42 research outputs found

    Psychological aspects of pre-adolescents or adolescents with precocious puberty: A systematic review

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    Precocious puberty (PP) is an illness that appears when puberty, begins some years earlier than usual, provoking inferences in preadolescents and adolescents and their families. Therefore, the aim is to analyze if psychological consequences can be observed in groups of preadolescents or adolescents with PP. Method: A bibliographic search of the scientific literature was made following the PRISMA guide in the following databases: ProQuest, Psychinfo, Web Of Science, and Scopus. 592 studies were found, were uploaded to Covidence to make a screening, of which finally 6 were included for the revision according to the inclusion and exclusion criteria. Two independent evaluators made the search, selection, data extraction and quality evaluation of studies independently. The agreement degree between both was excellent in all of the cases. Results: 211 preadolescents participated in total in all studies, of which 99 were preadolescents with PP, with a mean age of 8,94 years old. Studies evaluated so heterogeneous variables, such as psychopathology, selfimage, neuropsychological and cognitive variables, and reasons to delay or stop PP. The quality of studies was moderated especially due to the low quality of the studies design, which were mostly transversal, and the representativity of the sample, being selected by convenience. Conclusions and implications: More research is needed to evaluate the psychological consequences of the PP diagnosis in pediatrics, and its protection factors, because none of the studies approached this question. We consider that it is necessary to increment the quality of these studies, and that these take a biopsychosocial perspective

    The respiratory microbiome in bronchial mucosa and secretions from severe IgE-mediated asthma patients

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    Altres ajuts: This work was supported by Fundació Catalana de Neumología (FUCAP) and Centro de Investigación Biomédica en Red de Enfermedades Respiratorias(CIBERES). CIBERES is an initiative of the Instituto de Salud Carlos III.The bronchial microbiome in chronic lung diseases presents an abnormal pattern, but its microbial composition and regional differences in severe asthma have not been sufficiently addressed. The aim of the study was to describe the bacterial community in bronchial mucosa and secretions of patients with severe chronic asthma chronically treated with corticosteroids in addition to usual care according to Global Initiative for Asthma. Bacterial community composition was obtained by 16S rRNA gene amplification and sequencing, and functional capabilities through PICRUSt. Thirteen patients with severe asthma were included and provided 11 bronchial biopsies (BB) and 12 bronchial aspirates (BA) suitable for sequence analyses. Bacteroidetes, Firmicutes, Proteobacteria and Actinobacteria showed relative abundances (RAs) over 5% in BB, a cutoff that was reached by Streptococcus and Prevotella at genus level. Legionella genus attained a median RA of 2.7 (interquartile range 1.1-4.7) in BB samples. In BA a higher RA of Fusobacteria was found, when compared with BB [8.7 (5.9-11.4) vs 4.2 (0.8-7.5), p = 0.037], while the RA of Proteobacteria was lower in BA [4.3 (3.7-6.5) vs 17.1 (11.2-33.4), p = 0.005]. RA of the Legionella genus was also significantly lower in BA [0.004 (0.001-0.02) vs. 2.7 (1.1-4.7), p = 0.005]. Beta-diversity analysis confirmed the differences between the microbial communities in BA and BB (R 2 = 0.20, p = 0.001, Adonis test), and functional analysis revealed also statistically significant differences between both types of sample on Metabolism, Cellular processes, Human diseases, Organismal systems and Genetic information processing pathways. The microbiota in the bronchial mucosa of severe asthma has a specific pattern that is not accurately represented in bronchial secretions, which must be considered a different niche of bacteria growth. The online version of this article (doi:10.1186/s12866-017-0933-6) contains supplementary material, which is available to authorized users

    Colour of sputum is a marker for bacterial colonisation in chronic obstructive pulmonary disease

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    Background: Bacterial colonisation in chronic obstructive pulmonary disease (COPD) contributes to airway inflammation and modulates exacerbations. We assessed risk factors for bacterial colonisation in COPD. Methods: Patients with stable COPD consecutively recruited over 1 year gave consent to provide a sputum sample for microbiologic analysis. Bronchial colonisation by potentially pathogenic microorganisms (PPMs) was defined as the isolation of PPMs at concentrations of ≥102 colony-forming units (CFU)/mL on quantitative bacterial culture. Colonised patients were divided into high

