The purpose of the present study was to examine intergenerational transmission of adverse childhood experiences (ACEs) from parents to children and examine the buffering influence of forgiveness of oneself and others. Participants were 150 parents and children enrolled in Head Start in an upper midwestern, rural state who volunteered to complete questionnaires measuring ACEs and levels of forgiveness of oneself and others. Multiple correlation and regression were used to examine the associations between parent-reported parent and child ACEs and self-forgiveness and forgiveness of others. Analyses revealed that parental ACEs and child ACEs were positively correlated. Parents with low and medium levels of self-forgiveness and forgiveness of others had a stronger positive correlation between their own experience of ACEs and their child's, whereas, for parents with high levels of self-forgiveness and forgiveness of others, the correlation between parent and child ACEs was reduced statistically to zero. The cycle of intergenerational transmission of ACEs may be interrupted, or at very least notably buffered, by forgiving oneself and others.

Artificial intelligence (AI) has become a part of many image-based specialties, such as radiology and pathology, as well as medical specialties in which “oscopy” is the key to current practice. In gastroenterology, for example, AI is being explored as an aid to endoscopists to visually distinguish precancerous lesions in upper and lower endoscopy. Although there have been a variety of approaches to the employment of AI for this purpose, deep-learning algorithms, which combine the extraction and classification of image features using deep neural networks,1 have the capability of self-learning.

ABSTRACT Early childhood is a critical period to intervene for obesity, developmental and behavioural problems. Data from 1065 children in 14 Northeast Iowa Community Action Head Starts (HS) were collected between 2011 and 2018. Body mass index (BMI) and developmental scores were assessed at the beginning of each school year and compared after the first year in HS. Females showed a 3.5% decrease in BMI percentile (F = 2.46, P = .12, = .02), while males increased theirs by 4.4% (F = 7.41, P = .007, = .05). Females showed higher initial passing rates than males on the Brigance (85.9% vs 75.7%, p = .006), self-help (64.7% vs 49.1%, p = .001), but not socio-emotional outcomes. Females in HS showed a slight decrease in BMI, compared to a significant increase in males. Improvements in developmental and behavioural outcomes were similar for both. Further research should determine why such differences occurred.

This study examined the prospective relationships between preschoolers’ body mass index (BMI) and cognitive development. BMI, cognitive (i.e., Brigance), sex, and age data were collected from seven cohorts of children attending Head Start from 2012 to 2018. Children (N = 324) with two years of complete data were included. After controlling for the first year cognitive development scores, age, gender, and the cohort, the BMI was predictive of lower cognitive development scores in year two (B = −0.06, β = −0.14, t = −3.19, p = 0.002). Female sex (B = 2.69, β = 0.10, t = 2.30, p = 0.022) and older age (B = 0.02, β = 0.15, t = 3.20, p ≤ 0.001) were also shown to be statistically significant predictors of improved year two cognitive scores. The initial BMI scores were associated with poorer one year cognitive development scores in this sample of preschool children. Excessive body mass may contribute to numerous biological, psychological, and social factors that inhibit children with obesity from reaching their full cognitive potential, during a time in which brain development and cognitive skills development are at critical points of growth. Early childhood obesity interventions may have positive consequences for cognitive development, but additional prospective studies are needed to confirm these results.

Childhood obesity has reached epidemic rates nationwide and may be associated with impaired cognitive function. A growing body of evidence suggests that poorer academic performance for children with obesity and overweight is related to declines in executive function skills. This study aimed to identify biological mediators between obesity and overweight and cognitive function among children and adolescents. A total of 3323 children aged 6–16 years from the Third National Health and Nutrition Examination Survey between 1988 and 1994 (NHANES III) was used to measure associations between measures of obesity and overweight, cognitive function (IQ test batteries), iron deficiency, inflammation (c-reactive protein), and glucose metabolism (glycosylated hemoglobin) using multiple mediation models. Approximately 15% of the children were overweight and 11% were obese. Results showed lower scores for children who were obese or overweight than children of normal weight on several IQ subtest batteries. Obesity and overweight were also associated with biological mediators such as iron deficiency, elevated c-reactive protein and glycosylated hemoglobin. Several biomarkers of iron status were also related to measures of cognitive function. Early declines in cognitive function are associated with biomarkers of iron deficiency and inflammation in children and adolescents, and while some biological linkages between obesity and overweight and cognitive function are identified herein, further study is needed to identify additional biological mediators between obesity and overweight and cognitive function in pediatric populations.

