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        A new species of the genus Tanna Distant (Hemiptera: Cicadidae: Cicadinae: Leptopsaltriini) from Vietnam, with notes on taxonomic changes in Tanna

        Young June Lee,David Lyall Emery 국립중앙과학관 2020 Journal of Asia-Pacific Biodiversity Vol.13 No.1

        A new species of the genus Tanna Distant, 1905 (Hemiptera: Cicadidae), Tanna crassa sp. nov., is describedfrom Vietnam. Some taxonomic changes are made in Tanna. Tanna simultaneous (Chen, 1940) syn. nov. issynonymized with Tanna abdominalis (Kato, 1938). Tanna obliqua Liu, 1940 stat. rev. is resurrected fromthe junior synonym of Tanna auripennis Kato, 1930. Tanna shensiensis (Sanborn, 2006) is transferred toAetanna Lee, 2014 to become Aetanna shensiensis (Sanborn, 2006) comb. nov. Tanna bakeri Moulton, 1923is transferred to Purana Distant, 1905 to become Purana bakeri (Moulton, 1923) comb. nov.

      • Mapping Longitudinal Development of Local Cortical Gyrification in Infants from Birth to 2 Years of Age

        Li, Gang,Wang, Li,Shi, Feng,Lyall, Amanda E.,Lin, Weili,Gilmore, John H.,Shen, Dinggang Society for Neuroscience 2014 The Journal of neuroscience Vol.34 No.12

        <P>Human cortical folding is believed to correlate with cognitive functions. This likely correlation may have something to do with why abnormalities of cortical folding have been found in many neurodevelopmental disorders. However, little is known about how cortical gyrification, the cortical folding process, develops in the first 2 years of life, a period of dynamic and regionally heterogeneous cortex growth. In this article, we show how we developed a novel infant-specific method for mapping longitudinal development of local cortical gyrification in infants. By using this method, via 219 longitudinal 3T magnetic resonance imaging scans from 73 healthy infants, we systemically and quantitatively characterized for the first time the longitudinal cortical global gyrification index (GI) and local GI (LGI) development in the first 2 years of life. We found that the cortical GI had age-related and marked development, with 16.1% increase in the first year and 6.6% increase in the second year. We also found marked and regionally heterogeneous cortical LGI development in the first 2 years of life, with the high-growth regions located in the association cortex, whereas the low-growth regions located in sensorimotor, auditory, and visual cortices. Meanwhile, we also showed that LGI growth in most cortical regions was positively correlated with the brain volume growth, which is particularly significant in the prefrontal cortex in the first year. In addition, we observed gender differences in both cortical GIs and LGIs in the first 2 years, with the males having larger GIs than females at 2 years of age. This study provides valuable information on normal cortical folding development in infancy and early childhood.</P>

      • Cortical thickness and surface area in neonates at high risk for schizophrenia

        Li, G.,Wang, L.,Shi, F.,Lyall, A. E.,Ahn, M.,Peng, Z.,Zhu, H.,Lin, W.,Gilmore, J. H.,Shen, D. Springer Science + Business Media 2016 BRAIN STRUCTURE AND FUNCTION Vol.221 No.1

        <P>Schizophrenia is a neurodevelopmental disorder associated with subtle abnormal cortical thickness and cortical surface area. However, it is unclear whether these abnormalities exist in neonates associated with genetic risk for schizophrenia. To this end, this preliminary study was conducted to identify possible abnormalities of cortical thickness and surface area in the high-genetic-risk neonates. Structural magnetic resonance images were acquired from offspring of mothers (N = 21) who had schizophrenia (N = 12) or schizoaffective disorder (N = 9), and also matched healthy neonates of mothers who were free of psychiatric illness (N = 26). Neonatal cortical surfaces were reconstructed and parcellated as regions of interest (ROIs), and cortical thickness for each vertex was computed as the shortest distance between the inner and outer surfaces. Comparisons were made for the average cortical thickness and total surface area in each of 68 cortical ROIs. After false discovery rate (FDR) correction, it was found that the female high-genetic-risk neonates had significantly thinner cortical thickness in the right lateral occipital cortex than the female control neonates. Before FDR correction, the high-genetic-risk neonates had significantly thinner cortex in the left transverse temporal gyrus, left banks of superior temporal sulcus, left lingual gyrus, right paracentral cortex, right posterior cingulate cortex, right temporal pole, and right lateral occipital cortex, compared with the control neonates. Before FDR correction, in comparison with control neonates, male high-risk neonates had significantly thicker cortex in the left frontal pole, left cuneus cortex, and left lateral occipital cortex; while female high-risk neonates had significantly thinner cortex in the bilateral paracentral, bilateral lateral occipital, left transverse temporal, left pars opercularis, right cuneus, and right posterior cingulate cortices. The high-risk neonates also had significantly smaller cortical surface area in the right pars triangularis (before FDR correction), compared with control neonates. This preliminary study provides the first evidence that early development of cortical thickness and surface area might be abnormal in the neonates at genetic risk for schizophrenia.</P>

