Estimación de los factores de emisión de las fuentes Móviles de la ciudad de bogotá

Se seleccionó, adaptó y aplicó una metodología práctica y económica para determinar las emisiones del parque automotor de la ciudad de Bogotá. La metodología está basada en mediciones de calidad de aire, parámetros meteorológicos, conteos de vehículos y la aplicación inversa de un modelo de calidad de aire. Se presentan los resultados de un estudio de trazadores con el cual se validó la aplicación del modelo empleado. Se reportan los factores de emisión promedio de los contaminantes evaluados para vehículos livianos, pesados y para todos los vehículos. Las emisiones de los vehículos pesados son considerablemente mayores a las de los vehículos livianos.

Metamodeling approach for integrated assessment of air quality policies

A method is proposed to build integrated models (also called “Metamodels”) aimed at quantifying the economic efficiency of air quality policies. This “Metamodeling” approach is based on the coupling of two complementary models, that operate at different scales in space and time, and which represent the economic and the physical and chemical processes, respectively. The joint consideration of the physicochemical and techno-economic structure of the pollution control problems permits a comprehensive evaluation of air pollution abatement strategies. The motivating pollution control problems include urban-regional air quality management through efficient energy and traffic control policies. A pilot study, exploiting data collected in the Geneva canton (Switzerland), is used to demonstrate the potential of the approach

PM2.5 source allocation in European cities: A SHERPA modelling study

Many European cities suffer from poor air quality and still exceed the European standards prescribed by the Air Quality Directive, and the guidelines recommended by the World Health Organization (WHO). This is especially the case for PM2.5, focus of this work. While international, national and local level actions to reduce air pollution have undoubtedly resulted in an overall improvement of the air quality over the years, there are still problems, which are localised in specific regions and many cities. A key issue is to determine at which scale to act in order to abate these remaining air pollution problems most effectively. Central to this, for cities, is a quantitative assessment of the different origins of air pollution (urban, regional, national and transboundary) to support the design of efficient, effective air quality plans, which are a legal obligation for countries and regions whenever exceedances occur. The “Screening for High Emission Reduction Potentials for Air quality” tool (SHERPA) is used in this work to quantify the origins of air pollution in cities and regions, both from a spatial (urban, country…) and sectoral (transport, residential, agriculture…) perspectives. For PM2.5 we conclude that (1) for many cities, local actions at the city scale are an effective means of improving air quality in that city; (2) the target sectors and scales to abate air pollution are city specific, even for cities that are located in the same country. Consequently, it is important to take into account these city-specific circumstances when designing air quality plans and (3) for many cities, sectoral measures addressing agriculture at country or EU scale would have a clear benefit on urban air quality

A comprehensive inventory of TLX1 controlled long non-coding RNAs in T-cell acute lymphoblastic leukemia through polyA+ and total RNA sequencing

Graft-versus-host disease (GvHD) assessment has been shown to be a challenge for healthcare professionals, leading to the development of the eGVHD App (www.uzleuven.be/egvhd). In this study, we formally evaluated the accuracy of using the App compared to traditional assessment methods to assess GvHD. Our national multicenter randomized controlled trial involved seven Belgian transplantation centers and 78 healthcare professionals selected using a 2-stage convenience sampling approach between January and April 2017. Using a 1:1 randomization stratified by profession, healthcare professionals were assigned to use either the App ("APP") or their usual GvHD assessment aids ("No APP") to assess the diagnosis and severity score of 10 expert-validated clinical vignettes. Our main outcome measure was the difference in accuracy for GvHD severity scoring between both groups. The odds of being correct were 6.14 (95% CI: 2.83-13.34) and 6.29 (95% CI: 4.32-9.15) times higher in favor of the "APP" group for diagnosis and scoring, respectively (P<0.001). Appassisted GvHD severity scoring was significantly superior for both acute and chronic GvHD, with an Odds Ratio of 17.89 and 4.34 respectively (P<0.001) and showed a significantly increased inter-observer agreement compared to standard practice. Despite a mean increase of 24 minutes (95% CI: 20.45-26.97) in the time needed to score the whole GvHD test package in the "APP" group (P<0.001), usability feedback was positive. The eGVHD App shows superior GvHD assessment accuracy compared to standard practice and has the potential to improve the quality of outcome data registration in allogeneic stem cell transplantation

Differential impact of drugs on the outcome of ETV6-RUNX1 positive childhood B-cell precursor acute lymphoblastic leukaemia : results of the EORTC CLG 58881 and 58951 trials

info:eu-repo/semantics/publishe

Long-term in vitro maintenance of clonal abundance and leukaemia-initiating potential in acute lymphoblastic leukaemia

Lack of suitable in vitro culture conditions for primary acute lymphoblastic leukaemia (ALL) cells severely impairs their experimental accessibility and the testing of new drugs on cell material reflecting clonal heterogeneity in patients. We show that Nestin-positive human mesenchymal stem cells (MSCs) support expansion of a range of biologically and clinically distinct patient-derived ALL samples. Adherent ALL cells showed an increased accumulation in the S phase of the cell cycle and diminished apoptosis when compared with cells in the suspension fraction. Moreover, surface expression of adhesion molecules CD34, CDH2 and CD10 increased several fold. Approximately 20% of the ALL cells were in G0 phase of the cell cycle, suggesting that MSCs may support quiescent ALL cells. Cellular barcoding demonstrated long-term preservation of clonal abundance. Expansion of ALL cells for >3 months compromised neither feeder dependence nor cancer initiating ability as judged by their engraftment potential in immunocompromised mice. Finally, we demonstrate the suitability of this co-culture approach for the investigation of drug combinations with luciferase-expressing primograft ALL cells. Taken together, we have developed a preclinical platform with patient-derived material that will facilitate the development of clinically effective combination therapies for ALL

Distinct regulation of c-myb gene expression by HoxA9, Meis1 and Pbx proteins in normal hematopoietic progenitors and transformed myeloid cells

The proto-oncogenic protein c-Myb is an essential regulator of hematopoiesis and is frequently deregulated in hematological diseases such as lymphoma and leukemia. To gain insight into the mechanisms underlying the aberrant expression of c-Myb in myeloid leukemia, we analyzed and compared c-myb gene transcriptional regulation using two cell lines modeling normal hematopoietic progenitor cells (HPCs) and transformed myelomonocytic blasts. We report that the transcription factors HoxA9, Meis1, Pbx1 and Pbx2 bind in vivo to the c-myb locus and maintain its expression through different mechanisms in HPCs and leukemic cells. Our analysis also points to a critical role for Pbx2 in deregulating c-myb expression in murine myeloid cells cotransformed by the cooperative activity of HoxA9 and Meis1. This effect is associated with an intronic positioning of epigenetic marks and RNA polymerase II binding in the orthologous region of a previously described alternative promoter for c-myb. Taken together, our results could provide a first hint to explain the abnormal expression of c-myb in leukemic cells