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RISS 인기검색어
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- 저자 : Eberth, John (검색결과 2 건)
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David A. Eberth,Demchig Badamgarav,Philip J. Currie 한국고생물학회 2009 고생물학회지 Vol.25 No.1
The Baruungoyot and Nemegt formations interfinger through a minimum of 23 meters of stratigraphic section at Nemegt. This interfingering stratigraphic interval comprises the lower one-half of the Nemegt Formation's stratigraphic exposure in the area. This interfingering formational contact, as well as an upsection increase in conglomeratic sediments in the Nemegt Formation are evidence for progradation of the Nemegt clastics. We infer that during Nemegt "time," uplift in the paleo-Altan Nemegt source area increased both sediment supply and the depositional gradient, which, in tum, decreased accommodation. Decreased accommodation resulted in a preservational bias for channel-fill and sheet flood deposits. During progradation, a multi-kilometer-wide Nemegt meanderbelt episodically shifted its position to the southeast, and occasionally back-stepped to the northwest, thus leaving a succession of interfingering Baruungoyot and Nemegt tongues in the stratigraphic record. The meanderbelt hosted medium-size channels (~6 m deep and 75 m wide) that flowed to the southwest. Southeast of the meanderbelt, seasonally wet-dry distal-basin environments of the Baruungoyot Formation continued to exist during the time represented by the interfingering interval. The interfingering interval is the most vertebrate-fossil rich part of the stratigraphic section in this area (Nemegt meanderbelt tongues in particular). Rich fossil OCCUITences in this interfingering interval indicate that many of the Nemegt and Baruungoyot vertebrates from this interval co-existed.
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Sarkar, Sanjay,Bailey, Ernest,Go, Yun Young,Cook, R. Frank,Kalbfleisch, Ted,Eberth, John,Chelvarajan, R. Lakshman,Shuck, Kathleen M.,Artiushin, Sergey,Timoney, Peter J.,Balasuriya, Udeni B. R. Public Library of Science 2016 PLoS genetics Vol.12 No.12
<▼1><P>Equine arteritis virus (EAV) is the causative agent of equine viral arteritis (EVA), a respiratory, systemic, and reproductive disease of horses and other equid species. Following natural infection, 10–70% of the infected stallions can become persistently infected and continue to shed EAV in their semen for periods ranging from several months to life. Recently, we reported that some stallions possess a subpopulation(s) of CD3<SUP>+</SUP> T lymphocytes that are susceptible to <I>in vitro</I> EAV infection and that this phenotypic trait is associated with long-term carrier status following exposure to the virus. In contrast, stallions not possessing the CD3<SUP>+</SUP> T lymphocyte susceptible phenotype are at less risk of becoming long-term virus carriers. A genome wide association study (GWAS) using the Illumina Equine SNP50 chip revealed that the ability of EAV to infect CD3<SUP>+</SUP> T lymphocytes and establish long-term carrier status in stallions correlated with a region within equine chromosome 11. Here we identified the gene and mutations responsible for these phenotypes. Specifically, the work implicated three allelic variants of the equine orthologue of <I>CXCL16</I> (<I>EqCXCL16</I>) that differ by four non-synonymous nucleotide substitutions (XM_00154756; c.715 A → T, c.801 G → C, c.804 T → A/G, c.810 G → A) within exon 1. This resulted in four amino acid changes with EqCXCL16S (XP_001504806.1) having Phe, His, Ile and Lys as compared to EqCXL16R having Tyr, Asp, Phe, and Glu at 40, 49, 50, and 52, respectively. Two alleles (<I>EqCXCL16Sa</I>, <I>EqCXCL16Sb</I>) encoded identical protein products that correlated strongly with long-term EAV persistence in stallions (P<0.000001) and are required for <I>in vitro</I> CD3<SUP>+</SUP> T lymphocyte susceptibility to EAV infection. The third (<I>EqCXCL16R</I>) was associated with <I>in vitro</I> CD3<SUP>+</SUP> T lymphocyte resistance to EAV infection and a significantly lower probability for establishment of the long-term carrier state (viral persistence) in the male reproductive tract. <I>EqCXCL16Sa</I> and <I>EqCXCL16Sb</I> exert a dominant mode of inheritance. Most importantly, the protein isoform EqCXCL16S but not EqCXCL16R can function as an EAV cellular receptor. Although both molecules have equal chemoattractant potential, EqCXCL16S has significantly higher scavenger receptor and adhesion properties compared to EqCXCL16R.</P></▼1><▼2><P><B>Author Summary</B></P><P>A variable proportion of EAV infected stallions (10–70%) may become persistently infected and continuously shed the virus exclusively in their semen after recovery from acute infection. Previous studies in our laboratory have shown that stallions with the CD3<SUP>+</SUP> T lymphocyte susceptibility phenotype to <I>in vitro</I> EAV infection are at higher risk of becoming persistently infected carriers compared to those that lack this phenotype. Here genetic and experimental studies were used to demonstrate that <I>CXCL16</I> in the horse codes for two proteins, one associated with resistance and the other associated with susceptibility of CD3<SUP>+</SUP> T lymphocytes to EAV infection. The two proteins are the result of four nucleotide substitutions in exon 1 of the equine <I>CXCL16</I> gene. These alleles determine the outcome of <I>in vitro</I> infection of CD3<SUP>+</SUP> T lymphocytes with EAV and are strongly associated with the establishment and maintenance of long-term carrier state in stallions. <I>In vitro</I> studies demonstrated that one form of CXCL16 protein (CXCL16S) is one of the cellular receptors for EAV and has higher scavenger activity and adhesion ability as compared to the form of the protein associated with resistance (CXCL16R).</P></▼2>
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