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Simple Summary: Atrial natriuretic peptide (ANP) is a cardiac peptide hormone that was identified by Kangawa and Matsuo in 1984. In Japan, ANP has been used as an intravenous drug for the treatment of acute heart failure since 1995. Because ANP has a hypotensive effect, it is important to avoid excessive lowering of blood pressure when ANP is used. Recently, a compound that inhibits neutral endopeptidase, the enzyme that degrades ANP, has been developed (angiotensin receptor-neprilysin inhibitor (ARNI)). ARNI has been approved worldwide for the treatment of chronic heart failure and has been authorized in Japan as an antihypertensive drug. However, it is not understood exactly how ANP exerts its hypotensive effect. In this review, we discuss the molecular mechanism of the blood pressure-regulating effects of ANP, focusing on our recent findings. Natriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increased preload and afterload. Both hormones act through natriuretic peptide receptor 1 (NPR1). In contrast, CNP acts through natriuretic peptide receptor 2 (NPR2) and was found to be produced by the vascular endothelium, chondrocytes, and cardiac fibroblasts. Based on its relatively low plasma concentration compared with ANP and BNP, CNP is thought to function as both an autocrine and a paracrine factor in the vasculature, bone, and heart. The cytoplasmic domains of both NPR1 and NPR2 display a guanylate cyclase activity that catalyzes the formation of cyclic GMP. NPR3 lacks this guanylate cyclase activity and is reportedly coupled to Gi-dependent signaling. Recently, we reported that the continuous infusion of the peptide osteocrin, an endogenous ligand of NPR3 secreted by bone and muscle cells, lowered blood pressure in wild-type mice, suggesting that endogenous natriuretic peptides play major roles in the regulation of blood pressure. Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides. The increased worldwide clinical use of the angiotensin receptor-neprilysin inhibitor for the treatment of chronic heart failure has brought renewed attention to the physiological effects of natriuretic peptides. In this review, we provide an overview of the discovery of ANP and its translational research. We also highlight our recent findings on the blood pressure regulatory effects of ANP, focusing on its molecular mechanisms. [ABSTRACT FROM AUTHOR]

• 1200 μg/mL F. schisandrae inhibited the growth of V.alginolyticus ND-01. • V. alginolyticus under high concentrations of F. schisandrae stress had insufficient ability in the whole biofilm formation process. • DEGs was involved in the following functional categories: metabolic process, single-organism process, catalytic activity and localization. Due to the abusive use of antibiotics, bacterial resistance has become a global problem and poses severe threats to aquaculture. The drug-resistant diseases caused by Vibrio alginolyticus have caused significant economic losses to cultured marine fish. Fructus schisandrae is used to treat inflammatory diseases in China and Japan. There have been no reports of bacterial molecular mechanisms associated with F. schisandrae stress. In this study, the inhibiting effect of F. schisandrae on the growth of V. alginolyticus was detected to understand response mechanisms at the molecular level. The antibacterial tests were analyzed via next-generation deep sequencing technology (RNA sequencing, RNA-seq). Wild V. alginolyticus (CK) was compared with V. alginolyticus, F. schisandrae incubated for 2 h, and V. alginolyticus, F. schisandrae incubated for 4 h. Our results revealed that there were 582 genes (236 upregulated and 346 downregulated) and 1068 genes (376 upregulated and 692 downregulated), respectively. Differentially expressed genes (DEGs) were involved in the following functional categories: metabolic process, single-organism process, catalytic activity, cellular process, binding, membrane, cell part, cell, and localization. FS_2 h was compared with FS_4 h, and 21 genes (14 upregulated and 7 downregulated) were obtained. The RNA-seq results were validated by detecting the expression levels of 13 genes using quantitative real-time polymerase chain reaction (qRT-PCR). The qRT-PCR results matched those of the sequencing, which reinforced the reliability of the RNA-seq. The results revealed the transcriptional response of V. alginolyticus to F. schisandrae , which will provide new ideas for studying V. alginolyticus' complex virulence molecular mechanism and the possibility of developing Schisandra to prevent and treat drug-resistant diseases. [ABSTRACT FROM AUTHOR]

Minamata disease in Japan and the large-scale poisoning by methylmercury (MeHg) in Iraq caused wide public concerns about the risk emanating from mercury for human health. Nowadays, it is widely known that all forms of mercury induce toxic effects in mammals, and increasing evidence supports the concern that environmentally relevant levels of MeHg could impact normal biological functions in wildlife. The information of mechanism involved in mercurial toxicity is growing but knowledge gaps still exist between the adverse effects and mechanisms of action, especially at the molecular level. A body of data obtained from experimental studies on mechanisms of mercurial toxicity in vivo and in vitro points to that disruption of the antioxidant system may play an important role in the mercurial toxic effects. Moreover, the accumulating evidence indicates that signaling transduction, protein or/and enzyme activity, and gene regulation are involving in mediating toxic and adaptive response to mercury exposure. We conducted here a comprehensive review of mercurial toxic effects on wildlife and human, in particular synthesized key findings of molecular pathways involved in mercurial toxicity from the cells to human. We discuss the molecular evidence related mercurial toxicity to the adverse effects, with particular emphasis on the gene regulation. The further studies relying on Omic analysis connected to adverse effects and modes of action of mercury will aid in the evaluation and validation of causative relationship between health outcomes and gene expression., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2019 Elsevier Ltd. All rights reserved.)