The Formation of the Collisional Family around the Dwarf Planet Haumea

Haumea, a rapidly rotating elongated dwarf planet (~ 1500 km in diameter), has two satellites and is associated with a "family" of several smaller Kuiper Belt objects (KBOs) in similar orbits. All members of the Haumea system share a water ice spectral feature that is distinct from all other KBOs. The relative velocities between the Haumea family members are too small to have formed by catastrophic disruption of a large precursor body, which is the process that formed families around much smaller asteroids in the Main Belt. Here we show that all of the unusual characteristics of the Haumea system are explained by a novel type of giant collision: a graze-and-merge impact between two comparably sized bodies. The grazing encounter imparted the high angular momentum that spun off fragments from the icy crust of the elongated merged body. The fragments became satellites and family members. Giant collision outcomes are extremely sensitive to the impact parameters. Compared to the Main Belt, the largest bodies in the Kuiper Belt are more massive and experience slower velocity collisions; hence, outcomes of giant collisions are dramatically different between the inner and outer solar system. The dwarf planets in the Kuiper Belt record an unexpectedly large number of giant collisions, requiring a special dynamical event at the end of solar system formation.Comment: Accepted for publication in ApJ, 12 pages, 4 figures, 2 tables

Apparent mineralocorticoid excess syndrome: an overview

Apparent mineralocorticoid excess (AME) syndrome results from defective 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol (F) to its inactive metabolite cortisone (E). Its deficiency allows the unmetabolized cortisol to bind to the MR inducing sodium retention, hypokalemia, suppression of PRA and hypertension. Mutations in the gene encoding 11beta-HSD2 account for the inherited form, but a similar clinical picture to AME occurs following the ingestion of bioflavonoids, licorice and carbenoxolone, which are competitive inhibitors of 11beta-HSD2. Reduced 11beta-HSD2 activity may explain the increased sodium retention in preeclampsia, renal disease and liver cirrhosis. Relative deficiency of 11beta-HSD2 activity can occur in Cushing's syndrome due to saturation of the enzyme and explains the mineralocorticoid excess state that characterizes ectopic ACTH syndrome. Reduced placental 11beta-HSD2 expression might explain the link between reduced birth weight and adult hypertension. Polymorphic variability in the HSD11B2 gene in part determines salt sensitivity, a forerunner for adult hypertension onset. AME represents a spectrum of mineralocorticoid hypertension with severity reflecting the underlying genetic defect in the 11beta-HSD2; although AME is a genetic disorder, several exogenous compounds can bring about the symptoms by inhibiting 11beta-HSD2 enzyme. Substrate excess as seen in Cushing's syndrome and ACTH ectopic production can overwhelm the capacity of 11beta-HSD2 to convert F to E, leading up to an acquired form of AME

Inelastic electron tunneling via molecular vibrations in single-molecule transistors

In single-molecule transistors, we observe inelastic cotunneling features that correspond energetically to vibrational excitations of the molecule, as determined by Raman and infrared spectroscopy. This is a form of inelastic electron tunneling spectroscopy of single molecules, with the transistor geometry allowing in-situ tuning of the electronic states via a gate electrode. The vibrational features shift and change shape as the electronic levels are tuned near resonance, indicating significant modification of the vibrational states. When the molecule contains an unpaired electron, we also observe vibrational satellite features around the Kondo resonance.Comment: 5 pages, 4 figures. Supplementary information available upon reques

Northern Territory Heart Failure Initiative–Clinical Audit (NTHFI–CA)–a prospective database on the quality of care and outcomes for acute decompensated heart failure admission in the Northern Territory: study design and rationale

