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Mitigating climate change requires a global transition from fossil fuels to a “green economy” driven by renewable energies. This shift has fostered massive investments in mining resources, notably lithium in South America, needed to store renewable energies. These mining ventures often produce harmful externalities where lithium is located. In Argentina, a major producer, striking variation has occurred in the fortunes of lithium-mining projects. In some instances, mining companies offered concessions that mitigated environmental damage and improved local socioeconomic conditions. In others, companies made minimal concessions, and in a third set they halted projects in response to local resistance. Why do mining ventures result alternatively in negotiated, unnegotiated, or aborted extraction? The article proposes a new typology of modes of extraction together with a multilevel explanatory framework that centers on the strengths and strategies of transnational mining companies, subnational governments, and local communities in setting the terms for extracting lithium.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal lung disease. This disease is characterized by an excessive accumulation of extracellular matrix deposition that modify normal lung physiology. Up to date, there are not efficient therapeutic tools to fight IPF. Glucagon-like peptide-1 receptor (GLP-1R) activation plays an essential role in lung functions in normal and in pathological conditions. The aim of the present study was to study the possible beneficial effects of the administration of the GLP-1R agonist, liraglutide, in the pathogenesis of the fibrotic process in an animal model of pulmonary fibrosis induced by bleomycin. We observed that liraglutide decreased mRNA expression of collagen, hydroxyproline and key enzymes for the synthesis of collagen. In addition, GLP-1R activation restored the ACE2 mRNA levels modulating the activities of the RAS components, increased the production of surfactant proteins (SFTPa1, SFTPb, SFTPc) and promoted an improvement in pulmonary and cardiac functionality, including a partial restoration of lung alveolar structure. Liraglutide effects are shown at both the pro-inflammatory and fibrosis phases of the experimental disease. For these reasons, GLP-1 might be regarded as a promising drug for treating pulmonary fibrosis.

Glucagon like-peptide 1 (GLP-1) within the brain is produced by a population of preproglucagon neurons located in the caudal nucleus of the solitary tract. These neurons project to the hypothalamus and another forebrain, hindbrain, and mesolimbic brain areas control the autonomic function, feeding, and the motivation to feed or regulate the stress response and the hypothalamic-pituitary-adrenal axis. GLP-1 receptor (GLP-1R) controls both food intake and feeding behavior (hunger-driven feeding, the hedonic value of food, and food motivation). The activation of GLP-1 receptors involves second messenger pathways and ionic events in the autonomic nervous system, which are very relevant to explain the essential central actions of GLP-1 as neuromodulator coordinating food intake in response to a physiological and stress-related stimulus to maintain homeostasis. Alterations in GLP-1 signaling associated with obesity or chronic stress induce the dysregulation of eating behavior. This review summarized the experimental shreds of evidence from studies using GLP-1R agonists to describe the neural and endocrine integration of stress responses and feeding behavior.

When do oil-dependent governments spend oil rents in expanding political machines through patronage and clientelism, as rentier theories claim, or in providing better public services? Using regression analysis for panel data and two case studies of the Argentine provinces (1983-2013), this study shows that infrastructure can rise and patronage decline during oil booms. When rents are high and the oil sector creates new jobs, incumbents tend to increase capital investment. They cannot compete with oil salaries and use infrastructure to cope with the sector's pressures for basic services. When rents decline in contexts of job destruction in the oil sector, and the rest of the private sector cannot absorb the layoffs, incumbents tend to increase patronage to contain social turmoil and secure core voters.

Background Patients with liver cirrhosis and minimal hepatic encephalopathy (MHE) show mild cognitive impairment and spatial learning dysfunction. Hyperammonemia acts synergistically with inflammation to induce cognitive impairment in MHE. Hyperammonemia-induced neuroinflammation in hippocampus could contribute to spatial learning impairment in MHE. Two main aims of this work were: (1) to assess whether chronic hyperammonemia increases inflammatory factors in the hippocampus and if this is associated with microglia and/or astrocytes activation and (2) to assess whether hyperammonemia-induced neuroinflammation in the hippocampus is associated with altered membrane expression of glutamate and GABA receptors and spatial learning impairment. There are no specific treatments for cognitive alterations in patients with MHE. A third aim was to assess whether treatment with sulforaphane enhances endogenous the anti-inflammatory system, reduces neuroinflammation in the hippocampus of hyperammonemic rats, and restores spatial learning and if normalization of receptor membrane expression is associated with learning improvement. Methods We analyzed the following in control and hyperammonemic rats, treated or not with sulforaphane: (1) microglia and astrocytes activation by immunohistochemistry, (2) markers of pro-inflammatory (M1) (IL-1β, IL-6) and anti-inflammatory (M2) microglia (Arg1, YM-1) by Western blot, (3) membrane expression of GABA, AMPA, and NMDA receptors using the BS3 cross-linker, and (4) spatial learning using the radial maze. Results The results reported show that hyperammonemia induces astrocytes and microglia activation in the hippocampus, increasing pro-inflammatory cytokines IL-1β and IL-6. This is associated with altered membrane expression of AMPA, NMDA, and GABA receptors which would be responsible for altered neurotransmission and impairment of spatial learning in the radial maze. Treatment with sulforaphane promotes microglia differentiation from pro-inflammatory M1 to anti-inflammatory M2 phenotype and reduces activation of astrocytes in hyperammonemic rats. This reduces neuroinflammation, normalizes membrane expression of glutamate and GABA receptors, and restores spatial learning in hyperammonemic rats. Conclusions Hyperammonemia-induced neuroinflammation impairs glutamatergic and GABAergic neurotransmission by altering membrane expression of glutamate and GABA receptors, resulting in impaired spatial learning. Sulforaphane reverses all these effects. Treatment with sulforaphane could be useful to improve cognitive function in cirrhotic patients with minimal or clinical hepatic encephalopathy.

