Leptin, acylcarnitine metabolites and development of adiposity in the Rhea mother-child cohort in Crete, Greece.

OBJECTIVE: This study aims to investigate relations of serum leptin at age 4 with development of adiposity and linear growth during 3 years of follow-up among 75 Greek children and to identify serum metabolites associated with leptin at age 4 and to characterize their associations with adiposity gain and linear growth. METHODS: Linear regression models that accounted for maternal age, education and gestational weight gain and child's age and sex were used to examine associations of leptin and leptin-associated metabolites measured at age 4 with indicators of adiposity and linear growth at age 7. RESULTS: Each 1-unit increment in natural log-(ln)-transformed leptin corresponded with 0.33 (95% CI: 0.10, 0.55) units greater body mass index-for-age z-score gain during follow-up. Likewise, higher levels of the leptin-associated metabolites methylmalonyl-carnitine and glutaconyl-carnitine corresponded with 0.14 (95% CI: 0.01, 0.27) and 0.07 (95% CI: -0.01, 0.16) units higher body mass index-for-age z-score gain, respectively. These relationships did not differ by sex or baseline weight status and were independent of linear growth. CONCLUSIONS: These findings suggest that leptin, methylmalonyl-carnitine and possibly glutaconyl-carnitine are associated with weight gain during early childhood. Future studies are warranted to confirm these findings in other populations

Overweight and obesity status from the prenatal period to adolescence and its association with non- alcoholic fatty liver disease in young adults: cohort study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/16/bjo16199-sup-0005-ICMJES2.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/15/bjo16199-sup-0012-ICMJES12.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/14/bjo16199_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/13/bjo16199-sup-0010-ICMJES10.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/12/bjo16199-sup-0002-TableS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/11/bjo16199.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/10/bjo16199-sup-0007-ICMJES4.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/9/bjo16199-sup-0008-ICMJES5.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/8/bjo16199-sup-0006-ICMJES3.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/7/bjo16199-sup-0003-AppendixS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/6/bjo16199-sup-0011-ICMJES11.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/5/bjo16199-sup-0013-ICMJES13.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/4/bjo16199-sup-0014-ICMJES14.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/3/bjo16199-sup-0001-FigS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/2/bjo16199-sup-0009-ICMJES6.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156435/1/bjo16199-sup-0004-ICMJES1.pd

Anatomy of the Soft-Photon Approximation in Hadron-Hadron Bremsstrahlung

A modified Low procedure for constructing soft-photon amplitudes has been used to derive two general soft-photon amplitudes, a two-s-two-t special amplitude $M^{TsTts}_{\mu}$ and a two-u-two-t special amplitude $M^{TuTts}_{\mu}$, where s, t and u are the Mandelstam variables. $M^{TsTts}_{\mu}$ depends only on the elastic T-matrix evaluated at four sets of (s,t) fixed by the requirement that the amplitude be free of derivatives ($\partial$T/$\partial$s and /or $\partial$T/$\partial t$). Likewise $M^{TuTts}_{\mu}$ depends only on the elastic T-matrix evaluated at four sets of (u,t). In deriving these amplitudes, we impose the condition that $M^{TsTts}_{\mu}$ and $M^{TuTts}_{\mu}$ reduce to $\bar{M}^{TsTts}_{\mu}$ and $\bar{M}^{TuTts}_{\mu}$, respectively, their tree level approximations. The amplitude $\bar{M}^{TsTts}_{\mu}$ represents photon emission from a sum of one-particle t-channel exchange diagrams and one-particle s-channel exchange diagrams, while the amplitude $\bar{M}^{TuTts} _{\mu}$ represents photon emission from a sum of one-particle t-channel exchange diagrams and one-particle u-channel exchange diagrams. The precise expressions for $\bar{M}^{TsTts}_{\mu}$ and $\bar{M}^{TuTts}_{\mu}$ are determined by using the radiation decomposition identities of Brodsky and Brown. We point out that it is theoretically impossible to describe all bremsstrahlung processes by using only a single class of soft-photon amplitudes. At least two different classes are required: the amplitudes which depend on s and t or the amplitudes which depend on u and t. When resonance effects are important, the amplitude $M^{TsTts}_{\mu}$, not $M^{Low(st)}_{\mu}$, should be used. For processes with strong u-channel exchange effects, the amplitude $M^{TuTts}_{\mu}$ should be the first choice.Comment: 49 pages report # LA-UR-92-270

Plasma metabolite profiles in children with current asthma

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146270/1/cea13183.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146270/2/cea13183_am.pd

Maternal Diet Quality During Pregnancy and Offspring Hepatic Fat in Early Childhood: The Healthy Start Study

