5,012 research outputs found

    Taxonomic status of the Senkaku mole, Nesoscaptor uchidai, with special reference to variation in Mogera insularis from Taiwan (Mammalia : Insectivora)

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    The taxonomic status of the Senkaku mole, Nesoscaptor uchidai Abe, Shiraishi et Arai, 1991 (Mammalia: Insectivora: Talpidae), described from Uotsurijima in the Senkaku Group, Ryukyu Archipelago, was re-evaluated. Morphological analyses suggest that N. uchidai is most similar to Mogera insularis from Taiwan, although several morphological characters, such as the number of premolars and the shapes of the anterior portion of the palate, zygomatic arch, auditory bulla, and coronoid process, differentiate N. uchidai from M. insularis. Therefore, we synonymize the monotypic genus Nesoscaptor Abe, Shiraishi et Arai, 1991 with the genus Mogera Pomel, 1848, and define Mogera uchidai (Abe, Shiraishi et Arai, 1991) as a valid species endemic to Uotsurijima. In addition, we analyzed morphological variation within M. insularis, such as variation in the second upper premolar pair, overall cranial size, and the breadth of the rostrum and palate. Some of this variation may be associated with topographical and environmental factors in its habitat

    Glutamate transporter EAAT2: a new target for the treatment of neurodegenerative diseases

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    Glutamate is the primary excitatory amino acid neurotransmitter in the CNS. The concentration of glutamate in the synaptic cleft is tightly controlled by interplay between glutamate release and glutamate clearance. Abnormal glutamate release and/or dysfunction of glutamate clearance can cause overstimulation of glutamate receptors and result in neuronal injury known as excitotoxicity. The glial glutamate transporter EAAT2 plays a major role in glutamate clearance. Dysfunction or reduced expression of EAAT2 has been documented in many neurodegenerative diseases. In addition, many studies in animal models of disease indicate that increased EAAT2 expression provides neuronal protection. Here, we summarize these studies and suggest that EAAT2 is a potential target for the prevention of excitotoxicity. EAAT2 can be upregulated by transcriptional or translational activation. We discuss current progress in the search for EAAT2 activators, which is a promising direction for the treatment of neurodegenerative diseases

    The Size-Mass Relation of Post-Starburst Galaxies in the Local Universe

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    We present a study of the size--mass relation for local post-starburst (PSB) galaxies at z0.33z\lesssim0.33 selected from the Sloan Digital Sky Survey Data Release 8. We find that PSB galaxies with stellar mass (MM_*) at 109 M<M<1012 M10^9~M_{\odot}<M_*<10^{12}~M_{\odot} have their galaxy size smaller than or comparable with those of quiescent galaxies (QGs). After controlling redshift and stellar mass, the sizes of PSBs are 13%\sim 13\% smaller on average than those of QGs, such differences become larger and significant towards the low-MM_* end, especially at 109.5 MM1010.5 M10^{9.5}~M_{\odot} \lesssim M_*\lesssim 10^{10.5}~M_{\odot} where PSBs can be on average 19%\sim 19\% smaller than QGs. In comparison with predictions of possible PSB evolutionary pathways from cosmological simulations, we suggest that a fast quenching of star formation following a short-lived starburst event (might be induced by major merger) should be the dominated pathway of our PSB sample. Furthermore, by cross-matching with group catalogs, we confirm that local PSBs at M1010 MM_*\lesssim10^{10}~M_{\odot} are more clustered than more massive ones. PSBs resided in groups are found to be slightly larger in galaxy size and more disk-like compared to field PSBs, which is qualitatively consistent with and thus hints the environment-driven fast quenching pathway for group PSBs. Taken together, our results support multiple evolutionary pathways for local PSB galaxies: while massive PSBs are thought of as products of fast quenching following a major merger-induced starburst, environment-induced fast quenching should play a role in the evolution of less massive PSBs, especially at M1010 MM_*\lesssim 10^{10}~M_{\odot}.Comment: 16 pages, 7 figures; accepted for publication in Ap

    Dwarf galaxies with the highest concentration are not thicker than ordinary dwarf galaxies

