Microencapsulación de aceite de semilla de uva mediante secado por aspersión utilizando proteína de suero lácteo y pectina de tejocote

The use of O/W emulsions with well-functioning wall materials, such as whey protein and pectin from different origins, allows stabilization and protection of bioactive ingredients. The HP-protein interaction allowed the formation of thicker physical barriers, with high MEE and adequate morphology, which can stabilize GSO against oxidation processes. The GSO’s MEE was influenced by the TS content and the type of pectin used. The emulsions with hawthorn pectin from accessions 55 and 100, with 40 % TS, had the highest viscosities in the whole shear rate range. The EWPC-HP100,3:1 treatment produced microcapsules with the highest MEE (71.29 %) and the smallest emulsion droplet diameter (d3,2 = 1.45 μm). Generally, a reduction in droplet size is associated with greater stability for possible use in food matrices. The morphology of the capsules was affected by the type of biopolymer and the concentration of the wall materials. Microcapsules with HP100 had spherical particles with smaller dents on the outer surface than those formulated with CPObjective was to microencapsulate grape seed oil (GSO). GSO by spray drying of emulsions stabilized with biopolymer complexes formed from whey protein concentrate (WPC) and hawthorn pectin (HP) from two different cultivars Grape seed oil (GSO) contains unsaturated fatty acids that make it susceptible to degradation, causing it to deteriorate. In this sense, microencapsulation in biopolymer matrices is a good alternative to protect it. Emulsions were developed with different wall material: GSO ratios (2:1 and 3:1) and percentage of total solids (30 and 40 %). The wall materials were WPC-citrus pectin and WPC-HP from two cultivars (HP55 and HP100, with an esterification degree of 70.3 and 61 %, respectively). The factors evaluated were viscosity, mean surface diameter (d3,2) and morphology of the emulsions, and d3,2, microencapsulation efficiency (MEE) and electron microscopy of the microcapsules. The d3,2 of the emulsions ranged from 1.45 to 2.54 μm, where EWPC-HP100,3:1 exhibited the smallest d3,2. These values were related to the type of pectin and were inversely proportional to the viscosity and solids content. The highest MEE was presented by MWPC-HP100,3:1 (71.29 %), which had the highest viscosity and the lowest d3,2 in the emulsion

The PDZ-binding motif of severe acute respiratory syndrome coronavirus envelope protein is a determinant of viral pathogenesis

A recombinant severe acute respiratory syndrome coronavirus (SARS-CoV) lacking the envelope (E) protein is attenuated in vivo. Here we report that E protein PDZ-binding motif (PBM), a domain involved in protein-protein interactions, is a major determinant of virulence. Elimination of SARS-CoV E protein PBM by using reverse genetics caused a reduction in the deleterious exacerbation of the immune response triggered during infection with the parental virus and virus attenuation. Cellular protein syntenin was identified to bind the E protein PBM during SARS-CoV infection by using three complementary strategies, yeast two-hybrid, reciprocal coimmunoprecipitation and confocal microscopy assays. Syntenin redistributed from the nucleus to the cell cytoplasm during infection with viruses containing the E protein PBM, activating p38 MAPK and leading to the overexpression of inflammatory cytokines. Silencing of syntenin using siRNAs led to a decrease in p38 MAPK activation in SARS-CoV infected cells, further reinforcing their functional relationship. Active p38 MAPK was reduced in lungs of mice infected with SARS-CoVs lacking E protein PBM as compared with the parental virus, leading to a decreased expression of inflammatory cytokines and to virus attenuation. Interestingly, administration of a p38 MAPK inhibitor led to an increase in mice survival after infection with SARS-CoV, confirming the relevance of this pathway in SARS-CoV virulence. Therefore, the E protein PBM is a virulence domain that activates immunopathology most likely by using syntenin as a mediator of p38 MAPK induced inflammation

Severe acute respiratory syndrome coronavirus envelope protein ion channel activity promotes virus fitness and pathogenesis

