Childhood energy intake is associated with nonalcoholic fatty liver disease in adolescents

Background: Greater adiposity is an important risk factor for nonalcoholic fatty liver disease (NAFLD). Thus, it is likely that dietary intake is involved in the development of the disease. Prospective studies assessing the relation between childhood dietary intake and risk of NAFLD are lacking. Objective: This study was designed to explore associations between energy, carbohydrate, sugar, starch, protein, monounsaturated fat, polyunsaturated fat, saturated fat, and total fat intake by youth at ages 3, 7, and 13 y and subsequent (mean age: 17.8 y) ultrasound scan (USS)–measured liver fat and stiffness and serum alanine aminotransferase, aspartate aminotransferase, and γ-glutamyltransferase. We assessed whether observed associations were mediated through fat mass at the time of outcome assessment. Methods: Participants were from the Avon Longitudinal Study of Parents and Children. Trajectories of energy and macronutrient intake from ages 3–13 y were obtained with linear-spline multilevel models. Linear and logistic regression models examined whether energy intake and absolute and energy-adjusted macronutrient intake at ages 3, 7, and 13 y were associated with liver outcomes. Results: Energy intake at all ages was positively associated with liver outcomes; for example, the odds of having a USS-measured liver fat per 100 kcal increase in energy intake at age 3 y were 1.79 (95% CI: 1.14, 2.79). Associations between absolute macronutrient intake and liver outcomes were inconsistent and attenuated to the null after adjustment for total energy intake. The majority of associations attenuated to the null after adjustment for fat mass at the time liver outcomes were assessed. Conclusion: Higher childhood and early adolescent energy intake is associated with greater NAFLD risk, and the macronutrients from which energy intake is derived are less important. These associations appear to be mediated, at least in part, by fat mass at the time of outcome assessment

Does the Sigma(1580)3/2- resonance exist?

Precise new data for the reaction $K^- p \to \pi^0 \Lambda$ are presented in the c.m. energy range 1565 to 1600 MeV. Our analysis of these data sheds new light on claims for the $\Sigma(1580){3/2}^-$ resonance, which (if it exists with the specified quantum numbers) must be an exotic baryon because of its very low mass. Our results show no evidence for this state.Comment: 4 pages, 4 figure

Measurement of Inverse Pion Photoproduction at Energies Spanning the N(1440) Resonance

Differential cross sections for the process pi^- p -> gamma n have been measured at Brookhaven National Laboratory's Alternating Gradient Synchrotron with the Crystal Ball multiphoton spectrometer. Measurements were made at 18 pion momenta from 238 to 748 MeV/c, corresponding to E_gamma for the inverse reaction from 285 to 769 MeV. The data have been used to evaluate the gamma n multipoles in the vicinity of the N(1440) resonance. We compare our data and multipoles to previous determinations. A new three-parameter SAID fit yields 36 +/- 7 (GeV)^-1/2 X 10^-3 for the A^n_1/2 amplitude of the P_11.Comment: 14 pages, 8 figures, submitted to PR

ρ\rho - nucleus bound states in Walecka model

Possible formation of $\rho$ nucleus bound state is studied in the framework of Walecka model. The bound states are found in different nuclei ranging from $^3He$ to $^{208}Pb$. These bound states may have a direct bearing on the recent experiments on the photoproduction of $\rho$ meson in the nuclear medium.Comment: RevTeX fil

Subthreshold rho^0 photoproduction on 3He

A large reduction of the rho^0 mass in the nuclear medium is reported, inferred from dipion photoproduction spectra in the 1 GeV region, for the reaction 3He(gamma,pi+ pi-)X with a 10% duty factor tagged-photon beam and the TAGX multi-particle spectrometer. The energy range covered (800 < E(gamma) < 1120 MeV) lies mostly below the free rho^0 production threshold, a region which is believed sensitive to modifications of light vector-meson properties at nuclear-matter densities. The rho^0 masses extracted from the MC fitting of the data, m*(rho^0) = 642 +/- 40, 669 +/- 32, and 682 +/- 56 MeV/c^2 for E(gamma) in the 800-880, 880-960, and 960-1040 MeV regions respectively, are independently corroborated by a measured, assumption-free, kinematical observable. This mass shift, far exceeding current mean-field driven theoretical predictions, may be suggestive of rho^0 decay within the range of the nucleonic field.Comment: 40 pages, 13 figures, submitted to Phys. Rev.

Improving diagnosis and broadening the phenotypes in early-onset seizure and severe developmental delay disorders through gene panel analysis

BACKGROUND: We sought to investigate the diagnostic yield and mutation spectrum in previously reported genes for early-onset epilepsy and disorders of severe developmental delay. METHODS: In 400 patients with these disorders with no known underlying aetiology and no major structural brain anomaly, we analysed 46 genes using a combination of targeted sequencing on an Illumina MiSeq platform and targeted, exon-level microarray copy number analysis. RESULTS: We identified causative mutations in 71/400 patients (18%). The diagnostic rate was highest among those with seizure onset within the first two months of life (39%), although overall it was similar in those with and without seizures. The most frequently mutated gene was SCN2A (11 patients, 3%). Other recurrently mutated genes included CDKL5, KCNQ2, SCN8A (six patients each), FOXG1, MECP2, SCN1A, STXBP1 (five patients each), KCNT1, PCDH19, TCF4 (three patients each) and ATP1A3, PRRT2 and SLC9A6 (two patients each). Mutations in EHMT1, GABRB3, LGI1, MBD5, PIGA, UBE3A and ZEB2 were each found in single patients. We found mutations in a number of genes in patients where either the electroclinical features or dysmorphic phenotypes were atypical for the identified gene. In only 11 cases (15%) had the clinician sufficient certainty to specify the mutated gene as the likely cause before testing. CONCLUSIONS: Our data demonstrate the considerable utility of a gene panel approach in the diagnosis of patients with early-onset epilepsy and severe developmental delay disorders., They provide further insights into the phenotypic spectrum and genotype-phenotype correlations for a number of the causative genes and emphasise the value of exon-level copy number testing in their analysis