681 research outputs found

    Estudio de la viabilidad comercial para la creación de un spa para hombres de 25 a 59 años en la ciudad de Chiclayo, 2015

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    La presente tesis tuvo como objetivo principal investigar la viabilidad comercial de implementar un Spa exclusivamente para hombres en la ciudad de Chiclayo, debido a que diversos estudios indicaron que en la actualidad los índices de estrés, ya sea laboral o psicológico, son elevados y se requiere desarrollar modelos de negocio que permitan atenuarlos. Por ello, la presente investigación, basándose en una segmentación que abarca hombres de 25 a 59 años, de estilos de vida sofisticados y progresistas, realizó mediante encuestas, entrevistas y grupos focales, un estudio para verificar la viabilidad de ejecución del spa masculino, del cual se obtuvo resultados positivos con respecto al crecimiento de éste sector, demostrando la aceptación del proyecto como parte del cuidado masculino, de modo que éste pueda brindar un servicio innovador, exclusivo y necesario, que ayude a mejorar la calidad de vida y satisfacción de los clientes, a través de las preferencias, características y sugerencias recolectadas en el estudio y análisis del mercado Chiclayano, por lo que se concluyó del estudio que sí es viable la creación de un spa para hombres en dicha ciudad.Tesi

    Autism Risk Gene Cul3 Alters Neuronal Morphology via Caspase-3 Activity in Mouse Hippocampal Neurons

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    Autism Spectrum Disorders (ASDs) are neurodevelopmental disorders (NDDs) in which children display differences in social interaction/communication and repetitive stereotyped behaviors along with variable associated features. Cul3, a gene linked to ASD, encodes CUL3 (CULLIN-3), a protein that serves as a key component of a ubiquitin ligase complex with unclear function in neurons. Cul3 homozygous deletion in mice is embryonic lethal; thus, we examine the role of Cul3 deletion in early synapse development and neuronal morphology in hippocampal primary neuronal cultures. Homozygous deletion of Cul3 significantly decreased dendritic complexity and dendritic length, as well as axon formation. Synaptic spine density significantly increased, mainly in thin and stubby spines along with decreased average spine volume in Cul3 knockouts. Both heterozygous and homozygous knockout of Cul3 caused significant reductions in the density and colocalization of gephyrin/vGAT puncta, providing evidence of decreased inhibitory synapse number, while excitatory synaptic puncta vGulT1/PSD95 density remained unchanged. Based on previous studies implicating elevated caspase-3 after Cul3 deletion, we demonstrated increased caspase-3 in our neuronal cultures and decreased neuronal cell viability. We then examined the efficacy of the caspase-3 inhibitor Z-DEVD-FMK to rescue the decrease in neuronal cell viability, demonstrating reversal of the cell viability phenotype with caspase-3 inhibition. Studies have also implicated caspase-3 in neuronal morphological changes. We found that caspase-3 inhibition largely reversed the dendrite, axon, and spine morphological changes along with the inhibitory synaptic puncta changes. Overall, these data provide additional evidence that Cul3 regulates the formation or maintenance of cell morphology, GABAergic synaptic puncta, and neuronal viability in developing hippocampal neurons in culture

    The Schistosomiasis Research Agenda—What Now?

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    [Extract] As relatively new schistosomiasis researchers, we awaited with eagerness the publication of the "Schistosomiasis Research Agenda" SRA) put forward by Colley and Secor in the December 2007 issue of PLoS Neglected Tropical Diseases [1]. The SRA is a comprehensive, well-organized list of research activities that reflects the impressive diversity of interests that make up current schistosomiasis research. Colley and Secor went to admirable lengths to solicit the interests of researchers the world over, with special efforts to solicit the opinions of scientists in countries or regions where schistosomiasis is endemic, such as Brazil, China, and Africa. Having attended some of these meetings (11th International Congress of Parasitology, held in Glasgow, United Kingdom in August 2006; and the 55th Annual Meeting of the American Society of Tropical Medicine and Hygiene, held in Atlanta, United States in November 2006) and received the emails, we are confident that the SRA indeed reflects the richness and breadth of current schistosomiasis research

    A negative feedback loop mediated by the Bcl6-cullin 3 complex limits Tfh cell differentiation

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    Induction of Bcl6 (B cell lymphoma 6) is essential for T follicular helper (Tfh) cell differentiation of antigen-stimulated CD4(+) T cells. Intriguingly, we found that Bcl6 was also highly and transiently expressed during the CD4(+)CD8(+) (double positive [DP]) stage of T cell development, in association with the E3 ligase cullin 3 (Cul3), a novel binding partner of Bcl6 which ubiquitinates histone proteins. DP stage-specific deletion of the E3 ligase Cul3, or of Bcl6, induced the derepression of the Bcl6 target genes Batf (basic leucine zipper transcription factor, ATF-like) and Bcl6, in part through epigenetic modifications of CD4(+) single-positive thymocytes. Although they maintained an apparently normal phenotype after emigration, they expressed increased amounts of Batf and Bcl6 at basal state and produced explosive and prolonged Tfh responses upon subsequent antigen encounter. Ablation of Cul3 in mature CD4(+) splenocytes also resulted in dramatically exaggerated Tfh responses. Thus, although previous studies have emphasized the essential role of Bcl6 in inducing Tfh responses, our findings reveal that Bcl6-Cul3 complexes also provide essential negative feedback regulation during both thymocyte development and T cell activation to restrain excessive Tfh responses

    Accelerated elastin degradation by age-disease interaction:a common feature in age-related diseases

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    Aging is a major driving force for many diseases but the relationship between chronological age, the aging process and age-related diseases is not fully understood. Fragmentation and loss of ultra-long-lived elastin are key features in aging and several age-related diseases leading to increased mortality. By comparing the relationship between age and elastin turnover with healthy volunteers, we show that accelerated elastin turnover by age-disease interaction is a common feature of age-related diseases

    Accelerated elastin degradation by age-disease interaction:a common feature in age-related diseases

    Get PDF
    Aging is a major driving force for many diseases but the relationship between chronological age, the aging process and age-related diseases is not fully understood. Fragmentation and loss of ultra-long-lived elastin are key features in aging and several age-related diseases leading to increased mortality. By comparing the relationship between age and elastin turnover with healthy volunteers, we show that accelerated elastin turnover by age-disease interaction is a common feature of age-related diseases
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