Behavioral and Neural Correlates of Executive Functioning in Musicians and Non-Musicians

Executive functions (EF) are cognitive capacities that allow for planned, controlled behavior and strongly correlate with academic abilities. Several extracurricular activities have been shown to improve EF, however, the relationship between musical training and EF remains unclear due to methodological limitations in previous studies. To explore this further, two experiments were performed; one with 30 adults with and without musical training and one with 27 musically trained and untrained children (matched for general cognitive abilities and socioeconomic variables) with a standardized EF battery. Furthermore, the neural correlates of EF skills in musically trained and untrained children were investigated using fMRI. Adult musicians compared to non-musicians showed enhanced performance on measures of cognitive flexibility, working memory, and verbal fluency. Musically trained children showed enhanced performance on measures of verbal fluency and processing speed, and significantly greater activation in pre-SMA/SMA and right VLPFC during rule representation and task-switching compared to musically untrained children. Overall, musicians show enhanced performance on several constructs of EF, and musically trained children further show heightened brain activation in traditional EF regions during task-switching. These results support the working hypothesis that musical training may promote the development and maintenance of certain EF skills, which could mediate the previously reported links between musical training and enhanced cognitive skills and academic achievement

The Ages of Pre-main-sequence Stars

The position of pre-main-sequence or protostars in the Hertzsprung--Russell diagram is often used to determine their mass and age by comparison with pre-main-sequence evolution tracks. On the assumption that the stellar models are accurate, we demonstrate that, if the metallicity is known, the mass obtained is a good estimate. However, the age determination can be very misleading because it is significantly (generally different by a factor of two to five) dependent on the accretion rate and, for ages less than about one million years, the initial state of the star. We present a number of accreting protostellar tracks that can be used to determine age if the initial conditions can be determined and the underlying accretion rate has been constant in the past. Because of the balance established between the Kelvin-Helmholtz, contraction timescale and the accretion timescale a pre-main-sequence star remembers its accretion history. Knowledge of the current accretion rate, together with an H--R-diagram position gives information about the rate of accretion in the past but does not necessarily improve any age estimate. We do not claim that ages obtained by comparison with these particular accreting tracks are likely to be any more reliable than those from comparisons with non-accreting tracks. Instead we stress the unreliability of any such comparisons and use the disparities between various tracks to estimate the likely errors in age and mass estimates. We also show how a set of coeval accreting objects do not appear coeval when compared with non-accreting tracks. Instead accreting pre-main-sequence stars of around a solar mass are likely to appear older than those of either smaller or larger mass.Comment: Accepted by MNRA

Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2

Deficiency of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney. To examine this further, we produced mice with targeted disruption of the 11β-HSD2 gene. Homozygous mutant mice (11β-HSD2(–/–)) appear normal at birth, but ∼50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11β-HSD2(–/–) mice are markedly hypertensive, with a mean arterial blood pressure of 146 ± 2 mmHg, compared with 121 ± 2 mmHg in wild-type controls and 114 ± 4 mmHg in heterozygotes. The epithelium of the distal tubule of the nephron shows striking hypertrophy and hyperplasia. These histological changes do not readily reverse with mineralocorticoid receptor antagonism in adulthood. Thus, 11β-HSD2(–/–) mice demonstrate the major features of SAME, providing a unique rodent model to study the molecular mechanisms of kidney resetting leading to hypertension. J. Clin. Invest. 103:683–689 (1999

