Expression of the HPV18/E6 oncoprotein induces DNA damage

Abstract This study investigated possible variations in DNA damage in HeLa cells with silenced expression of the HPV/E6oncogene compared with HeLa cells with normal expression of the E6oncogene using the DNA breakage detection-fluorescence in situ hybridization (DBD-FISH) technique and a whole human genome DNA probe. The variable levels of DNA breaks present were measured quantitatively using image analysis after whole-genome DNA hybridization. HeLa cells with silenced expression of the HPV18/E6 oncogene showed a significant decrease in DNA damage compared with parental cells with normal expression of the E6oncogene. These results were confirmed by alkaline comet assay. In conclusion, we demonstrated a decrease in DNA damage in HeLa clones associated with low expression of the HPV/E6 oncogene

Comportamiento térmico del sistema SATE: análisis de la fachada de un edificio de los años 50 rehabilitado en Madrid

En España, según el Plan Nacional de Acción de eficiencia energética 2017-2020, el sector residencial supone un 18,5% del consumo de energía final. La normativa actual exige la reducción del consumo de energía en este sector a través de la implementación de estrategias de ahorro de energía. Actualmente existen 10 millones de edificios destinados a vivienda en nuestro país, de los cuales unos 800.000 tienen más de 50 años. En el caso de Madrid son más de 20.000 edificios construidos en esa época, presentando carencias en cuanto a confort y habitabilidad y, por ello, se hace necesario ver la rehabilitación como algo imprescindible para el cumplimiento de los objetivos de ahorro energético propuestos. Estas actuaciones tratan de adecuar el edificio a los requisitos de las nuevas normativas, mejorando su calidad y vida útil. Además, suponen un menor impacto económico y ambiental que la demolición y nueva construcción. En este caso, el objetivo de estudio es un edificio rehabilitado con un sistema de aislamiento térmico por el exterior (SATE). Este sistema consiste en la adición de aislamiento térmico por el exterior de las fachadas, ayudando así a crear una envolvente continua en la fachada del edificio. Se analiza el comportamiento térmico de las fachadas en una vivienda en la parte del edificio rehabilitado con este sistema, comparándolo con otra vivienda del edificio en su estado original, con el objetivo de analizar el comportamiento real de la fachada rehabilitada. El edificio está en San Cristóbal de los Ángeles, en el sur de Madrid y está construido al final de los años 50. Las dos viviendas están situadas en la tercera planta del edificio, en los portales 47 y 51, teniendo en cuenta las costumbres de uso de los inquilinos. Los datos de temperaturas para el análisis se obtienen a través de una monitorización con termopares tipo K, colocados tanto dentro como fuera de las fachadas, y en cada una de las orientaciones. Estos termopares están conectados a unos dataloggers que recogen los datos de temperatura durante la campaña de medición en marzo, mes caracterizado por tener condiciones climatológicas de temperaturas medias, pero con amplias oscilaciones entre el día y la noche. A través de esta comparativa se puede comprobar que existe una gran diferencia en el comportamiento térmico de la fachada en su estado original frente a la rehabilitada. La diferencia media de temperatura entre la superficie exterior e interior en la fachada original es de 3,5ºC y 2,5ºC, norte y sur respectivamente, mientras que en la rehabilitada es de 9,7ºC en el norte y 7,9ºC en el sur, mostrando una disminución de un 74,67% en la transmitancia con la colocación del SATE con respecto a la fachada original. En conclusión, el sistema SATE ayuda a que las temperaturas superficiales interiores sean más independientes de las temperaturas exteriores, y que su colocación como método de rehabilitación influye positivamente al mantenimiento de las temperaturas interiores ayudando a optimizar el consumo energético para mantener la temperatura de confort en las viviendas

SEN1990 is a predicted winged helix-turn-helix protein involved in the pathogenicity of Salmonella enterica serovar Enteritidis and the expression of the gene oafB in the SPI-17

