Like Parent, Like Child: Intergenerational Patterns of Cardiovascular Risk Factors at Midlife

Purpose: We aimed to assess the prevalence of four cardiovascular risk factors (obesity, diabetes, excessive alcohol intake, and cigarette smoking) for parents and their adult children at the same approximate midlife age. We also evaluated associations of parents' cardiovascular risk factors, childhood health exposures, and social contexts (i.e., family, school, and neighborhood) during adolescence with adult children's cardiovascular health at midlife. Methods: We used data from respondents at Wave V of the National Longitudinal Study of Adolescent to Adult Health who had corresponding parent (mostly mothers) data from Wave I. The final sample included 10,466 adult children with a mean age of 37.8 years. Descriptive statistics and logistic regression models were estimated, accounting for the National Longitudinal Study of Adolescent to Adult Health sampling design. Results: At similar ages (i.e., 35–45 years) to their parents, adult children had higher rates of excessive drinking and obesity than their parents, lower rates of diabetes, and similar rates of smoking. Adult children's health largely converged and correlated with their parents' health at similar ages. Cardiovascular risks for adult children were also significantly associated with their childhood health exposures and social contexts during adolescence. Some associations varied with respect to the health status of parents at Wave I. Conclusions: The cardiovascular risk of parents at midlife is strongly associated with the cardiovascular risk of their adult children at midlife. The status of parents' health during adolescence can also modify the significance and magnitude of associations between childhood health exposures or adolescent social contexts and adult children's cardiovascular risk factors

The Role of Family Health History in Predicting Midlife Chronic Disease Outcomes

Introduction: The generational relevance for determining disease risk for the leading causes of morbidity and mortality for U.S. adults is a source of debate. Methods: Data on 12,300 adults (Add Health Study Members) participating in Wave V (2016–2018) of the National Longitudinal Study of Adolescent to Adult Health (also known as Add Health) were merged with data from respondents’ parents (n=2,013) participating in the Add Health Parent Study (2015–2017). Analyses beginning in January 2020 examined the concordance in lifetime occurrence of chronic conditions across 4 generations, including cardiovascular disease, diabetes, hypertension, hyperlipidemia, obesity, cancer, and depression and examined the associations between individual disease history and ones’ family health history for the same condition. Results: Mean ages were 37.4 years for Add Health Study Members and 62.9 years for Add Health Parent Study mothers. The histories of mothers from the Add Health Parent Study on hyperlipidemia (AOR=1.61, 95% CI=1.04, 2.48), obesity (AOR=1.77, 95% CI=1.27, 2.48), and depression (AOR=1.87, 95% CI=1.19, 2.95) were significantly associated with increased odds of Add Health Study Member report of these conditions. Maternal great grandparent hyperlipidemia history was significantly associated with the Add Health Study Member hyperlipidemia (AOR=2.81, 95% CI=1.51, 5.21). Histories of diabetes in maternal grandfather (AOR=2.41, 95% CI=1.24, 4.69) and maternal great grandparent (AOR=3.05, 95% CI=1.45, 6.43) were significantly associated with Add Health Study Member diabetes. Each additional point in the Add Health Parent Study mothers’ cardiometabolic risk factor index was associated with an 11% increase (incidence rate ratio=1.11, 95% CI=1.04, 1.19) in the expected count of cardiometabolic risk conditions for the Add Health Study Members. Conclusions: Multigenerational health histories have value for quantifying the probability of diabetes, obesity, depression, and hyperlipidemia in early mid-adulthood. Family health history knowledge is relevant for health promotion and disease prevention strategies

Superlattice Growth via MBE and Green’s Function Techniques

A model has been developed to simulate the growth of arrays consisting of a substrate on which alternating layers of quantum dots (QDs) and spacer layers are epitaxially grown. The substrate and spacer layers are modeled as an anisotropic elastic half-space, and the QDs are modeled as point inclusions buried within the half-space. In this model, the strain at the free surface of this half-space due to the buried point QDs is calculated, and a scalar measure of the strain at the surface is subsequently determined. New point QDs are placed on the surface where the previously calculated scalar strain measure is a minimum. Following available DFT results, this scalar strain measure is a weighted average of the in-plane strains. This model is constructed under the assumption that diffusional anisotropy can be neglected, and thus, the results are more in agreement with results from experiments of growth of SiGe QDs than experiments involving QDs of (In,Ga)As

Role of Akt and c-Jun N-terminal Kinase 2 in Apoptosis Induced by Interleukin-4 Deprivation

We have shown previously that interleukin-4 (IL-4) protects TS1αβ cells from apoptosis, but very little is known about the mechanism by which IL-4 exerts this effect. We found that Akt activity, which is dependent on phosphatidylinositol 3 kinase, is reduced in IL-4-deprived TS1αβ cells. Overexpression of wild-type Akt or a constitutively active Akt mutant protects cells from IL-4 deprivation-induced apoptosis. Readdition of IL-4 before the commitment point is able to restore Akt activity. We also show expression and c-Jun N-terminal kinase 2 activation after IL-4 deprivation. Overexpression of the constitutively activated Akt mutant in IL-4-deprived cells correlates with inhibition of c-Jun N-terminal kinase 2 activity. Finally, TS1αβ survival is independent of Bcl-2, Bcl-x, or Bax

High Energy Photon-Nucleon and Photon-Nucleus Cross Sections

We re\,examine the theory of hadronic photon-nucleon interactions at the quark-gluon level. The possibility of multiple parton collisions in a single photon-nucleon collision requires an eikonal treatment of the high-energy scattering process. We give a general formulation of the theory in which the $\gamma p$ cross section is expressed as a sum over properly eikonalized cross sections for the interaction of the virtual hadronic components of the photon with the proton, with each cross section weighted by the probability with which that component appears in the photon, and then develop a detailed model which includes contributions from light vector mesons and from excited virtual states described in a quark-gluon basis. The parton distribution functions which appear can be related approximately to those in the pion, while a weighted sum gives the distribution functions for the photon. We use the model to make improved QCD-based predictions for the total inelastic photon-nucleon and photon-nucleus cross sections at energies relevant for HERA experiments and cosmic ray observations. We emphasize the importance in this procedure of including a soft-scattering background such that the calculated cross sections join smoothly with low-energy data.Comment: 34 pages, 6 figs. available on request from honjo@wishep. bitnet, MAD/TH/91-57, submitted to Phys. Rev.