Healthcare transition for adolescents and young adults with long-term conditions:Qualitative study of patients, parents and healthcare professionals’ experiences

Grades 4, 5, 6 Classroomhttps://egrove.olemiss.edu/phay_jon/1544/thumbnail.jp

Educational Attainment and Gestational Weight Gain among U.S. Mothers

BACKGROUND: Education is an important social determinant of many health outcomes, but the relationship between educational attainment and the amount of weight gained over the course of a woman's pregnancy (gestational weight gain (GWG)) has not been clearly established. METHODS: We used data from 1979-2010 for women in the National Longitudinal Survey of Youth 1979 cohort (n= 6344 pregnancies from 2769 women). We used generalized estimating equations to estimate the association between educational attainment and GWG adequacy (as defined by 2009 Institute of Medicine guidelines), controlling for diverse social factors from across the life course (e.g., income, wealth, educational aspirations and expectations) and considering effect measure modification by race/ethnicity and pre-pregnancy overweight status. RESULTS: In most cases, women with more education had increased odds of gaining a recommended amount of gestational weight, independent of educational aspirations and educational expectations and relatively robust to sensitivity analyses. This trend manifested itself in a few different ways. Those with less education had higher odds of inadequate GWG than those with more education. Among those who were not overweight pre-pregnancy, those with less education had higher odds of excessive GWG than college graduates. Among women who were white, those with less than a high school degree had higher odds of excessive GWG than those with more education. CONCLUSION: The relationship between educational attainment and GWG is nuanced and nonlinear

Apoptotic cell death in disease-Current understanding of the NCCD 2023

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease