Suchergebnisse

La situación actual de crisis sistémica global ha puesto de manifiesto la inviabilidad del modelo de desarrollo tradicional, basado en el crecimiento económico y la acumulación de capital como fin en sí mismo. Ante el fracaso de este modelo y la constatación de que sus dinámicas han resultado ser, en contra de lo esperado, "maldesarrolladoras", se hace necesaria la búsqueda de alternativas que propongan otras formas de relación más sostenibles y equilibradas. El ideal del Buen Vivir, originario de la cosmovisión indígena e incorporado en los nuevos textos constitucionales de Bolivia y Ecuador, promueve una nueva forma de entender el desarrollo, basada en la armonía entre los individuos y de éstos con la naturaleza. Este texto recoge las conclusiones fundamentales del seminario "Sumak Kawsay. Aprendiendo del Sur", organizado por el Instituto de Desarrollo Social y Paz de la Universidad de Alicante, precisamente con el fin de establecer espacios de discusión y análisis sobre el alcance de estas propuestas.

El cultivo del café (Coffea arabica L.) es de gran importancia económica, cultural y ambiental en el Sitio Ramsar Cascadas de Texolo y en su entorno, decretado como Área Natural Protegida. La degradación física, química y biológica del suelo en esta zona se ha incrementado; por lo que es prioritario realizar investigación tendiente a su manejo y conservación. El objetivo de este estudio fue conocer el historial y la actitud de cafeticultores del Sitio Ramsar Cascadas de Texolo hacia la adopción de prácticas de manejo y conservación del suelo. El estudio se realizó en localidades de Xico y Teocelo, Veracruz, mediante una encuesta que empleó un cuestionario aplicado a 40 cafeticultores cuya parcela se ubica dentro del polígono del Sitio Ramsar. Se encontró que las obras y prácticas de conservación de suelo fueron impulsadas al inicio de los años setenta por el desaparecido Instituto Mexicano del Café (INMECAFÉ) algunas de las cuales se siguen manteniendo y practicando. La edad promedio de los encuestados superó los 61 años, de los cuales 60 % son pequeños propietarios, 22 % medianos y 18 % grandes. De los productores 80 % alguna vez establecieron obras o ejecutaron prácticas de conservación. Sin embargo; actualmente sólo 45 % sigue realizando prácticas de conservación de suelo dentro del Sitio, a pesar de haber sido denominado Ramsar. Se encontró una actitud ligeramente positiva (3.3), en escala de Likert, hacia la conservación del agroecosistema cafetalero. Productores con mayor superficie cultivada presentan mejor actitud hacia la conservación de suelo (4.4), lo que podría estar relacionado con que son los que tienen mayor grado de escolaridad. Se concluyó que las actividades tendientes a la conservación de suelo que se practican en el Sitio Ramsar fueron producto de capacitaciones anteriores que aún tienen influencia y que han ido reduciéndose considerablemente a pesar de existir una actitud positiva entre los cafetaleros hacia el manejo y conservación del recurso.

This work was supported by grants from the Spanish Fondo de Investigaciones Sanitarias FIS09/01543, PI12/00281 and PI15/01471, Instituto de Salud Carlos III (ISCIII), European Regional Development Fund (ERDF) "Una manera de hacer Europa", Proyectos de Investigación del SACYL 355/ A/09, GRS/1172/A15, COST Action EuGESMA (BM0801), Fundación Manuel Solórzano, Obra Social Banca Cívica (Caja Burgos), Fundación Española de Hematología y Hemoterapia (FEHH), and by grants (RD12/0036/0069 and RD12/0036/0044) from Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness and European Regional Development Fund (ERDF) "Una manera de hacer Europa" (CEI 2010-1-0010). The research leading to these results has received funding from the European Union Seventh Framework Programme [FP7/2007-2013] under Grant Agreement nº 306242-NGS-PTL. ; Hernandez, JA; Hernandez-Sanchez, M; Rodriguez-Vicente, AE; Grossmann, V; Collado, R; Heras, C; Puiggros, A; Martin, AA; Puig, N; Benito, R; Robledo, C; Delgado, J; Gonzalez, T; Queizan, JA; Galende, J; de la Fuente, I; Martin-Nunez, G; Alonso, JM; Abrisqueta, P; Luno, E; Marugan, I; Gonzalez-Gason, I; Bosch, F; Kohlmann, A; Gonzalez, M; Espinet, B; Hernandez-Rivas, JM.