    Specific IgA against Pseudomonas aeruginosa in severe COPD

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    Background: The bronchial mucosa is protected by a specialized immune system focused on the prevention of colonization and infection by potentially pathogenic microorganisms (PPMs). Immunoglobulin A (IgA) is the principal antibody involved in this mechanism. A defective immune barrier may facilitate the recurrent presence of PPMs in COPD. Purpose: The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease. Methods: COPD patients with good-quality sputum samples obtained during stability were included and classified according to the presence or absence of chronic bronchial colonization by P. aeruginosa. Levels of specific IgA for P. aeruginosa in sputum were determined by ELISA and expressed as ratios, using the pooled level of 10 healthy subjects as reference (optical density450 patient/control). Results: Thirty-six stable COPD patients were included, 15 of whom had chronic colonization by P. aeruginosa. Levels of specific IgA against P. aeruginosa in stable non-colonized patients were lower than those in healthy subjects (IgA ratio: median =0.15 [interquartile range {IQR} 0.05-0.36]). Colonized patients had higher levels, (1.56 [IQR 0.59-2.79]) (p,0.001, Mann- Whitney U test), with figures equivalent but not exceeding the reference value. Conclusion: IgA-based immune response against P. aeruginosa was low in severe COPD patients. Levels of specific IgA against this microorganism were higher in colonized patients, but did not attain clear-cut levels above the reference. An impaired local response against P. aeruginosa may favor chronic colonization and recurrent infections in severe COPD

    Functional Metagenomics of the Bronchial Microbiome in COPD

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    Altres ajuts: Sociedad Catalana de Neumología; Fundació Catalana de Neumología; Fundació Parc Tauli; Marató de TV3; Sociedad Española de Neumología y Cirugía Torácica; Fundación Menarini; Generalitat Valenciana (Spain) [Prometeo/2009/092] i Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES)The course of chronic obstructive pulmonary disease (COPD) is frequently aggravated by exacerbations, and changes in the composition and activity of the microbiome may be implicated in their appearance. The aim of this study was to analyse the composition and the gene content of the microbial community in bronchial secretions of COPD patients in both stability and exacerbation. Taxonomic data were obtained by 16S rRNA gene amplification and pyrosequencing, and metabolic information through shotgun metagenomics, using the Metagenomics RAST server (MG-RAST), and the PICRUSt (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States) programme, which predict metagenomes from 16S data. Eight severe COPD patients provided good quality sputum samples, and no significant differences in the relative abundance of any phyla and genera were found between stability and exacerbation. Bacterial biodiversity (Chao1 and Shannon indexes) did not show statistical differences and beta-diversity analysis (Bray-Curtis dissimilarity index) showed a similar microbial composition in the two clinical situations. Four functional categories showed statistically significant differences with MG-RAST at KEGG level 2: in exacerbation, Cell growth and Death and Transport and Catabolism decreased in abundance [1.6 (0.2-2.3) vs 3.6 (3.3-6.9), p = 0.012; and 1.8 (0-3.3) vs 3.6 (1.8-5.1), p = 0.025 respectively], while Cancer and Carbohydrate Metabolism increased [0.8 (0-1.5) vs 0 (0-0.5), p = 0.043; and 7 (6.4-9) vs 5.9 (6.3-6.1), p = 0.012 respectively]. In conclusion, the bronchial microbiome as a whole is not significantly modified when exacerbation symptoms appear in severe COPD patients, but its functional metabolic capabilities show significant changes in several pathways

    Specific IgA against Pseudomonas aeruginosa in severe COPD

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    The bronchial mucosa is protected by a specialized immune system focused on the prevention of colonization and infection by potentially pathogenic microorganisms (PPMs). Immunoglobulin A (IgA) is the principal antibody involved in this mechanism. A defective immune barrier may facilitate the recurrent presence of PPMs in COPD. The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease. COPD patients with good-quality sputum samples obtained during stability were included and classified according to the presence or absence of chronic bronchial colonization by P. aeruginosa. Levels of specific IgA for P. aeruginosa in sputum were determined by ELISA and expressed as ratios, using the pooled level of 10 healthy subjects as reference (optical density patient/control). Thirty-six stable COPD patients were included, 15 of whom had chronic colonization by P. aeruginosa. Levels of specific IgA against P. aeruginosa in stable non-colonized patients were lower than those in healthy subjects (IgA ratio: median =0.15 [interquartile range {IQR} 0.05-0.36]). Colonized patients had higher levels, (1.56 [IQR 0.59-2.79]) (p 0.001, Mann-Whitney U test), with figures equivalent but not exceeding the reference value. IgA-based immune response against P. aeruginosa was low in severe COPD patients. Levels of specific IgA against this microorganism were higher in colonized patients, but did not attain clear-cut levels above the reference. An impaired local response against P. aeruginosa may favor chronic colonization and recurrent infections in severe COPD

