BUAP, modelo transformador en la mejora continua de la educación superior

Presentamos una práctica innovadora que transmite conocimientos y experiencias para la mejora continua de la educación superior, basados en el modelo de aseguramiento de la calidad desarrollado por la BUAP (2018), además del contenido teórico, se comparten experiencias exitosas  de  gestión académica, investigación y de responsabilidad social, con enfoque intercultural y de perspectiva de género, poniendo énfasis en la formación de profesionales plenos, responsables socialmente, humanistas, justos y democráticos. Los contenidos son flexibles, adaptables a cualquier tipo de institución, impartidos totalmente a distancia a través de plataformas educacionales, facilitando la participación de profesionales no solo de México, si no también de América Latina, promoviendo la cooperación y solidaridad entre instituciones. La transmisión de experiencias exitosas, se acompaña del uso del aprendizaje basado en proyectos, asesorando el desarrollo de proyectos de mejora contextualizados en las instituciones de interés del participante, promoviendo con la evaluación de pares, la crítica constructiva de los participantes. Ha generado alianzas de la BUAP con el principal organismo acreditador de México y con el Gobierno de Perú, la BUAP fue invitada para colaborar en la elaboración de política pública federal para la mejora de la educación superior de México. Genera cientos de beneficiarios directos en las comunidades académicas de los participantes e incontables beneficiarios por las acciones de impacto social en las regiones en donde las Instituciones tienen influencia. Su escalabilidad permanece en ascenso, genera innovaciones, mejoras educativas y estrategias de financiamiento e inversión para nuevos proyectos educativos que impactan en mejor calidad de vida

Análisis in silico de la interacción entre IclR y el regulador transcripcional de virulencia PerA de Escherichia coli enteropatógena

Escherichia coli enteropatógena (EPEC) es un patógeno causante de diarrea que afecta a menores de 6 meses de edad, pertenece a una familia de patógenos que forman la lesión AE (Attaching and Effacing), caracterizada por la destrucción de las microvellosidades y la formación de una estructura en forma de pedestal sobre la cual la bacteria se adhiere al enterocito. Uno de los factores de virulencia de EPEC es BFP (Bundle Forming Pilus), una fimbria tipo IV que contribuye a la adherencia inicial mediante la formación de microcolonias y la autoagregación. La expresión de BFP es activada a nivel transcripcional por PerA, un regulador tipo AraC/XylS. PerA activa también su propia expresión y la de PerC, un activador de los genes ubicados en la isla de patogenicidad LEE (Locus of enterocyte effacement). El mecanismo que emplea PerA como activador no es completamente entendido, recientemente demostramos que interactúa con la maquinaria transcripcional pero qué determina su función como activador todavía no ha sido analizado. Mediante estudios de proteómica, identificamos que PerA podría interactuar con diversas proteínas reguladoras de EPEC, lo que sugiere que dichas interacciones posiblemente modulan su función como activador. Una de estas proteínas es IclR, un regulador de la familia IclR que incluye a represores, activadores y de papel dual. Los miembros de esta familia regulan procesos involucrados en metabolismo, patogenicidad, percepción del quorum, entre otros. IclR reprime genes implicados en la vía del glioxilato y, aunque no hay una relación directa en la virulencia en EPEC, el objetivo de este trabajo fue evaluar mediante análisis bioinformáticos la interacción con PerA. Para esto, se obtuvo la secuencia primaria de IclR y PerA, se calculó la interacción con "PSOPIA". Posteriormente, se determinó la afinidad de unión con "PPA-Pred2", se analizaron los sitios de interacción con "iFrag" y se usó “HawkDock” para calcular la energía libre de unión. Para modelar la interacción, se utilizó “AlphaFold2” y se visualizaron con PyMOL. Los análisis de interacción entre las secuencias con PPA-Pred2 mostraron una ΔG de -5.2 kcal/mol y una kD 7.54e - 12 M. El modelo de acoplamiento molecular mostró una energía libre de unión de - 28,5 kcal/mol. En conjunto, los resultados obtenidos indican una potencial interacción entre IclR y PerA, estudios experimentales permitirán confirmar tal interacción y el papel de la misma en la modulación de PerA, lo que permitirá ampliar el conocimiento sobre el mecanismo que utiliza este importante regulador de virulencia de EPEC