BackgroundPhysiological factors such as age and sex have been shown to be risk factors for adverse effects in the liver, including liver diseases and drug-induced liver injury. Previously, we have reported age- and sex-related significant differences in hepatic basal gene expression in rats during the life span that may be related to susceptibility to such adverse effects. However, the underlying mechanisms of the gene expression changes were not fully understood. In recent years, increasing evidence for epigenetic mechanisms of gene regulation has fueled interest in the role of microRNAs (miRNAs) in toxicogenomics and biomarker discovery. We therefore proposed that significant age and sex differences exist in baseline liver miRNA expression, and that comprehensive profiling of miRNAs will provide insights into the epigenetic regulation of gene expression in rat liver.MethodsTo address this, liver tissues from male and female F344 rats were examined at 2, 5, 6, 8, 15, 21, 52, 78, and 104 weeks of age for the expression of 677 unique miRNAs. Following data processing, predictive pathway analysis was performed on selected miRNAs that exhibited prominent age and/or sex differences in expression.ResultsOf the 314 miRNAs found to be expressed, 214 were differentially expressed; 65 and 212 miRNAs showed significant (false discovery rate (FDR) <5% and ≥1.5-fold change) sex- and age-related differences in expression, respectively. Thirty-eight miRNAs showed 2-week-specific expression, of which 31 miRNAs were found to be encoded within the Dlk1-Dio3 cluster located on chromosome 6. This cluster has been associated with tissue proliferation and differentiation, and liver energy homeostasis in postnatal development. Predictive pathway analysis linked sex-biased miRNA expression with sexually dimorphic molecular functions and toxicological functions that may reflect sex differences in hepatic physiology and disease. The expression of miRNAs (miR-18a, miR-99a, and miR-203, miR-451) was also found to associate with specific sexually dimorphic hepatic histopathology. The expression of miRNAs involved in regulating cell death, cell proliferation, and cell cycle was found to change as the rats matured from adult to old age.ConclusionsOverall, significant age- and sex-related differences in liver miRNA expression were identified and linked to histopathological findings and predicted functional pathways that may underlie susceptibilities to liver toxicity and disease.

We tested whether African-American (AA) women are different from Caucasian women in regard to lipotoxicity, adipokines, and gene expression in adipose tissue and muscle. Insulin sensitivity (S(I)), plasma adipocytokine levels, intramyocellular lipid (IMCL), and the expression of candidate genes in adipose tissue and muscle were measured in AA and Caucasian women. This study was performed in an ambulatory general clinical research center. Subjects were healthy, nondiabetic AA and Caucasian women. There were no interventions. Comparison of S(I), IMCL, plasma adiponectin, and the expression of candidate genes regulating adipogenesis, lipogenesis, and inflammation in adipose tissue and muscle. AA had lower plasma adiponectin and IMCL when compared with Caucasian women with similar S(I). In sc adipose tissue (SAT), the expression of genes involved in adipogenesis including peroxisomal proliferator-activated receptor-gamma (PPARgamma) and lipin-1beta were also reduced in SAT of AA subjects (19%, P = 0.06, and 25%, P = 0.05, respectively). Similarly, 1-acylglycerol-3-phosphate acyltransferase 2 (AGPAT 2), stearoyl-coenzyme A desaturase-1 (SCD1), and CD36 mRNA expression was significantly reduced in SAT by 19, 54, and 28% respectively (P < 0.01 for all) in AA compared with Caucasian women. Yet the expression of CD68 in SAT was similar in both ethnic groups. Gene expression studies in muscle revealed a 31% reduction in expression of AGPAT 2 and a 72% reduction in SCD1 genes in AA. AA women demonstrated lower expression of several PPARgamma-responsive genes in adipose tissue, lower plasma adiponectin, and decreased IMCL levels as compared with Caucasians, which suggests that African-Americans may be protected from lipotoxicity. Together these data suggest significant ethnic differences in the pathophysiology of insulin resistance.