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Running bamboos are a group of clonal plants exhibiting rapid and widespread expansion. They possess two root subsystems, arising from different shoot parts, culm roots and rhizome roots. To date, it remains unclear what the functional differences are between the two root subsystems and what their relation is to the remarkably competitive ability of running bamboos.A typical running bamboo, Phyllostachys glauca, which dominates in a highly heterogeneous habitat of limestone hills, was sampled to compare the morphology, architecture, anatomy, chemical composition, mechanics and nutrient acquisition of the two root subsystems to explore their differences in functional traits.Compared with rhizome roots, culm roots possessed greater tensile strength, modulus of elasticity, stele diameter to root diameter ratio, root tissue density, root length density, rooting depth, basal diameter of shoot‐borne roots and more lignified cells. Culm roots also had a higher phosphorus (P) concentration (>0.4 mg g−1), which was nearly twice that of rhizome roots. By contrast, rhizome roots exhibited a greater specific root area, specific root length, cortex thickness to root radius ratio, total branch order and greater P‐uptake capacity than culm roots.Our findings revealed distinct differences in functional traits between culm roots and rhizome roots in P. glauca. Culm roots are considered to primarily provide anchorage, but also function in resource acquisition and nutrient storage, while rhizome roots mainly play a role in resource acquisition. Except for the anchorage and resource acquisition of culm roots, the extra resource acquisition by rhizome roots and the high concentration of a limiting nutrient (P) in culm roots enhance the performance in a highly heterogeneous habitat which offers a physiological explanation for P. glauca dominating on limestone hills.The functional differentiation between culm roots and rhizome roots provides insight into the mechanism underpinning the remarkable expansion of running bamboos and offers a new perspective to explain the strong competitive ability of clonal plants with dimorphic roots. Read the free Plain Language Summary for this article on the Journal blog. [ABSTRACT FROM AUTHOR]

In the paper, Poisson-Gamma mixture process is first brought forward, which is dynamically expanded from the well-known Poisson-Gamma mixture model. Some properties on Poisson-Gamma mixture process are presented, including the distribution of increment, Markov property, infinitesimal generator, joint density function of jump/waiting times, and the limit distribution of compound Poisson-Gamma mixture process, etc., which provide a thorough grounding in application of Poisson-Gamma mixture process. At last, some premium calculation principles are presented to show the application of Poisson-Gamma mixture process, which include expected value premium, stop-loss premium, mean-variance premium, and exponential premium. [ABSTRACT FROM AUTHOR]

Introduction: Our previous studies have demonstrated advanced glycation end products (AGEs) was an important mediator in osteoarthritis (OA) which may induce mitochondrial dysfunction. AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1), and its downstream target peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) are the critical sensors that regulate mitochondrial biogenesis and have been recognized as therapeutic targets in OA. This study was designed to test whether AGEs caused mitochondrial dysfunction through modulation of AMPKα/SIRT1/PGC-1α. Methods: We knocked down or overexpressed AMPKα, SIRT1, and PGC-1α by small interfering RNA or plasmid DNA transfection, respectively. Mitochondrial membrane potential (△Ψ) was detected by tetraethylbenzimidazolyl carbocyanine iodide (JC-1) fluorescence probe. Results: The results showed that AGEs impaired △Ψ, intracellular ATP level, and mitochondrial DNA content, linked to decreased AMPKα, SIRT1, and PGC-1α expression in chondrocyte. AMPKα pharmacologic activation or overexpression of AMPKα, SIRT1, and PGC-1α reversed impairments of mitochondrial biogenesis, oxidative stress, and inflammation in AGEs-induced chondrocytes. However, AMPKα activation using AICAR had decreased capacity to increase each of those same effect readouts in AGEs-treated SIRT1-siRNA or PGC-1α-siRNA chondrocyte. Conclusion: Taken together, AGEs reduced the AMPKα/SIRT1/PGC-1α signaling in chondrocytes, leading to mitochondrial dysfunction as a result of increased oxidative stress, inflammation, and apoptosis. These results indicated that target AMPK may be as a novel therapeutic strategy for AGEs-related OA prevention. [ABSTRACT FROM AUTHOR]

In this study, using the method of discounting the terminal expectation value into its initial value, the pricing formulas for European options are obtained under the assumptions that the financial market is risk-aversive, the risk measure is standard deviation, and the price process of underlying asset follows a geometric Brownian motion. In particular, assuming the option writer does not need the risk compensation in a risk-neutral market, then the obtained results are degenerated into the famous Black–Scholes model (1973); furthermore, the obtained results need much weaker conditions than those of the Black–Scholes model. As a by-product, the obtained results show that the value of European option depends on the drift coefficient μ of its underlying asset, which does not display in the Black–Scholes model only because μ = r in a risk-neutral market according to the no-arbitrage opportunity principle. At last, empirical analyses on Shanghai 50 ETF options and S&P 500 options show that the fitting effect of obtained pricing formulas is superior to that of the Black–Scholes model. [ABSTRACT FROM AUTHOR]

