Introducing MACEDA: New micro-data on an indigenous self-determination conflict

Replication data: The dataset, codebook, and do-files for the empirical analysis in this article, along with the Online appendix, are available at https://www.prio.org/journals/jpr/replicationdata All analyses were conducted using STATA. See also https://doi.org/10.7910/DVN/KXRYM3.This article introduces MACEDA, a micro-level dataset on the self-determination (SD) conflict between the Chilean state and the indigenous Mapuche. Although SD disputes are one of the most common conflicts in the world, and indigenous movements represent about 40% of all SD movements, this is the first micro-dataset focused on an indigenous SD conflict. MACEDA covers the period 1990–2016, including more than 2,600 events collected from local media. As indigenous conflicts are much less violent in terms of casualties, we take a flexible definition of conflict, based on its constituent events, and we discuss the comparability and generalization of our approach. To illustrate the usefulness of these micro-data in the analysis of conflict-related theories, we present a descriptive empirical analysis on the strategies of indigenous resistance, and we discuss how the data can be used in the causal analysis of conflicts.Institute for Research in Market Imperfections and Public Policy, ICM IS130002; Ministerio de Economía, Fomento y Turismo; the ANID Chile, project Fondecyt 1201737; ANID Chile through Fondecyt Iniciación project 11190283

Dihydropyridine Receptors as Voltage Sensors for a Depolarization-evoked, IP3R-mediated, Slow Calcium Signal in Skeletal Muscle Cells

The dihydropyridine receptor (DHPR), normally a voltage-dependent calcium channel, functions in skeletal muscle essentially as a voltage sensor, triggering intracellular calcium release for excitation-contraction coupling. In addition to this fast calcium release, via ryanodine receptor (RYR) channels, depolarization of skeletal myotubes evokes slow calcium waves, unrelated to contraction, that involve the cell nucleus (Jaimovich, E., R. Reyes, J.L. Liberona, and J.A. Powell. 2000. Am. J. Physiol. Cell Physiol. 278:C998–C1010). We tested the hypothesis that DHPR may also be the voltage sensor for these slow calcium signals. In cultures of primary rat myotubes, 10 μM nifedipine (a DHPR inhibitor) completely blocked the slow calcium (fluo-3-fluorescence) transient after 47 mM K+ depolarization and only partially reduced the fast Ca2+ signal. Dysgenic myotubes from the GLT cell line, which do not express the α1 subunit of the DHPR, did not show either type of calcium transient following depolarization. After transfection of the α1 DNA into the GLT cells, K+ depolarization induced slow calcium transients that were similar to those present in normal C2C12 and normal NLT cell lines. Slow calcium transients in transfected cells were blocked by nifedipine as well as by the G protein inhibitor, pertussis toxin, but not by ryanodine, the RYR inhibitor. Since slow Ca2+ transients appear to be mediated by IP3, we measured the increase of IP3 mass after K+ depolarization. The IP3 transient seen in control cells was inhibited by nifedipine and was absent in nontransfected dysgenic cells, but α1-transfected cells recovered the depolarization-induced IP3 transient. In normal myotubes, 10 μM nifedipine, but not ryanodine, inhibited c-jun and c-fos mRNA increase after K+ depolarization. These results suggest a role for DHPR-mediated calcium signals in regulation of early gene expression. A model of excitation-transcription coupling is presented in which both G proteins and IP3 appear as important downstream mediators after sensing of depolarization by DHPR

Contribution of polymorphisms in IFNG and TNF to complications of the allogeneic hematopoietic stem cell transplantation with sibling donors

