The Importance of Disk Structure in Stalling Type I Migration

As planets form they tidally interact with their natal disks. Though the tidal perturbation induced by Earth and super-Earth mass planets is generally too weak to significantly modify the structure of the disk, the interaction is potentially strong enough to cause the planets to undergo rapid type I migration. This physical process may provide a source of short-period super-Earths, though it may also pose a challenge to the emergence and retention of cores on long-period orbits with sufficient mass to evolve into gas giants. Previous numerical simulations have shown that the type I migration rate sensitively depends upon the circumstellar disk's properties, particularly the temperature and surface density gradients. Here, we derive these structure parameters for 1) a self-consistent viscous-disk model based on a constant \alpha-prescription, 2) an irradiated disk model that takes into account heating due to the absorption of stellar photons, and 3) a layered-accretion disk model with variable \alpha-parameter. We show that in the inner viscously-heated regions of typical protostellar disks, the horseshoe and corotation torques of super-Earths can exceed their differential Lindblad torque and cause them to undergo outward migration. However, the temperature profile due to passive stellar irradiation causes type I migration to be inwards throughout much of the disk. For disks in which there is outwards migration, we show that location and the mass range of the "planet traps" depends on some uncertain assumptions adopted for these disk models. Competing physical effects may lead to dispersion in super-Earths' mass-period distribution.Comment: 12 pages, Submitted to Ap

How a Diverse Research Ecosystem Has Generated New Rehabilitation Technologies: Review of NIDILRR’s Rehabilitation Engineering Research Centers

Over 50 million United States citizens (1 in 6 people in the US) have a developmental, acquired, or degenerative disability. The average US citizen can expect to live 20% of his or her life with a disability. Rehabilitation technologies play a major role in improving the quality of life for people with a disability, yet widespread and highly challenging needs remain. Within the US, a major effort aimed at the creation and evaluation of rehabilitation technology has been the Rehabilitation Engineering Research Centers (RERCs) sponsored by the National Institute on Disability, Independent Living, and Rehabilitation Research. As envisioned at their conception by a panel of the National Academy of Science in 1970, these centers were intended to take a “total approach to rehabilitation”, combining medicine, engineering, and related science, to improve the quality of life of individuals with a disability. Here, we review the scope, achievements, and ongoing projects of an unbiased sample of 19 currently active or recently terminated RERCs. Specifically, for each center, we briefly explain the needs it targets, summarize key historical advances, identify emerging innovations, and consider future directions. Our assessment from this review is that the RERC program indeed involves a multidisciplinary approach, with 36 professional fields involved, although 70% of research and development staff are in engineering fields, 23% in clinical fields, and only 7% in basic science fields; significantly, 11% of the professional staff have a disability related to their research. We observe that the RERC program has substantially diversified the scope of its work since the 1970’s, addressing more types of disabilities using more technologies, and, in particular, often now focusing on information technologies. RERC work also now often views users as integrated into an interdependent society through technologies that both people with and without disabilities co-use (such as the internet, wireless communication, and architecture). In addition, RERC research has evolved to view users as able at improving outcomes through learning, exercise, and plasticity (rather than being static), which can be optimally timed. We provide examples of rehabilitation technology innovation produced by the RERCs that illustrate this increasingly diversifying scope and evolving perspective. We conclude by discussing growth opportunities and possible future directions of the RERC program

Pericellular activation of hepatocyte growth factor by the transmembrane serine proteases matriptase and hepsin, but not by the membrane-associated protease uPA

