Adventitious roots are a post-embryonic root which arise from the stem and leaves and from non-pericycle tissues in old roots and it is one of the most important ways of vegetative propagation in plants. Many exogenous and endogenous factors regulate the formation of adventitious roots, such as Ca 2+ , sugars, auxin, polyamines, ethylene, nitric oxide, hydrogen peroxide, carbon monoxide, cGMP, MAPKs and peroxidase, etc. These mediators are thought to function as signaling and mediate auxin signal transduction during the formation of adventitious roots. To date, only a few genes have been identified that are associated with the general process of adventitious rooting, such as ARL1, VvPRP1, VvPRP2, HRGPnt3, LRP1 and RML, etc. Auxin has been shown to be intimately involved in the process of adventitious rooting and function as crucial role in adventitious rooting. Great progress has been made in elucidating the auxin-induced genes and auxin signaling pathway, especially in auxin response Aux/IAA and ARF genes family and the auxin receptor TIR1. Although, some of important aspects of adventitious rooting signaling have been revealed, the intricate signaling network remains poorly understood.

This article provides an overview of existing literature on the ultraviolet-B (UV-B) radiation effects on algae and cyanobacteria. We report on the effects of UV-B radiation to the growth and development, biomass, sensitivity, photosynthetic pigments, UV-B absorbing compounds, photosynthesis, protein and DNA damage, enzyme activity, nitrogen fixation and assimilation of nitrogen, protective mechanisms of algae and cyanobacteria, the accommodation of algae and cyanobacteria to environmental stress, and the effects to ecology system. Many of the studies show the dramatic effects of UV-B radiation; but typically these studies were conducted under conditions with supplemental UV-B irradiance that was higher than would ever occur outside experimental conditions or natural condition. A few of the studies reviewed used experimental conditions and supplemental UV-B irradiance that approached realism. Enhanced UV-B generally decreased chlorophyll content, whereas it increased UV-B absorbing compounds in many algae. Decrease in photosynthesis, particularly at higher UV-B doses, was due to both direct (effect on photosystem) and indirect (decrease in pigments) effects. The decreases in chlorophyll pigments and photosynthesis resulted in lower biomass. However, algae and cyanobacteria have evolved various avoidance and repair mechanisms to protect themselves against the damaging effects of UV radiation to acclimate to enhanced UV-B radiation. The review points to areas where further studies on the relationships among nitrogenase, Rubisco, antioxidase activity, signal, antioxidants, and free radicals under enhanced UV-B are needed to quantify the effects of UV-B radiation on algae and cyanobacteria. These studies are needed in order to develop dose response functions that can facilitate development of dynamic simulation models for use in UV-B and other environmental impact assessments.

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Background/Aims: Acute myocardial infarction (AMI) is a devastating cardiovascular disease with a high rate of morbidity and mortality, partly due to enhanced arrhythmogenicity. MicroRNAs (miRNAs) have been shown to participate in the regulation of cardiac ion channels and the associated arrhythmias. The purpose of this study was to test our hypothesis that miR-223-3p contributes to the electrical disorders in AMI via modulating KCND2, the gene encoding voltage-gated channel Kv4.2 that carries transient outward K⁺ current I_to. Methods: AMI model was established in male Sprague-Dawley (SD) rats by left anterior descending artery (LAD) ligation. Evans blue and TTC staining was used to measure infarct area. I_to was recorded in isolated ventricular cardiomyocytes or cultured neonatal rat ventricular cells (NRVCs) by whole-cell patch-clamp techniques. Western blot analysis was employed to detect the protein level of Kv4.2 and real-time RT-PCR to determine the transcript level of miR-223-3p. Luciferase assay was used to examine the interaction between miR-223-3p and KCND2 in cultured NRVCs. Results: Expression of miR-223-3p was remarkably upregulated in AMI relative to sham control rats. On the contrary, the protein level of Kv4.2 and I_to density were significantly decreased in AMI. Consistently, transfection of miR-223-3p mimic markedly reduced Kv4.2 protein level and Ito current in cultured NRVCs. Co-transfection of AMO-223-3p (an antisense inhibitor of miR-223-3p) reversed the repressive effect of miR-223-3p. Luciferase assay showed that miR-223-3p, but not the negative control, substantially suppressed the luciferase activity, confirming the direct binding of miR-223-3p to the seed site within the KCND2 sequence. Finally, direct intramuscular injection of AMO-223-3p into the ischemic myocardium to knockdown endogenous miR-223-3p decreased the propensity of ischemic arrhythmias. Conclusions: Upregulation of miR-223-3p in AMI repressed the expression of KCND2/Kv4.2 resulting in reduction of I_to density that can cause APD prolongation and promote arrhythmias in AMI, and therefore knockdown of endogenous miR-223-3p might be considered a new approach for antiarrhythmic therapy of ischemic arrhythmias.

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Hydrogen peroxide (H 2 O 2 ), an active oxygen species, is widely generated in many biological systems and mediates various physiological and biochemical processes in plants. In the present study, we present a signaling network involving H 2 O 2 , nitric oxide (NO), calcium (Ca 2+ ), cyclic guanosine monophosphate (cGMP), and the mitogen-activated protein kinase (MAPK) cascade during adventitious rooting in mung bean seedlings. Both exogenous H 2 O 2 and the NO donor sodium nitroprussiate were capable of promoting the formation and development of adventitious roots. H 2 O 2 and NO signaling pathways were elicited in parallel in auxin-induced adventitious rooting. Cytosolic Ca 2+ was required for adventitious rooting, and Ca 2+ served as a downstream component of H 2 O 2 , as well as cGMP or MAPK, signaling cascades. cGMP and MAPK cascades function downstream of H 2 O 2 signaling and depend on auxin responses in adventitious root signaling processes.

Salvianolic acid B has a significant protective effect on myocardial ischemia-reperfusion injury. It can alleviate oxidative stress, reduce calcium overload, improve endothelial function and so on.