Decolonizar la investigación sobre migraciones : apuntes desde una etnografía colaborativa

En este artículo analizamos los significados asumidos por la idea de "(in)migración(es)" y la categoría de "(in)migrante(s)" en los contextos sociales, políticos y académicos contemporáneos. Resaltando su estrecha relación con el pensamiento de Estado y la colonialidad del poder/saber, nos preguntamos por otros posibles acercamientos a la movilidad humana. Discutimos la etnografía colaborativa, entendida como una metodología decolonial que rechaza las representaciones pasivizantes hegemónicas y aspira a visibilizar los procesos de subjetivación política de las personas junto a las que se investiga. Aportando ejemplos de nuestra propia investigación colaborativa junto a Stop Desahucios-Granada 15M, ilustramos cómo la idea de (in)migración(es) y la categoría "(in)migrante(s)" se han materializado en nuestro contexto, que se encuentra definido por el activismo político y no había sido previamente alterizado como "migratorio". Concluimos resaltando la ambivalencia implícita en estas dos expresiones y reflexionamos sobre los pros y los contras implícitos en su uso.In this paper we analyze the meaning of "immigration" and "immigrant" within contemporary social, political and academic contexts. We emphasize their narrow relation with State thought and the coloniality of power/knowledge and search for alternative approaches to human mobility. With this aim, we discuss collaborative ethnography as a decolonial methodology addressed to visibilize the political subjectivation processes of the people we research with. Drawing on examples from our own collaborative research with Stop Evictions-Granada 15M, we show how the idea of "immigration" and the category "immigrants" have come into being within our field, a space of political activism which had not been previously constructed as a "migratory context". We conclude underlining the ambivalence implicit in the two aforementioned concepts and discuss the pros and cons of using them

Interchromosomal repeat array interactions between chromosomes 4 and 10: a model for subtelomeric plasticity.

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Interchromosomal repeat array interactions between chromosomes 4 and 10: a model for subtelomeric plasticity.

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Oxidatively modified proteins in bronchoalveolar lavage fluid of patients with ARDS and patients at-risk for ARDS.

Oxidative stress in acute respiratory distress syndrome (ARDS) is considered as an important pathophysiological mechanism in acute impairment of lung function. The present study investigated whether a pulmonary oxidant-antioxidant imbalance is indicated by substantial oxidative modification of proteins in bronchoalveolar lavage (BAL) fluid. Oxidatively modified proteins in BAL fluid, as measured by the reduction of protein carbonyl groups with tritiated borohydride, were studied in control subjects, patients with clinically established ARDS, and patients considered at-risk for ARDS because they had had coronary bypass surgery. Subsets of these at-risk patients were pretreated either with methylprednisolone or N-acetylcysteine. The carbonyl content of BAL fluid proteins was greatly increased in ARDS patients (5.0+/-13 nmol carbonyl x mL(-1) BAL fluid; mean+/-SEM; p=0.0004; n=10) and moderately increased in the untreated patients at-risk for ARDS (1.3+/-0.2 nmol x mL(-1); p=0.027; n=19) compared with controls (0.8+/-0.2 nmol x mL(-1); n=12). The two other at-risk groups pretreated either with methylprednisolone or N-acetylcysteine showed carbonyl values that were statistically not different from the controls (1.2+/-0.2 nmol x mL(-1); p=0.13; n=13, and 1.1+/-0.3 nmol x mL(-1); p=0.40; n=8, respectively). These results show that oxidatively modified proteins clearly accumulated in bronchoalveolar lavage fluid of acute respiratory distress syndrome patients, and to a minor extent in untreated at-risk patients. These data suggest a severe oxidant-antioxidant imbalance in acute respiratory distress syndrome

Variable hypomethylation of D4Z4 in facioscapulohumeral muscular dystrophy.

Item does not contain fulltextFacioscapulohumeral muscular dystrophy (FSHD) progressively affects the facial, shoulder, and upper arm muscles and is associated with contractions of the polymorphic D4Z4 repeat array in 4q35. Recently, we demonstrated that FSHD alleles are hypomethylated at D4Z4. To study potential relationships between D4Z4 hypomethylation and both residual repeat size and clinical severity, we compared the clinical severity score with D4Z4 methylation in unrelated FSHD patients. Correcting the clinical severity score for age at examination improves the parameter to define clinical severity and provides further support for hypomethylation of FSHD alleles. However, a linear relationship between repeat size and clinical severity of the disease cannot be established. Interestingly, FSHD can be separated in two clinical severity classes: patients with residual repeat sizes of 10 to 20 kb are severely affected and show pronounced D4Z4 hypomethylation. In contrast, patients with repeat sizes of 20 to 31kb show large interindividual variation in clinical severity and D4Z4 hypomethylation. Because the majority of familial FSHD cases are represented in this interval and considering the overt variation in clinical severity in these familial cases, it thus is imperative to develop comprehensive allele-specific assays monitoring total D4Z4 methylation to investigate whether interindividual variation in D4Z4 methylation can be translated into a prognostic factor for clinical severity

Hypomethylation of D4Z4 in 4q-linked and non-4q-linked facioscapulohumeral muscular dystrophy.

Item does not contain fulltextThe autosomal dominant myopathy facioscapulohumeral muscular dystrophy (FSHD1, OMIM 158900) is caused by contraction of the D4Z4 repeat array on 4qter. We show that this contraction causes marked hypomethylation of the contracted D4Z4 allele in individuals with FSHD1. Individuals with phenotypic FSHD1, who are clinically identical to FSHD1 but have an unaltered D4Z4, also have hypomethylation of D4Z4. These results strongly suggest that hypomethylation of D4Z4 is a key event in the cascade of epigenetic events causing FSHD1

Possible phenotypic dosage effect in patients compound heterozygous for FSHD-sized 4q35 alleles.

Item does not contain fulltextOBJECTIVE: Autosomal dominant facioscapulohumeral muscular dystrophy (FSHD) is associated with a contraction of the D4Z4 repeat array on chromosome 4. So far, homozygosity or compound heterozygosity for FSHD alleles has not been described, and it has been debated whether the absence of such subjects is because of the rarity or the lethality of the disorder. METHODS: Two unrelated families in which the probands are compound heterozygous for two FSHD-sized alleles were studied. Clinical examination, pulsed-field gel electrophoresis (PFGE) studies of DNA with probes proximal and distal to D4Z4, and cytogenetic analysis of metaphase chromosomes by FISH were performed. RESULTS: Complementary molecular and cytogenetic approaches confirmed the chromosome 4qA origin of all FSHD-sized repeat arrays that segregate in the families. CONCLUSIONS: Heterozygosity for FSHD-sized alleles is compatible with life in men and women. A possible dosage effect was observed in both probands in whom each 4qA allele contributed to the FSHD phenotype. Because at least one of the FSHD alleles in both families showed an unusual low penetrance, the authors propose that susceptibility for FSHD is partly determined by intrinsic properties of the disease allele other than the residual D4Z4 repeat size alone