Multiple positive solutions for boundary value problems of second order delay differential equations with one-dimensional p-Laplacian

AbstractWe consider the boundary value problems: (ϕp(x′(t)))′+q(t)f(t,x(t),x(t−1),x′(t))=0, ϕp(s)=|s|p−2s, p>1, t∈(0,1), subject to some boundary conditions. By using a generalization of the Leggett–Williams fixed-point theorem due to Avery and Peterson, we provide sufficient conditions for the existence of at least three positive solutions to the above problems

Tensor polarization of the deuteron at high momentum transfer in elastic (e,d) scattering

Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Physics, 1999.Includes bibliographical references (p. 202-209).by Wenxia Zhao.Ph.D

2-{[2-(2-Hy­droxy-3-meth­oxy­benzyl­idene)hydrazin-1-yl­idene]meth­yl}-6-meth­oxy­phenol

The title compound, C16H16N2O4, was obtained from the reaction of hydrazine hydrate and o-vanilin in absolute ethanol. The mol­ecule is almost planar (except for the methyl H atoms), with a mean deviation from the plane of 0.0259 Å. The mol­ecular structure also exhibits an approximate non-crystallographic twofold axis. Intra­molecular O—H⋯N hydrogen bonds occur. In the crystal, inter­molecular C—H⋯O hydrogen bonds generate mol­ecular zigzag sheets. The sheets stack through C—H⋯π inter­actions, leading to a three-dimensional-network

Fatigue crack propagation behavior of Ni-based superalloys after overloading at elevated temperatures

AbstractThe fatigue crack propagation behavior of three superalloys subjected to a single overloading at elevated temperatures was investigated. The fatigue crack propagation rate FCPR versus stress intensity factor range data da/dN—ΔK were calculated using the two-point secant method. It was found that the crack growth rates of the investigated materials were retarded after overloading with an overload ratio ROL=1.6. The size of the plastic zone in the front of the crack tip and its relation to loading level were discussed. The overload retardation effects are attributed to crack closure. The fatigue damage in the plastic zone can also be a factor to explain the overload retardation

Time duration of post-activation performance enhancement (PAPE) in elite male sprinters with different strength levels

(1) Purpose: This study aimed to explore the time duration of post-activation performance enhancement (PAPE) in elite male sprinters with different strength levels. (2) Methods: Thirteen elite male sprinters were divided into a strong group (relative strength: 1RM squat normalized by body mass of ≥ 2.5; n = 6) and a weak group (relative strength of < 2.5; n =7). All sprinters performed one static squat jump (SSJ) at baseline and 15 s, 3 min, 6 min, 9 min, and 12 min following an exercise protocol including three reps of a 90% 1RM back squat. Two force plates were used to determine the vertical jump height, the impulse output, and the power output for all SSJs. (3) Results: Significant improvements in vertical jump height and peak impulse were observed (p < 0.05) at 3, 6, and 9 min, without significant between-group differences. The peak power had a significant increase in 3 min (p < 0.01) and 6 min (p < 0.05), with also no significant difference between-group differences. Moreover, the stronger subjects induced a greater PAPE effect than the weaker counterparts at 3, 6, and 9 min after the intervention. The maximal benefit following the intervention occurred at 6 min and 3 min after the intervention in the stronger and weaker subjects, respectively. (4) Conclusions: The findings indicated that three reps of a 90% 1RM back squat augmented the subsequent explosive movement (SSJ) for 3–9 min in elite male sprinters, especially in stronger sprinters.info:eu-repo/semantics/publishedVersio

The Role of Tumour Metabolism in Cisplatin Resistance

Cisplatin is a chemotherapy drug commonly used in cancer treatment. Tumour cells are more sensitive to cisplatin than normal cells. Cisplatin exerts an antitumour effect by interfering with DNA replication and transcription processes. However, the drug-resistance properties of tumour cells often cause loss of cisplatin efficacy and failure of chemotherapy, leading to tumour progression. Owing to the large amounts of energy and compounds required by tumour cells, metabolic reprogramming plays an important part in the occurrence and development of tumours. The interplay between DNA damage repair and metabolism also has an effect on cisplatin resistance; the molecular changes to glucose metabolism, amino acid metabolism, lipid metabolism, and other metabolic pathways affect the cisplatin resistance of tumour cells. Here, we review the mechanism of action of cisplatin, the mechanism of resistance to cisplatin, the role of metabolic remodelling in tumorigenesis and development, and the effects of common metabolic pathways on cisplatin resistance

Characterization on microstructure of interface and failure analysis of SiC fiber reinforced Ti-17 composites under tension load

From IOP Publishing via Jisc Publications RouterHistory: ppub 2021-05, open-access 2021-05-01Publication status: PublishedAbstract: In this study, the ultimate tensile strength of unidirectional SiC-fiber/Ti-17 composites was measured in the as-produced condition at room temperature. Fracture and interfacial reaction zone was characterized by using laser confocal microscopy, field emission scanning electron microscopy (FE-SEM) and transmission electron microscopy. Elemental distribution maps of the interfacial reaction layer and titanium matrix were quantitatively examined by electron probe micro-analyzer (EPMA). Micromechanical properties of SiC fiber and titanium matrix was inspected by Nano-indentation. The Fracture failure mechanisms was show that the key microstructural parameters which dominate damage initiation, damage growth and fracture behavior of the composites were explained in detail

N-WASP Is Essential for the Negative Regulation of B Cell Receptor Signaling

Negative regulation of receptor signaling is essential for controlling cell activation and differentiation. In B-lymphocytes, the down-regulation of B-cell antigen receptor (BCR) signaling is critical for suppressing the activation of self-reactive B cells; however, the mechanism underlying the negative regulation of signaling remains elusive. Using genetically manipulated mouse models and total internal reflection fluorescence microscopy, we demonstrate that neuronal Wiskott–Aldrich syndrome protein (N-WASP), which is coexpressed with WASP in all immune cells, is a critical negative regulator of B-cell signaling. B-cell–specific N-WASP gene deletion causes enhanced and prolonged BCR signaling and elevated levels of autoantibodies in the mouse serum. The increased signaling in N-WASP knockout B cells is concurrent with increased accumulation of F-actin at the B-cell surface, enhanced B-cell spreading on the antigen-presenting membrane, delayed B-cell contraction, inhibition in the merger of signaling active BCR microclusters into signaling inactive central clusters, and a blockage of BCR internalization. Upon BCR activation, WASP is activated first, followed by N-WASP in mouse and human primary B cells. The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced WASP activation, and is restored by the activation of SH2 domain-containing inositol 5-phosphatase that inhibits WASP activation. Our results reveal a new mechanism for the negative regulation of BCR signaling and broadly suggest an actin-mediated mechanism for signaling down-regulation