A reconnaissance of the possible donor stars to the Kepler supernova

The identity of Type Ia supernova progenitors remains a mystery, with various lines of evidence pointing towards either accretion from a non-degenerate companion, or the rapid merger of two degenerate stars leading to the thermonuclear destruction of a white dwarf. In this paper we spectroscopically scrutinize 24 of the brightest stars residing in the central 38" x 38" of the SN 1604 (Kepler) supernova remnant to search for a possible surviving companion star. We can rule out, with high certainty, a red giant companion star - a progenitor indicated by some models of the supernova remnant. Furthermore, we find no star that exhibits properties uniquely consistent with those expected of a donor star down to L>10Lsun. While the distribution of star properties towards the remnant are consistent with unrelated stars, we identify the most promising candidates for further astrometric and spectroscopic follow-up. Such a program would either discover the donor star, or place strong limits on progenitor systems to luminosities with L<<Lsun.Comment: accepted by Ap

The promoter of human p22/PACAP response gene 1 (PRG1) contains functional binding sites for the p53 tumor suppressor and for NFκB

AbstractWe describe functional binding sites for the tumor suppressor p53 and for NFκB residing in the promoter of the novel human early response gene p22/PRG1 (IEX-1/DIF-2). Gel shift and supershift assays demonstrate binding of p53 and NFκB to their corresponding sites in vitro. CAT-reporter gene assays show transactivation of the human p22/PRG1 promoter by p53 in Hep3B cells stably transfected with a temperature-sensitive mutant p53, but not in p53-deficient Hep3B cells. TNFα induced NFκB dependent transactivation was shown in HepG2 cells or in 818-4 pancreatic cancer cells. These data imply that human p22/PRG1 is a target gene for p53 and NFκB involved in growth regulation and stress response

Excitation of Large Transverse Beam Oscillations without Emittance Blow-up using the AC-Dipole Principle

The so-called "AC-Dipole" principle allows the excitation of transverse oscillations to large (several sigma) excursions without emittance blow-up. The idea was originally proposed and tested at BNL for resonance crossing with polarized beams, using an orbit corrector dipole with an excitation frequency close to the betatron tune, hence "AC-Dipole". This method of beam excitation has several potential applications in teh LHC, such as phase advance and beta-measurements, dynamic aperture studies and the investigation of resonance strengths. The technique was recently tested in the CERN SPS using the transverse damper as an "AC-Dipole" providing the fixed frequency excitation. Results from this experiment are presented, along with an explanation of the underlying principle

Communication and signal exchange in the Rhizobium bradyrhizobium legume system

A new comprehensive communication concept in the Rhizobium/Bradyrhizobium legume symbiosis was developed. It includes a root zone specific flavonoid exudation, the differential activity of phenylpropane/acetate pathway derivatives on chemotaxis, nod-gene inducing activity and phytoalexin resistance induction on the microsymbiont side (Bradyrhizobium). Nod factor production from the microsymbiont affects the host plant in root hair curling and meristem induction. Phytoalexin production in the host plant is also an early response, however repressed to a low level after a few hours. Another strategy of the microsymbiont to overcome phytoalexin effects is degradation of phytoalexins in Rhizobium leguminosarum bv. vicieae. Competitiveness within the same infection group of the microsymbiont was studied with gus-gene fusion, using the blue coloured nodules to easily discriminate marked strains from unmarked competitors. New exopolysaccharide (EPS) mutants of Bradyrhizobium japonicum were reconstructed homologous with a DNA region to exoB gene of Rhizobium meliloti. Their clearly reduced competitiveness of nodulation, demonstrates that exopolysaccharides of Bradyrhizohium japonicum also have an important function during the early stages of this symbiotic interaction

Correction: A novel mutation of the calcium sensing receptor gene is associated with chronic pancreatitis in a family with heterozygous SPINK1 mutations

Abstract Background The role of mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene in chronic pancreatitis is still a matter of debate. Active SPINK1 is thought to antagonize activated trypsin. Cases of SPINK1 mutations, especially N34S, have been reported in a subset of patients with idiopathic chronic pancreatitis. However, the inheritance pattern is still unknown. Some cases with N34S heterozygosity have been reported with and without evidence for CP indicating neither an autosomal recessive nor dominant trait. Therefore SPINK1 mutations have been postulated to act as a disease modifier requiring additional mutations in a more complex genetic model. Familial hypocalciuric hypercalcemia (FHH) caused by heterozygous inactivating mutations in the calcium sensing receptor (CASR) gene is considered a benign disorder with elevated plasma calcium levels. Although hypercalcemia represents a risk factor for pancreatitis, increased rates of pancreatitis in patients with FHH have not been reported thus far. Methods We studied a family with a FHH-related hypercalcemia and chronic pancreatitis. DNA samples were analysed for mutations within the cationic trypsinogen (N29I, R122H) and SPINK1 (N34S) gene using melting curve analysis. Mutations within CASR gene were identified by DNA sequencing. Results A N34S SPINK1 mutation was found in all screened family members. However, only two family members developed chronic pancreatitis. These patients also had FHH caused by a novel, sporadic mutation in the CASR gene (518T>C) leading to an amino acid exchange (leucine->proline) in the extracellular domain of the CASR protein. Conclusion Mutations in the calcium sensing receptor gene might represent a novel as yet unidentified predisposing factor which may lead to an increased susceptibility for chronic pancreatitis. Moreover, this family analysis supports the hypothesis that SPINK1 mutations act as disease modifier and suggests an even more complex genetic model in SPINK1 related chronic pancreatitis.</p