Background: Overnutrition in utero may increase offspring risk of nonalcoholic fatty liver disease (NAFLD), but the specific contribution of maternal diet quality during pregnancy to this association remains understudied in humans. Objectives: This study aimed to examine the associations of maternal diet quality during pregnancy with offspring hepatic fat in early childhood (median: 5 y old, range: 4–8 y old). Methods: Data were from 278 mother–child pairs in the longitudinal, Colorado-based Healthy Start Study. Multiple 24-h recalls were collected from mothers during pregnancy on a monthly basis (median: 3 recalls, range: 1–8 recalls starting after enrollment), and used to estimate maternal usual nutrient intakes and dietary pattern scores [Healthy Eating Index-2010 (HEI-2010), Dietary Inflammatory Index (DII), and Relative Mediterranean Diet Score (rMED)]. Offspring hepatic fat was measured in early childhood by MRI. Associations of maternal dietary predictors during pregnancy with offspring log-transformed hepatic fat were assessed using linear regression models adjusted for offspring demographics, maternal/perinatal confounders, and maternal total energy intake. Results: Higher maternal fiber intake and rMED scores during pregnancy were associated with lower offspring hepatic fat in early childhood in fully adjusted models [Back-transformed β (95% CI): 0.82 (0.72, 0.94) per 5 g/1000 kcal fiber; 0.93 (0.88, 0.99) per 1 SD for rMED]. In contrast, higher maternal total sugar and added sugar intakes, and DII scores were associated with higher offspring hepatic fat [Back-transformed β (95% CI): 1.18 (1.05, 1.32) per 5% kcal/d added sugar; 1.08 (0.99, 1.18) per 1 SD for DII]. Analyses of dietary pattern subcomponents also revealed that lower maternal intakes of green vegetables and legumes and higher intake of “empty calories” were associated with higher offspring hepatic fat in early childhood. Conclusions: Poorer maternal diet quality during pregnancy was associated with greater offspring susceptibility to hepatic fat in early childhood. Our findings provide insights into potential perinatal targets for the primordial prevention of pediatric NAFLD

Spatial autocorrelation analysis of health care hotspots in Taiwan in 2006

<p>Abstract</p> <p>Background</p> <p>Spatial analytical techniques and models are often used in epidemiology to identify spatial anomalies (hotspots) in disease regions. These analytical approaches can be used to not only identify the location of such hotspots, but also their spatial patterns.</p> <p>Methods</p> <p>In this study, we utilize spatial autocorrelation methodologies, including Global Moran's I and Local Getis-Ord statistics, to describe and map spatial clusters, and areas in which these are situated, for the 20 leading causes of death in Taiwan. In addition, we use the fit to a logistic regression model to test the characteristics of similarity and dissimilarity by gender.</p> <p>Results</p> <p>Gender is compared in efforts to formulate the common spatial risk. The mean found by local spatial autocorrelation analysis is utilized to identify spatial cluster patterns. There is naturally great interest in discovering the relationship between the leading causes of death and well-documented spatial risk factors. For example, in Taiwan, we found the geographical distribution of clusters where there is a prevalence of tuberculosis to closely correspond to the location of aboriginal townships.</p> <p>Conclusions</p> <p>Cluster mapping helps to clarify issues such as the spatial aspects of both internal and external correlations for leading health care events. This is of great aid in assessing spatial risk factors, which in turn facilitates the planning of the most advantageous types of health care policies and implementation of effective health care services.</p

Developmental Splicing Deregulation in Leukodystrophies Related to EIF2B Mutations

Leukodystrophies (LD) are rare inherited disorders that primarily affect the white matter (WM) of the central nervous system. The large heterogeneity of LD results from the diversity of the genetically determined defects that interfere with glial cells functions. Astrocytes have been identified as the primary target of LD with cystic myelin breakdown including those related to mutations in the ubiquitous translation initiation factor eIF2B. EIF2B is involved in global protein synthesis and its regulation under normal and stress conditions. Little is known about how eIF2B mutations have a major effect on WM. We performed a transcriptomic analysis using fibroblasts of 10 eIF2B-mutated patients with a severe phenotype and 10 age matched patients with other types of LD in comparison to control fibroblasts. ANOVA was used to identify genes that were statistically significantly differentially expressed at basal state and after ER-stress. The pattern of differentially expressed genes between basal state and ER-stress did not differ significantly among each of the three conditions. However, 70 genes were specifically differentially expressed in eIF2B-mutated fibroblasts whatever the stress conditions tested compared to controls, 96% being under-expressed. Most of these genes were involved in mRNA regulation and mitochondrial metabolism. The 13 most representative genes, including genes belonging to the Heterogeneous Nuclear Ribonucleoprotein (HNRNP) family, described as regulators of splicing events and stability of mRNA, were dysregulated during the development of eIF2B-mutated brains. HNRNPH1, F and C mRNA were over-expressed in foetus but under-expressed in children and adult brains. The abnormal regulation of HNRNP expression in the brain of eIF2B-mutated patients was concomitant with splicing dysregulation of the main genes involved in glial maturation such as PLP1 for oligodendrocytes and GFAP in astrocytes. These findings demonstrate a developmental deregulation of splicing events in glial cells that is related to abnormal production of HNRNP, in eIF2B-mutated brains