Some Contributions to the Class of Two-Sex Branching Processes Depending on the Number of Couples in the Population

2000 Mathematics Subject Classification: 60J80We consider the class of two-sex branching processes with offspring and mating depending on the number of couples in the population introduced in Molina et al. (2008). In addition to its theoretical interest, this class also has clear practical implications, especially in population dynamics. We investigate its extinction probability and limiting behavior. By considering different probabilistic approaches, necessary and sufficient conditions for its almost sure extinction are determined. Assuming the nonextinction, some limiting results are derived.This research has been supported by the Ministerio de Ciencia e Innovaci´on of Spain, the Junta de Extremadura, and the FEDER (grants MTM2009-13248 and GR10118) and by the Natural Sciences Foundation of China (grant 10971048)

Free vibration analysis for wind turbine structure by component mode synthesis method

Based on free interface component modal synthesis method, the free vibration behavior of wind turbine structures is investigated. The wind turbine structure is divided into three parts including tower, wheel hub-cabin and rotor. The tower is modeled as an isotropic metal cantilever beam, the blade as thin-walled composite beam and the wheel hub-cabin as a rigid body due to its large extensional stiffness, bending stiffness and torsion stiffness compared with tower and blades. The displacements of the blades are described by thin-walled composite beam theory. Galerkin’s method is used to discretize blades and tower. Employing Lagrange method, the motion equations of blades are derived and then stiffness and mass matrices are obtained. The natural frequencies and mode shapes of the wind turbine structure are predicted by numerical simulations. Numerical results using the present model are validated by ANSYS software results

Comprehensive profiling of rhizome-associated alternative splicing and alternative polyadenylation in moso bamboo (Phyllostachys edulis).

Moso bamboo (Phyllostachys edulis) represents one of the fastest-spreading plants in the world, due in part to its well-developed rhizome system. However, the post-transcriptional mechanism for the development of the rhizome system in bamboo has not been comprehensively studied. We therefore used a combination of single-molecule long-read sequencing technology and polyadenylation site sequencing (PAS-seq) to re-annotate the bamboo genome, and identify genome-wide alternative splicing (AS) and alternative polyadenylation (APA) in the rhizome system. In total, 145 522 mapped full-length non-chimeric (FLNC) reads were analyzed, resulting in the correction of 2241 mis-annotated genes and the identification of 8091 previously unannotated loci. Notably, more than 42 280 distinct splicing isoforms were derived from 128 667 intron-containing full-length FLNC reads, including a large number of AS events associated with rhizome systems. In addition, we characterized 25 069 polyadenylation sites from 11 450 genes, 6311 of which have APA sites. Further analysis of intronic polyadenylation revealed that LTR/Gypsy and LTR/Copia were two major transposable elements within the intronic polyadenylation region. Furthermore, this study provided a quantitative atlas of poly(A) usage. Several hundred differential poly(A) sites in the rhizome-root system were identified. Taken together, these results suggest that post-transcriptional regulation may potentially have a vital role in the underground rhizome-root system

Liquiritin alleviates spinal cord injury through suppression of inflammation, oxidative stress, and cell apoptosis in a rat model

Purpose: Liquiritin is an extract from Glycyrrhiza Radix, one of the oldest traditional Chinese herbal medicines, which is commonly used to treat various injuries and swellings. This study is aimed to determine whether liquiritin can protect spinal cord injuries (SCIs) from secondary injuries. Methods: A rat SCI model was established. After liquiritin treatment, the neural-function of Rats was determined by Basso, Beattie and Bresnahan (BBB) scores, paw withdrawal threshold (PWT), and thermal withdrawal latency (PWL). The effects of anti-inflammation, anti-oxidation, and anti-apoptosis of liquiritin were also examined in the rats with SCI. Moreover, the activities of several signaling elements, such as, inflammation-associated nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), toll-like receptor 4 (TLR4), proliferative-related p38 mitogen-activated protein kinases (MAPK) and myeloid differentiation primary response 88 (MyD88) which was involved in the TLR4 signaling, were used for further investigation of the underlying molecular mechanisms. Results: Liquiritin improved locomotor function recovery, alleviated allodynia and hyperalgesia, and decreased water content of spinal cord in SCI rats. Also, liquiritin reduced SCI–induced inflammatory responses by decreasing the levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and IL-6. Liquiritin inhibited SCI–induced oxidative stress by decreasing malondialdehyde (MDA) level and increasing the levels of uperoxide dismutase (SOD) (p < 0.05), glutathione (GSH) (p < 0.01), and GSH-PX (p < 0.001). In addition, liquiritin alleviated spinal cord injury (SCI) –induced apoptosis of neural cells by decreasing the expression of cleaved caspase-9, -3 and cleaved poly ADP-ribose polymerase (PARP). Finally, liquiritin decreased spinal cord injury (SCI) -induced up-regulation of TLR4/MyD88/NF-κB and p38 MAPK signaling cascades. Conclusion: Liquiritin exerts protective role in SCI by reducing excessive inflammation, suppressing oxidative stress, and inhibiting neural cell apoptosis in a rat model of SCI. Thus, the agent can potentially be used for the management of SC

An analytical model for flutter behavior of composite panels with shape memory alloy fibers

An analytical model for predicting the effect of shape memory alloys (SMA) on the flutter behavior of composite panels is developed in the frequency and time domains. The laminated plate theory and piston theory are employed to model the aeroelastic response of the composite panels to aerodynamic loads. A thermo-mechanical constitutive equation of SMA proposed by Brinson et al. is used to calculate the recovery stress of the constrained SMA fibers. The approximate solution is obtained for supersonic flutter analysis of the composite panels based on the Galerkin approach. The parametric study is carried out to display the effect of the actuation temperature, volume fraction, the initial strain of SMA fibers and the length to width ratio of the panels on flutter boundaries

Chronically KIT-Stimulated Clonally-Derived Human Mast Cells Show Heterogeneity in Different Tissue Microenvironments

Human mast cell precursors arise in the bone marrow and circulate to different tissue microenvironments, where they develop distinct phenotypes that may be characterized by differential expression of the serine protease, chymase. The growth and development of mast cells is stimulated by mast cell growth factor, which is also known as kit ligand because its obligate receptor is KIT, the protein product of the c-KIT proto-oncogene. The in vivo influence of the KIT-kit ligand axis on the phenotype of human mast cells has not been determined. We used immunohistochemistry to detect in situ expression of tryptase and chymase by mast cells of a patient with urticaria pigmentosa and aggressive systemic mastocytosis, whose pathologic mast cells are clonally derived and chronically stimulated by KIT because they all contain the same point mutation causing constitutive activation of KIT. Mast cells in both spleen and skin expressed tryptase, but only in the skin did a majority of mast cells express chymase. We conclude that chronic stimulation of the KIT-kit ligand axis does not irrevocably commit mast cells to a chymase-positive or chymase-negative phenotype. These findings suggest that factors other than kit ligand predominate in determining mast cell phenotype