Aim: The present study was performed to investigate the effect of Aesculus hippocastanum (AH; Venoplant®) on concanavalin A (ConA)-induced acute liver injury and explore the mechanism in mice. Methods: ConA (20 mg/kg) was administered via tail vein injection to induce hepatic damage. The groups of AH (Venoplant®) were given at 65.8, 131.6, and 263.2 mg/kg by oral gavages for 20 days. The serum levels of aspartate transaminase (AST), alanine aminotransferase (ALT), total protein (TP), and albumin (Alb) were determined by automatic biochemical analyzer, and the Alb/globulin (A/G) ratio was calculated. Tumor necrosis factor-α (TNF-α) and IFN-γ levels were assayed by enzyme-linked immunosorbent assay. The liver tissue was attained by hematoxylin and eosin, and the histopathological changes were calculated. The cell apoptosis was assayed by terminal dUTP nick-end labeling. The malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) content of liver tissue were assayed by related kits. The activity of caspase-3 was detected by spectrophotometry. The expressions of cytochrome c, Bax, Bcl-2, c-Jun N-terminal kinase (JNK), and p-JNK were detected by western blot. Results: The results showed that the levels of ALT, AST, IFN-γ, and TNF-α in AH (Venoplant®) groups were significantly lower than those in ConA-injured group, while the levels of TP, Alb, and A/G were significantly higher. The SOD and GSH levels were significantly increased, and the MDA level was decreased; liver histopathology was changed consistently with the serological indicators, AH (Venoplant®) treatment significantly reduced the pathological damage and cell apoptosis; while in AH (Venoplant®) group, the expressions of cytochrome c, caspase-3, Bax/Bcl-2 ratio, and p-JNK were significantly decreased. Conclusion: AH (Venoplant®) could significantly protect the ConA-induced acute liver injury in mice via inhibition of reactive oxygen species and JNK pathway. [ABSTRACT FROM AUTHOR]

Aims: Recent studies have reported that intracellular calcium (Ca2+) mobilization is involved in homocysteine (Hcy)-induced endothelial dysfunction and the Na+/H+ exchanger (NHE) is responsible for an increase in the intracellular Ca2+ concentration in cardiovascular disease. We hypothesized that inhibition of the NHE had protective effects on Hcy-induced endothelial dysfunction. Methods: Acetylcholine-induced endothelium-dependent relaxation (EDR) and biochemical parameters were measured in the rat isolated aorta. The level of reactive oxygen species (ROS) was designed by a specific fluorescent probe. The phosphorylation of the nuclear factor-κB (NF-κB) system was studied by Western blot. Results: Cariporide significantly prevented Hcy-impaired EDR and increased nitric oxide (NO) release; endothelial NO synthase activity simultaneously decreased ROS production. We also found that cariporide blocked Hcy-induced NF-κB activation and inhibitor-κB degradation, thus inhibiting the production of tumor necrosis factor-α and intercellular adhesion molecule-1. Conclusions: The mechanisms of protective effects of cariporide may be related to the inhibition of NHE and the decrease in oxidative stress and inflammatory injury. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aims: The association between diabetes and neointimal expansion after vascular injury has been attributed to the accumulation of advanced glycation end products (AGEs). Here we investigated the inhibitory effect of cariporide, a specific Na+/H+ exchanger 1 blocker, on neointimal proliferation induced by AGEs in a balloon injury model. Methods: Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP) was monitored by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. The level of reactive oxygen species (ROS) was determined by specific fluorescent probe. The phosphorylation of the nuclear factor-ĸB (NF-ĸB) system was studied by Western blot. Results: Cariporide significantly suppressed AGE-induced neointimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation, COX-2, MMP-2 and MMP-9 expression. In addition, cariporide decreased AGE-induced ROS, malondiadehyde level and increased the superoxide dismutase and glutathione peroxidase activity. We also found that cariporide blocked AGE-induced NF-ĸB activation and inhibitor-ĸB degradation. Conclusions: The results indicated that cariporide inhibited AGE-induced neointimal formation by suppressing the VSMC proliferation and the up-regulation of COX-2, MMP-2, MMP-9 via inhibiting ROS and NF-ĸB activation. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aims: Accumulation of advanced glycation end products (AGEs) plays a pivotal role in the mechanism by which aging contributes to osteoarthritis (OA). In the present study, we examined the effect of curcumin, a pharmacologically safe phytochemical agent, on AGE-induced tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-13 (MMP-13) in rabbit chondrocytes. Methods: Chondrocytes were derived from rabbit articular cartilage by enzymatic digestion. TNF-α and MMP-13 mRNA was monitored by RT-PCR. TNF-α protein was determined using cytokine-specific ELISA. The reactive oxygen species was determined by the fluorescent probe 29,79-dichlorofluorescein diacetate. The phosphorylation and nuclear translocation of the nuclear factor-ĸB (NF-ĸB) system were studied by Western blot and immunofluorescence respectively. Results: Curcumin significantly decreased AGE-stimulated TNF-α and MMP-13 mRNA and suppressed the NF-ĸB activation via inhibition of ĸBα (I-ĸBα) phosphorylation, I-ĸBα degradation and p65 nuclear translocation. Conclusions: These novel pharmacological actions of curcumin on AGE-stimulated chondrocytes provide new suggestions that curcumin has nutritional potential as a naturally occurring anti-inflammatory agent for treating OA. [ABSTRACT FROM AUTHOR]

