Role of GSTM1 in resistance to lung inflammation

Lung inflammation resulting from oxidant/antioxidant imbalance is a common feature of many lung diseases. In particular, the role of enzymes regulated by the NF-E2-related factor 2 (Nrf2) transcription factor has recently received increased attention. Among these antioxidant genes, the glutathione S-transferase mu 1 (GSTM1) has been most extensively characterized since it has a null polymorphism which is highly prevalent in the population and associated with increased risk of inflammatory lung diseases. Present evidence suggests that GSTM1 acts through interactions with other genes and environmental factors, especially air pollutants. Here, we review GSTM1 gene expression and regulation and summarize the findings from epidemiological, clinical, animal and in vitro studies on the role played by GSTM1 in lung inflammation. We discuss limitations in the existing knowledge base and future perspectives and evaluate the potential of pharmacologic and genetic manipulation of the GSTM1 gene to modulate pulmonary inflammatory responses

eterminación del potencial de licuación de suelos; para mitigación de desastres en el casco urbano de la ciudad de San José, provincia de Lambayeque, departamento de Lambayeque

Llevamos a cabo estetrabajo de investigación con elprincipal objetivo de determinar el potencial de licuación de suelos en el casco urbano de la ciudad de San José, provincia de Lambayeque, departamento de Lambayeque. A través de ensayos de penetración standar (SPT), consistente en 14 puntos de exploración distribuidos estratégicamente por cuadrantes para así cubrir toda el área del casco urbano del distrito en mención. Para tal fin en el laboratorio de mecánica suelos de la UNPRG, se llevó a cabo ensayos de contenido de humedad, análisis granulométrico, límites de consistencia, sales totales, peso unitario de masa. Empleamos para hacer los cálculos el método empírico de Seed Idriss.La ciudad de San José está asentada sobre suelos arenosos y con presencia de nivel freático superficial, y su ubicación en el cinturón de fuego pueden originar dicho fenómeno por un movimiento sísmico considerable. Es por eso, que surge la necesidad de determinar el potencial de licuación de suelos en esta ciudad

Diesel Exhaust Exposure, Wheezing and Sneezing

The rising incidence of allergic disorders in developed countries is unexplained. Exposure to traffic related air pollutants may be an important cause of wheezing and asthma in childhood. Experimental evidence from human studies suggests that diesel exhaust particles, constituents of fine particulate matter less than 2.5 microns (PM2.5), may act to enhance IgE mediated aeroallergen sensitization and Th2 directed cytokine responses. To date, epidemiologic investigations indicate that children living in close proximity to heavily travelled roads are more likely to be atopic and wheeze. The Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort study was initiated to test the hypothesis that early high exposure to traffic related air pollutants is associated with early aeroallergen sensitization and allergic respiratory phenotypes. Using an exposure cohort design, more than 700 infants born to atopic parents were recruited at age 1 living either less than 400 meters (high traffic pollutant exposure) or greater than 1,500 meters (low exposure) from a major road. Children were medically evaluated and underwent skin prick testing with aeroallergen at screening, and re-evaluated sequentially at ages 1, 2, 3, 4, and 7. In this study, both proximity and land use regression (LUR) models of traffic air pollutant exposure have been assessed. Proximity to stop and go traffic with large concentrations of bus and truck traffic predicted persistent wheezing during infancy. The LUR model estimated elemental carbon attributable to traffic (ECAT) as a proxy for diesel exhaust particulate exposure. High ECAT was significantly associated with wheezing at age 1 as well as persistent wheezing at age 3. High mold exposure predicted a well defined asthma phenotype at age 7

Inteligencia artificial y heridas: avances, limitaciones y perspectivas en la educación médica

En este artículo, se aborda el tema de la inteligencia artificial (IA) aplicada a la detección y gestión de heridas en el campo de la medicina. Se revisan cinco estudios científicos que exploran el uso de IA en diversas áreas de la medicina relacionadas con heridas. El objetivo principal es analizar los avances, limitaciones y perspectivas de la IA en la educación médica para el manejo de heridas, considerando la IA como una herramienta potencialmente valiosa en el abordaje especifico de diferentes tipos de heridas

"Chemie im Kontext" in Spain : adaptation of a context based methodology for chemistry teaching

Chemie im Kontext (Chemistry in Context) is a German project that aims to improve the chemistry teaching in secondary education. It is a context-based methodology that uses a studentcentered approach. An ongoing research project in Madrid (Spain) is carried out in order to adapt this teaching concept to the Spanish educational system and to evaluate its effects. A context-based material was developed and used in 4 different schools. 4 teachers and 166 students participated in this study during the first year of the project. Their opinions were gathered with pre- and post-test questionnaires. Students showed an increase in their motivation and their perception of being immersed in a selfdirected learning process when using the Chemie im Kontext approach. Teachers considered that their students were more motivated when using this methodology

Impact of crestal and subcrestal implant placement upon changes in marginal peri-implant bone level. A systematic review

