School Programs and Characteristics and Their Influence on Student BMI: Findings from Healthy Passages

Background

Little is known about the contribution of school contextual factors to individual student body mass index (BMI). We set out to determine if school characteristics/resources: (1) are associated with student BMI; (2) explain racial/ethnic disparities in student BMI; and (3) explain school-level differences in student BMI.

Methods

Using gender-stratified multi-level modeling strategies we examined the association of school characteristics/resources and individual BMI in 4,387 5^th graders in the Healthy Passages Longitudinal Study of Adolescent Health. Additionally, we examined the association of race/ethnicity and individual BMI as well as the between-school variance in BMI before and after adding individual and school characteristics to test for attenuation.

Results

The school-level median household income, but not physical activity or nutrition resources, was inversely associated with female BMI (β = −0.12, CI: −0.21,−0.02). Neither school demographics nor physical activity/nutrition resources were predictive of individual BMI in males. In Black females, school characteristics attenuated the association of race/ethnicity and BMI. Individual student characteristics—not school characteristics/resources-reduced the between-school variation in BMI in males by nearly one-third and eliminated it in females.

Conclusions

In this cohort of 5^th graders, school SES was inversely associated with female BMI while school characteristics and resources largely explained Black/White disparities in female weight status. Between-school differences in average student weight status were largely explained by the composition of the student body not by school characteristics or programming.     

Insights into the Biology of Hearing and Deafness Revealed by Single-Cell RNA Sequencing

1. Download high-res image (267KB)
2. Download full-size image

     

Automatically Fixing Errors in Glycoprotein Structures with Rosetta

1. Download high-res image (143KB)
2. Download full-size image

     

Professor A. J. E. Cave 1900–2001

Few have served the Zoological Society of London longer or more faithfully than Alexander Cave who died on 17 May at the great age of 100.
As a Fellow, his record is outstanding: Member of Council, Vice President, Silver Medallist of the Society, Honorary Research Associate; and withal, an unending stream of original papers on various aspects of comparative anatomy. Unending? Well, almost, for he was still being published in his 95th year. Nor should be forgotten the great volume of work that he did in refereeing papers for the Journal of Zoology – an onerous and time-consuming task that he dealt with meticulously.     

Discriminating between the activities of human cathepsin G and chymase using fluorogenic substrates

Cathepsin G (CG) (EC 3.4.21.20) and chymase (EC 3.4.21.39) are two closely-related chymotrypsin-like proteases that are released from cytoplasmic granules of activated mast cells and/or neutrophils. We investigated the potential for their substrate-binding subsites to discriminate between their substrate specificities, aiming to better understand their respective role during the progression of inflammatory diseases. In addition to their preference for large aromatic residues at P1, both preferentially accommodate small hydrophilic residues at the S1' subsite. Despite significant structural differences in the S2' subsite, both prefer an acidic residue at that position. The Ala226/Glu substitution at the bottom of the CG S1 pocket, which allows CG but not chymase to accommodate a Lys residue at P1, is the main structural difference, allowing discrimination between the activities of these two proteases. However, a Lys at P1 is accommodated much less efficiently than a Phe, and the corresponding substrate is cleaved by β2-tryptase (EC 3.4.21.59). We optimized a P1 Lys-containing substrate to enhance sensitivity towards CG and prevent cleavage by chymase and β2-tryptase. The resulting substrate (ABZ-GIEPKSDPMPEQ-EDDnp) [where ABZ is O-aminobenzoic acid and EDDnp is N-(2,4-dinitrophenyl)-ethylenediamine] was cleaved by CG but not by chymase and tryptase, with a specificity constant of 190 mM(-1)·s(-1). This allows the quantification of active CG in cells or tissue extracts where it may be present together with chymase and tryptase, as we have shown using a HMC-1 cell homogenate and a sputum sample from a patient with severe asthma.     

Comparing Trends in BMI and Waist Circumference

The nature of excess body weight may be changing over time to one of greater central adiposity. The aim of this study is to determine whether BMI and waist circumference (WC) are increasing proportionately among population subgroups and the range of bodyweight, and to examine the public health implications of the findings. Our data are from two cross‐sectional surveys (the US National Health and Nutrition Examination Studies (NHANES) in 1988–1994 (NHANES III) and 2005–2006), from which we have used samples of 15,349 and 4,176 participants aged ≥20 years. Between 1988–1994 and 2005–2006 BMI increased by an average of 1.8 kg/m² and WC by 4.7 cm (adjusted for sex, age, race‐ethnicity, and education). The increase in WC was more than could be attributed simply to increases in BMI. This independent increase in WC (of on average, 0.9 cm) was consistent across the different BMI categories, sexes, education levels, and race‐ethnicity groups. It occurred in younger but not older age groups. Overall in each BMI category, the prevalence of low‐risk WC decreased and the prevalence of increased‐risk or substantially increased‐risk WC increased. These results suggest that the adverse health consequences associated with obesity may be increasingly underestimated by trends in BMI alone. Since WC is closely linked to adverse cardiovascular outcomes, it is important to know the prevailing trends in both of these parameters.     

Sexual orientation and bias in self-reported BMI

Our objective was to determine if sexual orientation groups differ in accuracy of BMI (kg/m(2)) calculated from self-reported height and weight and if weight status modifies possible differences. Using gender-stratified multiple linear regression to analyze Wave III of the National Longitudinal Study of Adolescent Health (n = 12,197), we examined the association of sexual orientation with BMI calculated from self-reported height and weight (self-reported BMI), controlling for BMI calculated from objectively measured height and weight (objectively measured BMI) as well as demographic, health, and behavioral variables. We tested for effect modification of the relationship between sexual orientation and self-reported BMI by objectively measured BMI. The population underestimated their BMI (females: β = 0.87, P < 0.001; males = 0.86, P < 0.001). Sexual orientation groups differed little in their accuracy of reporting; only gay males had significant underreporting (β = -0.37, P = 0.038) relative to their heterosexual peers. We found no evidence of effect modification of the relationship of sexual orientation and self-reported BMI by objectively measured BMI. With the exception of gay males, sexual orientation groups are consistent in their underreporting of BMI thus providing confidence in most comparisons of weight status based on self-report. Self-reporting of weight and height by gay males may exaggerate the differences in BMI between gay and heterosexual males.     

Swedish Alzheimer Mutation Induces Mitochondrial Dysfunction Mediated by HSP60 Mislocalization of Amyloid Precursor Protein (APP) and Beta-Amyloid

Alzheimer disease (AD) is a complex disorder that involves numerous cellular and subcellular alterations including impairments in mitochondrial homeostasis. To better understand the role of mitochondrial dysfunction in the pathogenesis of AD, we analyzed brains from clinically well-characterized human subjects and from the 3xTg-AD mouse model of AD. We find Aβ and critical components of the γ-secretase complex, presenilin-1, -2, and nicastrin, accumulate in the mitochondria. We used a proteomics approach to identify binding partners and show that heat shock protein 60 (HSP60), a molecular chaperone localized to mitochondria and the plasma membrane, specifically associates with APP. We next generated stable neural cell lines expressing human wild-type or Swedish APP, and provide corroborating in vitro evidence that HSP60 mediates translocation of APP to the mitochondria. Viral-mediated shRNA knockdown of HSP60 attenuates APP and Aβ mislocalization to the mitochondria. Our findings identify a novel interaction between APP and HSP60, which accounts for its translocation to the mitochondria.