PUSHing Core-Collapse Supernovae to Explosions in Spherical Symmetry: Nucleosynthesis Yields

Core-collapse supernovae (CCSNe) are the extremely energetic deaths of massive stars. They play a vital role in the synthesis and dissemination of many heavy elements in the universe. In the past, CCSN nucleosynthesis calculations have relied on artificial explosion methods that do not adequately capture the physics of the innermost layers of the star. The PUSH method, calibrated against SN1987A, utilizes the energy of heavy-flavor neutrinos emitted by the proto-neutron star (PNS) to trigger parametrized explosions. This makes it possible to follow the consistent evolution of the PNS and to ensure a more accurate treatment of the electron fraction of the ejecta. Here, we present the Iron group nucleosynthesis results for core-collapse supernovae, exploded with PUSH, for two different progenitor series. Comparisons of the calculated yields to observational metal-poor star data are also presented. Nucleosynthesis yields will be calculated for all elements and over a wide range of progenitor masses. These yields can be immensely useful for models of galactic chemical evolution.Comment: 3 pages, 3 figures, poster presentation to appear in the proceedings of the 14th International Symposium on Nuclei in the Cosmos (NIC-XIV), Ed. S. Kubono, JPS (Japan Physical Society

Explosion Dynamics of Parametrized Spherically Symmetric Core-Collapse Supernova Simulations

We report on a method, PUSH, for triggering core-collapse supernova (CCSN) explosions of massive stars in spherical symmetry. This method provides a framework to study many important aspects of core collapse supernovae: the effects of the shock passage through the star, explosive supernova nucleosynthesis and the progenitor-remnant connection. Here we give an overview of the method, compare the results to multi-dimensional simulations and investigate the effects of the progenitor and the equation of state on black hole formation.Comment: Proceedings for Nuclei in the Cosmos XIV, Niigata, Japan (2016

Glucose transporter-1 deficiency syndrome: the expanding clinical and genetic spectrum of a treatable disorder

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene in the majority of patients and results in impaired glucose transport into the brain. From 2004-2008, 132 requests for mutational analysis of the SLC2A1 gene were studied by automated Sanger sequencing and multiplex ligation-dependent probe amplification. Mutations in the SLC2A1 gene were detected in 54 patients (41%) and subsequently in three clinically affected family members. In these 57 patients we identified 49 different mutations, including six multiple exon deletions, six known mutations and 37 novel mutations (13 missense, five nonsense, 13 frame shift, four splice site and two translation initiation mutations). Clinical data were retrospectively collected from referring physicians by means of a questionnaire. Three different phenotypes were recognized: (i) the classical phenotype (84%), subdivided into early-onset (<2 years) (65%) and late-onset (18%); (ii) a non-classical phenotype, with mental retardation and movement disorder, without epilepsy (15%); and (iii) one adult case of glucose transporter-1 deficiency syndrome with minimal symptoms. Recognizing glucose transporter-1 deficiency syndrome is important, since a ketogenic diet was effective in most of the patients with epilepsy (86%) and also reduced movement disorders in 48% of the patients with a classical phenotype and 71% of the patients with a non-classical phenotype. The average delay in diagnosing classical glucose transporter-1 deficiency syndrome was 6.6 years (range 1 month-16 years). Cerebrospinal fluid glucose was below 2.5 mmol/l (range 0.9-2.4 mmol/l) in all patients and cerebrospinal fluid : blood glucose ratio was below 0.50 in all but one patient (range 0.19-0.52). Cerebrospinal fluid lactate was low to normal in all patients. Our relatively large series of 57 patients with glucose transporter-1 deficiency syndrome allowed us to identify correlations between genotype, phenotype and biochemical data. Type of mutation was related to the severity of mental retardation and the presence of complex movement disorders. Cerebrospinal fluid : blood glucose ratio was related to type of mutation and phenotype. In conclusion, a substantial number of the patients with glucose transporter-1 deficiency syndrome do not have epilepsy. Our study demonstrates that a lumbar puncture provides the diagnostic clue to glucose transporter-1 deficiency syndrome and can thereby dramatically reduce diagnostic delay to allow early start of the ketogenic die