The rapid progress in next-generation sequencing technologies has significantly contributed to our knowledge of the genetic events associated with the development, progression and treatment resistance of chronic lymphocytic leukemia patients. Together with the discovery of new driver mutations, next-generation sequencing has revealed an immense degree of both intra- and inter-tumor heterogeneity and enabled us to describe marked clonal evolution. Advances in immunogenetics may be implemented to detect minimal residual disease more sensitively and to track clonal B cell populations, their dynamics and molecular characteristics. The interpretation of these aspects is indispensable to thoroughly examine the genetic background of chronic lymphocytic leukemia. We review and discuss the recent results provided by the different next-generation sequencing techniques used in studying the chronic lymphocytic leukemia genome, as well as future perspectives in the methodologies and applications. ; This work received funding from the European Union Seventh Framework Programme [FP7/2007-2013] under Grant Agreement n°306242-NGS-PTL and MSMT CR (2013–2015/no.7E13008). It was also supported by grants from the Spanish Fondo de Investigaciones Sanitarias FIS 09/01543, PI12/00281 and PI15/01471, Proyectos de Investigación del SACYL 355/A/09, COST Action EuGESMA (BM0801), Fundación Manuel Solórzano, Obra Social Banca Cívica (Caja Burgos), Fundación Española de Hematología y Hemoterapia (FEHH), and by grants (RD12/0036/0069 and RD12/0036/0044) from the Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness and European Regional Development Fund (ERDF) "Una manera de hacer Europa" (CEI 2010-1-0010). AERV is supported by a grant from the Fundación Ramón Areces. MHS is fully supported by an Ayuda Predoctoral de la Junta de Castilla y León from the Fondo Social Europeo (JCYL-EDU/346/2013 PhD scholarship). SP, VB and JM were supported by AZV grants from the Ministry of Health of the Czech Republic No. 15-31834A, 15-30015A and 16-29447A, MH CR project 65269705 and MSMT CR project CEITEC2020 LQ1601 under the National Sustainability Programme II. ; Peer Reviewed

This is an open access article distributed under the terms of the Creative Commons Attribution License.-- et al. ; To analyze the impact of the 11q deleted (11q-) cells in CLL patients on the time to first therapy (TFT) and overall survival (OS), 2,493 patients with CLL were studied. 242 patients (9.7%) had 11q-. Fluorescence in situ hybridization (FISH) studies showed a threshold of 40% of deleted cells to be optimal for showing that clinical differences in terms of TFT and OS within 11q- CLLs. In patients with ≥40% of losses in 11q (11q-H) (74%), the median TFT was 19 months compared with 44 months in CLL patients with <40% del(11q) (11q-L) (P<0.0001). In the multivariate analysis, only the presence of 11q-L, mutated IGHV status, early Binet stage and absence of extended lymphadenopathy were associated with longer TFT. Patients with 11q-H had an OS of 90 months, while in the 11q-L group the OS was not reached (P = 0.008). The absence of splenomegaly (P = 0.02), low LDH (P = 0.018) or β2M (P = 0.006), and the presence of 11q-L (P = 0.003) were associated with a longer OS. In addition, to detect the presence of mutations in the ATM, TP53, NOTCH1, SF3B1, MYD88, FBXW7, XPO1 and BIRC3 genes, a select cohort of CLL patients with losses in 11q was sequenced by next-generation sequencing of amplicons. Eighty %of CLLs with 11qshowed mutations and fewer patients with low frequencies of 11q- had mutations among genes examined (50% vs 94.1%, P = 0.023). In summary, CLL patients with <40% of 11qhad a long TFT and OS that could be associated with the presence of fewer mutated genes. ; This work was supported by grants from the Spanish Fondo de Investigaciones Sanitarias FIS 09/01543, PI12/00281 and PI15/01471, Instituto de Salud Carlos III (ISCIII), European Regional Development Fund (ERDF) "Una manera de hacer Europa", Proyectos de Investigación del SACYL 355/A/09, GRS/1172/A15, COST Action EuGESMA (BM0801), Fundación Manuel Solórzano, Obra Social Banca Cívica (Caja Burgos), Fundación Española de Hematología y Hemoterapia (FEHH), and by grants (RD12/0036/0069 and RD12/0036/0044) from Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness and European Regional Development Fund (ERDF) "Una manera de hacer Europa" (CEI 2010-1-0010). The research leading to these results has received funding from the European Union Seventh Framework Programme [FP7/2007-2013] under Grant Agreement n°306242-NGS-PTL. María Hernández-Sánchez is fully supported by an Ayuda Predoctoral de la Junta de Castilla y León from the Fondo Social Europeo (JCYL-EDU/346/2013 Ph.D. scholarship). Vera Grossmann was supported by MLL Munich and Alexander Kohlmann was supported by MLL Munich and AstraZeneca in terms of salary. ; Peer Reviewed

