Game Based Learning on Urban Sustainability: The "Sustain" Project

SUSTAIN is an ERASMUS+ project with an innovative perspective on urban sustainability. Its target is to promote the importance of sustainability on the everyday problems of the cities among the students of higher education, which are the policy makers of tomorrow and the ones that will shape the future. In order to achieve its goals, the research team will develop a course that will be based on an interactive game with an analytical style of education. This game will allow students to learn about transportation sustainability and societal metabolism through playing. In addition, the research team will develop small and illustrative simulation models, which will make the definitions more concrete and allow students to experiment in a consequence-free environment. It is a quite innovative and hybrid perspective way of learning, in the sense that it will combine game-based learning with a cognitive and analytical style of education

DESCRIBING THE VERTICAL STRUCTURE OF INFORMAL SETTLEMENTS ON THE BASIS OF LIDAR DATA – A CASE STUDY FOR <i>FAVELAS</i> (SLUMS) IN SAO PAULO CITY

Cadastral mapping of favela’s agglomerated buildings in informal settlements at Level of Detail 1 (LoD1) usually requires specific surveys and extensive manual data processing. Therefore, there is a demand for including the favelas in the city map production on the basis of Lidar surveys, as well as the detection of their vertical growth. However, the currently developed algorithms for automatically extracting buildings from airborne Lidar data have mainly been tested only for regular building reconstruction. This study aims to develop a Lidar data processing pipeline enabling to compute metrics related to intraurban informal settlements. To do so, we present a procedure to generate favela’s buildings delineation, height, floors’ number and built area and apply them to six case studies in favela typo-morphologies. We conducted an exploratory analysis in order to obtain the adequate parameters of the processing pipeline and its evaluation, using open source, free license and self-developed software. The results are compared to reference data from the manual stereo plotting, achieving a quality index in the building reconstruction about 70%. We also calculated the growth density, measured by gross Floor Area Ratio index inside settlement, revealing values from 29% to 74% considering different time periods

MiR-137 Targets Estrogen-Related Receptor Alpha and Impairs the Proliferative and Migratory Capacity of Breast Cancer Cells

ERRα is an orphan nuclear receptor emerging as a novel biomarker of breast cancer. Over-expression of ERRα in breast tumor is considered as a prognostic factor of poor clinical outcome. The mechanisms underlying the dysexpression of this nuclear receptor, however, are poorly understood. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level and play important roles in tumor initiation and progression. In the present study, we have identified that the expression of ERRα is regulated by miR-137, a potential tumor suppressor microRNA. The bioinformatics search revealed two putative and highly conserved target-sites for miR-137 located within the ERRα 3′UTR at nt 480–486 and nt 596–602 respectively. Luciferase-reporter assay demonstrated that the two predicted target sites were authentically functional. They mediated the repression of reporter gene expression induced by miR-137 in an additive manner. Moreover, ectopic expression of miR-137 down-regulated ERRα expression at both protein level and mRNA level, and the miR-137 induced ERRα-knockdown contributed to the impaired proliferative and migratory capacity of breast cancer cells. Furthermore, transfection with miR-137mimics suppressed at least two downstream target genes of ERRα–CCNE1 and WNT11, which are important effectors of ERRα implicated in tumor proliferation and migration. Taken together, our results establish a role of miR-137 in negatively regulating ERRα expression and breast cancer cell proliferation and migration. They suggest that manipulating the expression level of ERRα by microRNAs has the potential to influence breast cancer progression

Patient-derived glioblastoma cells show significant heterogeneity in treatment responses to the inhibitor-of-apoptosis-protein antagonist birinapant.

BACKGROUND: Resistance to temozolomide (TMZ) greatly limits chemotherapeutic effectiveness in glioblastoma (GBM). Here we analysed the ability of the Inhibitor-of-apoptosis-protein (IAP) antagonist birinapant to enhance treatment responses to TMZ in both commercially available and patient-derived GBM cells. METHODS: Responses to TMZ and birinapant were analysed in a panel of commercial and patient-derived GBM cell lines using colorimetric viability assays, flow cytometry, morphological analysis and protein expression profiling of pro- and antiapoptotic proteins. Responses in vivo were analysed in an orthotopic xenograft GBM model. RESULTS: Single-agent treatment experiments categorised GBM cells into TMZ-sensitive cells, birinapant-sensitive cells, and cells that were insensitive to either treatment. Combination treatment allowed sensitisation to therapy in only a subset of resistant GBM cells. Cell death analysis identified three principal response patterns: Type A cells that readily activated caspase-8 and cell death in response to TMZ while addition of birinapant further sensitised the cells to TMZ-induced cell death; Type B cells that readily activated caspase-8 and cell death in response to birinapant but did not show further sensitisation with TMZ; and Type C cells that showed no significant cell death or moderately enhanced cell death in the combined treatment paradigm. Furthermore, in vivo, a Type C patient-derived cell line that was TMZ-insensitive in vitro and showed a strong sensitivity to TMZ and TMZ plus birinapant treatments. CONCLUSIONS: Our results demonstrate remarkable differences in responses of patient-derived GBM cells to birinapant single and combination treatments, and suggest that therapeutic responses in vivo may be greatly affected by the tumour microenvironment