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INTRODUCTION: Food security and nutrition have been severely impacted during the COVID-19 pandemic, particularly in low- and middle-income countries (LMICs). We aimed to quantify the impacts of the pandemic on food security and diet diversity within Chilanga District in Zambia and identify target areas for high-impact social protection and safety net programs. METHODS: We conducted a cross-sectional study in Chilanga district immediately after the Omicron variant surge in February 2022. Diet quality and food security were assessed based on a household diet questionnaire and a Minimum Dietary Diversity-Women (MDD-W) score was calculated. A paired t-test was used to determine whether there was a statistically significant change in the MDD-W score and McNemar test was used to investigate the change in food security between the pre- and peri-COVID-19 period. RESULTS: Compared to the pre-COVID-19 period, there were increases in food prices across the board in the peri-COVID-19 period and decreased consumption of key food categories including legumes, dairy and vitamin A rich foods. Despite high rates of food insecurity, only 6.6% of surveyed households received any cash or in-kind assistance from a government agency, non-profit, or other organization in the post-COVID-19 period. CONCLUSION: The COVID-19 pandemic had significant impacts on food security and dietary diversity in Chilanga district. This is particularly relevant in the low-income communities that we surveyed, which had pre-existing challenges with food security. Additional resources must be invested in Chilanga District and similarly affected areas to address this gap in access to food and promote national equity. Trial Registration N/A.
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COVID-19 , Pandemias , Humanos , Femenino , Zambia/epidemiología , Estudios Transversales , Abastecimiento de Alimentos , COVID-19/epidemiología , SARS-CoV-2 , Dieta , Verduras , Seguridad AlimentariaRESUMEN
Background: Adolescents make up roughly a quarter of the population in Zambia; however, most nutrition-related programming is targeted at the under-five population. Understanding the scale of undernutrition in older children and adolescents is fundamental to alleviating food insecurity and addressing undernutrition across all age groups. Methods: A cross-sectional survey was performed in four low-income, peri-urban compounds in Chilanga District which included anthropometric measurements of children between ages 6 months-19 years and a household-level diet diversity and food security questionnaire. Wasting was used for children under 5 and thinness for children 5-19 years. Descriptive analysis and multivariate logistic regression were conducted to quantify the prevalence and distribution of malnutrition and understand the impact of food security. Results: We surveyed 393 households and 1,004 children between the ages of 6 months and 19 years. Children aged 6-9 years had the highest prevalence of severe thinness (5.2%) and adolescents (10-19 years) had the highest rates of moderate thinness (6.5%). Across all age groups, more than 75% of children were in households that worried about running out of food in the previous month. 24.9% of adolescents and 28.4% of older children were in households were more likely to go a whole day without eating compared to 16.9% of children under 5. Conclusion: Our survey indicated that malnutrition in adolescents and older children living in Chilanga district was comparable to those under 5. Interventions to address undernutrition must be targeted at older children and adolescents in order to ameliorate this burden.
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Desnutrición , Delgadez , Humanos , Niño , Adolescente , Lactante , Delgadez/epidemiología , Estudios Transversales , Zambia/epidemiología , Trastornos del Crecimiento/epidemiología , Abastecimiento de Alimentos , Desnutrición/epidemiologíaRESUMEN
Despite a series of high-profile media reports of sexual abuse in sport over the past few years, little research has been done to explore the scope of the problem in the United States. The current article reports on prevalence of child sexual assault in elite athletes in the United States. Using a retrospective web survey, adults answered questions on their experiences in sport. Of the 473 elite athletes surveyed, 3.8% (n = 18) reported being sexual assaulted as a minor in the sporting context. Of those reporting assault, most (61%) reported being abused by an adult authority figure (usually a coach) and 44% reported being assaulted by a peer. Abused athletes were significantly more likely to report having been diagnosed with a mental disorder (Fisher's exact test; p < .001). The findings can be utilized to improve prevention and child protection measures and other safeguarding initiatives in sport.
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Abuso Sexual Infantil , Adulto , Niño , Humanos , Prevalencia , Salud Mental , Estudios Retrospectivos , AtletasRESUMEN
Folliculin interacting protein 1 (Fnip1) is a cytoplasmic protein originally discovered through its interaction with the master metabolic sensor 5' AMP-activated protein kinase (AMPK) and Folliculin, a protein mutated in individuals with Birt-Hogg-Dubé Syndrome. In response to low energy, AMPK stimulates catabolic pathways such as autophagy to enhance energy production while inhibiting anabolic pathways regulated by the mechanistic target of rapamycin complex 1 (mTORC1). We previously found that constitutive disruption of Fnip1 in mice resulted in a lack of peripheral B cells because of a block in B cell development at the pre-B cell stage. Both AMPK and mTORC1 were activated in Fnip1-deficient B cell progenitors. In this study, we found inappropriate mTOR localization at the lysosome under nutrient-depleted conditions. Ex vivo lysine or arginine depletion resulted in increased apoptosis. Genetic inhibition of AMPK, inhibition of mTORC1, or restoration of cell viability with a Bcl-xL transgene failed to rescue B cell development in Fnip1-deficient mice. Fnip1-deficient B cell progenitors exhibited increased nuclear localization of transcription factor binding to IgHM enhancer 3 (TFE3) in developing B cells, which correlated with an increased expression of TFE3-target genes, increased lysosome numbers and function, and increased autophagic flux. These results indicate that Fnip1 modulates autophagy and energy response pathways in part through the regulation of AMPK, mTORC1, and TFE3 in B cell progenitors.
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Proteínas Quinasas Activadas por AMP/metabolismo , Linfocitos B/metabolismo , Factores de Transcripción Básicos con Cremalleras de Leucinas y Motivos Hélice-Asa-Hélice/metabolismo , Proteínas Portadoras/metabolismo , Homeostasis , Diana Mecanicista del Complejo 1 de la Rapamicina/metabolismo , Animales , Ratones , Ratones Endogámicos C57BL , Ratones NoqueadosRESUMEN
Birt-Hogg-Dube' Syndrome (BHDS) is a rare genetic disorder in humans characterized by skin hamartomas, lung cysts, pneumothorax, and increased risk of renal tumors. BHDS is caused by mutations in the BHD gene, which encodes for Folliculin, a cytoplasmic adapter protein that binds to Folliculin interacting proteins-1 and -2 (Fnip1, Fnip2) as well as the master energy sensor AMP kinase (AMPK). Whereas kidney-specific deletion of the Bhd gene in mice is known to result in polycystic kidney disease (PKD) and renal cell carcinoma, the roles of Fnip1 in renal cell development and function are unclear. In this study, we utilized mice with constitutive deletion of the Fnip1 gene to show that the loss of Fnip1 is sufficient to result in renal cyst formation, which was characterized by decreased AMPK activation, increased mTOR activation, and metabolic hyperactivation. Using RNAseq, we found that Fnip1 disruption resulted in many cellular and molecular changes previously implicated in the development of PKD in humans, including alterations in the expression of ion and amino acid transporters, increased cell adhesion, and increased inflammation. Loss of Fnip1 synergized with Tsc1 loss to hyperactivate mTOR, increase Erk activation, and greatly accelerate the development of PKD. Our results collectively define roles for Fnip1 in regulating kidney development and function, and provide a model for how loss of Fnip1 contributes to PKD and perhaps renal cell carcinoma.