Effect and safety of treatment with ACE-inhibitor Enalapril and β-blocker metoprolol on the onset of left ventricular dysfunction in Duchenne muscular dystrophy - a randomized, double-blind, placebo-controlled trial

Background: X-linked Duchenne muscular dystrophy (DMD), the most frequent human hereditary skeletal muscle myopathy, inevitably leads to progressive dilated cardiomyopathy. We assessed the effect and safety of a combined treatment with the ACE-inhibitor enalapril and the β-blocker metoprolol in a German cohort of infantile and juvenile DMD patients with preserved left ventricular function. Methods, Trial design: Sixteen weeks single-arm open run-in therapy with enalapril and metoprolol followed by a two-arm 1:1 randomized double-blind placebo-controlled treatment in a multicenter setting. Inclusion criteria: DMD boys aged 10–14 years with left ventricular fractional shortening [LV-FS] ≥ 30% in echocardiography. Primary endpoint: time from randomization to first occurrence of LV-FS &lt; 28%. Secondary: changes of a) LV-FS from baseline, b) blood pressure, c), heart rate and autonomic function in ECG and Holter-ECG, e) cardiac biomarkers and neurohumeral serum parameters, f) quality of life, and g) adverse events. Results: From 3/2010 to 12/2013, 38 patients from 10 sites were centrally randomized after run-in, with 21 patients continuing enalapril and metoprolol medication and 17 patients receiving placebo. Until end of study 12/2015, LV-FS &lt; 28% was reached in 6/21 versus 7/17 patients. Cox regression adjusted for LV-FS after run-in showed a statistically non-significant benefit for medication over placebo (hazard ratio: 0.38; 95% confidence interval: 0.12 to 1.22; p = 0.10). Analysis of secondary outcome measures revealed a time-dependent deterioration of LV-FS with no statistically significant differences between the two study arms. Blood pressure, maximal heart rate and mean-NN values were significantly lower at the end of open run-in treatment compared to baseline. Outcome analysis 19 months after randomization displayed significantly lower maximum heart rate and higher noradrenalin and renin values in the intervention group. No difference between treatments was seen for quality of life. As a single, yet important adverse event, the reversible deterioration of walking abilities of one DMD patient during the run-in period was observed. Conclusions: Our analysis of enalapril and metoprolol treatment in DMD patients with preserved left ventricular function is suggestive to delay the progression of the intrinsic cardiomyopathy to left ventricular failure, but did not reach statistical significance, probably due to insufficient sample size. Clinical trial registration: DRKS-number 00000115, EudraCT-number 2009–009871-36

Inhibition of Voriconazole Metabolism by Chloramphenicol in an Adolescent with Central Nervous System Aspergillosis▿

For an adolescent with bacterial meningitis and subsequent cerebral aspergillosis, intravenous voriconazole dose requirements substantially decreased during coadministration with intravenous chloramphenicol and considerably rose after discontinuation of the antibiotic. In agreement with in vitro evidence, these data suggest that chloramphenicol is a rather significant inhibitor of hepatic CYP3A4 and/or CYP2C19

PUSHing Core-collapse Supernovae to Explosions in Spherical Symmetry. II. Explodability and Remnant Properties

In a previously presented proof-of-principle study we established a parametrized spherically symmetric explosion method (PUSH) that can reproduce many features of core-collapse supernovae. The present paper goes beyond a specific application that is able to reproduce observational properties of SN1987A and performs a systematic study of the explosion properties for an extensive set of non-rotating, solar metallicity stellar progenitor models in the mass range from 10.8 to 120 M$_\odot$.This includes the transition from neutron stars to black holes as the final result of the collapse of massive stars, and the relation of the latter to supernovae and faint/failed supernovae. The present paper provides the basis for extended nucleosynthesis predictions in a forthcoming paper to be employed in galactic evolution models.Comment: 24 pages, 18 figures, 5 tables. Accepted to Ap