Deletion of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) envelope (E) gene attenuates the virus. E gene encodes a small multifunctional protein that possesses ion channel (IC) activity, an important function in virus-host interaction. To test the contribution of E protein IC activity in virus pathogenesis, two recombinant mouse-adapted SARS-CoVs, each containing one single amino acid mutation that suppressed ion conductivity, were engineered. After serial infections, mutant viruses, in general, incorporated compensatory mutations within E gene that rendered active ion channels. Furthermore, IC activity conferred better fitness in competition assays, suggesting that ion conductivity represents an advantage for the virus. Interestingly, mice infected with viruses displaying E protein IC activity, either with the wild-type E protein sequence or with the revertants that restored ion transport, rapidly lost weight and died. In contrast, mice infected with mutants lacking IC activity, which did not incorporate mutations within E gene during the experiment, recovered from disease and most survived. Knocking down E protein IC activity did not significantly affect virus growth in infected mice but decreased edema accumulation, the major determinant of acute respiratory distress syndrome (ARDS) leading to death. Reduced edema correlated with lung epithelia integrity and proper localization of Na+/K+ ATPase, which participates in edema resolution. Levels of inflammasome-activated IL-1β were reduced in the lung airways of the animals infected with viruses lacking E protein IC activity, indicating that E protein IC function is required for inflammasome activation. Reduction of IL-1β was accompanied by diminished amounts of TNF and IL-6 in the absence of E protein ion conductivity. All these key cytokines promote the progression of lung damage and ARDS pathology. In conclusion, E protein IC activity represents a new determinant for SARS-CoV virulence

Epithelial to mesenchymal transition trajectories in developmental and disease

Resumen del trabajo presentado al 19th International Congress of Developmental Biology, celebrado en El Algarve (Portugal) del 16 al 20 de octubre de 2022.The Epithelial to Mesenchymal transition (EMT) triggers cell plasticity during embryonic development and tissue repair, but it can also promote tumor progression and organ degeneration. The reactivation of EMT in the adult promotes cell dedifferentiation and profound remodeling of the epithelial program, leading to multiple phenotypes, observed in response to injury, during organ fibrosis and cancer cell dissemination. Despite recent advances, identifying universal EMT molecular signatures and understanding how EMT can instructs different outcomes have remained elusive due to the intrinsic complexity and heterogeneity of the process. We have dissected how EMT transcription factors (EMT-TFs) orchestrate TGFBinduced EMT including phenotypic and behavioral states. Further, we have combined lineage tracing and single-cell transcriptomics in three EMT contexts, namely the neural crest, renal fibrosis, and breast cancer to reveal conserved EMT transcription factor codes and signaling pathways that discriminate different EMT states. After inferring cellular trajectories, we have reconstructed the evolution of EMT phenotypic and functional states in all these contexts. Finally, multiplex labeling allowed to spatially allocate distinct EMT programs in mouse and human tumor samples. Altogether, this work unveils distinct EMT trajectories in development and disease, which should also help propase improved therapeutic strategies for organ fibrosis and cancer.Peer reviewe

Two distinct epithelial to mesenchymal transition programmes. Control invasion and inflammation in segregated tumour cell populations

Resumen del trabajo presentado al 19th Christmas Meeting del Instituto de Neurociencias (CSIC-UMH) celebrado el 21 de diciembre de 2022.Epithelial plasticity is at the core of crucial processes including embryonic cell migration, cancer progression, organ tibrosis and tissue repair. The epithelial to mesenchymal transition (EMT) triggers cell plasticity in all these contexts, highlighting its pleiotropy and intrinsic complcxity. Seminal studies have classified EMT states in cancer celllines and animal modcls. This varicty ofEMT phenotypes necds further investigation, particularly those relevant to the progression ofprevalent and dcvastating diseases such as cancer. Our objcctive is to analyse at single-cell level how different EMT states are established in tumours and if different EMT states pcrform different functions during tumour progression.Peer reviewe

Memoria del segundo simposium sobre historia, sociedad y cultura de México y América Latina

La presente obra reúne 20 ponencias de las 27 que se presentaron en el “Segundo simposium sobre historia, sociedad y cultura de México y América Latina”, realizado el 8 y 9 de noviembre de 2006, en el Centro de Investigación en Ciencias Sociales y Humanidades (CICSyH) de la Universidad Autónoma del Estado de México (UAEM), en Toluca, Estado de México

Regulation of cell death receptor S-nitrosylation and apoptotic signaling by Sorafenib in hepatoblastoma cells