Social prescribing is a mechanism for connecting patients with non-medical forms of support within the community and has been shown to improve loneliness. Yet uptake from young people (YP) has been lower than for adults. That is thought to be the case because young people are less likely to engage with primary care for wellbeing support, where social prescribing is based. The INACT study will pilot a social prescribing pathway via schools to support young people who are lonely, testing its feasibility and acceptability of delivering, and evaluating its impact on loneliness through a randomised controlled trial. This pilot study utilises a two-group (intervention vs. active control) parallel randomised design, with YP as the unit of randomisation. Approximately 78 pupils reporting loneliness will be recruited across 12 mainstream (6 primary and 6 secondary) schools in England. The co-produced social prescribing intervention includes 6-12 sessions over an 8-week period with a Link Worker who will work with individuals, on a one-to-one basis, to understand 'what matters to them' and connect them with local sources of support. Pupils in the control group will receive signposting to sources of support from school staff. Data will be collected at baseline, 3- and 6-month follow-up. Acceptability and feasibility will be assessed via participant recruitment and retention, and via qualitative interviews. Interviews will also explore barriers and facilitators to engagement and implementation and mechanisms of change. Primary and secondary outcomes will be completed to assess response and completeness, including measures of loneliness, mental health and wellbeing. The INACT study will provide preliminary evidence of the feasibility and acceptability of both the research design and social prescribing intervention. Results will inform a planned future randomised trial. ClinicalTrials.gov NCT06656663.

Has the global energy transition opened new opportunities for natural resource extraction to foster development? To address this question we propose the concept “developmental extraction” (DE), an intermediate option between neoliberal and anti-extraction. For proponents of DE, mining can be a development-enhancing activity that triggers virtuous economic linkages. Focusing on South America’s Lithium Triangle countries (Argentina, Bolivia, and Chile), we find that the results of DE are mixed, with modest advances in fostering developmental linkages at the local level coupled with uneven outcomes at translocal scales. To explain the contrasting outcomes of DE projects, we offer a multilevel framework that highlights political and territorial challenges of forging developmental linkages. The fortunes of DE depend on the distribution of bargaining power among states, mining companies, and communities and, in turn, on the results of local and translocal negotiations over the terms of extraction.

This article analyses the relation between mineral rents and development outcomes at the subnational level. The classical literature suggests that natural resource abundance has negative effects on well-being, a situation referred to as the resource curse. However, a novel strand of research emphasizes that rentier states worldwide exhibit contrasting outcomes. To account for such variation, this investigation aligns with approaches stressing the significance of contextual (place and institutional) factors to studying the resource curse. The main claim in this work is that both structural and institutional factors related to the extractive industry help account for variation in development outcomes. It contends that mineral rents are positively associated with human development and economic industrialization when the extractive sector is not geographically concentrated in enclave economies, and subnational fiscal institutions redistribute enough rents from producing to non-producing districts. It empirically tests this argument using a time series cross-sectional analysis, a difference-in-difference (DiD) estimation, and two case studies in Argentina, a country where subnational territorial units collect mineral royalties and have exogenously created their own rent-sharing regimes. It finally provides some comparative implications that may contribute to current debates on the socioeconomic impact of natural resource wealth.

Numerous reports showed that the epididymis plays key roles in the acquisition of sperm fertilizing ability but its contribution to embryo development remains less understood. Female mice mated with males with simultaneous mutations in Crisp1 and Crisp3 genes exhibited normal in vivo fertilization but impaired embryo development. In this work, we found that this phenotype was not due to delayed fertilization, and it was observed in eggs fertilized by epididymal sperm either in vivo or in vitro . Of note, eggs fertilized in vitro by mutant sperm displayed impaired meiotic resumption unrelated to Ca 2+ oscillations defects during egg activation, supporting potential sperm DNA defects. Interestingly, cauda but not caput epididymal mutant sperm exhibited increased DNA fragmentation, revealing that DNA integrity defects appear during epididymal transit. Moreover, exposing control sperm to mutant epididymal fluid or to Ca 2+ -supplemented control fluid significantly increased DNA fragmentation. This, together with the higher intracellular Ca 2+ levels detected in mutant sperm, supports a dysregulation in Ca 2+ homeostasis within the epididymis and sperm as the main factor responsible for embryo development failure. These findings highlight the contribution of the epididymis beyond fertilization and identify CRISP1 and CRISP3 as novel factors essential for sperm DNA integrity and early embryo development.

Maternal and perinatal undernutrition affects the lung development of litters and it may produce long-lasting alterations in respiratory health. This can be demonstrated using animal models and epidemiological studies. During pregnancy, maternal diet controls lung development by direct and indirect mechanisms. For sure, food intake and caloric restriction directly influence the whole body maturation and the lung. In addition, the maternal food intake during pregnancy controls mother, placenta, and fetal endocrine systems that regulate nutrient uptake and distribution to the fetus and pulmonary tissue development. There are several hormones involved in metabolic regulations, which may play an essential role in lung development during pregnancy. This review focuses on the effect of metabolic hormones in lung development and in how undernutrition alters the hormonal environment during pregnancy to disrupt normal lung maturation. We explore the role of GLP-1, ghrelin, and leptin, and also retinoids and cholecalciferol as hormones synthetized from diet precursors. Finally, we also address how metabolic hormones altered during pregnancy may affect lung pathophysiology in the adulthood.