Articles

<b>Background:</b> Chronic kidney disease (CKD) affects over 35.5 million US adults. Serum α1-acid glycoprotein (α1-AGP), an acute-phase protein, exhibits anti-inflammatory properties in animal models, but its association with CKD in younger women remains underexplored. This study investigated the relationship between serum α1-AGP and CKD risk in US women aged 20–49 years. <b>Methods:</b> This nationally representative cross-sectional study used data on female adults in the US aged 20–49 years from the National Health and Nutrition Examination Survey 2015–2018 cycles. 2,137 individuals were included in the study after excluding individuals without serum α1-AGP, urine albumin, and creatinine data. Multivariate logistic regression models evaluated the association between serum α1-AGP and CKD. Moreover, we performed stratified and interaction analyses to see if the relationship was stable in different subgroups. <b>Results:</b> Among 2,137 participants (mean age 34.6 years, mean eGFR 111.7 mL/min/1.73 m²), CKD prevalence was 8.8% (n=188). Higher serum α1-AGP levels were associated with lower CKD risk in the fully adjusted model (OR 0.37, 95% CI 0.16–0.84, P = 0.017), with a dose-response trend across quartiles (P = 0.041). The association was stronger in women aged 40–49 years (OR 0.20, 95% CI 0.05–0.76) and Mexican Americans (OR 0.07, 95% CI 0.01–0.56), though interaction terms were not significant (P > 0.05). <b>Conclusions:</b> Higher serum α1-AGP levels are associated with lower CKD prevalence in young women, suggesting a protective role. Longitudinal studies are needed to confirm causality and explore α1-AGP as a biomarker for CKD risk stratification.

<b>Background:</b> Hepatocellular carcinoma (HCC) faces significant challenges in early diagnosis and prognostic assessment, necessitating novel molecular biomarkers. The role of GCN1 in tumorigenesis remains unclear, warranting systematic investigation of its clinical value. <b>Methods</b><b>:</b><b> </b>Utilizing multi-omics data from 164 HCC patients in the TCGA database, we comprehensively evaluated the diagnostic and prognostic value of GCN1 through differential expression analysis, Cox proportional hazards regression, and gene set enrichment analysis (GSEA). <b>Results</b><b>:</b><b> </b>GCN1 expression was significantly upregulated in tumor tissues (P<0.001), with ROC analysis demonstrating an AUC of 0.921 (95% CI: 0.893-0.950) for discriminating tumor from normal tissue. Clinical correlation analysis revealed that high GCN1 expression significantly associated with advanced T stage (OR=1.941, P=0.002) and AFP levels >400 ng/ml (OR=3.697, P<0.001). Multivariate survival analysis confirmed its independent prognostic value (HR=1.454, P=0.038). Functional analysis indicated GCN1 promotes tumor progression by regulating cell cycle (NES=2.385) and axon guidance (NES=2.307) pathways. <b>Conclusion</b><b>:</b><b> </b>This study first elucidates the dual clinical value of GCN1 in HCC, providing a theoretical foundation for developing novel diagnostic biomarkers and prognostic evaluation systems. Future research should validate its molecular mechanisms and explore potential targeted therapies.

<b>Background: </b>Dysphagia is a common functional impairment in elderly populations, often leading to severe complications such as malnutrition and aspiration pneumonia, significantly increasing healthcare burdens. Currently, effective prognostic assessment tools are lacking. The absolute lymphocyte count (ALC), a biomarker reflecting immune-nutritional status, has potential predictive value in this context, though its role in dysphagia prognosis remains unclear. <b>Methods: </b>This retrospective cohort study included 253 dysphagic patients who received percutaneous endoscopic gastrostomy (PEG) or total parenteral nutrition (TPN) between 2014 and 2017. Five patients with missing ALC were excluded. Cox regression models assessed the association between ALC and mortality. ALC was analyzed as both continuous variable (using restriocted cubic splines) and categorical tertiles, with additional threshold analyses to assess non-linearity. Kaplan–Meier survival curves and subgroup analyses were also performed. <b>Results: </b>Lower ALC was associated with poorer nutritional status, higher inflammatory markers, and greater comorbidity burden. Higher ALC was independently associated with reduced mortality (adjusted HR: 0.60; 95% CI: 0.44–0.83; <i>p</i> = 0.002). Patients in the highest tertile had significantly better survival than those in the lowest (HR: 0.37; 95% CI: 0.23–0.59; <i>P</i> < 0.001). A non-linear threshold effect was identified at ALC = 1.899×10<SUP>9</SUP>/L (<i>p</i> for non-linearity = 0.009). Kaplan–Meier analysis confirmed improved survival with higher ALC (<i>p</i> < 0.0001). Subgroup analyses showed the protective effect of higher ALC was consistent across age, sex, BMI, PEG use, and comorbidity strata, with no significant interactions. <b>Conclusions: </b>ALC is an independent, non-linear predictor of mortality in older dysphagic patients and may aid clinical risk stratification across diverse patient subgroups.