To systematically assess studies analyzing peri-implant bone loss in implants placed in crestal and subcrestal position. Following the recommended methods for systematic reviews and meta-analyses (PRISMA), an electronic search was conducted in the PubMed (MEDLINE), EMBASE and LILACS databases to identify all relevant articles published up until April 2017. The search included human studies comparing marginal bone loss (MBL) between a control group and a study group with a minimum of 10 patients and a minimum follow-up of 6 months after prosthetic loading with rough neck implants. Two independent reviewers assessed the risk of bias in the selected studies based on the Newcastle-Ottawa scale for observational studies and the Cochrane Collaboration for clinical trials. Of 342 potentially eligible items, 7 complied with the inclusion criteria. One article was retrieved through the manual search. Eight articles were finally included: five experimental and three observational studies. The risk of bias assessed by the Cochrane Collaboration and Newcastle-Ottawa showed a high risk of bias. The mean follow-up period was 21 months (range 6-36 months). In four studies, implants placed in a crestal position presented higher MBL than subcrestal implants - the differences being significant in one study, while in three studies, implants placed in a subcrestal position presented greater MBL than crestal implants, with significant differences in only one study. Despite its limitations, the present systematic review did not find better outcomes between crestal and subcrestal implant placement, however, new studies will be needed, involving improved designs and the standardization of protocols to allow statistical comparisons and the drawing of firm conclusions

Effects of air pollutants on innate immunity: The role of Toll-like receptors and nucleotide-binding oligomerization domain–like receptors

Interactions between exposure to ambient air pollutants and respiratory pathogens have been shown to modify respiratory immune responses. Emerging data suggest key roles for Toll-like receptor (TLR) and nucleotide-binding oligomerization domain–like receptor (NLR) signaling in pathogen-induced immune responses. Similarly, immune responses elicited by exposure to air pollutants are mediated by specific TLR- and NLR-dependent mechanisms. This review article will summarize current knowledge about how air pollutants modify TLR- and NLR-dependent signaling and host defense responses in the lung

Validation of a Dietary Questionnaire to Screen Omega-3 Fatty Acids Levels in Healthy Adults

To facilitate a clinical observational study to identify healthy volunteers with low (defined as ≤4%) and high (defined as ≥5.5%) omega-3 indices, a dietary questionnaire to rapidly assess habitual dietary intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) was developed. This study aimed to determine the validity of this newly developed dietary questionnaire. One hundred and eight volunteers were included and were assessed for habitual dietary intake of EPA and DHA using the questionnaire. The United States Department of Agriculture food products database and nutrition fact label was referenced for calculation. Blood samples were collected for the analysis of fatty acids in whole blood specimens and to derive omega-3 indices. A linear correlation was observed between reported dietary consumption of EPA, DHA, EPA+DHA and the whole blood levels of EPA, DHA, and the omega-3 indices ( = 0.67, 0.62, 0.67, respectively, \u3c 0.001 for all). The findings also suggested that the questionnaire was substantially better at identifying volunteers with high omega-3 indices (sensitivity 89%, specificity 84%, and agreement 86%) compared to volunteers with low omega-3 indices (sensitivity 100%, specificity 66%, and agreement 42%). In conclusion, this newly developed questionnaire is an efficient tool for the assessment of omega-3 indices in study populations and is particularly effective in identifying individuals with high omega-3 indices

Glutathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells

Background Diesel exhaust particles (DEP) contribute substantially to ambient particulate matter (PM) air pollution in urban areas. Inhalation of PM has been associated with increased incidence of lung disease in susceptible populations. We have demonstrated that the glutathione S-transferase M1 (GSTM1) null genotype could aggravate DEP-induced airway inflammation in human subjects. Given the critical role airway epithelial cells play in the pathogenesis of airway inflammation, we established the GSTM1 deficiency condition in primary bronchial epithelial cells from human volunteers with GSTM1 sufficient genotype (GSTM1+) using GSTM1 shRNA to determine whether GSTM1 deficiency could exaggerate DEP-induced expression of interleukin-8 (IL-8) and IL-1β proteins. Furthermore, the mechanisms underlying GSTM1 regulation of DEP-induced IL-8 and IL-1β expression were also investigated. Methods IL-8 and IL-1β protein levels were measured using enzyme-linked immunosorbent assay. GSTM1 deficiency in primary human bronchial epithelial cells was achieved using lentiviral GSTM1 shRNA particles and verified using real-time polymerase chain reaction and immunoblotting. Intracellular reactive oxygen species (ROS) production was evaluated using flow cytometry. Phosphorylation of protein kinases was detected using immunoblotting. Results Exposure of primary human bronchial epithelial cells (GSTM1+) to 25-100 μg/ml DEP for 24 h significantly increased IL-8 and IL-1β protein expression. Knockdown of GSTM1 in these cells further elevated DEP-induced IL-8 and IL-1β expression, implying that GSTM1 deficiency aggravated DEP-induced pro-inflammatory response. DEP stimulation induced the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, the downstream kinase of phosphoinositide 3-kinase (PI3K), in GSTM1+ bronchial epithelial cells. Pharmacological inhibition of ERK kinase and PI3K activity blocked DEP-induced IL-8 and IL-1β expression. DEP-induced ERK and Akt phosphorylation could be increased by GSTM1 knockdown. In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1β expression. Conclusion GSTM1 regulates DEP-induced IL-8 and IL-1β expression in primary human bronchial epithelial cells by modulation of ROS, ERK and Akt signaling