HGF (hepatocyte growth factor) is a pleiotropic cytokine homologous to the serine protease zymogen plasminogen that requires canonical proteolytic cleavage to gain functional activity. The activating proteases are key components of its regulation, but controversy surrounds their identity. Using quantitative analysis we found no evidence for activation by uPA (urokinase plasminogen activator), despite reports that this is a principal activator of pro-HGF. This was unaffected by a wide range of experimental conditions, including the use of various molecular forms of both HGF and uPA, and the presence of uPAR (uPA receptor) or heparin. In contrast the catalytic domains of the TTSPs (type-II transmembrane serine proteases) matriptase and hepsin were highly efficient activators (50% activation at 0.1 and 3.4 nM respectively), at least four orders of magnitude more efficient than uPA. PS-SCL (positional-scanning synthetic combinatorial peptide libraries) were used to identify consensus sequences for the TTSPs, which in the case of hepsin corresponded to the pro-HGF activation sequence, demonstrating a high specificity for this reaction. Both TTSPs were also found to be efficient activators at the cell surface. Activation of pro-HGF by PC3 prostate carcinoma cells was abolished by both protease inhibition and matriptase-targeting siRNA (small interfering RNA), and scattering of MDCK (Madin–Darby canine kidney) cells in the presence of pro-HGF was abolished by inhibition of matriptase. Hepsin-transfected HEK (human embryonic kidney)-293 cells also activated pro-HGF. These observations demonstrate that, in contrast with the uPA/uPAR system, the TTSPs matriptase and hepsin are direct pericellular activators of pro-HGF, and that together these proteins may form a pathway contributing to their involvement in pathological situations, including cancer

Olfactory perireceptor and receptor events in moths: a kinetic model revised

Modelling reveals that within about 3 ms after entering the sensillum lymph, 17% of total pheromone is enzymatically degraded while 83% is bound to the pheromone-binding protein (PBP) and thereby largely protected from enzymatic degradation. The latter proceeds within minutes, 20,000-fold more slowly than with the free pheromone. In vivo the complex pheromone–PBP interacts with the receptor molecule. At weak stimulation the half-life of the active complex is 0.8 s due to the postulated pheromone deactivation. Most likely this process is enzymatically catalysed; it changes the PBP into a scavenger form, possibly by interference with the C-terminus. The indirectly determined PBP concentration (3.8 mM) is close to direct measurements. The calculated density of receptor molecules within the plasma membrane of the receptor neuron reaches up to 6,000 units per μm2. This is compared with the estimated densities of the sensory-neuron membrane protein and of ion channels. The EC50 of the model pheromone–PBP complex interacting with the receptor molecules is 6.8 μM, as compared with the EC50 = 1.5 μM of bombykol recently determined using heterologous expression. A possible mechanism widening the range of stimulus intensities covered by the dose–response curve of the receptor-potential is proposed

Navigating in the Landscape of Care: A Critical Reflection on Theory and Practise of Care and Ethics

The theory and practise of care is defined and enacted differently in different national as well as cultural contexts, illuminating how differently constructed the personal and societal structures in Europe are. A common trait is however that care work paid or non-paid, private or public is identified with women. To navigate in the landscape of care and ethics requires taking into account the constitutive relation between one’s identity, embodiment and position. The author suggests conceiving care as an existential condition of life demanded from all human beings. This will free care from the identification with women and pave a way towards a more gender equal and just society with less gender segregation in the labour market and at the arena of education

Recent Walker Circulation strengthening and Pacific cooling amplified by Atlantic warming

An unprecedented strengthening of Pacific trade winds since the late 1990s (ref. 1) has caused widespread climate perturbations, including rapid sea-level rise in the western tropical Pacific, strengthening of Indo-Pacific ocean currents, and an increased uptake of heat in the equatorial Pacific thermocline. The corresponding intensification of the atmospheric Walker circulation is also associated with sea surface cooling in the eastern Pacific, which has been identified as one of the contributors to the current pause in global surface warming. In spite of recent progress in determining the climatic impacts of the Pacific trade wind acceleration, the cause of this pronounced trend in atmospheric circulation remains unknown. Here we analyse a series of climate model experiments along with observational data to show that the recent warming trend in Atlantic sea surface temperature and the corresponding trans-basin displacements of the main atmospheric pressure centres were key drivers of the observed Walker circulation intensification, eastern Pacific cooling, North American rainfall trends and western Pacific sea-level rise. Our study suggests that global surface warming has been partly offset by the Pacific climate response to enhanced Atlantic warming since the early 1990s

