The Growth of Oligarchy in a Yard-Sale Model of Asset Exchange: A Logistic Equation for Wealth Condensation

The addition of wealth-attained advantage (WAA) to the Yard-Sale Model (YSM) of asset exchange has been demonstrated to induce wealth condensation. In a model of WAA for which the bias is a continuous function of the wealth difference of the transacting agents, the condensation was shown to arise from a second-order phase transition to a coexistence regime. In this paper, we present the first analytic time-dependent results for this model, by showing that the condensed wealth obeys a logistic equation in time.Comment: 15 pages, 2 figure

Erosion patterns in a sediment layer

We report here on a laboratory-scale experiment which reproduces a rich variety of natural patterns with few control parameters. In particular, we focus on intriguing rhomboid structures often found on sandy shores and flats. We show that the standard views based on water surface waves come short to explain the phenomenon and we evidence a new mechanism based on a mud avalanche instability.Comment: 4 pages, 4 figures, to appear as Phys. Rev. E rapid com

Short stature, hyperkalemia and acidosis: A defect in renal transport of potassium

Short stature, hyperkalemia, and acidosis: A defect in renal transport of potassium. An eleven-year-old boy presented with short stature, hyperkalemia, and metabolic acidosis. No endocrine cause for a short stature could be demonstrated. Renal function, as assessed by inulin and PAH clearances, concentrating and diluting capacity, and ability to acidify the urine and to excrete net acid, was normal. No defect was detected in adrenal secretion of, or renal responsiveness to, aldosterone. A low renal threshold for bicarbonate was documented which apparently explained the acidosis. However, correction of the acidosis by administration of sodium bicarbonate did not influence the hyperkalemia, making it unlikely that an abnormality in bicarbonate reabsorption was the primary defect. Chlorothiazide induced a fall in serum potassium and a rise in serum bicarbonate to normal levels. During bicarbonate loading the rates of excretion of potassium in urine were consistently below those observed in control subjects. It appeared, therefore, that the patient had a primary abnormality in potassium excretion. The resulting hyperkalemia caused urinary loss of bicarbonate and systemic acidosis. Correction of both the acidosis and hyperkalemia by chronic administration of chlorothiazide and sodium bicarbonate has resulted in resumption of normal growth.Retard de croissance, hyperkaliéme et acidose: Un déficit du transport rénal du potassium. Un enfant de 11 ans avait un retard de croissance, une hyperkaliémie et une acidose métabolique. Aucune cause endocrine du retard de croissance n'a été trouvée. La fonction rénale, estimée par les clearances de l'inuline et du PAH, la capacité de concentration et de dilution et la capacité d'acidifier l'urine, était normales. Aucun déficit de la secrétion d'aldostérone ou de la réponse rénale à l'aldostérone n'a été mis en évidence. Un seuil rénal bas des bicarbonates a été découvert, qui explique apparemment l'acidose. Cependant la correction de l'acidose par l'administration de bicarbonate de sodium n'a pas influencé l'hyperkaliémie, ce qui rend peu probable que le déficit de la réabsorption de bicarbonate soit la cause de l'ensemble. Le Chlorothiazide a déterminé une baisse de la kaliéme et une augmentation du bicarbonate plasmatique jusqu'à des valeurs normales. Pendant une charge en bicarbonate les débits d'excretion du potassium dans les urines ont été nettement inférieurs à ceux obtenus chez des sujets témoins. Il apparaît donc que le malade a une anomalie primitive de l'excrétion de potassium. L'hyperkaliémie qui en est la conséquence a déterminé une perte de bicarbonate dans les urines et une acidose systémique. La correction de l'acidose et de l'hyperkaliémie par l'administration permanente de Chlorothiazide et de bicarbonate de sodium a eu pour résultat une reprise de la croissance normale