This is an open access article distributed under the terms of the Creative Commons Attribution License.-- et al. ; The presence of SF3B1 gene mutations is a hallmark of refractory anemia with ring sideroblasts (RARS). However, the mechanisms responsible for iron accumulation that characterize the Myelodysplastic Syndrome with ring sideroblasts (MDS-RS) are not completely understood. In order to gain insight in the molecular basis of MDS-RS, an integrative study of the expression and mutational status of genes related to iron and mitochondrial metabolism was carried out. A total of 231 low-risk MDS patients and 81 controls were studied. Gene expression analysis revealed that iron metabolism and mitochondrial function had the highest number of genes deregulated in RARS patients compared to controls and the refractory cytopenias with unilineage dysplasia (RCUD). Thus mitochondrial transporters SLC25 (SLC25A37 and SLC25A38) and ALAD genes were over-expressed in RARS. Moreover, significant differences were observed between patients with SF3B1 mutations and patients without the mutations. The deregulation of genes involved in iron and mitochondrial metabolism provides new insights in our knowledge of MDS-RS. New variants that could be involved in the pathogenesis of these diseases have been identified. ; This work was partially supported by grants from: the Spanish Fondo de Investigaciones Sanitarias (PI14/1971, PI12/00281); Proyectos de Investigación del SACYL (BIO/SA52/14, BIO/SA10/14, BIO/SA31/13, GRS 994/A/14); Consejería Educación, Junta Castilla y León (HUS272U13); COST Action "EuGESMA" (BM0801); Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness & European Regional Development Fund (ERDF) "Una manera de hacer Europa" (Innocampus) (RD12/0036/0069, RD12/0036/0029, RD12/0036/0044); European Union's Seventh Framework Programme (FP7/2007-2013 nº 306242- NGS-PTL). MDR is fully supported by a "Grant from Fundación Española de Hematología y Hemoterapia". MA was fully supported by a "Grant from the Spanish Consejo Superior de Investigaciones Científicas, Junta para la Ampliación de Estudios (JAE Predoctoral) [09-02402]". MH is fully suported by an "Ayuda predoctoral de la Junta de Castilla y León" from "European Regional Development Fund". DMZ was funded by the Spanish Ministry of Science and Innovation (PI082025) and Junta de Castilla y León (CSI224A11-2, SAN/103/2011). ; Peer Reviewed

© The Author(s). ; CRISPR-Cas9 gene editing has transformed our ability to rapidly interrogate the functional impact of somatic mutations in human cancers. Droplet-based technology enables the analysis of Cas9-introduced gene edits in thousands of single cells. Using this technology, we analyze Ba/F3 cells engineered to express single or multiplexed loss-of-function mutations recurrent in chronic lymphocytic leukemia. Our approach reliably quantifies mutational co-occurrences, zygosity status, and the occurrence of Cas9 edits at single-cell resolution. ; C.J.W. acknowledges support from the NIH/National Cancer Institute (NIH/NCI) (R01 CA216273, U10 CA180861, P01 CA206978, and P01-CA081534) and is a scholar of the Leukemia and Lymphoma Society. E.t.H. is a Special Fellow of the Leukemia and Lymphoma Society and a Scholar of the American Society of Hematology. S.L. is supported by the NCI Research Specialist Award (R50CA251956-01). L.P. is supported by the National Human Genome Research Institute (NHGRI) Career Development Award (R00HG008399), Genomic Innovator Award (R35HG010717), and CEGS (RM1HG009490). MHS holds a Sara Borrell post-doctoral contract (CD19/00222) from the Instituto de Salud Carlos III (ISCIII) co-founded by Fondo Social Europeo (FSE) "El Fondo Social Europeo invierte en tu futuro". M.G. was supported by a Marie-Curie International Outgoing Fellowship from the European Union (PIOF-2013-624924).