Acute Kawasaki Disease: Not Just for Kids

Kawasaki Disease is a small-to-medium-vessel vasculitis that preferentially affects children. Kawasaki Disease can occur in adults, but the presentation may differ from that observed in children. Typical findings in both adults and children include fever, conjunctivitis, pharyngitis, and skin erythema progressing to a desquamating rash on the palms and soles. Adults more frequently present with cervical adenopathy (93% of adults vs. 15% of children), hepatitis (65% vs. 10%), and arthralgia (61% vs. 24–38%). In contrast, adults are less frequently affected by meningitis (10% vs. 34%), thrombocytosis (55% vs. 100%), and coronary artery aneurysms (5% vs. 18–25%). We report a case of acute Kawasaki Disease in a 24-year-old man who presented with rash, fever, and arthritis. He was successfully treated with high-dose aspirin and intravenous immunoglobulin (IVIG). Our case highlights the importance of considering Kawasaki Disease in adults presenting with symptoms commonly encountered in a general medical practice

Identification of strontium in the merger of two neutron stars.

Half of all of the elements in the Universe that are heavier than iron were created by rapid neutron capture. The theory underlying this astrophysical r-process was worked out six decades ago, and requires an enormous neutron flux to make the bulk of the elements1. Where this happens is still debated2. A key piece of evidence would be the discovery of freshly synthesized r-process elements in an astrophysical site. Existing models3-5 and circumstantial evidence6 point to neutron-star mergers as a probable r-process site; the optical/infrared transient known as a 'kilonova' that emerges in the days after a merger is a likely place to detect the spectral signatures of newly created neutron-capture elements7-9. The kilonova AT2017gfo-which was found following the discovery of the neutron-star merger GW170817 by gravitational-wave detectors10-was the first kilonova for which detailed spectra were recorded. When these spectra were first reported11,12, it was argued that they were broadly consistent with an outflow of radioactive heavy elements; however, there was no robust identification of any one element. Here we report the identification of the neutron-capture element strontium in a reanalysis of these spectra. The detection of a neutron-capture element associated with the collision of two extreme-density stars establishes the origin of r-process elements in neutron-star mergers, and shows that neutron stars are made of neutron-rich matter13

Identification of p.A684V missense mutation in the WFS1 gene as a frequent cause of autosomal dominant optic atrophy and hearing impairment

Optic atrophy (OA) and sensorineural hearing loss (SNHL) are key abnormalities in several syndromes, including the recessively inherited Wolfram syndrome, caused by mutations in WFS1 . In contrast, the association of autosomal dominant OA and SNHL without other phenotypic abnormalities is rare, and almost exclusively attributed to mutations in the Optic Atrophy-1 gene ( OPA1 ), most commonly the p.R445H mutation. We present eight probands and their families from the US, Sweden, and UK with OA and SNHL, whom we analyzed for mutations in OPA1 and WFS1 . Among these families, we found three heterozygous missense mutations in WFS1 segregating with OA and SNHL: p.A684V (six families), and two novel mutations, p.G780S and p.D797Y, all involving evolutionarily conserved amino acids and absent from 298 control chromosomes. Importantly, none of these families harbored the OPA1 p.R445H mutation. No mitochondrial DNA deletions were detected in muscle from one p.A684V patient analyzed. Finally, wolframin p.A684V mutant ectopically expressed in HEK cells showed reduced protein levels compared to wild-type wolframin, strongly indicating that the mutation is disease-causing. Our data support OA and SNHL as a phenotype caused by dominant mutations in WFS1 in these additional eight families. Importantly, our data provide the first evidence that a single, recurrent mutation in WFS1 , p.A684V, may be a common cause of ADOA and SNHL, similar to the role played by the p.R445H mutation in OPA1 . Our findings suggest that patients who are heterozygous for WFS1 missense mutations should be carefully clinically examined for OA and other manifestations of Wolfram syndrome. © 2011 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/84383/1/33970_ftp.pd