NGC 346 in the Small Magellanic Cloud. III. Recent Star Formation and Stellar Clustering Properties in the Bright HII Region N 66

In the third part of our photometric study of the star-forming region NGC 346/N~66 and its surrounding field in the Small Magellanic Cloud (SMC), we focus on the large number of low-mass pre-main sequence (PMS) stars revealed by the Hubble Space Telescope Observations with the Advanced Camera for Surveys. We investigate the origin of the observed broadening of the pre-main sequence population in the $V-I$, $V$ CMD. The most likely explanations are either the presence of differential reddening or an age spread among the young stars. Assuming the latter, simulations indicate that we cannot exclude the possibility that stars in NGC 346 might have formed in two distinct events occurring about 10 and 5 Myr ago, respectively. We find that the PMS stars are not homogeneously distributed across NGC 346, but instead are grouped in at least five different clusters. On spatial scales from 0.8$''$ to 8$''$ (0.24 to 2.4 pc at the distance of the SMC) the clustering of the PMS stars as computed by a two-point angular correlation function is self-similar with a power law slope $\gamma \approx -0.3$. The clustering properties are quite similar to Milky Way star forming regions like Orion OB or $\rho$ Oph. Thus molecular cloud fragmentation in the SMC seems to proceed on the same spatial scales as in the Milky Way. This is remarkable given the differences in metallicity and hence dust content between SMC and Milky Way star forming regions.Comment: Accepted for publication in ApJ. 16 pages, 13 (low-resolution) figures, emulateapj.cls LaTeX styl

Evidence of mild founder LMOD3 mutations causing nemaline myopathy 10 in Germany and Austria

Objective To expand the clinical and genetic spectrum of nemaline myopathy 10 by a series of Austrian and German patients with a milder disease course and missense mutations in LMOD3. Methods We characterized the clinical features and the genetic status of 4 unrelated adolescent or adult patients with nemaline myopathy. Results The 4 patients showed a relatively mild disease course. They all have survived into adulthood, 3 of 4 have remained ambulatory, and all showed marked facial weakness. Muscle biopsy specimens gave evidence of nemaline bodies. All patients were unrelated but originated from Austria (Tyrol and Upper Austria) and Southern Germany (Bavaria). All patients carried the missense variant c.1648C>T, p.(Leu550Phe) in the LMOD3 gene, either on both alleles or in trans with another missense variant (c.1004A>G, p.Gln335Arg). Both variants were not reported previously. Conclusions In 2014, a severe form of congenital nemaline myopathy caused by disrupting mutations in LMOD3 was identified and denoted as NEM10. Unlike the previously reported patients, who had a severe clinical picture with a substantial risk of early death, our patients showed a relatively mild disease course. As the missense variant c.1648C>T is located further downstream compared to all previously published LMOD3 mutations, it might be associated with higher protein expression compared to the reported loss-of-function mutations. The apparent clusters of 2 mild mutations in Germany and Austria in 4 unrelated families may be explained by a founder effect

A High-Resolution Spectroscopic Search for the Remaining Donor for Tycho's Supernova

In this paper, we report on our analysis using Hubble Space Telescope astrometry and Keck-I HIRES spectroscopy of the central six stars of Tycho's supernova remnant (SN 1572). With these data, we measured the proper motions, radial velocities, rotational velocities, and chemical abundances of these objects. Regarding the chemical abundances, we do not confirm the unusu- ally high [Ni/Fe] ratio previously reported for Tycho-G. Rather, we find that for all metrics in all stars, none exhibit the characteristics expected from traditional SN Ia single-degenerate-scenario calculations. The only possible exception is Tycho-B, a rare, metal-poor A-type star; however, we are unable to find a suitable scenario for it. Thus, we suggest that SN 1572 cannot be explained by the standard single-degenerate model.Comment: 34 pages, 11 Figures, revised and resubmitted to Ap

Tumor necrosis factor-mediated inhibition of interleukin-18 in the brain: a clinical and experimental study in head-injured patients and in a murine model of closed head injury.

Tumor necrosis factor (TNF) and interleukin-(IL)-18 are important mediators of neuroinflammation after closed head injury (CHI). Both mediators have been previously found to be significantly elevated in the intracranial compartment after brain injury, both in patients as well as in experimental model systems. However, the interrelation and regulation of these crucial cytokines within the injured brain has not yet been investigated. The present study was designed to assess a potential regulation of intracranial IL-18 levels by TNF based on a clinical study in head-injured patients and an experimental model in mice. In the first part, we investigated the interrelationship between the daily TNF and IL-18 cerebrospinal fluid levels in 10 patients with severe CHI for up to 14 days after trauma. In the second part of the study, the potential TNF-dependent regulation of intracerebral IL-18 levels was further characterized in an experimental set-up in mice: (1) in a standardized model of CHI in TNF/lymphotoxin-α gene-deficient mice and wild-type (WT) littermates, and (2) by intracerebro-ventricular injection of mouse recombinant TNF in WT C57BL/6 mice. The results demonstrate an inverse correlation of intrathecal TNF and IL-18 levels in head-injured patients and a TNF-dependent inhibition of IL-18 after intracerebral injection in mice. These findings imply a potential new anti-inflammatory mechanism of TNF by attenuation of IL-18, thus confirming the proposed "dual" function of this cytokine in the pathophysiology of traumatic brain injury