Applying Topographic Classification, Based on the Hydrological Process, to Design Habitat Linkages for Climate Change

The use of biodiversity surrogates has been discussed in the context of designing habitat linkages to support the migration of species affected by climate change. Topography has been proposed as a useful surrogate in the coarse-filter approach, as the hydrological process caused by topography such as erosion and accumulation is the basis of ecological processes. However, some studies that have designed topographic linkages as habitat linkages, so far have focused much on the shape of the topography (morphometric topographic classification) with little emphasis on the hydrological processes (generic topographic classification) to find such topographic linkages. We aimed to understand whether generic classification was valid for designing these linkages. First, we evaluated whether topographic classification is more appropriate for describing actual (coniferous and deciduous) and potential (mammals and amphibians) habitat distributions. Second, we analyzed the difference in the linkages between the morphometric and generic topographic classifications. The results showed that the generic classification represented the actual distribution of the trees, but neither the morphometric nor the generic classification could represent the potential animal distributions adequately. Our study demonstrated that the topographic classes, according to the generic classification, were arranged successively according to the flow of water, nutrients, and sediment; therefore, it would be advantageous to secure linkages with a width of 1 km or more. In addition, the edge effect would be smaller than with the morphometric classification. Accordingly, we suggest that topographic characteristics, based on the hydrological process, are required to design topographic linkages for climate change

Real-time visualization of clustering and intracellular transport of gold nanoparticles by correlative imaging.

Mechanistic understanding of the endocytosis and intracellular trafficking of nanoparticles is essential for designing smart theranostic carriers. Physico-chemical properties, including size, clustering and surface chemistry of nanoparticles regulate their cellular uptake and transport. Significantly, even single nanoparticles could cluster intracellularly, yet their clustering state and subsequent trafficking are not well understood. Here, we used DNA-decorated gold (fPlas-gold) nanoparticles as a dually emissive fluorescent and plasmonic probe to examine their clustering states and intracellular transport. Evidence from correlative fluorescence and plasmonic imaging shows that endocytosis of fPlas-gold follows multiple pathways. In the early stages of endocytosis, fPlas-gold nanoparticles appear mostly as single particles and they cluster during the vesicular transport and maturation. The speed of encapsulated fPlas-gold transport was critically dependent on the size of clusters but not on the types of organelle such as endosomes and lysosomes. Our results provide key strategies for engineering theranostic nanocarriers for efficient health management

Iron-Fur complex suppresses the expression of components of the cyclo-(Phe-Pro)-signaling regulatory pathway in Vibrio vulnificus

In the human pathogen Vibrio vulnificus, the quorum-sensing (QS) signal molecule cyclo-(L-phenylalanine-L-proline) (cFP) plays a critical role in triggering a signaling pathway involving the components LeuO-vHUαβ-RpoS-KatG via the membrane signal receptor ToxR. In this study, we investigated the impact of iron on the expression of these signaling components. We found that the transcription of the membrane sensor protein ToxR was not significantly affected by Fur-iron. However, Fur-iron repressed the transcription of genes encoding all the downstream cytoplasmic components in this pathway by binding to the upstream regions of these genes. Consequently, the expression of genes regulated by the alternative sigma factor RpoS, as well as the resistance to hydrogen peroxide conferred by KatG, were repressed. Additionally, we observed that in Vibrio cholerae, genes dependent on ToxR showed higher expression levels in a fur-deletion mutant compared to the wild type. These findings indicate that iron, in association with Fur, represses virtually all the cytoplasmic components responsible for the ToxR-dependent cFP-signaling pathways in these two pathogenic Vibrio species. This study, along with our previous reports demonstrating the repression of components involved in AI-2 dependent QS signaling by Fur-iron, highlights the crucial role of iron in quorum-sensing regulation, which is closely associated with the pathogenicity of this human pathogen

An in situ study on the coalescence of monolayer-protected Au-Ag nanoparticle deposits upon heating