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.-- et al. ; [Background]: MicroRNAs are known to inhibit gene expression by binding to the 3'UTR of the target transcript. Downregulation of miR-223 has been recently reported to have prognostic significance in CLL. However, there is no evidence of the pathogenetic mechanism of this miRNA in CLL patients. [Methods]: By applying next-generation sequencing techniques we have detected a common polymorphism (rs2307842), in 24% of CLL patients, which disrupts the binding site for miR-223 in HSP90B1 3'UTR. We investigated whether miR-223 directly targets HSP90B1 through luciferase assays and ectopic expression of miR-223. Quantitative real-time polymerase chain reaction and western blot were used to determine HSP90B1 expression in CLL patients. The relationship between rs2307842 status, HSP90B1 expression and clinico-biological data were assessed. [Results]: HSP90B1 is a direct target for miR-223 by interaction with the putative miR-223 binding site. The analysis in paired samples (CD19+ fraction cell and non-CD19+ fraction cell) showed that the presence of rs2307842 and IGHV unmutated genes determined HSP90B1 overexpression in B lymphocytes from CLL patients. These results were confirmed at the protein level by western blot. Of note, HSP90B1 overexpression was independently predictive of shorter time to the first therapy in CLL patients. By contrast, the presence of rs2307842 was not related to the outcome. [Conclusions]: HSP90B1 is a direct target gene of miR-223. Our results provide a plausible explanation of why CLL patients harboring miR-223 downregulation are associated with a poor outcome, pointing out HSP90B1 as a new pathogenic mechanism in CLL and a promising therapeutic target. ; This work was partially supported by grants from the Spanish Fondo de Investigaciones Sanitarias FIS 09/01543 and PI12/00281, Proyectos de Investigación del SACYL 355/A/09, COST Action EuGESMA (BM0801), Fundación Manuel Solórzano, Obra Social Banca Cívica (Caja Burgos), Fundación Española de Hematología y Hemoterapia (FEHH) and by a grant (RD12/0036/0069) from the Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness & European Regional Development Fund (ERDF) "Una manera de hacer Europa" (Innocampus). The research leading to these results has received funding from the European Union Seventh Framework Programme [FP7/2007-2013] under Grant Agreement n°306242-NGS-PTL. MHS is fully supported by an Ayuda predoctoral de la Junta de Castilla y Leon by the Fondo Social Europeo. ME Sarasquete is supported by Contrato Miguel Servet (CP13/00080). ; Peer Reviewed

The research leading to these results has mainly received funding from the European Union Seventh Framework Programme [FP7/2007–2013] under Grant Agreement no 306242-NGS-PTL. In addition, this work was supported by grants from the Spanish Fondo de Investigaciones Sanitarias PI15/01471, PI18/01500, Instituto de Salud Carlos III (ISCIII), European Regional Development Fund (ERDF) "Una manera de hacer Europa", "Consejería de Educación, Junta de Castilla y León" (SA085U16), "Proyectos de Investigación del SACYL", Spain: GRS 994/A/14, BIO/SA10/14, BIO/SA31/13, GRS 1172/A/15,"Fundación Memoria Don Samuel Solórzano Barruso", by grants (RD12/0036/0069) from Red Temática de Investigación Cooperativa en Cáncer (RTICC), Centro de Investigación Biomédica en Red de Cáncer (CIBERONC) CB16/12/00233 and USAL "Programa XIII". M. Hernández-Sánchez is supported by FEHH-Janssen ("Sociedad Española de Hematología y Hemoterapia"). M Quijada-Álamo is supported by an "Ayuda Predoctoral de la Junta de Castilla y León" (JCYL-EDU/529/2017). We are grateful to I. Rodríguez, S. González, T.Prieto, M. Á. Ramos, A. Martín, A. Díaz, A. Simón, M.del Pozo, V. Gutiérrez and S. Pujante from Centro de Investigación del Cáncer, Salamanca, for their technical assistance. D. Tamborero is supported by project SAF2015–74072-JUN, which is funded by the Agencia Estatal de Investigación (AEI) and Fondo Europeo de Dearrollo Regional (FEDER). This work was supported by Seventh Framework Programme (NGS-PTL/2012–2015/no.306242) and Ministry of Education, Youth and Sports (2013–2015, no. 7E13008); by the Ministry of Education, Youth and Sports of the Czech Republic under the CEITEC 2020 project (LQ1601); by the Ministry of Health, Czech Republic - conceptual development of research organization (FNBr, 65269705); by the Specific University Research (nr. MUNI/A/0968/2017) provided by MEYS; and by the project CZ.02.1.01/0.0/0.0/16_013/0001634 National Center for Medical Genomic - modernization of infrastructure and research of genetic variation in the population, funded by OP RDE. We acknowledge the CF Genomics CEITEC MU supported by the NCMG research infrastructure (LM2015091 funded by MEYS CR) for their support with obtaining the scientific data presented in this paper. We acknowledge S. Takacova from CEITEC MU for her help with the sample selection and processing.