Hepatitis C virus infection in blood donors from the state of Puebla, Mexico

<p>Abstract</p> <p>Background</p> <p>Worldwide, 130 million persons are estimated to be infected with HCV. Puebla is the Mexican state with the highest mortality due to hepatic cirrhosis. Therefore, it is imperative to obtain epidemiological data on HCV infection in asymptomatic people of this region. The objective of present study was to analyze the prevalence of antibodies and genotypes of hepatitis C virus (HCV) in blood donors from Puebla, Mexico.</p> <p>Results</p> <p>The overall prevalence was 0.84% (515/61553). Distribution by region was: North, 0.86% (54/6270); Southeast, 1.04% (75/7197); Southwest, 0.93% (36/3852); and Central, 0.79% (350/44234). Ninety-six donors were enrolled for detection and genotyping of virus, from which 37 (38.5%) were HCV-RNA positive. Detected subtypes were: 1a (40.5%), 1b (27.0%), mixed 1a/1b (18.9%), undetermined genotype 1 (5.4%), 2a (2.7%), 2b (2.7%), and mixed 1a/2a (2.7%). All recovered donors with S/CO > 39 were HCV-RNA positive (11/11) and presented elevated ALT; in donors with S/CO < 39 HCV-RNA, positivity was of 30.4%; and 70% had normal values of ALT. The main risk factors associated with HCV infection were blood transfusion and surgery.</p> <p>Conclusions</p> <p>HCV prevalence of donors in Puebla is similar to other Mexican states. The most prevalent genotype is 1, of which subtype 1a is the most frequent.</p

Epigenetic mechanisms of particulate matter exposure: air pollution and hazards on human health

Environmental pollution nowadays has not only a direct correlation with human health changes but a direct social impact. Epidemiological studies have evidenced the increased damage to human health on a daily basis because of damage to the ecological niche. Rapid urban growth and industrialized societies importantly compromise air quality, which can be assessed by a notable accumulation of air pollutants in both the gas and the particle phases. Of them, particulate matter (PM) represents a highly complex mixture of organic and inorganic compounds of the most variable size, composition, and origin. PM being one of the most complex environmental pollutants, its accumulation also varies in a temporal and spatial manner, which challenges current analytical techniques used to investigate PM interactions. Nevertheless, the characterization of the chemical composition of PM is a reliable indicator of the composition of the atmosphere, the quality of breathed air in urbanized societies, industrial zones and consequently gives support for pertinent measures to avoid serious health damage. Epigenomic damage is one of the most promising biological mechanisms of air pollution-derived carcinogenesis. Therefore, this review aims to highlight the implication of PM exposure in diverse molecular mechanisms driving human diseases by altered epigenetic regulation. The presented findings in the context of pan-organic cancer, fibrosis, neurodegeneration and metabolic diseases may provide valuable insights into the toxicity effects of PM components at the epigenomic level and may serve as biomarkers of early detection for novel targeted therapies

Simulated LCSLM with Inducible Diffractive Theory to Display Super-Gaussian Arrays Applying the Transport-of-Intensity Equation

We simulate a liquid crystal spatial light modulator (LCSLM), previously validated by Fraunhofer diffraction to observe super-Gaussian periodic profiles and analyze the wavefront of optical surfaces applying the transport-of-intensity equation (TIE). The LCSLM represents an alternative to the Ronchi Rulings, allowing to avoid all the related issues regarding diffractive and refractive properties, and noise. To this aim, we developed and numerically simulated a LCSLM resembling a fractal from a generating base. Such a base is constituted by an active square (values equal to one) and surrounded by eight switched-off pixels (zero-valued). We replicate the base in order to form 1 ×N-pixels and the successive rows to build the 1024×1024 LCSLM of active pixels. We visually test the LCSLM with calibration images as a diffractive object that is mathematically inducible, using mathematical induction over the N×N-shape (1×1, 2×2, 3×3, …, n×n pixels for the generalization). Finally, we experimentally generate periodic super-Gaussian profiles to be visualized in the LCSLM (transmission SLM, 1024×768-pixels LC 2012 Translucent SLM), modifying the TIE as an optical test in order to analyze the optical elements by comparing the results with ZYGO/APEX

The Assembly of Flagella in Enteropathogenic Escherichia coli Requires the Presence of a Functional Type III Secretion System

In enteropathogenic Escherichia coli (EPEC), the production of flagella and the type III secretion system (T3SS) is activated in the presence of host cultured epithelial cells. The goal of this study was to investigate the relationship between expression of flagella and the T3SS. Mutants deficient in assembling T3SS basal and translocon components (&Delta;espA, &Delta;espB, &Delta;espD, &Delta;escC, &Delta;escN, and &Delta;escV), and in secreting effector molecules (&Delta;sepD and &Delta;sepL) were tested for flagella production under several growth conditions. The &Delta;espA mutant did not produce flagella in any condition tested, although fliC was transcribed. The remaining mutants produced different levels of flagella upon growth in LB or in the presence of cells but were significantly diminished in flagella production after growth in Dulbecco&rsquo;s minimal essential medium. We also investigated the role of virulence and global regulator genes in expression of flagella. The &Delta;qseB and &Delta;qseC mutants produced abundant flagella only when growing in LB and in the presence of HeLa cells, indicating that QseB and QseC act as negative regulators of fliC transcription. The &Delta;grlR, &Delta;perA, &Delta;ler, &Delta;hns, and &Delta;fis mutants produced low levels of flagella, suggesting these regulators are activators of fliC expression. These data suggest that the presence of an intact T3SS is required for assembly of flagella highlighting the existence in EPEC of a cross-talk between these two virulence-associated T3SSs

