1,751,186 research outputs found

    Table_2_CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis.XLS

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    This study aimed to investigate the potential roles of circRNAs in regulating osteoarthritis (OA)-related ghrelin synthesis, autophagy induction, and the relevant molecular mechanisms. Results showed that Col2a1, Acan, ghrelin, and autophagy-related markers expression were downregulated, while matrix metalloproteinase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) expressions increased in both IL-1β-induced rat chondrocytes and cartilage tissues of OA rats. A total of 130 circRNAs and 731 mRNAs were differentially expressed in IL-1β-induced rat chondrocytes. Among them, we found that circPan3 expression was significantly decreased in both cellular and animal OA models. CircPan3 directly targeted miR-667-5p. CircPan3 overexpression promoted Col2a1, Acan, ghrelin, beclin 1, and LC3-II expression but reduced MMP13 and ADAMTS5 expression in rat chondrocytes, whereas overexpression of miR-667-5p exhibited opposite effects on the above markers. Furthermore, we found that miR-667-5p bound directly to the 3′-UTR sequence of ghrelin gene. Moreover, the circPan3-induced alterations in chondrocytes were antagonized by miR-667-5p overexpression. Taken together, our findings demonstrate that circPan3 promotes ghrelin synthesis and chondrocyte autophagy via targeting miR-667-5p, protecting against OA injury. This study provided experimental evidence that circPan3/miR-667-5p/ghrelin axis might serve as targets of drug development for the treatment of OA.</p

    Table_1_CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis.XLS

    No full text
    This study aimed to investigate the potential roles of circRNAs in regulating osteoarthritis (OA)-related ghrelin synthesis, autophagy induction, and the relevant molecular mechanisms. Results showed that Col2a1, Acan, ghrelin, and autophagy-related markers expression were downregulated, while matrix metalloproteinase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) expressions increased in both IL-1β-induced rat chondrocytes and cartilage tissues of OA rats. A total of 130 circRNAs and 731 mRNAs were differentially expressed in IL-1β-induced rat chondrocytes. Among them, we found that circPan3 expression was significantly decreased in both cellular and animal OA models. CircPan3 directly targeted miR-667-5p. CircPan3 overexpression promoted Col2a1, Acan, ghrelin, beclin 1, and LC3-II expression but reduced MMP13 and ADAMTS5 expression in rat chondrocytes, whereas overexpression of miR-667-5p exhibited opposite effects on the above markers. Furthermore, we found that miR-667-5p bound directly to the 3′-UTR sequence of ghrelin gene. Moreover, the circPan3-induced alterations in chondrocytes were antagonized by miR-667-5p overexpression. Taken together, our findings demonstrate that circPan3 promotes ghrelin synthesis and chondrocyte autophagy via targeting miR-667-5p, protecting against OA injury. This study provided experimental evidence that circPan3/miR-667-5p/ghrelin axis might serve as targets of drug development for the treatment of OA.</p

    Table_3_CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis.XLS

    No full text
    This study aimed to investigate the potential roles of circRNAs in regulating osteoarthritis (OA)-related ghrelin synthesis, autophagy induction, and the relevant molecular mechanisms. Results showed that Col2a1, Acan, ghrelin, and autophagy-related markers expression were downregulated, while matrix metalloproteinase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) expressions increased in both IL-1β-induced rat chondrocytes and cartilage tissues of OA rats. A total of 130 circRNAs and 731 mRNAs were differentially expressed in IL-1β-induced rat chondrocytes. Among them, we found that circPan3 expression was significantly decreased in both cellular and animal OA models. CircPan3 directly targeted miR-667-5p. CircPan3 overexpression promoted Col2a1, Acan, ghrelin, beclin 1, and LC3-II expression but reduced MMP13 and ADAMTS5 expression in rat chondrocytes, whereas overexpression of miR-667-5p exhibited opposite effects on the above markers. Furthermore, we found that miR-667-5p bound directly to the 3′-UTR sequence of ghrelin gene. Moreover, the circPan3-induced alterations in chondrocytes were antagonized by miR-667-5p overexpression. Taken together, our findings demonstrate that circPan3 promotes ghrelin synthesis and chondrocyte autophagy via targeting miR-667-5p, protecting against OA injury. This study provided experimental evidence that circPan3/miR-667-5p/ghrelin axis might serve as targets of drug development for the treatment of OA.</p

    Nephi Arsenal P.02

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    Nephi Arsenal, 1938. Salt Lake Tribune #667

    El Tlacuache Núm. 667 (2015). 667 Año 13 (2015) marzo. El Tlacuache

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    El Vaso de la Ventilla: Nuevos datos para el estudio del cuchillo curvo en Teotihuacan por Jaime Delgado Rubio, Norma, transgresión y sentencia en una población Nahua de la Huasteca por Jonatan Cerros C

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Resolución UNRN N° 667/2009. Convocar para el Curso de extensión "Derecho Laboral Colectivo y Derecho Laboral Individual"

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    Fil: Universidad Nacional de Río Negro (U). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución UNRN N° 667/2009. Convocar para el Curso de extensión "Derecho Laboral Colectivo y Derecho Laboral Individual"fals

    El derecho a la defensa y el inciso 7 del artículo 667 del código civil Peruano.

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    La presente investigación tiene como objetivo general analizar la manera en que se relaciona el derecho a la defensa con el inciso 7 del artículo 667° del Código Civil peruano, de allí que, nuestra pregunta general de investigación sea: ¿ De qué manera se relaciona el derecho a la defensa con el inciso 7 del artículo 667° del Código Civil peruano?, y nuestra hipótesis general: “El derecho a la defensa se relaciona de manera negativa con el inciso 7 del artículo 667° del Código Civil peruano”; asimismo, guarda un método de investigación de corte jurídico dogmático, esto es con un método general denominado la hermenéutica, asimismo presenta un tipo de investigación básico o fundamental, con un nivel correlacional y un diseño observacional, por tal motivo es que la investigación por su naturaleza expuesta, utilizará la técnica del análisis documental de leyes, códigos, sentencias y libros doctrinarios que serán procesados mediante la argumentación jurídica a través de los instrumentos de recolección de datos como la ficha textual y de resumen que se obtengan de cada libro con información relevante; asimismo, la tesis obtuvo los siguientes resultados: El derecho a la defensa, en sentido amplio, es en un derecho subjetivo constitucionalmente respaldado, en donde, la persona tiene el poder de solicitar ante un órgano de justicia igualdad de condiciones para la solución de un conflicto intersubjetivo, a fin de alcanzar una justicia equilibrada en contexto del derecho; finalmente la conclusión más importante de la investigación fue: Las causales de indignidad, deben de ser contenidos abiertos, en donde se pueda adecuar mejor la conducta inmoral del heredero o legatario, a fin de que no sea rígido y casuístico
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