The selenized glutelin (Se-G) from Se-enriched chickpea sprouts has demonstrated high antioxidant potential. In this study, the response surface methodology was employed to optimize Se-G content (1–4%) and grape or rosehip oils (10–40%) for the preparation of W/O emulsions with strong antioxidant activity. In the optimal emulsions (Se-GG with grape oil and Se-GR with rosehip oil), antioxidant, photoprotective, and antiaging properties were evaluated. Non-Se glutelin was used in the control emulsions. The optimal conditions determined (4.0% Se-G/10.0% rosehip oil and 3.39% Se-G/12.50% grape oil) allowed for the preparation of emulsions with higher antioxidant capacity. The Se-GR with rosehip oil had greater antioxidant capacity than the Se-GG with grape oil. The optimal emulsions with Se, compared to their Se-free controls, had significantly higher antioxidant activity. The zeta potential value increased with the presence of Se. A positive effect on the inhibition of ROS production and lipid peroxidation was observed, as well as the inhibition of collagenase, elastase, and hyaluronidase activity, mainly due to the presence of selenium. Se-G represents a powerful tool for preventing damage to the skin caused by UV exposure.

This study examined how residents of Culiacán, México, adapted over time to prolonged community violence and perceived insecurity. We evaluated a two-speed adaptation theory, which proposes that indicators of acute psychological distress and economic strain decline over time, whereas protective behavioral responses persist as a state of chronic vigilance. A mixed-longitudinal design was employed, consisting of a baseline survey of 1163 residents conducted in October 2024 and a longitudinal cohort of 100 participants followed in February and June 2025. Longitudinal changes were evaluated using Cochran’s Q tests with exact McNemar post hoc comparisons, proportions were reported with 95% Clopper–Pearson confidence intervals, and multivariable logistic regression was used to examine predictors of migration intent. Pharmacologic treatment utilization declined significantly from 36% to 20%, and reported economic strain decreased from 62% to 35% over the study period. In contrast, behavioral routine modifications remained persistently high, decreasing only from 95% to 88%, with no statistically significant longitudinal change. These findings are consistent with the proposed theory, suggesting that while acute psychosocial and economic impacts may diminish over time, protective behavioral adaptations remain comparatively stable. Regarding migration intent, individual economic strain was not significantly associated with the intention to leave the city. Instead, participants who attributed insecurity primarily to social contract collapse, conceptualized as the perceived erosion of community trust, institutional legitimacy, social polarization, and the breakdown of social order, had substantially greater odds of reporting migration intent than those primarily concerned with economic factors (OR = 11.56, 95% CI 1.55–85.98). Overall, these findings suggest that prolonged community violence produces distinct trajectories of psychosocial adaptation, in which acute distress decreases while chronic vigilance persists. Furthermore, migration intentions appear to be more strongly associated with perceived deterioration of the social environment than with individual economic hardship, highlighting the importance of restoring community trust and institutional legitimacy alongside traditional public health and economic interventions.

Background: T2DM and AD are major public health concerns characterized by metabolic and cognitive impairments, respectively, with growing evidence suggesting that gut microbiota alterations contribute to their pathogenesis. Metagenomic and metabolomic analyses provide valuable insights into the microbiota's role in glucose regulation, inflammation, and dementia risk, offering potential for early diagnosis and targeted interventions. Understanding the interplay between gut microbiota and metabolic pathways could lead to novel therapeutic strategies to improve patient outcomes. Method: A descriptive study with a quantitative approach, cross‐sectional observational comparative, of relational scope will be conducted. The study population will be segmented into four groups and two subgroups: Control (CTRL) ( n = 30), Type 2 Diabetes Mellitus (T2DM) ( n = 30), Alzheimer's Disease (AD) without T2DM ( n = 30), and AD with T2DM ( n = 30). Subgroups include Control (Young adults) ( n = 30) and T2DM (Young adults) ( n = 30). All groups will undergo characterization, which includes blood chemistry, and clinical, mental, nutritional, and anthropometric evaluations. We obtained urine and stool samples for DNA extraction and library preparation. We used Magnetic Resonance Mass Spectrometry (MRMS) for metabolomic analysis, which uses eluents to detect metabolites. We will apply MetaHit bioinformatics tools to assess sample diversity and perform metabolomic analysis in RStudio. Result: The study revealed distinct patterns of intestinal dysbiosis and metabolic changes in patients with T2DM and AD, categorized by age. A comprehensive taxonomic and functional representation of the gut microbiome highlighted condition‐specific differences. Significant correlations were found between microbiological, metabolomic, and clinical biomarkers, particularly those related to cognitive decline. Key metabolic pathways and molecular processes underlying dysbiosis were identified. Fecal metabolite analysis uncovered distinctive compounds such as (+/‐)‐Ethylketocyclazocine, (‐)‐Quebrachamine, and (‐)‐jasmonoyl‐L‐isoleucine, while urinary metabolites like (Phenylthio) acetic acid and 2,3‐Diketo‐L‐gulonate showed disease‐associated variations. These findings support the development of personalized interventions to mitigate cognitive decline through microbiota and metabolomic profile modifications. Conclusion: The study identifies distinct gut microbiota and metabolic patterns linked to cognitive decline in T2DM and AD, offering insights into disease mechanisms and supporting the development of personalized therapeutic strategies to improve patient outcomes.