Radio interferometric observations of two core-dominated triple radio sources at z>3

Aims. We selected two radio quasars (J1036+1326 and J1353+5725) based on their 1.4-GHz radio structure, which is dominated by a bright central core and a pair of weaker and nearly symmetric lobes at ~10" angular separation. They are optically identified in the Sloan Digital Sky Survey (SDSS) at spectroscopic redshifts z>3. We investigate the possibility that their core-dominated triple morphology can be a sign of restarted radio activity in these quasars, involving a significant repositioning of the radio jet axis. Methods. We present the results of high-resolution radio imaging observations of J1036+1326 and J1353+5725, performed with the European Very Long Baseline Interferometry (VLBI) Network (EVN) at 1.6 GHz. These data are supplemented by archive observations from the Very Large Array (VLA).We study the large- and small-scale radio structures and the brightness temperatures, then estimate relativistic beaming parameters. Results. We show that the central emission region of these two high-redshift, core-dominated triple sources is compact but resolved at ~10 milli-arcsecond resolution. We find that it is not necessary to invoke large misalignment between the VLBI jet and the large-scale radio structure to explain the observed properties of the sources.Comment: 5 pages, 4 figures, accepted for publication in A&

Silencing of Sex Chromosomes: from meiosis to early embryonic development

__Abstract__ In order to fit the whole genome into the cell nucleus, the DNA has to be organized into a condensed structure. The basic structure is the double helix structure of the DNA. The formation of nucleosomes mediates the first level of condensation: 147 base pairs of the double helix of DNA is wrapped around an octamer of two of each of the his tones H2A, H2B, H3 and H4 in 1.67 turns The complex of core histone proteins and the DNA that is folded around it, is the most simple form of chromatin. The nucleosomes are org

Molecular spectrum of TSHβ subunit gene defects in central hypothyroidism in the UK and Ireland.

OBJECTIVE: Homozygous mutations in the TSH beta subunit gene (TSHB) result in severe, isolated, central congenital hypothyroidism (CCH). This entity evades diagnosis in TSH-based congenital hypothyroidism (CH) screening programmes in the UK and Ireland. Accordingly, genetic diagnosis, enabling ascertainment of affected relatives in families, is critical for prompt diagnosis and treatment of the disorder. DESIGN, PATIENTS AND MEASUREMENTS: Four cases of isolated TSH deficiency from three unrelated families in the UK and Ireland were investigated for mutations or deletions in TSHB. Haplotype analysis, to investigate a founder effect, was undertaken in cases with identical mutations (c.373delT). RESULTS: Two siblings in kindred 1 were homozygous for a previously described TSHB mutation (c.373delT). In kindreds 2 and 3, the affected individuals were compound heterozygous for TSHB c.373delT and either a 5·4-kB TSHB deletion (kindred 2, c.1-4389_417*195delinsCTCA) or a novel TSHB missense mutation (kindred 3, c.2T>C, p.Met1?). Neurodevelopmental retardation, following delayed diagnosis and treatment, was present in 3 cases. In contrast, the younger sibling in kindred 1 developed normally following genetic diagnosis and treatment from birth. CONCLUSIONS: This study, including the identification of a second, novel, TSHB deletion, expands the molecular spectrum of TSHB defects and suggests that allele loss may be a commoner basis for TSH deficiency than previously suspected. Delayed diagnosis and treatment of profound central hypothyroidism in such cases result in neurodevelopmental retardation. Inclusion of thyroxine (T4) plus thyroxine-binding globulin (TBG), or free thyroxine (FT4) in CH screening, together with genetic case ascertainment enabling earlier therapeutic intervention, could prevent such adverse sequelae.Wellcome Trust (Grant IDs: 100585/Z/12/Z, 095564/Z/11/Z), National Institute for Health Research Biomedical Research Centre CambridgeThis is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1111/cen.1314

Predictors of intact and C-terminal fibroblast growth factor 23 in Gambian children