The Transcription of Flagella of Enteropathogenic Escherichia coli O127:H6 Is Activated in Response to Environmental and Nutritional Signals

The flagella of enteropathogenic Escherichia coli (EPEC) O127:H6 E2348/69 mediate adherence to host proteins and epithelial cells. What environmental and nutritional signals trigger or down-regulate flagella expression in EPEC are largely unknown. In this study, we analyzed the influence of pH, oxygen tension, cationic and anionic salts (including bile salt), carbon and nitrogen sources, and catecholamines on the expression of the flagellin gene (fliC) of E2348/69. We found that sodium bicarbonate, which has been shown to induce the expression of type III secretion effectors, down-regulated flagella expression, explaining why E2348/69 shows reduced motility and flagellation when growing in Dulbecco&rsquo;s Minimal Essential Medium (DMEM). Further, growth under a 5% carbon dioxide atmosphere, in DMEM adjusted to pH 8.2, in M9 minimal medium supplemented with 80 mM glucose or sucrose, and in DMEM containing 150 mM sodium chloride, 0.1% sodium deoxycholate, or 30 &micro;M epinephrine significantly enhanced fliC transcription to different levels in comparison to growth in DMEM alone. When EPEC was grown in the presence of HeLa cells or in supernatants of cultured HeLa cells, high levels (4-fold increase) of fliC transcription were detected in comparison to growth in DMEM alone. Our data suggest that nutritional and host signals that EPEC may encounter in the intestinal niche activate fliC expression in order to favor motility and host colonization

The EcpD Tip Adhesin of the <i>Escherichia coli</i> Common Pilus Mediates Binding of Enteropathogenic <i>E. coli</i> to Extracellular Matrix Proteins

The attachment of enteropathogenic Escherichia coli (EPEC) to intestinal epithelial cells is facilitated by several adhesins; however, the individual host-cell receptors for pili-mediated adherence have not been fully characterized. In this study, we evaluated the hypothesis that the E. coli common pilus (ECP) tip adhesin protein EcpD mediates attachment of EPEC to several extracellular matrix (ECM) glycoproteins (fibronectin, laminin, collagens I and IV, and mucin). We found that the ΔecpA mutant, which lacks production of the EcpA filament but retains EcpD on the surface, adhered to these glycoproteins below the wild-type levels, while the ΔecpD mutant, which does not display EcpA or EcpD, bound significantly less to these host glycoproteins. In agreement, a purified recombinant EcpD subunit bound significantly more than EcpA to laminin, fibronectin, collagens I and IV, and mucin in a dose-dependent manner. These are compelling data that strongly suggest that ECP-producing EPEC may bind to host ECM glycoproteins and mucins through the tip adhesin protein EcpD. This study highlights the versatility of EPEC to bind to different host proteins and suggests that the interaction of ECP with the host’s ECM glycoproteins may facilitate colonization of the intestinal mucosal epithelium

Regulatory Control of the Escherichia coli O157:H7 lpf1 Operon by H-NS and Ler▿

Long polar fimbriae 1 (Lpf1) of Escherichia coli O157:H7 is a tightly regulated adhesin, with H-NS silencing the transcriptional expression of the lpf1 operon while Ler (locus of enterocyte effacement-encoded regulator) acts as an antisilencer. We mapped the minimal regulatory region of lpf1 required for H-NS- and Ler-mediated regulation and found that it is 79% AT rich. Three putative sites for H-NS binding were identified. Two of them, named silencer regulatory sequence 1 (SRS1) and SRS2, are located on a region that covers both of the lpf1 promoters (P1 and P2). The third putative H-NS binding site is located within the lpfA1 gene in a region extending from +258 bp to +545 bp downstream of ATG; however, this site does not seem to play a role in lpfA1 regulation under the conditions tested in this work. Ler was also found to interact with Ler binding sites (LBSs). Ler binding site 1 (LBS1) and LBS2 are located upstream of the two promoters. LBS1 overlaps SRS1, while LBS3 overlaps the P1 promoter and SRS2. Based on the experimental data, we propose that H-NS silences lpf1 expression by binding to both of the SRSs on the promoter region, forming an SRS-H-NS complex that prevents RNA polymerase-mediated transcription. A model of the regulation of the lpfA1 operon of E. coli O157:H7 by H-NS and Ler is discussed