The structural evolution of thiolate-protected nanoparticles of gold, silver, and their alloys with various Au/Ag ratios (3:1, 1:1, and 1:3) upon heating was investigated by means of in situ synchrotron radiation X-ray diffraction. The relationships between the coalescence and composition of nanoparticles, as well as the surfactant reactions, were clarified. Experimental results show that there existed a critical temperature ranging from 120°C to 164°C, above which the tiny broad X-ray diffraction peaks became sharp and strong due to particle coalescence. The coalescence temperatures for alloy nanoparticle deposits were clearly lower than those for pure metals, which can be ascribed to the rivalry between the thermodynamic effect due to alloying and the interactions between surface-assembled layers and the surface atoms of the nanoparticles. The strong affinity of thiolates to Ag and thus complex interactions give rise to a greater energy barrier for the coalescence of nanoparticles into the bulk and subsequent high coalescence temperature. The influences of particle coalescence on the optical and electrical properties of the nanoparticle deposits were also explored

Atypical Antipsychotic Drug Olanzapine Deregulates Hepatic Lipid Metabolism and Aortic Inflammation and Aggravates Atherosclerosis

Background/Aims: Olanzapine, an atypical antipsychotic drug, has therapeutic effects for schizophrenia. However, clinical reports indicate that patients taking atypical antipsychotic drugs are at high risk of metabolic syndrome with unclear mechanisms. We investigated the effect of olanzapine on atherosclerosis and the mechanisms in apolipoprotein E-null (apoE-/-) mice. Methods: ApoE-/- mice were used as in vivo models. Western blot analysis was used to evaluate protein expression. Conventional assay kits were applied to assess the levels of cholesterol, triglycerides, free cholesterol, cholesteryl ester, fatty acids, glycerol, and cytokines. Results: Daily treatment with olanzapine (3 mg/kg body weight) for four weeks increased mean arterial blood pressure and the whitening of brown adipose tissue in mice. In addition, olanzapine impaired aortic cholesterol homeostasis and exacerbated hyperlipidemia and aortic inflammation, which accelerated atherosclerosis in mice. Moreover, lipid accumulation in liver, particularly total cholesterol, free cholesterol, fatty acids, and glycerol, was increased with olanzapine treatment in apoE-/- mice by upregulating the expression of de novo lipid synthesis-related proteins and downregulating that of cholesterol clearance- or very low-density lipoprotein secretion-related proteins. Conclusion: Olanzapine may exacerbate atherosclerosis by deregulating hepatic lipid metabolism and worsening hyperlipidemia and aortic inflammation

Enhanced expression of microrna-1273g-3p contributes to alzheimer’s disease pathogenesis by regulating the expression of mitochondrial genes

Alzheimer’s disease (AD) is the most common form of dementia in the elderly population, but its underlying cause has not been fully elucidated. Recent studies have shown that microRNAs (miRNAs) play important roles in regulating the expression levels of genes associated with AD development. In this study, we analyzed miRNAs in plasma and cerebrospinal fluid (CSF) from AD patients and cognitively normal (including amyloid positive) individuals. miR-1273g-3p was identified as an AD-associated miRNA and found to be elevated in the CSF of early-stage AD patients. The overexpression of miR-1273g-3p enhanced amyloid beta (Aβ) production by inducing oxidative stress and mitochondrial impairments in AD model cell lines. A biotin-streptavidin pull-down assay demonstrated that miR-1273g-3p primarily interacts with mitochondrial genes, and that their expression is downregulated by miR-1273g-3p. In particular, the miR-1273g-3p-target gene TIMM13 showed reduced expression in brain tissues from human AD patients. These results suggest that miR1273g-3p expression in an early stage of AD notably contributes to Aβ production and mitochondrial impairments. Thus, miR-1273g-3p might be a biomarker for early diagnosis of AD and a potential therapeutic target to prevent AD progression