PUSHing Core-collapse Supernovae to Explosions in Spherical Symmetry. III. Nucleosynthesis Yields

In a previously presented proof-of-principle study, we established a parametrized spherically symmetric explosion method (PUSH) that can reproduce many features of core-collapse supernovae for a wide range of pre-explosion models. The method is based on the neutrino-driven mechanism and follows collapse, bounce and explosion. There are two crucial aspects of our model for nucleosynthesis predictions. First, the mass cut and explosion energy emerge simultaneously from the simulation (determining, for each stellar model, the amount of Fe-group ejecta). Second, the interactions between neutrinos and matter are included consistently (setting the electron fraction of the innermost ejecta). In the present paper, we use the successful explosion models from Ebinger et al. (2018) which include two sets of pre-explosion models at solar metallicity, with combined masses between 10.8 and 120 M$_{\odot}$. We perform systematic nucleosynthesis studies and predict detailed isotopic yields. The resulting $^{56}$Ni ejecta are in overall agreement with observationally derived values from normal core-collapse supernovae. The Fe-group yields are also in agreement with derived abundances for metal-poor star HD84937. We also present a comparison of our results with observational trends in alpha element to iron ratios.Comment: 24 pages, 10 figures, 8 tables (Accepted, ApJ

Combinations of caudal myxopapillary ependymoma and dermal sinus: A single shared embryologic lesion?

A female child presenting with acute flaccid paraparesis at 18 months was found to have a dermal sinus in combination with a dermoid cyst and a myxopapillary ependymoma of the cauda equina and conus medullaris. A possible embryologic relation between these lesions is discussed

Diffuse cortical necrosis in a neonate with incontinentia pigmenti and an encephalitis-like presentation

Incontinentia pigmenti is a rare neurocutaneous disorder that may present with neurologic symptoms, in addition to a characteristic vesicular rash within the first days of life. We describe a neonate girl presenting with a rash and an encephalopathy who was first thought to suffer from a viral infection and was only later recognized as being affected by incontinentia pigmenti. Cerebral MR imaging showed extensive cortical necrosis in the acute period. Incontinentia pigmenti should be included in the differential diagnosis of encephalopathy and cutaneous involvement in neonates, after a viral infection has been ruled out

Roles of Lactose and Fructose Malabsorption and Dietary Outcomes in Children Presenting with Chronic Abdominal Pain

Intolerance to lactose or fructose is frequently diagnosed in children with chronic abdominal pain (CAP). However, the causal relationship remains a matter of discussion. A cohort of 253 patients, aged 7&ndash;12 years, presenting with unexplained CAP received standardized diagnostics. Additional diagnostic tests were performed based on their medical history and physical and laboratory investigations. Fructose and lactose hydrogen breath tests (H2BT) as well as empiric diagnostic elimination diets were performed in 135 patients reporting abdominal pain related to the consumption of lactose or fructose to evaluate carbohydrate intolerance as a potential cause of CAP. Carbohydrate malabsorption by H2BT was found in 55 (41%) out of 135 patients. An abnormal increase in H2BT was revealed in 30% (35/118) of patients after fructose consumption and in 18% (20/114) of patients after lactose administration. Forty-six percent (25/54) reported pain relief during a diagnostic elimination diet. In total, 17 patients had lactose malabsorption, 29 fructose malabsorption, and nine combined carbohydrate malabsorption. Carbohydrate intolerance as a cause of CAP was diagnosed at follow-up in only 18% (10/55) of patients with malabsorption after the elimination of the respective carbohydrate. Thus, carbohydrate malabsorption appears to be an incidental finding in children with functional abdominal pain disorders, rather than its cause. Therefore, testing of carbohydrate intolerance should only be considered in children with a strong clinical suspicion and with the goal to prevent long-term unnecessary dietary restrictions in children suffering from CAP