Elevated C-terminal fibroblast growth factor 23 (C-FGF23) concentrations have been reported in Gambian children with and without putative Ca-deficiency rickets. The aims of this study were to investigate whether i) elevated C-FGF23 concentrations in Gambian children persist long term; ii) they are associated with higher intact FGF23 concentrations (I-FGF23), poor iron status and shorter 25-hydroxyvitamin D half-life (25OHD-t1/2); and iii) the persistence and predictors of elevated FGF23 concentrations differ between children with and without a history of rickets. Children (8-16 years, n=64) with a history of rickets and a C-FGF23 concentration >125 RU/ml (bone deformity (BD), n=20) and local community children with a previously measured elevated C-FGF23 concentration (LC+, n=20) or a previously measured C-FGF23 concentration within the normal range (LC-, n=24) participated. BD children had no remaining signs of bone deformities. C-FGF23 concentration had normalised in BD children, but remained elevated in LC+ children. All the children had I-FGF23 concentration within the normal range, but I-FGF23 concentration was higher and iron status poorer in LC+ children. 1,25-dihydroxyvitamin D was the strongest negative predictor of I-FGF23 concentration (R(2)=18%; P=0.0006) and soluble transferrin receptor was the strongest positive predictor of C-FGF23 concentration (R(2)=33%; P≤0.0001). C-FGF23 and I-FGF23 concentrations were poorly correlated with each other (R(2)=5.3%; P=0.07). 25OHD-t1/2 was shorter in BD children than in LC- children (mean (s.d.): 24.5 (6.1) and 31.5 (11.5) days respectively; P=0.05). This study demonstrated that elevated C-FGF23 concentrations normalised over time in Gambian children with a history of rickets but not in local children, suggesting a different aetiology; that children with resolved rickets had a shorter 25OHD-t1/2, suggesting a long-standing increased expenditure of 25OHD, and that iron deficiency is a predictor of elevated C-FGF23 concentrations in both groups of Gambian children

Recent advances in central congenital hypothyroidism.

Central congenital hypothyroidism (CCH) may occur in isolation, or more frequently in combination with additional pituitary hormone deficits with or without associated extrapituitary abnormalities. Although uncommon, it may be more prevalent than previously thought, affecting up to 1:16 000 neonates in the Netherlands. Since TSH is not elevated, CCH will evade diagnosis in primary, TSH-based, CH screening programs and delayed detection may result in neurodevelopmental delay due to untreated neonatal hypothyroidism. Alternatively, coexisting growth hormones or ACTH deficiency may pose additional risks, such as life threatening hypoglycaemia. Genetic ascertainment is possible in a minority of cases and reveals mutations in genes controlling the TSH biosynthetic pathway (TSHB, TRHR, IGSF1) in isolated TSH deficiency, or early (HESX1, LHX3, LHX4, SOX3, OTX2) or late (PROP1, POU1F1) pituitary transcription factors in combined hormone deficits. Since TSH cannot be used as an indicator of euthyroidism, adequacy of treatment can be difficult to monitor due to a paucity of alternative biomarkers. This review will summarize the normal physiology of pituitary development and the hypothalamic-pituitary-thyroid axis, then describe known genetic causes of isolated central hypothyroidism and combined pituitary hormone deficits associated with TSH deficiency. Difficulties in diagnosis and management of these conditions will then be discussed.This work was supported by funding from the Wellcome Trust (Grant 100585/Z/12/Z, to N.S., Grant 095564/Z/11/Z, to K.C.)This is the final version of the article. It first appeared from Society for Endocrinology via http://dx.doi.org/10.1530/JOE-15-034

Double-double radio galaxies: remnants of merger of supermassive binary black holes

The activity of active galaxy may be triggered by the merge of galaxies and present-day galaxies are probably the product of successive minor mergers. The frequent galactic merges at high redshift imply that active galaxy harbors supermassive unequal-mass binary black holes in its center at least once during its life time. In this paper, we showed that the recently discovered double-lobed FR II radio galaxies are the remnants of such supermassive binary black holes. The inspiraling secondary black hole opens a gap in the accretion disk and removes the inner accretion disk when it merges into the primary black hole, leaving a big hole of about several hundreds of Schwarzschild radius in the vicinity of the post-merged supermassive black hole and leading to an interruption of jet formation. When the outer accretion disk slowly refills the big hole on a viscous time scale, the jet formation restarts and the interaction of the recurrent jets and the inter-galactic medium forms a secondary pair of lobes. We applied the model to a particular double-lobed radio source B1834+620 and showed that the orbit of the secondary is elliptical with a typical eccentricity $e \simeq 0.68$ and the mass ratio $q$ of the secondary and the primary is 0.01 \la q \la 0.4. The accretion disk is a standard $\alpha$-disk with 0.01 \la \alpha \la 0.04 and the ratio of disk half height $H$ and radius $r$ is $\delta \simeq 0.01$. The model predicates that double-lobed radio structure forms only in FR II radio galaxies.Comment: 6 pages, 2 figure