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/Introduction Congestive heart failure is a significant cause of morbidity and mortality in Australia. Accurate data for the Northern Territory and Indigenous Australians are not presently available. The economic burden of this chronic cardiovascular disease is felt by all funding bodies and it still remains unclear what impact current measures have on preventing the ongoing disease burden and how much of this filters down to more remote areas. Clear differentials also exist in rural areas including a larger Indigenous community, greater disease burden, differing aetiologies for heart failure as well as service and infrastructure discrepancies. It is becoming increasingly clear that urban solutions will not affect regional outcomes. To understand regional issues relevant to heart failure management, an understanding of the key performance indicators in that setting is critical. Methods and analysis The Northern Territory Heart Failure Initiative—Clinical Audit (NTHFI-CA) is a prospective registry of acute heart failure admissions over a 12-month period across the two main Northern Territory tertiary hospitals. The study collects information across six domains and five dimensions of healthcare. The study aims to set in place an evidenced and reproducible audit system for heart failure and inform the developing heart failure disease management programme. The findings, is believed, will assist the development of solutions to narrow the outcomes divide between remote and urban Australia and between Indigenous and Non-Indigenous Australians, in case they exist. A combination of descriptive statistics and mixed effects modelling will be used to analyse the data. Ethics and dissemination This study has been approved by respective ethics committees of both the admitting institutions. All participants will be provided a written informed consent which will be completed prior to enrolment in the study. The study results will be disseminated through local and international health conferences and peer reviewed manuscripts

Correlations between Ground and Excited State Spectra of a Quantum Dot

We have studied the ground and excited state spectra of a semiconductor quantum dot for successive numbers of electron occupancy using linear and nonlinear magnetoconductance measurements. We present the first observation of direct correlation between the mth excited state of the N electron system and the ground state of the N+m electron system for m up to 4. Results are consistent with a non-spin-degenerate single particle picture of the filling of levels. Electron-electron interaction effects are also observed as a perturbation to this model. Magnetoconductance fluctuations of ground states are shown as anticrossings where wavefunction characteristics are exchanged between adjacent levels.Comment: 8 pages pdf; gzipped ps available at http://www-leland.stanford.edu/group/MarcusLab/grouppubs.htm

Associations Between Left Ventricular Dysfunction and Brain Structure and Function: Findings From the SABRE (Southall and Brent Revisited) Study

Background Subclinical left ventricular (LV) dysfunction has been inconsistently associated with early cognitive impairment, and mechanistic pathways have been poorly considered. We investigated the cross‐sectional relationship between LV dysfunction and structural/functional measures of the brain and explored the role of potential mechanisms. Method and Results A total of 1338 individuals (69±6 years) from the Southall and Brent Revisited study underwent echocardiography for systolic (tissue Doppler imaging peak systolic wave) and diastolic (left atrial diameter) assessment. Cognitive function was assessed and total and hippocampal brain volumes were measured by magnetic resonance imaging. Global LV function was assessed by circulating N‐terminal pro–brain natriuretic peptide. The role of potential mechanistic pathways of arterial stiffness, atherosclerosis, microvascular disease, and inflammation were explored. After adjusting for age, sex, and ethnicity, lower systolic function was associated with lower total brain (beta±standard error, 14.9±3.2 cm3; P<0.0001) and hippocampal volumes (0.05±0.02 cm3, P=0.01). Reduced diastolic function was associated with poorer working memory (−0.21±0.07, P=0.004) and fluency scores (−0.18±0.08, P=0.02). Reduced global LV function was associated with smaller hippocampal volume (−0.10±0.03 cm3, P=0.004) and adverse visual memory (−0.076±0.03, P=0.02) and processing speed (0.063±0.02, P=0.006) scores. Separate adjustment for concomitant cardiovascular risk factors attenuated associations with hippocampal volume and fluency only. Further adjustment for the alternative pathways of microvascular disease or arterial stiffness attenuated the relationship between global LV function and visual memory. Conclusions In a community‐based sample of older people, measures of LV function were associated with structural/functional measures of the brain. These associations were not wholly explained by concomitant risk factors or potential mechanistic pathways

Bidirectional relationship between functional connectivity and amyloid-β deposition in mouse brain