      • Regulatory Effects of Ca<sup>2+</sup> and H<sup>+</sup> on the Rat Chorda Tympani Response to NaCl and KCl

        DeSimone, John A.,Phan, Tam-Hao T.,Mummalaneni, Shobha,Rhyu, Mee-Ra,Heck, Gerard L.,Lyall, Vijay Oxford University Press 2015 Chemical senses Vol.40 No.6

        <P>Modulatory effects of pH<SUB>i</SUB> and [Ca<SUP>2+</SUP>]<SUB>i</SUB> on taste receptor cell (TRC) epithelial sodium channel (ENaC) were investigated by monitoring chorda tympani (CT) responses to NaCl and KCl at various lingual voltages, before and after lingual application of ionomycin and with 0–10mM CaCl<SUB>2</SUB> in the stimulus and rinse solutions adjusted to pH<SUB>o</SUB> 2.0–9.7. 0.1 and 0.5M KCl responses varied continuously with voltage and were fitted to an apical ion channel kinetic model using the same parameters. ENaC-dependent NaCl CT response was fitted to the same channel model but with parameters characteristic of ENaC. A graded increase in TRC [Ca<SUP>2+</SUP>]<SUB>i</SUB> decreased the ENaC-dependent NaCl CT response, and inhibited and ultimately eliminated its pH sensitivity. CT responses to KCl were pH<SUB>i</SUB>- and [Ca<SUP>2+</SUP>]<SUB>i</SUB>-independent. Between ±60 mV applied lingual potential, the data were well described by a linear approximation to the nonlinear channel equation and yielded 2 parameters, the open-circuit response and the negative of the slope of the line in the CT response versus voltage plot, designated the response conductance. The ENaC-dependent NaCl CT response conductance was a linear function of the open-circuit response for all pH<SUB>i</SUB>-[Ca<SUP>2+</SUP>]<SUB>i</SUB> combinations examined. Analysis of these data shows that pH<SUB>i</SUB> and [Ca<SUP>2+</SUP>]<SUB>i</SUB> regulate TRC ENaC exclusively through modulation of the maximum CT response.</P>

      • TRPM5-dependent amiloride- and benzamil-insensitive NaCl chorda tympani taste nerve response

        Ren, ZuoJun,Rhyu, Mee-Ra,Phan, Tam-Hao T.,Mummalaneni, Shobha,Murthy, Karnam S.,Grider, John R.,DeSimone, John A.,Lyall, Vijay American Physiological Society 2013 American journal of physiology, Gastrointestinal a Vol.305 No.1

        <P>Transient receptor potential (TRP) subfamily M member 5 (TRPM5) cation channel is involved in sensing sweet, bitter, umami, and fat taste stimuli, complex-tasting divalent salts, and temperature-induced changes in sweet taste. To investigate if the amiloride- and benzamil (Bz)-insensitive NaCl chorda tympani (CT) taste nerve response is also regulated in part by TRPM5, CT responses to 100 mM NaCl + 5 μM Bz (NaCl + Bz) were monitored in Sprague-Dawley rats, wild-type (WT) mice, and TRP vanilloid subfamily member 1 (TRPV1) and TRPM5 knockout (KO) mice in the presence of resiniferatoxin (RTX), a TRPV1 agonist. In rats, NaCl + Bz + RTX CT responses were also monitored in the presence of triphenylphosphine oxide, a specific TRPM5 blocker, and capsazepine and <I>N</I>-(3-methoxyphenyl)-4-chlorocinnamid (SB-366791), specific TRPV1 blockers. In rats and WT mice, RTX produced biphasic effects on the NaCl + Bz CT response, enhancing the response at 0.5–1 μM and inhibiting it at >1 μM. The NaCl + Bz + SB-366791 CT response in rats and WT mice and the NaCl + Bz CT response in TRPV1 KO mice were inhibited to baseline level and were RTX-insensitive. In rats, blocking TRPV1 by capsazepine or TRPM5 by triphenylphosphine oxide inhibited the tonic NaCl + Bz CT response and shifted the relationship between RTX concentration and the magnitude of the tonic CT response to higher RTX concentrations. TRPM5 KO mice elicited no constitutive NaCl + Bz tonic CT response. The relationship between RTX concentration and the magnitude of the tonic NaCl + Bz CT response was significantly attenuated and shifted to higher RTX concentrations. The results suggest that pharmacological or genetic alteration of TRPM5 activity modulates the Bz-insensitive NaCl CT response and its modulation by TRPV1 agonists.</P>

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