Las complicaciones del trasplante alogénico de células progenitoras hematopoyéticas (TACPH) relacionado incluyen tiempos variables de engraftment,enfermedad injerto contra huésped (EICH), infeccionesbacterianas y reactivación de citomegalovirus(CMV), entre otras. La existencia de polimorfismosen genes no HLA que codifican citoquinas proinflamatoriastales como el factor de necrosis tumoralalfa (TNF) e interferón gamma (IFNG) condicionaría la aparición de estas complicaciones. Se evaluóel impacto de la variante +1349 CAn del gen INFG y del polimorfismo -308 G/A de TNF en el engraftment y en la EICH en 148 receptores de TACPHrealizados en los centros participantes. Con respecto al engraftment tardío (≥15 días), el análisis multivariado confirmó el poder predictivo desfavorable del genotipo CAno12/no12 (baja producción) de IFNG(OR 3,9; p=0,003), médula ósea (MO) como fuente de células progenitoras (OR 4,6; p=0,013) y bacteriemia (OR 3,0; p=0,033). En relación a EICHa 3-4,las variables independientes fueron el genotipo de baja producción de IFNG (OR 0,1; p=0,008), bacteriemia (OR 3,3; p=0,048) y presencia de CMV(OR3,3; p=0,046). Y con respecto a EICHc, el riesgo fue influenciado por el genotipo -308 GG (producción baja) de TNF (OR 3,3; p=0,038), SP como fuente (OR 5,0; p=0,028), acondicionamiento mieloablativo (OR 3,3; p=0,014) y antecedente de EICHa 2-4 (OR 2,6; p=0,029). Aunque es necesario confirmar estos hallazgos, el genotipo de baja producción de IFNG se asoció con engraftment tardío y menor EICHa, mientras que los genotipos de baja producción de TNF se relacionaron con mayor incidencia de EICHc. Las variantes polimórficas estudiadas contribuirían al desarrollo de complicaciones en pacientes con TACPH relacionado.Complications of allogeneic hematopoietic stem cell transplantation (allo-HSCT) include variable engraftment times, acute (aGVHD) and chronic (cGVHD) graft-versus-host diseases, bacterial infections and reactivation of cytomegalovirus (CMV), among others. The existence of polymorphisms in non-HLA genes that encode pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF) and interferon gamma (IFNG) would condition the appearance of these complications. The impact of polymorphic variants +1349 CAn of INFG gene and -308 G/A of TNF was evaluated on the engraftment and GVHD in 148 allo-HSCT recipients with sibling donors. In the multivariate analysis, the genotype CAno12/no12 (low production) of INFG (OR 3.9, p=0.003), bone marrow (BM) as source of progenitor cells (OR 4.6, p=0.013) and bacteremia (OR 3.0, p=0.033) maintained their predictive power with respect to late engraftment (≥15 days). Genotype of low IFNG production (OR 0.1, p=0.008), bacteremia (OR 3.3, p=0.048) and presence of CMV (OR 3.3, p=0.046) showed a significant association with aGVHD 3-4. And with respect to cGVHD, the genotype -308 GG (low production) of TNF (OR 3.3, p=0.038), PB as source (OR 5.0, p=0.028), myeloablative conditioning (OR 3.3, p=0.014) and previous aGVHD 2-4 (OR 2.6, p=0.029). Although it is necessary to confirm these findings, the genotype of lower IFNG production was associated with a later engraftment and less severe aGVHD and genotypes of lower TNF production was related to a higher incidence of cGVHD contributing to the development of complications in allo-HSCT.Fil: Palau Nagore, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Berro, Mariano. Universidad Austral; ArgentinaFil: Bestach, Yesica Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Rivas, M.M.. Universidad Austral; ArgentinaFil: Foncuberta, C.. Instituto Alexander Fleming; ArgentinaFil: Vitriu, A.. Instituto Alexander Fleming; ArgentinaFil: Remaggi, G.. Fundaleu; ArgentinaFil: Martínez Rolón, J.. Fundaleu; ArgentinaFil: Jaimovich, Sebastian Gaston. Fundación Favaloro; ArgentinaFil: Requejo, A.. Fundación Favaloro; ArgentinaFil: Padros, K.. Primer Centro Argentino de Inmunogenética; ArgentinaFil: Rodríguez, M.B.. Primer Centro Argentino de Inmunogenética; ArgentinaFil: Kusminsky, G.. Universidad Austral; ArgentinaFil: Larripa, Irene Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Belli, Carolina Bárbara. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentin