Virtual Planetary Analysis Environment for Remote Science

All of the data for NASA's current planetary missions and most data for field experiments are collected via orbiting spacecraft, aircraft, and robotic explorers. Mission scientists are unable to employ traditional field methods when operating remotely. We have developed a virtual exploration tool for remote sites with data analysis capabilities that extend human perception quantitatively and qualitatively. Scientists and mission engineers can use it to explore a realistic representation of a remote site. It also provides software tools to "touch" and "measure" remote sites with an immediacy that boosts scientific productivity and is essential for mission operations

3D Visualization for Phoenix Mars Lander Science Operations

Planetary surface exploration missions present considerable operational challenges in the form of substantial communication delays, limited communication windows, and limited communication bandwidth. A 3D visualization software was developed and delivered to the 2008 Phoenix Mars Lander (PML) mission. The components of the system include an interactive 3D visualization environment called Mercator, terrain reconstruction software called the Ames Stereo Pipeline, and a server providing distributed access to terrain models. The software was successfully utilized during the mission for science analysis, site understanding, and science operations activity planning. A terrain server was implemented that provided distribution of terrain models from a central repository to clients running the Mercator software. The Ames Stereo Pipeline generates accurate, high-resolution, texture-mapped, 3D terrain models from stereo image pairs. These terrain models can then be visualized within the Mercator environment. The central cross-cutting goal for these tools is to provide an easy-to-use, high-quality, full-featured visualization environment that enhances the mission science team s ability to develop low-risk productive science activity plans. In addition, for the Mercator and Viz visualization environments, extensibility and adaptability to different missions and application areas are key design goals

Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disease caused by defective prelamin A processing, leading to nuclear lamina alterations, severe cardiovascular pathology, and premature death. Prelamin A alterations also occur in physiological aging. It remains unknown how defective prelamin A processing affects the cardiac rhythm. We show age-dependent cardiac repolarization abnormalities in HGPS patients that are also present in the Zmpste24-/- mouse model of HGPS. Challenge of Zmpste24-/- mice with the ß-adrenergic agonist isoproterenol did not trigger ventricular arrhythmia but caused bradycardia-related premature ventricular complexes and slow-rate polymorphic ventricular rhythms during recovery. Patch-clamping in Zmpste24-/- cardiomyocytes revealed prolonged calcium-transient duration and reduced sarcoplasmic reticulum calcium loading and release, consistent with the absence of isoproterenol-induced ventricular arrhythmia. Zmpste24-/- progeroid mice also developed severe fibrosis-unrelated bradycardia and PQ interval and QRS complex prolongation. These conduction defects were accompanied by overt mislocalization of the gap junction protein connexin43 (Cx43). Remarkably, Cx43 mislocalization was also evident in autopsied left ventricle tissue from HGPS patients, suggesting intercellular connectivity alterations at late stages of the disease. The similarities between HGPS patients and progeroid mice reported here strongly suggest that defective cardiac repolarization and cardiomyocyte connectivity are important abnormalities in the HGPS pathogenesis that increase the risk of arrhythmia and premature death.Peer ReviewedPostprint (published version

SelfPub 2.0

The self-publishing revolution has created a drastic increase in the number or works being published in the social sciences and humanities. This windfall of content has created an abundance that can be overwhelming, but it ultimately presents an opportunity for libraries to develop deeper and more unique collections. The preconference at the 2013 Charleston Conference focused on several interrelated topics in the self-publishing world: navigating the abundance of self-published material, libraries’ adoption of the role of publisher, vendor perspectives on self-published content and plans for the future, issues in humanities and social science acquisitions of self-published works, and an agent’s perspective on how self-publishing fits into the traditional publishing world. Speakers include librarians, publishers, vendors, and academics involved with a number of projects and efforts to pioneer this emerging field

Writing in Britain and Ireland, c. 400 to c. 800

No abstract available

Possible patterns of marine primary productivity during the Great Ordovician Biodiversification Event