<b>Background: </b>Maternal nutrition plays a crucial role in fetal brain development, with vitamin B12 being essential for neuronal myelination and cognitive function. The paper by Hrezova et al. entitled “Vitamin B12 Intake During Pregnancy Linked to Child Speech Development and Intelligence Quotient”, examines the association between maternal B12 intake and early childhood neurodevelopment. <b>Methods: </b>Using data from 5,151 mother-child pairs in the ELSPAC-CZ cohort, maternal B12 intake was assessed through dietary questionnaires, and child cognitive outcomes were evaluated at 18 months, 3 years, and 8 years. Multivariate adjustments were applied to control for potential confounders. <b>Results: </b>The research reports that higher maternal B12 intake was positively associated with improved language comprehension at 18 months (B=0.20,95% CI 0.06,0.34) and increased verbal IQ at 8 years (B=1.08,95% CI 0.09,2.08). However, no significant relationship was observed between maternal B12 intake and speech intelligibility at age 3 (OR=1.03,95% CI 0.99,1.07). Findings suggest B12’s role in early cognitive development but highlight gaps in its long-term effects. <b>Conclusions: </b>Ensuring adequate maternal B12 intake is vital for optimizing early neurodevelopment. Public health initiatives should promote B12 supplementation, especially for pregnant women at risk of deficiency. Further research with objective biomarkers is needed to clarify long-term effects.

<b>Background</b><b>: </b>Epigenetic aging, measured through various DNA methylation-based clocks, may have implications for predicting disease risk. However, the sensitivity of different epigenetic clocks that have emerged as biomarkers for biological aging and in predicting physical and mental health outcomes remains uncertain. This study examines the age and sex-adjusted associations between multiple epigenetic age acceleration measures and three key health indicators, including self-rated health, depressive symptoms, and body mass index (BMI), in a nationally representative sample of U.S. middle-aged and older adults. <b>Methods</b><b>: </b>We analyzed data from 4,018 adults in the 2016 wave of the Health and Retirement Study (HRS), which included several epigenetic age acceleration measures: HORVATH, HANNUM, LEVINE, HORVATHSKIN, LIN, WEIDNER, VIDALBRALO, YANG, ZHANG, BOCKLANDT, GARAGNANI, and GRIMAGE. Linear regression models were used to assess the associations between epigenetic age acceleration and self-rated health (poor health), depressive symptoms, and BMI, adjusting for age and sex. <b>Results</b><b>: </b>We found significant positive associations between epigenetic age acceleration and worse self-rated health, higher depressive symptoms, and increased BMI. However, these associations varied across different epigenetic clocks, with some measures potentially having more consistent utility for specific health outcomes than others. <b>Conclusion</b><b>: </b>Epigenetic age acceleration is linked to poorer self-rated health, greater depressive symptoms, and higher BMI, but choosing which epigenetic clock(s) to use is also important. These findings underscore the need to consider multiple epigenetic aging markers when assessing health risks and highlight the potential for particular clocks to serve as more sensitive indicators of physical and mental health outcomes.

<b>Background</b>: Type 2 Diabetes Mellitus (T2DM) and Alzheimer’s Disease (AD) are increasingly linked through shared pathophysiological mechanisms, giving rise to the concept of Type 3 Diabetes Mellitus (T3DM). Brain insulin resistance, oxidative stress, and neuroinflammation are central to both conditions, contributing to cognitive decline and AD progression. <b>Aim:</b> This review aims to explore this emerging relationship and its implications for prevention and management. <b>Methods</b>: Using an integrative review, 21 studies were systematically analyzed. The review focused on identifying demographic, genetic, and lifestyle factors contributing to T2DM and AD and examined shared molecular pathways such as insulin dysregulation and amyloid-beta accumulation. <b>Results</b>: The findings reveal that T3DM shares key features with T2DM and AD, including insulin resistance and chronic inflammation. Lifestyle interventions, such as diet and exercise, alongside routine cognitive and metabolic screenings, are critical in mitigating progression. <b>Conclusions</b>: Further research into diagnostic biomarkers and targeted therapies is essential to manage T3DM and its impact on AD. The role of nursing professionals in early detection, education, and holistic management is emphasized as vital in addressing this dual disease burden. This review offers actionable insights into integrated strategies for addressing these interconnected conditions.