Inclined Surface Locomotion Strategies for Spherical Tensegrity Robots

This paper presents a new teleoperated spherical tensegrity robot capable of performing locomotion on steep inclined surfaces. With a novel control scheme centered around the simultaneous actuation of multiple cables, the robot demonstrates robust climbing on inclined surfaces in hardware experiments and speeds significantly faster than previous spherical tensegrity models. This robot is an improvement over other iterations in the TT-series and the first tensegrity to achieve reliable locomotion on inclined surfaces of up to 24\degree. We analyze locomotion in simulation and hardware under single and multi-cable actuation, and introduce two novel multi-cable actuation policies, suited for steep incline climbing and speed, respectively. We propose compelling justifications for the increased dynamic ability of the robot and motivate development of optimization algorithms able to take advantage of the robot's increased control authority.Comment: 6 pages, 11 figures, IROS 201

Lack of interaction between ErbB2 and insulin receptor substrate signaling in breast cancer

Background: ErbB2 Receptor Tyrosine Kinase 2 (ErbB2, HER2/Neu) is amplified in breast cancer and associated with poor prognosis. Growing evidence suggests interplay between ErbB2 and insulin-like growth factor (IGF) signaling. For example, ErbB2 inhibitors can block IGF-induced signaling while, conversely, IGF1R inhibitors can inhibit ErbB2 action. ErbB receptors can bind and phosphorylate insulin receptor substrates (IRS) and this may be critical for ErbBmediated anti-estrogen resistance in breast cancer. Herein, we examined crosstalk between ErbB2 and IRSs using cancer cell lines and transgenic mouse models. Methods: MMTV-ErbB2 and MMTV-IRS2 transgenic mice were crossed to create hemizygous MMTV-ErbB2/MMTVIRS2 bigenic mice. Signaling crosstalk between ErbB2 and IRSs was examined in vitro by knockdown or overexpression followed by western blot analysis for downstream signaling intermediates and growth assays. Results: A cross between MMTV-ErbB2 and MMTV-IRS2 mice demonstrated no enhancement of ErbB2 mediated mammary tumorigenesis or metastasis by elevated IRS2. Substantiating this, overexpression or knockdown of IRS1 or IRS2 in MMTV-ErbB2 mammary cancer cell lines had little effect upon ErbB2 signaling. Similar results were obtained in human mammary epithelial cells (MCF10A) and breast cancer cell lines. Conclusion: Despite previous evidence suggesting that ErbB receptors can bind and activate IRSs, our findings indicate that ErbB2 does not cooperate with the IRS pathway in these models to promote mammary tumorigenesis

Modelling semi-attributable toxicity in dual-agent phase I trials with non-concurrent drug administration.

In oncology, combinations of drugs are often used to improve treatment efficacy and/or reduce harmful side effects. Dual-agent phase I clinical trials assess drug safety and aim to discover a maximum tolerated dose combination via dose-escalation; cohorts of patients are given set doses of both drugs and monitored to see if toxic reactions occur. Dose-escalation decisions for subsequent cohorts are based on the number and severity of observed toxic reactions, and an escalation rule. In a combination trial, drugs may be administered concurrently or non-concurrently over a treatment cycle. For two drugs given non-concurrently with overlapping toxicities, toxicities occurring after administration of the first drug yet before administration of the second may be attributed directly to the first drug, whereas toxicities occurring after both drugs have been given some present ambiguity; toxicities may be attributable to the first drug only, the second drug only or the synergistic combination of both. We call this mixture of attributable and non-attributable toxicity semi-attributable toxicity. Most published methods assume drugs are given concurrently, which may not be reflective of trials with non-concurrent drug administration. We incorporate semi-attributable toxicity into Bayesian modelling for dual-agent phase I trials with non-concurrent drug administration and compare the operating characteristics to an approach where this detail is not considered. Simulations based on a trial for non-concurrent administration of intravesical Cabazitaxel and Cisplatin in early-stage bladder cancer patients are presented for several scenarios and show that including semi-attributable toxicity data reduces the number of patients given overly toxic combinations. © 2016 The Authors. Statistics in Medicine Published by John Wiley & Sons Ltd.G.M. Wheeler and A.P. Mander are supported by the Medical Research Council (grant number G0800860). M.J. Sweeting is supported by a European Research Council Advanced Investigator Award: EPIC-Heart (grant number 268834), the UK Medical Research Council (grant number MR/L003120/1), the British Heart Foundation and the Cambridge National Institute for Health Research Biomedical Research Centre. S.M. Lee is supported by the American Cancer Society (grant number MRSG-13-146-01-CPHPS).This is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1002/sim.691

Relationship of national institutes of health stroke scale to 30-day mortality in medicare beneficiaries with acute ischemic stroke.