Excisable genomic islands (EGIs) are horizontally acquired genetic elements that harbor an array of genes with diverse functions. ROD21 is an EGI found integrated in the chromosome of Salmonella enterica serovar Enteritidis (Salmonella ser. Enteritidis). While this island is known to be involved in the capacity of Salmonella ser. Enteritidis to cross the epithelial barrier and colonize sterile organs, the role of most ROD21 genes remains unknown, and thus, the identification of their function is fundamental to understanding the impact of this EGI on bacterium pathogenicity. Therefore, in this study, we used a bioinformatical approach to evaluate the function of ROD21-encoded genes and delve into the characterization of SEN1990, a gene encoding a putative DNA-binding protein. We characterized the predicted structure of SEN1990, finding that this protein contains a three-stranded winged helix-turn-helix (wHTH) DNA-binding domain. Additionally, we identified homologs of SEN1990 among other members of the EARL EGIs. Furthermore, we deleted SEN1990 in Salmonella ser. Enteritidis, finding no differences in the replication or maintenance of the excised ROD21, contrary to what the previous Refseq annotation of the protein suggests. High-throughput RNA sequencing was carried out to evaluate the effect of the absence of SEN1990 on the bacterium’s global transcription. We found a downregulated expression of oafB, an SPI-17-encoded acetyltransferase involved in O-antigen modification, which was restored when the deletion mutant was complemented ectopically. Additionally, we found that strains lacking SEN1990 had a reduced capacity to colonize sterile organs in mice. Our findings suggest that SEN1990 encodes a wHTH domain-containing protein that modulates the transcription of oafB from the SPI-17, implying a crosstalk between these pathogenicity islands and a possible new role of ROD21 in the pathogenesis of Salmonella ser. Enteritidis

Geographical Distribution and Risk Association of Human Papillomavirus Genotype 52–Variant Lineages

Human papillomavirus (HPV) genotype 52 is commonly found in Asian cases of cervical cancer but is rare elsewhere. Analysis of 611 isolates collected worldwide revealed a remarkable geographical distribution, with lineage B predominating in Asia (89.0% vs 0%–5.5% ; Pcorrected < .001), whereas lineage A predominated in Africa, the Americas, and Europe. We propose that the name “Asian lineage” be used to denote lineage B, to signify this feature. Preliminary analysis suggested a higher disease risk for lineage B, although ethnogeographical confounders could not be excluded. Further studies are warranted to verify whether the reported high attribution of disease to HPV52 in Asia is due to the high prevalence of lineage B

Métodos y técnicas de monitoreo y predicción temprana en los escenarios de riesgos socionaturales

Esta obra concentra los métodos y las técnicas fundamentales para el seguimiento y monitoreo de las dinámicas de los escenarios de riesgos socionaturales (geológicos e hidrometeorológicos) y tiene como objetivo general orientar, apoyar y acompañar a los directivos y operativos de protección civil en aterrizar las acciones y políticas públicas enfocadas a la gestión del riesgo local de desastre

Virus de papiloma humano y polimorfismos del gen TP53 en cáncer cervical uterino /\ua0tesis que para obtener el grado de Doctor en Ciencias Biomédicas, presenta Patricia Piña Sánchez ; asesor Mauricio Salcedo Vargas, Patricia Ostrosky Wegman, Alfonso Dueñas González

. ii, 103, 11, [15] páginas :\ua0ilustraciones. Doctorado en Ciencias Biomédicas\ua0UNAM, Instituto de Investigaciones Biomédicas,\ua0201

Histone code and long non-coding RNAs (lncRNAs) aberrations in lung cancer: implications in the therapy response

Abstract Respiratory diseases hold several genome, epigenome, and transcriptional aberrations as a cause of the accumulated damage promoted by, among others, environmental risk factors. Such aberrations can also come about as an adaptive response when faced with therapeutic oncological drugs. In epigenetic terms, aberrations in DNA methylation patterns, histone code marks balance, and/or chromatin-remodeling complexes recruitment, among Polycomb Repressive Complex-2 (PRC2) versus Trithorax (TRX) Activator Complex, have been proposed to be affected by several previously characterized functional long non-coding RNAs (lncRNAs). Such molecules are involved in modulating and/or controlling lung cancer epigenome and genome expression, as well as in malignancy and clinical progression in lung cancer. Several recent reports have described diverse epigenetic modifications in lung cancer cells and solid tumors, among others genomic DNA methylation and post-translational modifications (PTMs) on histone tails, as well as lncRNAs patterns and levels of expression. However, few systematic approaches have attempted to demonstrate a biological function and clinical association, aiming to improve therapeutic decisions in basic research and lung clinical oncology. A widely used example is the lncRNA HOTAIR and its functional histone mark H3K27me3, which is directly associated to the PRC2; however, few systematic pieces of solid evidence have been experimentally performed, conducted and/or validated to predict lung oncological therapeutic efficacy. Recent evidence suggests that chromatin-remodeling complexes accompanied by lncRNAs profiles are involved in several comprehensive lung carcinoma clinical parameters, including histopathology progression, prognosis, and/or responsiveness to unique or combined oncological therapies. The present manuscript offers a systematic revision of the current knowledge about the major epigenetic aberrations represented by changes in histone PTMs and lncRNAs expression levels and patterns in human lung carcinomas in cancer drug-based treatments, as an important comprehensive knowledge focusing on better oncological therapies. In addition, a new future direction must be refocusing on several gene target therapies, mainly on pharmaceutical EGFR-TKIs compounds, widely applied in lung cancer, currently the leading cause of death by malignant diseases