Nitric oxide (NO) plays a relevant role during cell death regulation in tumor cells. The overexpression of nitric oxide synthase type III (NOS-3) induces oxidative and nitrosative stress, p53 and cell death receptor expression and apoptosis in hepatoblastoma cells. S-nitrosylation of cell death receptor modulates apoptosis. Sorafenib is the unique recommended molecular-targeted drug for the treatment of patients with advanced hepatocellular carcinoma. The present study was addressed to elucidate the potential role of NO during Sorafenib-induced cell death in HepG2 cells. We determined the intra- and extracellular NO concentration, cell death receptor expression and their S-nitrosylation modifications, and apoptotic signaling in Sorafenib-treated HepG2 cells. The effect of NO donors on above parameters has also been determined. Sorafenib induced apoptosis in HepG2 cells. However, low concentration of the drug (10nM) increased cell death receptor expression, as well as caspase-8 and -9 activation, but without activation of downstream apoptotic markers. In contrast, Sorafenib (10 µM) reduced upstream apoptotic parameters but increased caspase-3 activation and DNA fragmentation in HepG2 cells. The shift of cell death signaling pathway was associated with a reduction of S-nitrosylation of cell death receptors in Sorafenib-treated cells. The administration of NO donors increased S-nitrosylation of cell death receptors and overall induction of cell death markers in control and Sorafenib-treated cells. In conclusion, Sorafenib induced alteration of cell death receptor S-nitrosylation status which may have a relevant repercussion on cell death signaling in hepatoblastoma cells.Instituto de Salud Carlos III PI13/00021Ministerio de Economía y Competitividad BFU2012-32056Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía BIO-0216Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía CTS-6264Consejería de Salud, Junta de Andalucía PI13/ 0002

Comunicación educación un campo de resistencias

El presente libro obedece a la imperiosa necesidad de desplegar la potencia de la Facultad de Ciencias de la Comunicación en la Corporación Universitaria Minuto de Dios -UNIMINUTO, de otras comunidades académicas y de los espacios de movimiento social interesados en deconstruir los discursos de comunicación y educación desde la perspectiva del pensamiento crítico. En este caso entendemos potencia como la fuerza individual y colectiva capaz de rebasar la racionalidad dominante en la sociedad contemporánea, colonizada por la economía como única mirada del mundo; esto es, potencia como ímpetu insospechado por el poder. Por otra parte, el libro tiene como eje articulador el concepto de resistencia, definido este como el acto de recrear la realidad a partir de las posibilidades que ofrece la comunicación, para generar producción de sentido y dinamizar el cambio social. Propone realizar el ejercicio de concebir el mundo desde una perspectiva diferente a la hegemónica y de crear multiplicidades que trabajen unidas, reconociendo sus diferencias pero vinculándose en un “lugar común” del cual, cada una de ellas, regrese a su lugar cotidiano transformada por la acción colectiva del campo de Comunicación - Educación

Clustering COVID-19 ARDS patients through the first days of ICU admission. An analysis of the CIBERESUCICOVID Cohort

Background Acute respiratory distress syndrome (ARDS) can be classified into sub-phenotypes according to different inflammatory/clinical status. Prognostic enrichment was achieved by grouping patients into hypoinflammatory or hyperinflammatory sub-phenotypes, even though the time of analysis may change the classification according to treatment response or disease evolution. We aimed to evaluate when patients can be clustered in more than 1 group, and how they may change the clustering of patients using data of baseline or day 3, and the prognosis of patients according to their evolution by changing or not the cluster.Methods Multicenter, observational prospective, and retrospective study of patients admitted due to ARDS related to COVID-19 infection in Spain. Patients were grouped according to a clustering mixed-type data algorithm (k-prototypes) using continuous and categorical readily available variables at baseline and day 3.Results Of 6205 patients, 3743 (60%) were included in the study. According to silhouette analysis, patients were grouped in two clusters. At baseline, 1402 (37%) patients were included in cluster 1 and 2341(63%) in cluster 2. On day 3, 1557(42%) patients were included in cluster 1 and 2086 (57%) in cluster 2. The patients included in cluster 2 were older and more frequently hypertensive and had a higher prevalence of shock, organ dysfunction, inflammatory biomarkers, and worst respiratory indexes at both time points. The 90-day mortality was higher in cluster 2 at both clustering processes (43.8% [n = 1025] versus 27.3% [n = 383] at baseline, and 49% [n = 1023] versus 20.6% [n = 321] on day 3). Four hundred and fifty-eight (33%) patients clustered in the first group were clustered in the second group on day 3. In contrast, 638 (27%) patients clustered in the second group were clustered in the first group on day 3.Conclusions During the first days, patients can be clustered into two groups and the process of clustering patients may change as they continue to evolve. This means that despite a vast majority of patients remaining in the same cluster, a minority reaching 33% of patients analyzed may be re-categorized into different clusters based on their progress. Such changes can significantly impact their prognosis