    Plasma miRNA profile at COVID-19 onset predicts severity status and mortality

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    BACKGROUND: MicroRNAs (miRNAs) have a crucial role in regulating immune response against infectious diseases, showing changes early in disease onset and before the detection of the pathogen. Thus, we aimed to analyze the plasma miRNA profile at COVID-19 onset to identify miRNAs as early prognostic biomarkers of severity and survival. METHODS AND RESULTS: Plasma miRNome of 96 COVID-19 patients that developed asymptomatic/mild, moderate and severe disease was sequenced together with a group of healthy controls. Plasma immune-related biomarkers were also assessed. COVID-19 patients showed 200 significant differentially expressed (SDE) miRNAs concerning healthy controls, with upregulated putative targets of SARS-CoV-2, and inflammatory miRNAs. Among COVID-19 patients, 75 SDE miRNAs were observed in asymptomatic/mild compared to symptomatic patients, which were involved in platelet aggregation and cytokine pathways, among others. Moreover, 137 SDE miRNAs were identified between severe and moderate patients, where miRNAs targeting the SARS CoV-2 genome were the most strongly disrupted. Finally, we constructed a mortality predictive risk score (miRNA-MRS) with ten miRNAs. Patients with higher values had a higher risk of 90-days mortality (hazard ratio = 4.60; p-value < 0.001). Besides, the discriminant power of miRNA-MRS was significantly higher than the observed for age and gender (AUROC = 0.970 vs. 0.881; p = 0.042). CONCLUSIONS: SARS-CoV-2 infection deeply disturbs the plasma miRNome from an early stage of COVID-19, making miRNAs highly valuable as early predictors of severity and mortality

    Interacción microorganismo-paciente en la enfermedad pulmonar obstructiva crónica

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    A pesar de que tradicionalmente se pensaba que la vía aérea era estéril, hoy en día, gracias a las nuevas técnicas de microbiología independientes de cultivo, se sabe que presenta una microbiota característica, que podría estar alterada en los procesos patológicos. Además, la presencia de microorganismos potencialmente patógenos en la vía aérea de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) es un hecho reconocido durante muchos años, sin embargo su efecto no está definido. En los trabajos que conforman esta tesis se pretende profundizar en el efecto de los microorganismos en la EPOC. En el primer trabajo se analizó el efecto de la colonización bronquial por Haemophilus influenzae en la respuesta inmune bronquial mediada por IgA, así como en los niveles de metaloproteinasa 9 (MMP-9) y su inhibidor, inhibidor tisular de metalopreoteinasas-1 (TIMP-1), en los pacientes con EPOC estable. El análisis de la respuesta inmunitaria contra este microorganismo demostró una deficiencia que puede favorecer la persistencia de la colonización y su recurrencia. Los niveles de MMP-9 y su ratio molar con TIMP-1 fueron significativamente más altos en los pacientes colonizados, lo que puede favorecer el remodelado de la vía aérea en los pacientes con EPOC. Por tanto, defectos en el sistema inmune bronquial pueden facilitar la presencia de H. influenzae en la vía aérea, que además parece estimular la actividad de MMP-9, lo que podría asociarse a daño estructural. El segundo trabajo examinó las diferencias entre el microbioma bronquial de los pacientes con EPOC severa en estabilidad y exacerbación en función de la presencia de colonización por Pseudomonas aeruginosa. Los pacientes colonizados presentaron una biodiversidad similar a los no colonizados, a pesar de la mayor abundancia relativa del género Pseudomonas. Las exacerbaciones tuvieron el mismo espectro bacterial causal en los dos grupos de pacientes, lo que permite asumir que los MPPs que causan exacerbación en la EPOC severa son los mismos en pacientes colonizados y no colonizados. En el tercer trabajo se evaluó el cambio en la microbiota en la EPOC severa respecto a formas más moderadas de la enfermedad. Se detectó una pérdida de diversidad microbiana en la etapa más severa, con una mayor abundancia de los géneros que incluyen los microorganismos potencialmente patógenos más reconocidos de la enfermedad avanzada. Estos trabajos ponen de manifiesto el efecto que los microorganismos tienen en la EPOC tanto en situación de estabilidad clínica como durante exacerbación.Although the airway has traditionally been considered sterile, nowadays, due to the new culture-independent microbiological techniques, it is known that the airway presents a characteristic microbiota, which may be altered in pathological processes. Moreover, bronchial colonization by potentially pathogenic microorganisms (PPMs) in patients with Chronic Obstructive Pulmonary Disease (COPD) has been recognized for years, but its effect is not defined. The studies that form this thesis aim to investigate the effect of the microorganisms on COPD. In the first study, the effect of bronchial colonization by Haemophilus influenzae on the immune response mediated by IgA, and on the levels of metaloproteinase 9 (MMP-9) and its inhibitor, tissue inhibitor of metaloproteinases 1 (TIMP-1) was analyzed, in patients with stable COPD. Analysis of the immune response against this microorganism showed a deficiency that may favor the persistence of colonization. The levels of MMP-9 and its molar ratio with TIMP-1 were significantly higher in colonized patients, which may promote airway remodeling in COPD patients. Therefore, defects in the immune system may facilitate bronchial colonization by H. influenzae. This colonization also seems to stimulate the activity of MMP-9, which could be associated with structural damage. The second study examined the differences between bronchial microbiome of patients with severe COPD in stability and during exacerbation, depending on the presence of bronchial colonization by Pseudomonas aeruginosa. Colonized patients had similar biodiversity than non-colonized patients, despite the higher relative abundance of Pseudomonas genus and, in both groups of patients, exacerbations had the same causative bacterial spectrum. Therefore, in severe COPD patients colonized by P. aeruginosa and non-colonized patients, the same MPPs may cause exacerbation, independently of previous colonization. In the third study we evaluated the changes in bronchial microbiota in severe COPD patients compared to patients with moderate disease. A loss of microbial diversity in the severe stage of the disease was seen, with a greater abundance of genera that include the most important pathogens related to the disease. These works show the effect of the microorganisms on COPD in either stable or exacerbated states