[Background]: Chronic lymphocytic leukemia (CLL) is a highly genetically heterogeneous disease. Although CLL has been traditionally considered as a mature B cell leukemia, few independent studies have shown that the genetic alterations may appear in CD34+ hematopoietic progenitors. However, the presence of both chromosomal aberrations and gene mutations in CD34+ cells from the same patients has not been explored. [Methods]: Amplicon-based deep next-generation sequencing (NGS) studies were carried out in magnetically activated-cell-sorting separated CD19+ mature B lymphocytes and CD34+ hematopoietic progenitors (n = 56) to study the mutational status of TP53, NOTCH1, SF3B1, FBXW7, MYD88, and XPO1 genes. In addition, ultra-deep NGS was performed in a subset of seven patients to determine the presence of mutations in flow-sorted CD34+CD19− early hematopoietic progenitors. Fluorescence in situ hybridization (FISH) studies were performed in the CD34+ cells from nine patients of the cohort to examine the presence of cytogenetic abnormalities. [Results]: NGS studies revealed a total of 28 mutations in 24 CLL patients. Interestingly, 15 of them also showed the same mutations in their corresponding whole population of CD34+ progenitors. The majority of NOTCH1 (7/9) and XPO1 (4/4) mutations presented a similar mutational burden in both cell fractions; by contrast, mutations of TP53 (2/2), FBXW7 (2/2), and SF3B1 (3/4) showed lower mutational allele frequencies, or even none, in the CD34+ cells compared with the CD19+ population. Ultra-deep NGS confirmed the presence of FBXW7, MYD88, NOTCH1, and XPO1 mutations in the subpopulation of CD34+CD19− early hematopoietic progenitors (6/7). Furthermore, FISH studies showed the presence of 11q and 13q deletions (2/2 and 3/5, respectively) in CD34+ progenitors but the absence of IGH cytogenetic alterations (0/2) in the CD34+ cells. Combining all the results from NGS and FISH, a model of the appearance and expansion of genetic alterations in CLL was derived, suggesting that most of the genetic events appear on the hematopoietic progenitors, although these mutations could induce the beginning of tumoral cell expansion at different stage of B cell differentiation. [Conclusions]: Our study showed the presence of both gene mutations and chromosomal abnormalities in early hematopoietic progenitor cells from CLL patients. ; This work was partially supported by grants from the Spanish Fondo de Investigaciones Sanitarias PI12/00281, PI15/01471, Instituto de Salud Carlos III (ISCIII), European Regional Development Fund (ERDF) "Una manera de hacer Europa," Consejería de Educación, Junta de Castilla y León (SA085U16), Proyectos de Investigación del SACYL, Spain: GRS 1172/A/15, BIO/SA10/14, GRS 1343/A/16, and Fundación Española de Hematología y Hemoterapia (FEHH) and by a grant (RD12/0036/0069) from the Red Temática de Investigación Cooperativa en Cáncer (RTICC), Instituto de Salud Carlos III (ISCIII), Spanish Ministry of Economy and Competitiveness & European Regional Development Fund (ERDF) "Una manera de hacer Europa" (Innocampus; CEI-2010-1-0010), Fundación "Memoria Don Samuel Solórzano Barruso" 2016, and the European Union Seventh Framework Programme [FP7/2007–2013] under Grant Agreement no. 306242-NGS-PTL. MHS is fully supported by an "Ayuda predoctoral de la Junta de Castilla y León" by the Fondo Social Europeo (JCYL-EDU/346/2013 PhD scholarship). ; Peer Reviewed