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    The formation mechanism of high-concentration dwarf galaxies is still a mystery. We perform a comparative study of the intrinsic shape of nearby low-mass galaxies with different stellar concentration. The intrinsic shape is parameterized by the intermediate-to-major axis ratios B/A and the minor-to-major axis ratios C/A of triaxial ellipsoidal models. Our galaxies (107.5M10^{7.5} M_\odot < MM_\star < 1010.0M10^{10.0} M_\odot) are selected to have spectroscopic redshift from SDSS or GAMA, and have broadband optical images from the HSC-SSP Wide layer survey. The deep HSC-SSP images allow to measure the apparent axis ratios qq at galactic radii beyond the central star-forming area of our galaxies. We infer the intrinsic axis ratios based on the qq distributions. We find that 1) our galaxies have typical intrinsic shape similarly close to be oblate (μB/A\mu_{B/A} \sim 0.9--1), regardless of the concentration, stellar mass, star formation activity, and local environment (being central or satellite); 2) galaxies with the highest concentration tend to have intrinsic thickness similar to or (in virtually all cases) slightly thinner (i.e. smaller mean μC/A\mu_{C/A} or equivalently lower triaxiality) than ordinary galaxies, regardless of other properties explored here. This appears to be in contrast with the expectation of the classic merger scenario for high-concentration galaxies. Given the lack of a complete understanding of dwarf-dwarf merger, we cannot draw a definite conclusion about the relevance of mergers in the formation of high-concentration dwarfs. Other mechanisms such as halo spin may also play important roles in the formation of high-concentration dwarf galaxies.Comment: 12 pages, 8 figures, 2 tables, accepted for publication in Ap

    Morphometric variation in the pusillus group of the genus Rhinolophus (Mammalia: Chiroptera: Rhinolophidae) in East Asia.

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    Based on 203 specimens belonging to the Rhinolophus "pusillus group" (Mammalia: Chiroptera: Rhinolophidae), univariate and multivariate morphometric analyses using 19 characters were performed to assess the confused species taxonomy. The results indicated that R. pusillus (including calidus, parcus, and szechuanus) in the continental region and Hainan Island of China and "R. cornutus" in Japan are morphologically divergent species. Rhinolophus cornutus should be further split into R. cornutus (including orii, pumilus, and miyakonis) in the main islands of Japan, the Amami and Okinawa Group of the central Ryukyu Archipelago, and Miyako Group of the southern Ryukyus; and R. perditus and R. imaizumii from the Yaeyama Group in the southern Ryukyus. Rhinolophus monoceros from Taiwan is morphologically more similar to species in Japan than to R. pusillus. In addition to R. pusillus, another form that is morphologically similar to species in Japan was recognized from Langzhong in Sichuan Province; this may represent an undescribed species, and further examination is necessary to determine its taxonomic status. Specimens from Guang'an in Sichuan Province, China, are also different from the others, and are characterized by the smallest skull size. Although further studies are required, these specimens were tentatively identified as R. subbadius

    High Throughput Sequencing Identifies MicroRNAs Mediating α-Synuclein Toxicity by Targeting Neuroactive-Ligand Receptor Interaction Pathway in Early Stage of Drosophila Parkinson\u27s Disease Model.

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    Parkinson\u27s disease (PD) is a prevalent neurodegenerative disorder with pathological features including death of dopaminergic neurons in the substantia nigra and intraneuronal accumulations of Lewy bodies. As the main component of Lewy bodies, α-synuclein is implicated in PD pathogenesis by aggregation into insoluble filaments. However, the detailed mechanisms underlying α-synuclein induced neurotoxicity in PD are still elusive. MicroRNAs are ~20nt small RNA molecules that fine-tune gene expression at posttranscriptional level. A plethora of miRNAs have been found to be dysregulated in the brain and blood cells of PD patients. Nevertheless, the detailed mechanisms and their in vivo functions in PD still need further investigation. By using Drosophila PD model expressing α-synuclein A30P, we examined brain miRNA expression with high-throughput small RNA sequencing technology. We found that five miRNAs (dme-miR-133-3p, dme-miR-137-3p, dme-miR-13b-3p, dme-miR-932-5p, dme-miR-1008-5p) were upregulated in PD flies. Among them, miR-13b, miR-133, miR-137 are brain enriched and highly conserved from Drosophila to humans. KEGG pathway analysis using DIANA miR-Path demonstrated that neuroactive-ligand receptor interaction pathway was most likely affected by these miRNAs. Interestingly, miR-137 was predicted to regulate most of the identified targets in this pathway, including dopamine receptor (DopR, D2R), γ-aminobutyric acid (GABA) receptor (GABA-B-R1, GABA-B-R3) and N-methyl-D-aspartate (NMDA) receptor (Nmdar2). The validation experiments showed that the expression of miR-137 and its targets was negatively correlated in PD flies. Further experiments using luciferase reporter assay confirmed that miR-137 could act on specific sites in 3\u27 UTR region of D2R, Nmdar2 and GABA-B-R3, which downregulated significantly in PD flies. Collectively, our findings indicate that α-synuclein could induce the dysregulation of miRNAs, which target neuroactive ligand-receptor interaction pathway in vivo. We believe it will help us further understand the contribution of miRNAs to α-synuclein neurotoxicity and provide new insights into the pathogenesis driving PD
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