    The Microbiome in COPD : Emerging Potential for Microbiome-Targeted Interventions

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    The aim of interventions over the respiratory microbiome in COPD is to preserve the original microbial flora, focusing in taxa with a demonstrated impact on the prognosis of the disease. Inhaled therapy is the main treatment for COPD, and chronic corticosteroid use is recommended for patients with frequent exacerbations. This therapy, however, increases both the bronchial microbial load and the abundance of potentially pathogenic bacteria in patients with low peripheral eosinophil counts, and to minimize its use in patients without peripheral eosinophilia, when possible, may avoid increases in bacterial loads of microorganisms as Haemophilus influenzae and Streptococcus pneumoniae. In exacerbations antibiotics determine a decrease in the microbial diversity, a change that persists during stability periods in frequent exacerbators. High-diversity bronchial microbiomes are enriched in non-dominant genera and determine low exacerbation frequencies and survival improvement. Limiting the antibiotic use to the treatment of exacerbations which would clearly benefit would favor the diversity of the respiratory microbiome and may have a positive impact on quality of life and survival. Oral antiseptics have shown and effect on the bronchial microbiome that was associated with improvements in quality of life, and the gut microbiome may be also modified through the oral administration of probiotics or prebiotics, that potentially may determine decreases in lung inflammation and bronchial hyperreactivity. High fiber diets also favor the production of anti-inflammatory molecules by the digestive flora, which would reach the respiratory system through the bloodstream. Interventional approaches favoring the preservation of the respiratory microbiome in COPD need first to select accurately the patients who would benefit from long-term inhaled corticosteroids and antibiotic treatments during exacerbations, under the hypothesis that keeping a respiratory microbiome close to the healthy subject would favor the respiratory health. Additionally, high fiber diets may be able to modify the gut microbiome and influence the respiratory system through the gut-lung axis. Therapeutic approaches targeting the microbiome to improve COPD, however, still require clinical validation and the identification of patient subtypes who would benefit the most with their use

    Comparación de las concepciones de la verdad de Tarski y Kripke: interpretaciones y avances de Kripke sobre Tarski

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    Desde su publicación en 1944, La concepción semántica de la verdad y los fundamentos de la semántica, del lógico polaco Alfred Tarski, ha sido fuente de debates e interpretaciones. El filósofo norteamericano Saul Kripke, al publicar en 1975 su Esbozo de una teoría de la verdad, basado en el trabajo sobre la verdad del polaco, se enmarca entre los numerosos intérpretes de dicha tesis. Es por esto que el objetivo del presente trabajo de grado es triple. En primer lugar, se busca hacer una comparación entre ambas propuestas. En segundo lugar, analizar cómo Kripke interpreta a Tarski en relación a tres preguntas: si construyó su teoría con uno o varios conceptos de verdad en mente; si su teoría es correspondentista; y, en caso de que sea correspondentista, si se trata de una correspondencia fuerte o débil. Por último, en tercer lugar, procurar responder a la pregunta sobre en qué avanza Kripke respecto de Tarski en su propuesta sobre una teoría de la verdad. Como principales conclusiones se obtuvieron que Kripke consideró que Tarski pensaba en un solo concepto de verdad y que era correspondentista débil; se concluyó también que como avances de la propuesta de Kripke con respecto a la de Tarski están la introducción de la noción formal de fundamentación, no asegurada en la propuesta tarskiana; la construcción de un lenguaje que contiene su propio predicado de verdad y la creación de una correspondencia más sofisticada o precisa.PregradoPROFESIONAL EN FILOSOFÍ
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