Brain region-specific deposition of extracellular amyloid plaques principally composed of aggregated amyloid-β (Aβ) peptide is a pathological signature of Alzheimer’s disease (AD). Recent human neuroimaging data suggest that resting-state functional connectivity strength is reduced in patients with AD, cognitively normal elderly harboring elevated amyloid burden, and in advanced aging. Interestingly, there exists a striking spatial correlation between functional connectivity strength in cognitively normal adults and the location of Aβ plaque deposition in AD. However, technical limitations have heretofore precluded examination of the relationship between functional connectivity, Aβ deposition, and normal aging in mouse models. Using a novel functional connectivity optical intrinsic signal (fcOIS) imaging technique, we demonstrate that Aβ deposition is associated with significantly reduced bilateral functional connectivity in multiple brain regions of older APP/PS1 transgenic mice. The amount of Aβ deposition in each brain region was associated with the degree of local, age-related bilateral functional connectivity decline. Normal aging was associated with reduced bilateral functional connectivity specifically in retrosplenial cortex. Furthermore, we found that the magnitude of regional bilateral functional correlation in young APP/PS1 mice prior to Aβ plaque formation was proportional to the amount of region-specific plaque deposition seen later in older APP/PS1 mice. Together, these findings suggest that Aβ deposition and normal aging are associated with region-specific disruption of functional connectivity and that the magnitude of local bilateral functional connectivity predicts regional vulnerability to subsequent Aβ deposition in mouse brain

Charge Solitons in 1-D Arrays of Serially Coupled Josephson Junctions

We study a 1-D array of Josephson coupled superconducting grains with kinetic inductance which dominates over the Josephson inductance. In this limit the dynamics of excess Cooper pairs in the array is described in terms of charge solitons, created by polarization of the grains. We analyze the dynamics of these topological excitations, which are dual to the fluxons in a long Josephson junction, using the continuum sine-Gordon model. We find that their classical relativistic motion leads to saturation branches in the I-V characteristic of the array. We then discuss the semi-classical quantization of the charge soliton, and show that it is consistent with the large kinetic inductance of the array. We study the dynamics of a quantum charge soliton in a ring-shaped array biased by an external flux through its center. If the dephasing length of the quantum charge soliton is larger than the circumference of the array, quantum phenomena like persistent current and coherent current oscillations are expected. As the characteristic width of the charge soliton is of the order of 100 microns, it is a macroscopic quantum object. We discuss the dephasing mechanisms which can suppress the quantum behaviour of the charge soliton.Comment: 26 pages, LaTex, 7 Postscript figure

Coulomb Blockade Fluctuations in Strongly Coupled Quantum Dots

Quantum fluctuations of Coulomb blockade are investigated as a function of the coupling to reservoirs in semiconductor quantum dots. We use fluctuations in the distance between peaks $\Delta N$ apart to characterize both the amplitude and correlation of peak motion. For strong coupling, peak motion is greatly enhanced at low temperature, but does not show an increase in peak-to-peak correlation. These effects can lead to anomalous temperature dependence in the Coulomb valleys, similar to behavior ascribed to Kondo physics.Comment: figures made smaller so download works. Revised, including new data. Related papers at http://www.stanford.edu/group/MarcusLab/grouppubs.htm

Favorable outcome of early treatment of new onset child and adolescent migraine-implications for disease modification.

There is evidence that the prevalence of migraine in children and adolescents may be increasing. Current theories of migraine pathophysiology in adults suggest activation of central cortical and brainstem pathways in conjunction with the peripheral trigeminovascular system, which ultimately results in release of neuropeptides, facilitation of central pain pathways, neurogenic inflammation surrounding peripheral vessels, and vasodilatation. Although several risk factors for frequent episodic, chronic, and refractory migraine have been identified, the causes of migraine progression are not known. Migraine pathophysiology has not been fully evaluated in children. In this review, we will first discuss the evidence that early therapeutic interventions in the child or adolescent new onset migraineur, may halt or limit progression and disability. We will then review the evidence suggesting that many adults with chronic or refractory migraine developed their migraine as children or adolescents and may not have been treated adequately with migraine-specific therapy. Finally, we will show that early, appropriate and optimal treatment of migraine during childhood and adolescence may result in disease modification and prevent progression of this disease