Background:</b> Early life socioeconomic conditions and race/ethnicity are critical determinants of long-term health and behavioral outcomes. Epigenetic changes, particularly those measured by the GrimAge biomarker, may mediate the impact of these early adversities on later life outcomes. This study investigates the relationships between race/ethnicity, poverty at birth, epigenetic aging at age 15, and subsequent self-rated health, school discipline, depression, and school dropout at age 22. We explored sex differences in these paths. <b>Methods:</b> Data were drawn from the Fragile Families and Child Wellbeing Study (FFCWS), which included 733 youth with comprehensive follow-up data up to age 22. Structural Equation Modeling (SEM) was employed to assess the pathways from race/ethnicity and poverty at birth to epigenetic aging (GrimAge) at age 15, and subsequently to self-rated health and school discipline at age 22. The model controlled for potential confounders including sex, family structure, and parental education. <b>Results:</b> Race/ethnicity and poverty at birth were significantly associated with higher GrimAge scores at age 15 (p < 0.05). Higher GrimAge scores were predictive of poorer self-rated health (β = -0.08, p < 0.05) and increased instances of school discipline (β = 0.13, p < 0.01) at age 22. The indirect effects of race/ethnicity and poverty at birth on self-rated health and school discipline through GrimAge were also significant (p < 0.05), suggesting that epigenetic aging partially mediates these relationships. Sex differences were also observed. Poverty at birth predicted faster epigenetic aging at age 15 for males not females. We also observed that faster epigenetic aging at age 15 was predictive of school discipline of male not female participants at age 22. In contrast, faster epigenetic aging at age 15 was predictive of self-rated health (SRH) of female not male participants at age 22. <b>Conclusions:</b> This study provides evidence that with some sex differences, race/ethnicity and poverty at birth contribute to accelerated epigenetic aging (GrimAge) by age 15, which in turn predicts poorer self-rated health and increased school discipline issues by age 22. These findings emphasize the importance of early interventions targeting social determinants to mitigate long-term health and behavioral disparities. Addressing these early life conditions is crucial for improving health equity and outcomes in young adulthood.

<b>Background</b>: Telomere length is a critical biomarker of cellular aging and overall health. While childhood socioeconomic status (SES) indicators such as education and poverty can have long-lasting effects on biological aging, research has shown contradictory results regarding the impact of adulthood SES on future telomere length, particularly in racially and ethnically diverse individuals. This study investigates the effects of baseline adulthood SES indicators such as education and poverty on telomere length nine years later in women, using data from the Future of Families and Child Wellbeing Study (FFCWS). <b>Methods: </b>We analyzed data from the FFCWS, a longitudinal cohort study. The sample included baseline adulthood SES and follow-up telomere length measure of women (n = 2,421) with varying socioeconomic conditions. Telomere length was measured from saliva samples nine years after the baseline measure of adulthood SES. Education, poverty, and marital status at baseline were assessed. Multivariate linear regression models were used to examine the association between adulthood SES indicators at baseline and future telomere length, controlling for potential confounders. <b>Results:</b><b> </b>From the total 2,421 women, 675 were Latino White, 1,158 were non-Latino Black, and 588 were non-Latino White. Our findings indicate that for non-Latino White women poverty at certain level, and childbirth weight, and for non-Latino Black maternal age were predictors of telomere lengths nine years later. <b>Conclusion:</b><b> </b>Poverty at a specific level, maternal age and childbirth weight serve as predictors of telomere lengths nine years later in some women. These findings underscore the importance of socioeconomic factors and early-life influences in understanding telomere dynamics and aging processes among women from varied racial and ethnic backgrounds.

<b>Background:</b> Telomere length is a critical biomarker of cellular aging and overall health. While childhood socioeconomic status (SES) indicators such as education and poverty can have long-lasting effects on biological aging, research has shown contradictory results regarding the impact of adulthood SES on future telomere length, particularly in racially and ethnically diverse individuals. This study investigates the effects of baseline adulthood SES indicators such as education and poverty on telomere length nine years later in women, using data from the Future of Families and Child Wellbeing Study (FFCWS). <b>Methods:</b> We analyzed data from the FFCWS, a longitudinal cohort study. The sample included baseline adulthood SES and follow-up telomere length measure of women (n = 2,421) with varying socioeconomic conditions. Telomere length was measured from saliva samples nine years after the baseline measure of adulthood SES. Education, poverty, and marital status at baseline were assessed. Multivariate linear regression models were used to examine the association between adulthood SES indicators at baseline and future telomere length, controlling for potential confounders. <b>Results:</b> From the total 2,421 women, 675 were Latino White, 1,158 were non-Latino Black, and 588 were non-Latino White. Our findings indicate that for women in our study, no adulthood SES indicators such as poverty status, education, or marital status at baseline were predictive of telomere lengths nine years later. <b>Conclusion: </b>Our observations challenge that expected longitudinal association between adulthood SES indicators and subsequent telomere length almost a decade later in racially and ethnically diverse group of women. These findings underscore the need for additional research on the validity of TL as a mediator of the effects of adulthood SES on future rate of biological aging.