Abstract: In this present study, we examined the role of Na+/H+ exchanger 1 (NHE1) in the cultured rat vascular smooth muscle cell (VSMC) proliferation induced by advanced glycation end products (AGEs). AGEs significantly increased the [3H] thymidine incorporation of VSMC. Cariporide, an NHE1 inhibitor, dose-dependently attenuated the AGEs-induced increase in cell DNA synthesis. Thus the effect of AGEs on NHE1 activity was next examined. The cariporide-dependent intracellular pH (pHi) was significantly increased after 24h exposure to AGEs (10μg/ml). The direct AGEs-induced NHE1 activation was measured by the Na+-dependent intracellular pH recovery from intracellular acidosis. AGEs can increase the NHE1 activity in a time- and concentration-dependent manner. Inhibition of either the receptor for AGEs (RAGE) by anti-RAGE or mitogen-activated protein kinases (MAPK) by PD98059 reversed the effect of AGEs on NHE1 activity. Reverse transcription (RT)-PCR analysis revealed that AGEs dose-dependently increased NHE1 mRNA at 24h. These findings demonstrate NHE1 is required for in AGEs-induced proliferation of VSMC, and AGEs increase NHE1 activity via the MAPK pathway. [Copyright &y& Elsevier]

Great efforts have been devoted to two-sided exponentially weighted moving average (EWMA) control charts, while less attention has been paid to one-sided EWMA charts. This article proposes an improved one-sided EWMA chart (IEWMA) for rapid detection of upward or downward changes in the process mean. The basic idea is to accumulate positive (or negative) observations only and reset negative (or positive) observations to zero in the iterative computation of the EWMA estimate for the purpose of quickly catching the upward (or downward) change in the process mean. The comparison result of the IEWMA chart with other control charts favors the former. [ABSTRACT FROM AUTHOR]

By means of Liapunov's direct method coupled with Razumikhin technique some sufficient conditions for (uniform, uniform and globally asymptotic, uniformly globally asymptotic, and globally exponential) p-moment stability of the zero solution of functional differential equations with random impulses are presented, where the parameter λ(t) in (dV(t, x(t)))/dt is not required to be negative definite. Thus the obtained results are convenient to apply. [Copyright &y& Elsevier]

Abstract: The model of second-order linear differential systems with random impulses is brought forward in this paper. Then, necessary and sufficient conditions for oscillation in mean, p-moment stability and p-moment boundedness are obtained by several theorems that compare solutions of this system with the corresponding nonimpulsive differential system. At last, an example is presented to show the application of obtained results. [Copyright &y& Elsevier]

In the paper, p-moment stability of stochastic differential equations with jumps is considered. First, some preliminary notes are given. Then, several theorems on p-moment stability of these equations are established using Liapunov function. At last, an example is present to show application of the obtained results. [Copyright &y& Elsevier]

Through the use of the so-called variational Lyapunov method, which is developed by combining the method of variation of parameters and the Lyapunov second method, stability and instability properties in terms of two measures for impulsive differential equations with variable moments of impulsive effects are discussed. Some stability and instability criteria are established. These theorems, together with an example, show that perturbation and impulsive effects may make a stable system uniformly asymptotically stable or unstable. These results significantly generalize the known ones. [ABSTRACT FROM PUBLISHER]

