Maternal nicotine dependence is associated with longitudinal increases in child obesogenic eating behaviors

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/152014/1/ijpo12541.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/152014/2/ijpo12541_am.pd

Experimental and observational studies on alcohol use and dietary intake: a systematic review

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153599/1/obr12950_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/153599/2/obr12950.pd

Associations of Appetitive Traits and Parental Feeding Style with Diet Quality During Early Childhood.

BackgroundAppetitive traits and parent feeding styles are associated with body mass index in children, yet their associations with child diet quality are unclear.ObjectiveThe objective was to examine relations of appetitive traits and parental feeding style with diet quality in 3.5-year-old children.DesignThe study was a secondary, cross-sectional analysis of data from Sprouts, a follow-up study of the Pregnancy Eating Attributes Study (PEAS). Birthing parents completed the Child Eating Behavior Questionnaire, Caregiver's Feeding Styles Questionnaire, and proxy 24-hour dietary recalls for their children from February 2019 to December 2020.Participants/settingParticipants were 162 birthing parents (early pregnancy BMI ≥18.5 kg/m2 and absence of pre-existing diabetes, any medical condition contraindicating study participation, self-reported eating disorder, and medications that could affect diet or weight) and their children living in North Carolina.Main outcome measuresHealthy Eating Index-2015 (HEI-2015) total scores were calculated.Statistical analyses performedPath modeling was conducted using PROC CALIS with full information maximum likelihood (FIML) to account for missing data (ResultsA 1-SD greater food fussiness was associated with a 2.4-point lower HEI-2015 total score [p = .02, 95% CI (-4.32, -0.48)] in children. When parental feeding style was authoritarian, a 1-SD greater food responsiveness was associated a 4.1-point higher HEI-2015 total score [p = .007, 95% CI (1.12, 7.01)] in children. When parental feeding style was authoritative, a 1-SD greater slowness in eating was associated with a 5.8-point lower HEI-2015 total score [p = .01, 95% CI (-10.26, -1.33)] in children.ConclusionsParental feeding style may modify the association of appetitive traits with diet quality in young children. Future research could determine whether matching parent feeding styles to child appetitive trait profiles improves child diet quality

Developmental trajectory of appetitive traits and their bidirectional relations with body mass index from infancy to early childhood.

Appetitive traits, including food responsiveness, enjoyment of food, satiety responsiveness and slowness in eating, are associated with childhood body mass index. Change in appetitive traits from infancy to childhood and the direction of causality between appetitive traits and body mass index are unclear. The present study examined the developmental trajectory of appetitive traits and their bidirectional relations with body mass index, from infancy to early childhood. Mothers in the Pregnancy Eating Attributes Study and follow-up (n = 162) reported child appetitive traits using the Baby and Child Eating Behaviour Questionnaires at ages 6 months and 3.5 years, respectively. Standardized body mass index (zBMI) was calculated from child anthropometrics. Cross-lagged panel models estimated bidirectional relations between appetitive traits and zBMI. Food responsiveness, satiety responsiveness and slowness in eating increased from infancy to early childhood. In cross-lagged panel models, lower infant satiety responsiveness (B ± SE = -0.45 ± 0.19, p = .02) predicted greater child zBMI. Infant zBMI did not predict child appetitive traits (p-values >.36). From infancy to early childhood, appetitive traits may amplify. Appetitive traits, particularly satiety responsiveness, appear to influence body mass index during this period, suggesting early intervention targeting these traits may reduce childhood obesity

Human B Cell Differentiation Is Characterized by Progressive Remodeling of O-Linked Glycans

Germinal centers (GC) are microanatomical niches where B cells proliferate, undergo antibody affinity maturation, and differentiate to long-lived memory B cells and antibody-secreting plasma cells. For decades, GC B cells have been defined by their reactivity to the plant lectin peanut agglutinin (PNA), which binds serine/threonine (O-linked) glycans containing the asialylated disaccharide Gal-β1,3-GalNAc-Ser/Thr (also called T-antigen). In T cells, acquisition of PNA binding by activated T cells and thymocytes has been linked with altered tissue homing patterns, cell signaling, and survival. Yet, in GC B cells, the glycobiological basis and significance of PNA binding remains surprisingly unresolved. Here, we investigated the basis for PNA reactivity of GC B cells. We found that GC B cell binding to PNA is associated with downregulation of the α2,3 sialyltransferase, ST3GAL1 (ST3Gal1), and overexpression of ST3Gal1 was sufficient to reverse PNA binding in B cell lines. Moreover, we found that the primary scaffold for PNA-reactive O-glycans in B cells is the B cell receptor-associated receptor-type tyrosine phosphatase CD45, suggesting a role for altered O-glycosylation in antigen receptor signaling. Consistent with similar reports in T cells, ST3Gal1 overexpression in B cells in vitro induced drastic shortening in O-glycans, which we confirmed by both antibody staining and mass spectrometric O-glycomic analysis. Unexpectedly, ST3Gal1-induced changes in O-glycan length also correlated with altered binding of two glycosylation-sensitive CD45 antibodies, RA3-6B2 (more commonly called B220) and MEM55, which (in humans) have previously been reported to favor binding to naïve/GC subsets and memory/plasmablast subsets, respectively. Analysis of primary B cell binding to B220, MEM55, and several plant lectins suggested that B cell differentiation is accompanied by significant loss of O-glycan complexity, including loss of extended Core 2 O-glycans. To our surprise, decreased O-glycan length from naïve to post-GC fates best correlated not with ST3Gal1, but rather downregulation of the Core 2 branching enzyme GCNT1. Thus, our data suggest that O-glycan remodeling is a feature of B cell differentiation, dually regulated by ST3Gal1 and GCNT1, that ultimately results in expression of distinct O-glycosylation states/CD45 glycoforms at each stage of B cell differentiation

The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer

Abstract: Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and p.Arg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM−/− patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Commensality and Food Choice in the United States

Cross-sectional survey assessing frequency of eating different types of food with different co-eaters (friends, family, coworkers, romantic partners, children