A new generation of sodium chloride porogen for tissue engineering

Porogen leaching is a widely used and simple technique for the creation of porous scaffolds in tissue engineering. Sodium chloride (NaCl) is the most commonly used porogen, but the current grinding and sieving methods generate salt particles with huge size variations and cannot generate porogens in the submicron size range. We have developed a facile method based on the principles of crystallization to precisely control salt crystal sizes down to a few microns within a narrow size distribution. The resulting NaCl crystal size could be controlled through the solution concentration, crystallization temperature, and crystallization time. A reduction in solution temperature, longer crystallization times, and an increase in salt concentration resulted in an increase in NaCl crystal sizes due to the lowered solubility of the salt solution. The nucleation and crystallization technique provides superior control over the resulting NaCl size distribution (13.78 ± 1.18 μm), whereas the traditional grinding and sieving methods produced NaCl porogens 13.89 ± 12.49 μm in size. The resulting NaCl porogens were used to fabricate scaffolds with increased interconnectivity, porous microchanneled scaffolds, and multiphasic vascular grafts. This new generation of salt porogen provides great freedom in designing versatile scaffolds for various tissue-engineering applications.     

心得安对实验性心肌梗塞大鼠心肌膜β受体的影响

本文采用受体放射自显影术,以银粒数的分布与数量变化作为观察指标,对β受体阻滞剂心得安治疗实验性急性心肌梗塞(AMI)大鼠的心肌膜β肾上腺素能受体(β受体)的影响进行研究.左冠状动脉前降支(LAD)结扎后一周引起心肌梗塞区内[3H]DHA结合位点数显著降低,在非梗塞区亦降低.结扎LAD应用心得安(100ug/kg)治疗一周后梗塞区[3H]DHA结合位点数明显回升,而非梗塞区则进一步降低.引人注目的是,心得安治疗后,[3H]DHA结合位点数在梗塞区/非梗塞区的比值由LAD结扎时的0.24上升为0.87,接近于假手术对照组的0.97.结果证明,心得安是直接作用于心脏的β受体,可能还通过调整了梗塞区与非梗塞区β受体的平衡,改善了心室的顺应性和提高了梗塞心脏的收缩协同作用.从而对AMI的心脏起到保护和治疗作用.     

A MAP Kinase Dependent Feedback Mechanism Controls Rho1 GTPase and Actin Distribution in Yeast

In the yeast Saccharomyces cerevisiae the guanosine triphosphatase (GTPase) Rho1 controls actin polarization and cell wall expansion. When cells are exposed to various environmental stresses that perturb the cell wall, Rho1 activates Pkc1, a mammalian Protein Kinase C homologue, and Mpk1, a mitogen activated protein kinase (MAPK), resulting in actin depolarization and cell wall remodeling. In this study, we demonstrate a novel feedback loop in this Rho1-mediated Pkc1-MAPK pathway that involves regulation of Rom2, the guanine nucleotide exchange factor of Rho1, by Mpk1, the end kinase of the pathway. This previously unrecognized Mpk1-depedent feedback is a critical step in regulating Rho1 function. Activation of this feedback mechanism is responsible for redistribution of Rom2 and cell wall synthesis activity from the bud to cell periphery under stress conditions. It is also required for terminating Rho1 activity toward the Pkc1-MAPK pathway and for repolarizing actin cytoskeleton and restoring growth after the stressed cells become adapted.     

Adaptive Evolution and the Birth of CTCF Binding Sites in the Drosophila Genome

Changes in the physical interaction between cis-regulatory DNA sequences and proteins drive the evolution of gene expression. However, it has proven difficult to accurately quantify evolutionary rates of such binding change or to estimate the relative effects of selection and drift in shaping the binding evolution. Here we examine the genome-wide binding of CTCF in four species of Drosophila separated by between ∼2.5 and 25 million years. CTCF is a highly conserved protein known to be associated with insulator sequences in the genomes of human and Drosophila. Although the binding preference for CTCF is highly conserved, we find that CTCF binding itself is highly evolutionarily dynamic and has adaptively evolved. Between species, binding divergence increased linearly with evolutionary distance, and CTCF binding profiles are diverging rapidly at the rate of 2.22% per million years (Myr). At least 89 new CTCF binding sites have originated in the Drosophila melanogaster genome since the most recent common ancestor with Drosophila simulans. Comparing these data to genome sequence data from 37 different strains of Drosophila melanogaster, we detected signatures of selection in both newly gained and evolutionarily conserved binding sites. Newly evolved CTCF binding sites show a significantly stronger signature for positive selection than older sites. Comparative gene expression profiling revealed that expression divergence of genes adjacent to CTCF binding site is significantly associated with the gain and loss of CTCF binding. Further, the birth of new genes is associated with the birth of new CTCF binding sites. Our data indicate that binding of Drosophila CTCF protein has evolved under natural selection, and CTCF binding evolution has shaped both the evolution of gene expression and genome evolution during the birth of new genes.     

Induction of priming by cold stress via inducible volatile cues in neighboring tea plants

Plants have evolved sophisticated defense mechanisms to overcome their sessile nature. However, if and how volatiles from cold‐stressed plants can trigger interplant communication is still unknown. Here, we provide the first evidence for interplant communication via inducible volatiles in cold stress. The volatiles, including nerolidol, geraniol, linalool, and methyl salicylate, emitted from cold‐stressed tea plants play key role(s) in priming cold tolerance of their neighbors via a C‐repeat‐binding factors‐dependent pathway. The knowledge will help us to understand how plants respond to volatile cues in cold stress and agricultural ecosystems.