BackgroundThe National Institutes of Health Stroke Scale (NIHSS), a well-validated tool for assessing initial stroke severity, has previously been shown to be associated with mortality in acute ischemic stroke. However, the relationship, optimal categorization, and risk discrimination with the NIHSS for predicting 30-day mortality among Medicare beneficiaries with acute ischemic stroke has not been well studied.Methods and resultsWe analyzed data from 33102 fee-for-service Medicare beneficiaries treated at 404 Get With The Guidelines-Stroke hospitals between April 2003 and December 2006 with NIHSS documented. The 30-day mortality rate by NIHSS as a continuous variable and by risk-tree determined or prespecified categories were analyzed, with discrimination of risk quantified by the c-statistic. In this cohort, mean age was 79.0 years and 58% were female. The median NIHSS score was 5 (25th to 75th percentile 2 to 12). There were 4496 deaths in the first 30 days (13.6%). There was a strong graded relation between increasing NIHSS score and higher 30-day mortality. The 30-day mortality rates for acute ischemic stroke by NIHSS categories were as follows: 0 to 7, 4.2%; 8 to 13, 13.9%; 14 to 21, 31.6%; 22 to 42, 53.5%. A model with NIHSS alone provided excellent discrimination whether included as a continuous variable (c-statistic 0.82 [0.81 to 0.83]), 4 categories (c-statistic 0.80 [0.79 to 0.80]), or 3 categories (c-statistic 0.79 [0.78 to 0.79]).ConclusionsThe NIHSS provides substantial prognostic information regarding 30-day mortality risk in Medicare beneficiaries with acute ischemic stroke. This index of stroke severity is a very strong discriminator of mortality risk, even in the absence of other clinical information, whether used as a continuous or categorical risk determinant. (J Am Heart Assoc. 2012;1:42-50.)

Patterns, predictors, variations, and temporal trends in emergency medical service hospital prenotification for acute ischemic stroke.

BACKGROUND#ENTITYSTARTX02014;: Emergency medical services (EMS) hospital prenotification of an incoming stroke patient is guideline recommended as a means of increasing the timeliness with which stroke patients are evaluated and treated. Still, data are limited with regard to national use of, variations in, and temporal trends in EMS prenotification and associated predictors of its use. METHODS AND RESULTS#ENTITYSTARTX02014;: We examined 371 988 patients with acute ischemic stroke who were transported by EMS and enrolled in 1585 hospitals participating in Get With The Guidelines-Stroke from April 1, 2003, through March 31, 2011. Prenotification occurred in 249 197 EMS-transported patients (67.0%) and varied widely by hospital (range, 0% to 100%). Substantial variations by geographic regions and by state, ranging from 19.7% in Washington, DC, to 93.4% in Montana, also were noted. Patient factors associated with lower use of prenotification included older age, diabetes mellitus, and peripheral vascular disease. Prenotification was less likely for black patients than for white patients (adjusted odds ratio 0.94, 95% confidence interval 0.92-0.97, P<0.0001). Hospital factors associated with greater EMS prenotification use were absence of academic affiliation, higher annual volume of tissue plasminogen activator administration, and geographic location outside the Northeast. Temporal improvements in prenotification rates showed a modest general increase, from 58.0% in 2003 to 67.3% in 2011 (P temporal trend <0.0001). CONCLUSIONS#ENTITYSTARTX02014;: EMS hospital prenotification is guideline recommended, yet among patients transported to Get With The Guidelines-Stroke hospitals it is not provided for 1 in 3 EMS-arriving patients with acute ischemic stroke and varies substantially by hospital, state, and region. These results support the need for enhanced implementation of stroke systems of care. (J Am Heart Assoc. 2012;1:e002345 doi: 10.1161/JAHA.112.002345.)