[Background]: In B-cell precursor acute lymphoblastic leukaemia (B-ALL), the identification of additional genetic alterations associated with poor prognosis is still of importance. We determined the frequency and prognostic impact of somatic mutations in children and adult cases with B-ALL treated with Spanish PETHEMA and SEHOP protocols. [Methods]: Mutational status of hotspot regions of TP53, JAK2, PAX5, LEF1, CRLF2 and IL7R genes was determined by next-generation deep sequencing in 340 B-ALL patients (211 children and 129 adults). The associations between mutation status and clinicopathological features at the time of diagnosis, treatment outcome and survival were assessed. Univariate and multivariate survival analyses were performed to identify independent prognostic factors associated with overall survival (OS), event-free survival (EFS) and relapse rate (RR). [Results]: A mutation rate of 12.4% was identified. The frequency of adult mutations was higher (20.2% vs 7.6%, P=0.001). TP53 was the most frequently mutated gene (4.1%), followed by JAK2 (3.8%), CRLF2 (2.9%), PAX5 (2.4%), LEF1 (0.6%) and IL7R (0.3%). All mutations were observed in B-ALL without ETV6-RUNX1 (P=0.047) or BCR-ABL1 fusions (P<0.0001). In children, TP53mut was associated with lower OS (5-year OS: 50% vs 86%, P=0.002) and EFS rates (5-year EFS: 50% vs 78.3%, P=0.009) and higher RR (5-year RR: 33.3% vs 18.6% P=0.037), and was independently associated with higher RR (hazard ratio (HR)=4.5; P=0.04). In adults, TP53mut was associated with a lower OS (5-year OS: 0% vs 43.3%, P=0.019) and a higher RR (5-year RR: 100% vs 61.4%, P=0.029), whereas JAK2mut was associated with a lower EFS (5-year EFS: 0% vs 30.6%, P=0.035) and a higher RR (5-year RR: 100% vs 60.4%, P=0.002). TP53mut was an independent risk factor for shorter OS (HR=2.3; P=0.035) and, together with JAK2mut, also were independent markers of poor prognosis for RR (TP53mut: HR=5.9; P=0.027 and JAK2mut: HR=5.6; P=0.036). [Conclusions]: TP53mut and JAK2mut are potential biomarkers associated with poor prognosis in B-ALL patients. ; This work was supported in part by a grant from the European Union's Seventh Framework Programme (FP7/2007–2013) under Grant Agreement 306242-NGS-PTL, the Consejeria de Educacion, Junta de Castilla y León (HUS272U13, SA085U16 to JMHR and JCYL-EDU/346/2013 PhD scholarship to MHS), Fundación Castellano Leonesa de Hematología y Hemoterapia (FUCALHH 2013) to JMHR, Proyectos de Investigacion del SACYL, Spain (BIO/SA31/13 and BIO/SA10/14) to RB; The Instituto de Salud Carlos III from Spanish Ministry of Economy and Competitiveness and the European Regional Development Fund (ISCIII-FEDER) ''Una manera de hacer Europa'' Spanish Cancer Network (RD12/0036/0069 and RD12/0036/0061 to JM) and FIS grants PI15/01471 to JMHR and PI15/00032 to EFR. Universidad Pedagogica y Tecnologica de Colombia—Vicerrectoría de Investigacion y Extension (Grupo de Investigacion en Ciencias Biomedicas UPTC—GICBUPTC, Escuela de Ciencias Biologicas) to MFC. ; Peer Reviewed

Los textos presentados reflejan el espíritu del encuentro que los reunió. Juntos expresan un ejercicio de interdisciplinariedad, pluralidad, debate de ideas, y difusión de diferentes puntos de vista, sobre temas relacionados con la cultura de paz, la violencia, el desarrollo y la democracia. Y contribuyen a la comprensión sobre los límites, heterogeneidades y lagunas del proceso de instauración y consolidación de las instituciones democráticas de los países de América Latina. También analizan la marginación, la desigualdad, la inequidad, la violencia, la inseguridad cotidiana y otros asuntos relacionados con la falta de recursos y opciones para los habitates de la región .