High-spatial-resolution imaging of thermal emission from debris disks

We have obtained sub-arcsec mid-IR images of a sample of debris disks within 100 pc. For our sample of nineteen A-type debris disk candidates chosen for their IR excess, we have resolved, for the first time, five sources plus the previously resolved disk around HD 141569. Two other sources in our sample have been ruled out as debris disks since the time of sample selection. Three of the six resolved sources have inferred radii of 1-4 AU (HD 38678, HD 71155, and HD 181869), and one source has an inferred radius ~10-30 AU (HD 141569). Among the resolved sources with detections of excess IR emission, HD 71155 appears to be comparable in size (r~2 AU) to the solar system's asteroid belt, thus joining Zeta Lep (HD 38678, reported previously) to comprise the only two resolved sources of that class. Two additional sources (HD 95418 and HD 139006) show spatial extent that implies disk radii of ~1-3 AU, although the excess IR fluxes are not formally detected with better than 2-sigma significance. For the unresolved sources, the upper limits on the maximum radii of mid-IR disk emission are in the range ~1-20 AU, four of which are comparable in radius to the asteroid belt. We have compared the global color temperatures of the dust to that expected for the dust in radiative equilibrium at the distances corresponding to the observed sizes or limits on the sizes. In most cases, the temperatures estimated via these two methods are comparable, and therefore, we see a generally consistent picture of the inferred morphology and the global mid-IR emission. Finally, while our sample size is not statistically significant, we notice that the older sources (>200 Myr) host much warmer dust (T > 400 K) than younger sources (in the 10s of Myr).Comment: 46 pages, 12 figure

Transiting Disintegrating Planetary Debris around WD 1145+017

More than a decade after astronomers realized that disrupted planetary material likely pollutes the surfaces of many white dwarf stars, the discovery of transiting debris orbiting the white dwarf WD 1145+017 has opened the door to new explorations of this process. We describe the observational evidence for transiting planetary material and the current theoretical understanding (and in some cases lack thereof) of the phenomenon.Comment: Invited review chapter. Accepted March 23, 2017 and published October 7, 2017 in the Handbook of Exoplanets. 15 pages, 10 figure

Fragmentation of Massive Protostellar Disks

We examine whether massive-star accretion disks are likely to fragment due to self-gravity. Rapid accretion and high angular momentum push these disks toward fragmentation, whereas viscous heating and the high protostellar luminosity stabilize them. We find that for a broad range of protostar masses and for reasonable accretion times, massive disks larger than ~150 AU are prone to fragmentation. We develop an analytical estimate for the angular momentum of accreted material, extending the analysis of Matzner and Levin (2005) to account for strongly turbulent initial conditions. In a core-collapse model, we predict that disks are marginally prone to fragmentation around stars of about four to 15 solar masses -- even if we adopt conservative estimates of the disks' radii and tendency to fragment. More massive stars are progressively more likely to fragment, and there is a sharp drop in the stability of disk accretion at the very high accretion rates expected above 110 solar masses. Fragmentation may starve accretion in massive stars, especially above this limit, and is likely to create swarms of small, coplanar companions.Comment: 15 pages, 7 figures, accepted for publication in MNRAS, updated version with minor changes to tex

A Rare Case of a Systemic Non-Langerhans Histiocytosis Presenting with Diabetes Insipidus and a Tentorial Mass

Introduction The histiocytoses are a group of clinically diverse diseases distinguished from one another based on the specific immunophenotype of the lesional cells, implying derivation from the same precursor cell. Langerhans cell histiocytoses (LCH) diseases stem from abnormal dendritic cell lineages, while the non-Langerhans cell histiocytoses (non-LCH) are usually derived from an abnormal monocyte/macrophage cell line.1 Non-LCH with central nervous system (CNS) involvement is predictive of poor outcome. Histopathology is used to make a diagnosis of non-LCH. Immunohistochemistry and the clinical setting are used to differentiate between the various subtypes of non-LCH.1 The non-LCH can be divided into cutaneous non-LCH, cutaneous with a major systemic component, and systemic non-LCH.1 Erdheim-Chester disease (ECD) and Rosai-Dorfman disease (RDD) are systemic non-LCH diseases. First described in 1930, ECD is characterized by xanthogranulomatous accumulations. The extent of infiltration is heterogeneous and can include skin, bones, lungs, kidneys, and the CNS. Approximately 500 cases have been reported so far.2 The majority of ECD patients harbor an activating mutation of the proto-oncogene BRAF, namely BRAF-V600E.3 Recent studies indicate CNS involvement as a predictor of highest mortality among ECD patients.4 First described in 1969, RDD is characterized by accumulation of histiocytes exhibiting emperipolesis in lymph nodes, in the head and neck or in extranodal sites. Extranodal sites include the CNS, skin, soft tissue and gastrointestinal tract. The clinical presentation is typically painless cervical lymphadenopathy with leukocytosis and a fever.5 The etiology of RDD is unknown.6 RDD with CNS involvement is rare and approximately 210 cases have been reported. CNS involvement typically lacks extracranial lymphadenopathy and resembles meningioma radiologically and clinically. 1 Select cases have demonstrated a combined presentation of ECD and RDD.2 In this report we describe a rare case presenting with headache and with clinically and pathologically overlapping features of RDD and ECD. We describe treatment and complications and review the existing literature regarding diagnosis and treatment for these rare conditions

