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In the face of extreme violence, some Indigenous women-led social movement organisations defending human rights from the abuses related to mega-projects have achieved favourable changes in corporate practices. In the predominantly patriarchal, capitalist and racist context of Latin America, what explains the success (or not) of Indigenous women-led mobilisations regarding the most politically and economically powerful actors? Although there is a well-established literature on social movements, some dedicated to the influence on corporate practices, there is a lacuna concerning the agency, leadership and impact of Indigenous women-led movements in the context of mega-projects. This thesis uses a multi-level qualitative research methodology to develop a theoretical framework to explain their outcomes. It involves three main comparisons of cases of success and non-success: (1) within-country variation comparing Lenca women-led organisations contesting abuses related to hydroelectric dam projects in Honduras; (2) within-case variation over time of a Binni'za women-led mobilisation against violations connected to wind farm projects in Mexico; and (3) a small-N cross-national comparison of mobilisations in Ecuador, Peru and Colombia led by Sarayaku, Asháninka and Wayuu women challenging the abuses related to oil extractives, hydroelectric dam projects, and coal mining respectively. Also, I develop a qualitative comparative analysis of all these cases, which includes a Boolean minimisation process. The thesis finds that in a minimally favourable context the following four factors operating together in a braid of action lead to success (i.e., a favourable change in corporate behaviour): (1) transforming the territory into power; (2) Indigenous women's effective leadership; (3) human rights framing; and, (4) reacting to a grave violation overtly involving corporations. These four strands interweaved in a tough braid of action are capable of harnessing mobilisation power, achieving success over much materially powerful corporate forces. If some of the strands are weak or frayed, the braid cannot achieve this success.

Background/Aims Bariatric surgery can increase the risk of addictive disorders and nutritional deficiencies. The aim of this study was to evaluate the association between bariatric surgery and alcohol use disorder (AUD), alcohol-related liver disease (ALD), and psychiatric disorders associated with AUD. The impact of vitamin D deficiency in these associations was also investigated.Methods A cross-sectional study was performed using the National Inpatient Sample database and its ICD-9 codes information. Diagnostic and comorbidity data from hospital discharges were obtained from patients with bariatric surgery and other abdominal surgeries between 2005 and 2015. The two groups were then compared for alcohol-related outcomes after propensity-score matching.Results The final study cohort included 537,757 patients with bariatric surgery and 537,757 with other abdominal surgeries. The bariatric surgery group had an increased risk of AUD [odds ratio (OR): 1.90; 95% CI: 1.85-1.95], ALD [OR: 1.29; 95% CI: 1.22-1.37], cirrhosis [OR, 1.39; 95% CI: 1.37-1.42], and psychiatric disorders associated with AUD [OR, 3.59; 95% CI: 3.37-3.84]. Vitamin D deficiency did not impact in the association between bariatric surgery and AUD, ALD, or psychiatric disorders associated with AUD.Conclusions Bariatric surgery is associated with an increased prevalence of AUD, ALD, and psychiatric disorders associated with AUD. These associations appear to be independent from vitamin D deficiency.

Spx is a transcription factor present in low G+C Gram-positive bacteria, including Bacillus subtilis and several human pathogens. By direct binding to the αCTD domain of the RNA polymerase, Spx modulates the expression of a large set of genes in B. subtilis. The Spx regulon is active in growing cells, and its expression is further induced in response to some stresses. Spx activation has been typically studied using diamide to generate disulfide stress. By using molecular biology, genetic, and biochemistry techniques, I show that the Spx regulon is also induced in response to cell wall stress, and that Spx is critical for survival of B. subtilis upon treatment with cell wall antibiotics. I further show the molecular mechanisms that lead to activation of Spx. Unlike disulfide stress, induction of the Spx regulon in response to cell wall stress requires transcriptional induction of the spx gene. This induction is mediated by the alternative extracytoplasmic sigma factor σM, and occurs at a promoter upstream of the yjbC-spx operon (i.e. PM1). Interestingly, activation of the Spx regulon in response to cell wall stress also requires stabilization; however, unlike disulfide stress, this process is mediated by a small protein called YirB. YirB is an anti-adaptor protein that binds with high affinity to YjbH, the adaptor protein required for ClpXP-mediated proteolysis, and therefore reduces the rate of Spx degradation. Transcriptional induction and post-translational stabilization are thus required for activation of the Spx regulon in response to antibiotics that inhibit peptidoglycan biosynthesis. Then, I show that yirB is also induced in response to cell wall stress, and that its activation requires the coordinated action of the YuxN repressor and the CssRS two-component system. Finally, I show that Spx is not only degraded through ClpXP, but also by ClpCP. The adaptor that mediates this degradation in unstressed cells appears to be MecA, and the evidence comes from the Spx-dependent synthetic lethality of ClpX and MecA. The McsB arginine kinase, which also acts as a ClpCP adaptor, as well as the YwlE arginine phosphatase are also shown to play an important role in Spx regulation. Overall, this work expands the regulatory mechanisms that control the activity of a pleiotropic transcription factor in B. subtilis.