Aims: The association between diabetes and neointimal expansion after vascular injury has been attributed to the accumulation of advanced glycation end products (AGEs). Here we investigated the inhibitory effect of cariporide, a specific Na(+)/H(+) exchanger 1 blocker, on neointimal proliferation induced by AGEs in a balloon injury model., Methods: Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP) was monitored by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. The level of reactive oxygen species (ROS) was determined by specific fluorescent probe. The phosphorylation of the nuclear factor-ĸB (NF-ĸB) system was studied by Western blot., Results: Cariporide significantly suppressed AGE-induced neointimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation, COX-2, MMP-2 and MMP-9 expression. In addition, cariporide decreased AGE-induced ROS, malondiadehyde level and increased the superoxide dismutase and glutathione peroxidase activity. We also found that cariporide blocked AGE-induced NF-ĸB activation and inhibitor-ĸB degradation., Conclusions: The results indicated that cariporide inhibited AGE-induced neointimal formation by suppressing the VSMC proliferation and the up-regulation of COX-2, MMP-2, MMP-9 via inhibiting ROS and NF-ĸB activation., (Copyright © 2013 S. Karger AG, Basel.)

Aims: Recent studies have reported that intracellular calcium (Ca(2+)) mobilization is involved in homocysteine (Hcy)-induced endothelial dysfunction and the Na(+)/H(+) exchanger (NHE) is responsible for an increase in the intracellular Ca(2+) concentration in cardiovascular disease. We hypothesized that inhibition of the NHE had protective effects on Hcy-induced endothelial dysfunction., Methods: Acetylcholine-induced endothelium-dependent relaxation (EDR) and biochemical parameters were measured in the rat isolated aorta. The level of reactive oxygen species (ROS) was designed by a specific fluorescent probe. The phosphorylation of the nuclear factor-κB (NF-κB) system was studied by Western blot., Results: Cariporide significantly prevented Hcy-impaired EDR and increased nitric oxide (NO) release; endothelial NO synthase activity simultaneously decreased ROS production. We also found that cariporide blocked Hcy-induced NF-κB activation and inhibitor-κB degradation, thus inhibiting the production of tumor necrosis factor-α and intercellular adhesion molecule-1., Conclusions: The mechanisms of protective effects of cariporide may be related to the inhibition of NHE and the decrease in oxidative stress and inflammatory injury.

We investigated the effect of paraoxon on vascular contractility using organ baths in thoracic aortic rings of rabbits and examined the effect of paraoxon on calcium homeostasis using a whole-cell patch-clamp technique in isolated aortic smooth muscle cells of rabbits. The findings show that administration of paraoxon (30 microM) attenuated thoracic aorta contraction induced by phenylephrine (1 microM) and/or a high K+ environment (80 mM) in both the presence and absence of thoracic aortic endothelium. This inhibitory effect of paraoxon on vasoconstrictor-induced contraction was abolished in the absence of extracellular Ca2+, or in the presence of the Ca2+ channel inhibitor, verapamil. But atropine had little effect on the inhibitory effect of paraoxon on phenylephrine-induced contraction. Paraoxon also attenuated vascular smooth muscle contraction induced by the cumulative addition of CaCl2 and attenuated an increase of intracellular Ca2+ concentration induced by K+ in vascular smooth muscle cells. Moreover, paraoxon (30 microM) inhibited significantly L-type calcium current in isolated aortic smooth muscle cells of rabbits. In conclusion, our results demonstrate that paraoxon attenuates vasoconstrictor-induced contraction through inhibiting Ca2+ influx in the rabbits thoracic aorta.

In this present study, we examined the role of Na(+)/H(+) exchanger 1 (NHE1) in the cultured rat vascular smooth muscle cell (VSMC) proliferation induced by advanced glycation end products (AGEs). AGEs significantly increased the [(3)H] thymidine incorporation of VSMC. Cariporide, an NHE1 inhibitor, dose-dependently attenuated the AGEs-induced increase in cell DNA synthesis. Thus the effect of AGEs on NHE1 activity was next examined. The cariporide-dependent intracellular pH (pH(i)) was significantly increased after 24h exposure to AGEs (10mug/ml). The direct AGEs-induced NHE1 activation was measured by the Na(+)-dependent intracellular pH recovery from intracellular acidosis. AGEs can increase the NHE1 activity in a time- and concentration-dependent manner. Inhibition of either the receptor for AGEs (RAGE) by anti-RAGE or mitogen-activated protein kinases (MAPK) by PD98059 reversed the effect of AGEs on NHE1 activity. Reverse transcription (RT)-PCR analysis revealed that AGEs dose-dependently increased NHE1 mRNA at 24h. These findings demonstrate NHE1 is required for in AGEs-induced proliferation of VSMC, and AGEs increase NHE1 activity via the MAPK pathway.