimization

Postendocytotic traffic of the galanin R1 receptor: A lysosomal signal motif on the cytoplasmic terminus

The neuropeptide galanin R1 receptor (GalR1) was tagged at its C terminus with EGFP (GalR1–EGFP) to study receptor localization and trafficking. In PC12 and HEK293 cells, functional GalR1–EGFP was expressed on the plasma membrane and internalized into cytoplasmic vesicles after galanin stimulation. The internalization was blocked by 0.4 M sucrose and by silencing of clathrin with siRNA methodology. Internalized GalR1–EGFP and LysoTracker, a lysosomal marker, overlapped in intracellular vesicles after prolonged galanin stimulation. This colocalization was strongly reduced after site-directed mutagenesis of the motif YXXØ on the C terminus of GalR1 (where Ø is a bulky hydrophobic residue and X any amino acid). Taken together, these data suggest that GalR1 is internalized via the clathrin-dependent, endocytic pathway and then, to a large extent, delivered to lysosomes for degradation through the lysosome-targeting signal YXXØ