Large-Scale Immigration Worksite Raids and Mixed-Status Families: Separation, Financial Crisis, and Family Role Rearrangement.

Mixed-status families-whose members have multiple immigration statuses-are common in US immigrant communities. Large-scale worksite raids, an immigration enforcement tactic used throughout US history, returned during the Trump administration. Yet, little research characterizes the impacts of these raids, especially as related to mixed-status families.

[Parsonage-Turner syndrome. Report of one case].

We report a 59-year-old male who, three weeks after a coronary revascularization surgery, reported a sudden intense burning pain in his left upper limb. Two weeks later, he reports a paresis with difficulty to extend his left wrist and fingers. The electromyography showed a severe axonal damage of the radial nerve with distal denervation signs.

Iron toxicity in neurodegeneration.

Iron is an essential element for life on earth, participating in a plethora of cellular processes where one-electron transfer reactions are required. Its essentiality, coupled to its scarcity in aqueous oxidative environments, has compelled living organisms to develop mechanisms that ensure an adequate iron supply, at times with disregard to long-term deleterious effects derived from iron accumulation. However, iron is an intrinsic producer of reactive oxygen species, and increased levels of iron promote neurotoxicity because of hydroxyl radical formation, which results in glutathione consumption, protein aggregation, lipid peroxidation and nucleic acid modification.

Effect of mitochondrial complex I inhibition on Fe-S cluster protein activity.

Iron-sulfur (Fe-S) clusters are small inorganic cofactors formed by tetrahedral coordination of iron atoms with sulfur groups. Present in numerous proteins, these clusters are involved in key biological processes such as electron transfer, metabolic and regulatory processes, DNA synthesis and repair and protein structure stabilization. Fe-S clusters are synthesized mainly in the mitochondrion, where they are directly incorporated into mitochondrial Fe-S cluster-containing proteins or exported for cytoplasmic and nuclear cluster-protein assembly.

Divalent metal transporter 1 (DMT1) contributes to neurodegeneration in animal models of Parkinson's disease.

Dopaminergic cell death in the substantia nigra (SN) is central to Parkinson's disease (PD), but the neurodegenerative mechanisms have not been completely elucidated. Iron accumulation in dopaminergic and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation, and neuronal death. The mechanisms involved in iron accumulation also remain unclear.

The alpha2-adrenoceptor antagonist dexefaroxan enhances hippocampal neurogenesis by increasing the survival and differentiation of new granule cells.

The generation of new neurons in the hippocampus is a dynamic process regulated by environmental, endocrine, and pharmacological factors. Since enhancement of hippocampal neurogenesis has been associated with learning and memory, and the locus coeruleus-noradrenergic system has been shown to modulate these cognitive functions, we hypothesized that activation of noradrenergic neurotransmission might enhance neurogenesis in the adult hippocampus. To test this hypothesis in vivo, we induced the release of noradrenaline in the hippocampus by blocking presynaptic inhibitory autoreceptors with the selective alpha2-adrenoceptor antagonist dexefaroxan.

Progressive iron accumulation induces a biphasic change in the glutathione content of neuroblastoma cells.

Glutathione (GSH) constitutes the single most important antioxidant in neurons, whereas iron causes oxidative stress that leads to cell damage and death. Although GSH and iron produce opposite effects on redox cell status, no mechanistic relationships between iron and GSH metabolism are known. In this work, we evaluated in SH-SY5Y neuroblastoma cells the effects of iron accumulation on intracellular GSH metabolism.