Following the appearance of numerous animal phyla during the ‘Cambrian Explosion’, the ‘Great Ordovician Biodiversification Event’ (GOBE) records their rapid diversification at the lower taxonomic levels, constituting the most significant rise in biodiversity in Earth's history. Recent studies suggest that the rapid rise in phytoplankton diversity observed at the Cambrian–Ordovician boundary may have profoundly restructured marine trophic chains, paving the way for the subsequent flourishing of plankton-feeding groups during the Ordovician. Unfortunately, the fossil record of plankton is incomplete. Its smaller members represent the bulk of the modern marine biomass, but they are usually not documented in Palaeozoic sediments, preventing any definitive assumption with regard to an eventual correlation between biodiversity and biomass at that time. Here, we use an up-to-date ocean general circulation model with biogeochemical capabilities (MITgcm) to simulate the spatial patterns of marine primary productivity throughout the Ordovician, and we compare the model output with available palaeontological and sedimentological data

Mutations in HYAL2, Encoding Hyaluronidase 2, Cause a Syndrome of Orofacial Clefting and Cor Triatriatum Sinister in Humans and Mice.

Orofacial clefting is amongst the most common of birth defects, with both genetic and environmental components. Although numerous studies have been undertaken to investigate the complexities of the genetic etiology of this heterogeneous condition, this factor remains incompletely understood. Here, we describe mutations in the HYAL2 gene as a cause of syndromic orofacial clefting. HYAL2, encoding hyaluronidase 2, degrades extracellular hyaluronan, a critical component of the developing heart and palatal shelf matrix. Transfection assays demonstrated that the gene mutations destabilize the molecule, dramatically reducing HYAL2 protein levels. Consistent with the clinical presentation in affected individuals, investigations of Hyal2-/- mice revealed craniofacial abnormalities, including submucosal cleft palate. In addition, cor triatriatum sinister and hearing loss, identified in a proportion of Hyal2-/- mice, were also found as incompletely penetrant features in affected humans. Taken together our findings identify a new genetic cause of orofacial clefting in humans and mice, and define the first molecular cause of human cor triatriatum sinister, illustrating the fundamental importance of HYAL2 and hyaluronan turnover for normal human and mouse development

Antiplatelet therapy with aspirin, clopidogrel, and dipyridamole versus clopidogrel alone or aspirin and dipyridamole in patients with acute cerebral ischaemia (TARDIS): a randomised, open-label, phase 3 superiority trial

Background: Intensive antiplatelet therapy with three agents might be more effective than guideline treatment for preventing recurrent events in patients with acute cerebral ischaemia. We aimed to compare the safety and efficacy of intensive antiplatelet therapy (combined aspirin, clopidogrel, and dipyridamole) with that of guideline-based antiplatelet therapy. Methods: We did an international, prospective, randomised, open-label, blinded-endpoint trial in adult participants with ischaemic stroke or transient ischaemic attack (TIA) within 48 h of onset. Participants were assigned in a 1:1 ratio using computer randomisation to receive loading doses and then 30 days of intensive antiplatelet therapy (combined aspirin 75 mg, clopidogrel 75 mg, and dipyridamole 200 mg twice daily) or guideline-based therapy (comprising either clopidogrel alone or combined aspirin and dipyridamole). Randomisation was stratified by country and index event, and minimised with prognostic baseline factors, medication use, time to randomisation, stroke-related factors, and thrombolysis. The ordinal primary outcome was the combined incidence and severity of any recurrent stroke (ischaemic or haemorrhagic; assessed using the modified Rankin Scale) or TIA within 90 days, as assessed by central telephone follow-up with masking to treatment assignment, and analysed by intention to treat. This trial is registered with the ISRCTN registry, number ISRCTN47823388. Findings: 3096 participants (1556 in the intensive antiplatelet therapy group, 1540 in the guideline antiplatelet therapy group) were recruited from 106 hospitals in four countries between April 7, 2009, and March 18, 2016. The trial was stopped early on the recommendation of the data monitoring committee. The incidence and severity of recurrent stroke or TIA did not differ between intensive and guideline therapy (93 [6%] participants vs 105 [7%]; adjusted common odds ratio [cOR] 0·90, 95% CI 0·67–1·20, p=0·47). By contrast, intensive antiplatelet therapy was associated with more, and more severe, bleeding (adjusted cOR 2·54, 95% CI 2·05–3·16, p<0·0001). Interpretation: Among patients with recent cerebral ischaemia, intensive antiplatelet therapy did not reduce the incidence and severity of recurrent stroke or TIA, but did significantly increase the risk of major bleeding. Triple antiplatelet therapy should not be used in routine clinical practice