32 research outputs found
The home environment and childhood obesity in low-income households: indirect effects via sleep duration and screen time
Background
Childhood obesity disproportionally affects children from low-income households. With the aim of informing interventions, this study examined pathways through which the physical and social home environment may promote childhood overweight/obesity in low-income households.
Methods
Data on health behaviors and the home environment were collected at home visits in low-income, urban households with either only normal weight (n = 48) or predominantly overweight/obese (n = 55) children aged 6–13 years. Research staff conducted comprehensive, in-person audits of the foods, media, and sports equipment in each household. Anthropometric measurements were collected, and children’s physical activity was assessed through accelerometry. Caregivers and children jointly reported on child sleep duration, screen time, and dietary intake of foods previously implicated in childhood obesity risk. Path analysis was used to test direct and indirect associations between the home environment and child weight status via the health behaviors assessed.
Results
Sleep duration was the only health behavior associated with child weight status (OR = 0.45, 95% CI: 0.27, 0.77), with normal weight children sleeping 33.3 minutes/day longer on average than overweight/obese children. The best-fitting path model explained 26% of variance in child weight status, and included paths linking chaos in the home environment, lower caregiver screen time monitoring, inconsistent implementation of bedtime routines, and the presence of a television in children’s bedrooms to childhood overweight/obesity through effects on screen time and sleep duration.
Conclusions
This study adds to the existing literature by identifying aspects of the home environment that influence childhood weight status via indirect effects on screen time and sleep duration in children from low-income households. Pediatric weight management interventions for low-income households may be improved by targeting aspects of the physical and social home environment associated with sleep
Identification and Expression of the Family of Classical Protein-Tyrosine Phosphatases in Zebrafish
Protein-tyrosine phosphatases (PTPs) have an important role in cell survival, differentiation, proliferation, migration and other cellular processes in conjunction with protein-tyrosine kinases. Still relatively little is known about the function of PTPs in vivo. We set out to systematically identify all classical PTPs in the zebrafish genome and characterize their expression patterns during zebrafish development. We identified 48 PTP genes in the zebrafish genome by BLASTing of human PTP sequences. We verified all in silico hits by sequencing and established the spatio-temporal expression patterns of all PTPs by in situ hybridization of zebrafish embryos at six distinct developmental stages. The zebrafish genome encodes 48 PTP genes. 14 human orthologs are duplicated in the zebrafish genome and 3 human orthologs were not identified. Based on sequence conservation, most zebrafish orthologues of human PTP genes were readily assigned. Interestingly, the duplicated form of ptpn23, a catalytically inactive PTP, has lost its PTP domain, indicating that PTP activity is not required for its function, or that ptpn23b has lost its PTP domain in the course of evolution. All 48 PTPs are expressed in zebrafish embryos. Most PTPs are maternally provided and are broadly expressed early on. PTP expression becomes progressively restricted during development. Interestingly, some duplicated genes retained their expression pattern, whereas expression of other duplicated genes was distinct or even mutually exclusive, suggesting that the function of the latter PTPs has diverged. In conclusion, we have identified all members of the family of classical PTPs in the zebrafish genome and established their expression patterns. This is the first time the expression patterns of all members of the large family of PTP genes have been established in a vertebrate. Our results provide the first step towards elucidation of the function of the family of classical PTPs
The interaction between heteroditopic pyridine–nitrogen NHC with novel sulfur NHC ligands in palladium(0) derivatives: Synthesis and structural characterization of a bis-carbene palladium(0) olefin complex and formation in solution of an alkene–alkyne mixed intermediate as a consequence of the ligandshemilability
We have synthesized a new class of heteroditopic chelating ligands bearing the phenylthiomethyl group
and variously substituted imidazole derivatives and the corresponding complexes [Pd(eta2-ma)(R-NHCCH2-
SPh) (ma = maleic anhydride; R = methyl, mesityl, di-i-propylphenyl). We have compared their
chemical characteristics and reactivity with those of similar palladium(0) complexes bearing the RNHC-
CH2-Py ligands.
The hemilability of the above-mentioned moieties is apparent when their palladium derivatives react
with an excess of the same or different heteroditopic ligands. In these cases, we obtained complexes bearing
maleic anhydride and two mono-coordinated heteroditopic ligands bound to the same metal center.
However, at variance with the generally accepted opinion, precipitation of AgBr does not warrant the
quantitative formation of the bis-heteroditopic Pd(0) derivative and in some cases, a reaction involving
a heterogeneous equilibrium is observed.
The reaction of the palladium(0) carbene–sulfur or carbene–nitrogen complexes with the alkyne
dimethyl-2-butynedioate (dmbd) to give palladacyclometallate derivatives is not always warranted
and formation of the intermediate [Pd(eta2-ma)(eta2-dmdb)(chi1-Mes-NHC-CH2-SPh)] is detected only in
one case.
Finally, we have carried out a diffractometric study on the solid-state structures of two derivatives and
in particular we describe the configurations of the complex [Pd(eta2-ma)(j1-Me-NHC-CH2-SPh)2] and of
[Pd(eta2-ma)(Me-NHC-CH2-SPh)]