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Spatial memory is significant in modeling animal movement. For a diffusive consumer-resource model, a memory-based diffusion of consumer can result in richer and more realistic dynamics. In fact, memory-based diffusion is related to the resource distributions in past times because the memory decays over time. We originally propose a consumer-resource model with distributed memory, and then investigate the influence of the weak memory kernel on the stability of the positive constant steady state. When the memory-based diffusion coefficient is negative, the mean delay does not affect the stability of the positive constant steady state; however, when the memory-based diffusion coefficient is positive, the mean delay can lead to the spatially inhomogeneous periodic oscillation patterns. The direction and stability of Turing bifurcation induced by the memory-based diffusion coefficient are calculated by using the methods of Crandall and Rabinowitz, and the direction and stability of Hopf bifurcation induced by the mean delay are determined by the normal form theory. • Propose a consumer-resource model with distributed memory. • Investigate the influence of the mean delay on the stability of positive constant steady state. • Find the stability induced by the average delay. • Investigate the properties of Turing bifurcation and derive the normal form associated with the Hopf bifurcation. [ABSTRACT FROM AUTHOR]

The limited cardiomyocyte proliferation is insufficient for repair of the myocardium. Therefore, activating cardiomyocyte proliferation might be a reasonable option for myocardial regeneration. Here, we investigated effect of retinoic acid (RA) on inducing adult cardiomyocyte proliferation and assessed efficacy of self-assembling peptide (SAP)-released RA in activating regeneration of the infarcted myocardium. Effect of RA on inducing cardiomyocyte proliferation was examined with the isolated cardiomyocytes. Expression of the cell cycle-associated genes and paracrine factors in the infarcted myocardium was examined at one week after treatment with SAP-carried RA. Cardiomyocyte proliferation, myocardial regeneration and improvement of cardiac function were assessed at four weeks after treatment. In the adult rat myocardium, expression of RA synthetase gene Raldh2 and RA concentration were decreased significantly. After treatment with RA, the proliferated cardiomyocytes were increased. The formulated SAP could sustainedly release RA. After treatment with SAP-carried RA, expression of the pro-proliferative genes in cell cycle and paracrine factors in the infarcted myocardium were up-regulated. Myocardial regeneration was enhanced, and cardiac function was improved significantly. These results demonstrate that RA can induce adult cardiomyocytes to proliferate effectively. The sustained release of RA with SAP is a promise strategy to enhance repair of the infarcted myocardium. [Display omitted] • Synthesis of retinoic acid in adult myocardium is decreased. • Retinoic acid can induce proliferation of adult cardiomyocytes. • Sustained release of retinoic acid is effective for repair of the infarcted myocardium. [ABSTRACT FROM AUTHOR]

We consider a directed polymer model in dimension 1 + 1 , where the disorder is given by the occupation field of a Poisson system of independent random walks on Z. In a suitable continuum and weak disorder limit, we show that the family of quenched partition functions of the directed polymer converges to the Stratonovich solution of a multiplicative stochastic heat equation (SHE) with a Gaussian noise, whose space-time covariance is given by the heat kernel. In contrast to the case with space-time white noise where the solution of the SHE admits a Wiener-Itô chaos expansion, we establish an L 1 -convergent chaos expansions of iterated integrals generated by Picard iterations. Using this expansion and its discrete counterpart for the polymer partition functions, the convergence of the terms in the expansion is proved via functional analytic arguments and heat kernel estimates. The Poisson random walk system is amenable to careful moment analysis, which is an important input to our arguments. [ABSTRACT FROM AUTHOR]

Regions affected by heavy metal contamination frequently encounter phosphorus (P) deficiency. Numerous studies highlight crucial role of P in facilitating cadmium (Cd) accumulation in woody plants. However, the regulatory mechanism by which P affects Cd accumulation in roots remains ambiguous. This study aims to investigate the effects of phosphorus (P) deficiency on Cd accumulation, Cd subcellular distribution, and cell wall components in the roots of Salix caprea under Cd stress. The results revealed that under P deficiency conditions, there was a 35.4% elevation in Cd content in roots, coupled with a 60.1% reduction in Cd content in shoots, compared to the P sufficiency conditions. Under deficient P conditions, the predominant response of roots to Cd exposure was the increased sequestration of Cd in root cell walls. The sequestration of Cd in root cell walls increased from 37.1% under sufficient P conditions to 66.7% under P deficiency, with pectin identified as the primary Cd binding site under both P conditions. Among cell wall components, P deficiency led to a significant 31.7% increase in Cd content within pectin compared to P sufficiency conditions, but did not change the pectin content. Notably, P deficiency significantly increased pectin methylesterase (PME) activity by regulating the expression of PME and PMEI genes, leading to a 10.4% reduction in the degree of pectin methylesterification. This may elucidate the absence of significant changes in pectin content under P deficiency conditions and the concurrent increase in Cd accumulation in pectin. Fourier transform infrared spectroscopy (FTIR) results indicated an increase in carboxyl groups in the root cell walls under P deficiency compared to sufficient P treatment. The results provide deep insights into the mechanisms of higher Cd accumulation in root mediated by P deficiency. [Display omitted] • Phosphorus (P) deficiency increases cadmium (Cd) accumulation in roots but inhibits translocation to shoots. • P deficiency increases Cd deposition in root cell walls. • Cd primarily binds to pectin in root cell walls. • P deficiency promotes pectin demethylesterification in root cell walls. [ABSTRACT FROM AUTHOR]