Transgenic amplification of glucocorticoid action in adipose tissue causes high blood pressure in mice

Obesity is closely associated with the metabolic syndrome, a combination of disorders including insulin resistance, diabetes, dyslipidemia, and hypertension. A role for local glucocorticoid reamplification in obesity and the metabolic syndrome has been suggested. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regenerates active cortisol from inactive 11-keto forms, and aP2-HSD1 mice with relative transgenic overexpression of this enzyme in fat cells develop visceral obesity with insulin resistance and dyslipidemia. Here we report that aP2-HSD1 mice also have high arterial blood pressure (BP). The mice have increased sensitivity to dietary salt and increased plasma levels of angiotensinogen, angiotensin II, and aldosterone. This hypertension is abolished by selective angiotensin II receptor AT-1 antagonist at a low dose that does not affect BP in non-Tg littermates. These findings suggest that activation of the circulating renin-angiotensin system (RAS) develops in aP2-HSD1 mice. The long-term hypertension is further reflected by an appreciable hypertrophy and hyperplasia of the distal tubule epithelium of the nephron, resembling salt-sensitive or angiotensin II–mediated hypertension. Taken together, our findings suggest that overexpression of 11β-HSD1 in fat is sufficient to cause salt-sensitive hypertension mediated by an activated RAS. The potential role of adipose 11β-HSD1 in mediating critical features of the metabolic syndrome extends beyond obesity and metabolic complications to include the most central cardiovascular feature of this disorder

11β-HSD1 suppresses cardiac fibroblast CXCL2, CXCL5 and neutrophil recruitment to the heart post MI

We have previously demonstrated that neutrophil recruitment to the heart following myocardial infarction (MI) is enhanced in mice lacking 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) that regenerates active glucocorticoid within cells from intrinsically inert metabolites. The present study aimed to identify the mechanism of regulation. In a mouse model of MI, neutrophil mobilization to blood and recruitment to the heart were higher in 11β-HSD1-deficient (Hsd11b1(-)(/)(-) ) relative to wild-type (WT) mice, despite similar initial injury and circulating glucocorticoid. In bone marrow chimeric mice, neutrophil mobilization was increased when 11β-HSD1 was absent from host cells, but not when absent from donor bone marrow-derived cells. Consistent with a role for 11β-HSD1 in 'host' myocardium, gene expression of a subset of neutrophil chemoattractants, including the chemokines Cxcl2 and Cxcl5, was selectively increased in the myocardium of Hsd11b1(-)(/)(-) mice relative to WT. SM22α-Cre directed disruption of Hsd11b1 in smooth muscle and cardiomyocytes had no effect on neutrophil recruitment. Expression of Cxcl2 and Cxcl5 was elevated in fibroblast fractions isolated from hearts of Hsd11b1(-)(/)(-) mice post MI and provision of either corticosterone or of the 11β-HSD1 substrate, 11-dehydrocorticosterone, to cultured murine cardiac fibroblasts suppressed IL-1α-induced expression of Cxcl2 and Cxcl5 These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11β-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury