4,454 research outputs found

    Cownose Ray (Rhinoptera Bonasus) Predation Relative To Bivalve Ontogeny

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    The purpose of this study was to determine the ability of the cownose ray, Rhinoptera bonasus (Mitchill, 1815), to manipulate oysters and clams, to test for relative prey preference, and to investigate whether susceptibility to cownose ray predation changes with bivalve ontogeny. We investigated patterns of predation for captive adult and young-of-year cownose rays on 4 species of bivalves, including Crassostrea virginica (Gmelin, 1791), Crassostrea ariakensis (Fujita, 1913), Mercenaria mercenaria (Linnaeus, 1758), and Mya arenaria Linnaeus, 1758. In oyster (C. virginica) trials, predation probabilities by adult rays were highest at shell heights of 30-70 mm and shell depths of 8-22 mm. The rates of predation by adult rays in trials in which same-size oysters were used were higher than rates in most comingled trials. Adult rays showed no differences in predation between native oysters (C. virginica) and nonnative oysters (C. ariakensis; P \u3e 0.05). Adult rays selected hard- and soft-shell clams (Manly-Chesson index M. mercenaria, alpha = 0.736 +/- 0.002, electivity = 0.473 +/- 0.007; M. arenaria, alpha = 0.742 +/- 0.003, electivity = 0.485 +/- 0.013) over oysters (C. virginica, alpha = 0.263 +/- 0.002, electivity = -0.473 +/- 0.007; alpha = 0.257 +/- 0.003, electivity = -0.485 +/- 0.003). In young-of-year feeding trials, oysters with a shell height of 10-35 mm and a shell depth of 3-12 mm had the highest probability of predation. Native oyster and hard clam peak force or load crush tests resulted in forces of 200-1,500 N and 400-1,400 N across shell depths of 10-35 mm and 21-34 mm, respectively, before valve failure. The results of this study indicate that cownose ray predation on shellfish is limited by shell size and is likely related to ray jaw gape and bite force

    Brownian Motion in wedges, last passage time and the second arc-sine law

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    We consider a planar Brownian motion starting from OO at time t=0t=0 and stopped at t=1t=1 and a set F={OIi;i=1,2,...,n}F= \{OI_i ; i=1,2,..., n\} of nn semi-infinite straight lines emanating from OO. Denoting by gg the last time when FF is reached by the Brownian motion, we compute the probability law of gg. In particular, we show that, for a symmetric FF and even nn values, this law can be expressed as a sum of arcsin⁥\arcsin or (arcsin⁥)2(\arcsin)^2 functions. The original result of Levy is recovered as the special case n=2n=2. A relation with the problem of reaction-diffusion of a set of three particles in one dimension is discussed

    Incidence and Characteristics of Total Stroke in the United States

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    BACKGROUND AND PURPOSE: Stroke, increasingly referred to as a "brain attack", is one of the leading causes of death and the leading cause of adult disability in the United States. It has recently been estimated that there were three quarters of a million strokes in the United States in 1995. The aim of this study was to replicate the 1995 estimate and examine if there was an increase from 1995 to 1996 by using a large administrative claims database representative of all 1996 US inpatient discharges. METHODS: We used the Nationwide Inpatient Sample of the Healthcare Cost and Utilization Project, release 5, which contains ≈ 20 percent of all 1996 US inpatient discharges. We identified stroke patients by using the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes from 430 to 438, and we compared the 1996 database with that of 1995. RESULTS: There were 712,000 occurrences of stroke with hospitalization (95% CI 688,000 to 737,000) and an estimated 71,000 occurrences of stroke without hospitalization. This totaled 783,000 occurrences of stroke in 1996, compared to 750,000 in 1995. The overall rate for occurrence of total stroke (first-ever and recurrent) was 269 per 100,000 population (age- and sex-adjusted to 1996 US population). CONCLUSIONS: We estimate that there were 783,000 first-ever or recurrent strokes in the United States during 1996, compared to the figure of 750,000 in 1995. This study replicates and confirms the previous annual estimates of approximately three quarters of a million total strokes. This slight increase is likely due to the aging of the population and the population gain in the US from 1995 to 1996

    Individual participant data meta-analysis to examine interactions between treatment effect and participant-level covariates: statistical recommendations for conduct and planning

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    Precision medicine research often searches for treatment‐covariate interactions, which refers to when a treatment effect (eg, measured as a mean difference, odds ratio, hazard ratio) changes across values of a participant‐level covariate (eg, age, gender, biomarker). Single trials do not usually have sufficient power to detect genuine treatment‐covariate interactions, which motivate the sharing of individual participant data (IPD) from multiple trials for meta‐analysis. Here, we provide statistical recommendations for conducting and planning an IPD meta‐analysis of randomized trials to examine treatment‐covariate interactions. For conduct, two‐stage and one‐stage statistical models are described, and we recommend: (i) interactions should be estimated directly, and not by calculating differences in meta‐analysis results for subgroups; (ii) interaction estimates should be based solely on within‐study information; (iii) continuous covariates and outcomes should be analyzed on their continuous scale; (iv) nonlinear relationships should be examined for continuous covariates, using a multivariate meta‐analysis of the trend (eg, using restricted cubic spline functions); and (v) translation of interactions into clinical practice is nontrivial, requiring individualized treatment effect prediction. For planning, we describe first why the decision to initiate an IPD meta‐analysis project should not be based on between‐study heterogeneity in the overall treatment effect; and second, how to calculate the power of a potential IPD meta‐analysis project in advance of IPD collection, conditional on characteristics (eg, number of participants, standard deviation of covariates) of the trials (potentially) promising their IPD. Real IPD meta‐analysis projects are used for illustration throughout

    Probability that a chromosome is lost without trace under the neutral Wright-Fisher model with recombination

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    I describe an analytical approximation for calculating the short-term probability of loss of a chromosome under the neutral Wright-Fisher model with recombination. I also present an upper and lower bound for this probability. Exact analytical calculation of this quantity is difficult and computationally expensive because the number of different ways in which a chromosome can be lost, grows very large in the presence of recombination. Simulations indicate that the probabilities obtained using my approximate formula are always comparable to the true expectations provided that the number of generations remains small. These results are useful in the context of an algorithm that we recently developed for simulating Wright-Fisher populations forward in time. C++ programs that can efficiently calculate these formulas are available on request.Comment: Additional Information, Padhukasahasram et al. 2008, Genetics, FORWSIM algorith

    Necrosis correlates with high vascular density and focal macrophage infiltration in invasive carcinoma of the breast

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    Necrosis is a common feature of invasive carcinoma of the breast and is caused by chronic ischaemia leading to infarction. Although necrosis was previously assumed to be due to a generally poor blood supply in the tumour, in this study we show that it is present in tumours with focal areas of high vascular density situated away from the actual sites of necrosis. This may account, in part, for the previous observation that necrosis is linked to poor prognosis in this disease. Highly angiogenic tumours often display blood vessel shunting from one tumour area to another, which further exacerbates ischaemia and the formation of tumour necrosis. We have recently demonstrated that high focal microphage infiltration into breast tumours is significantly associated with increased tumour angiogenesis and poor prognosis and that the macrophages accumulate in poorly vascularized, hypoxic areas within breast tumours. In order to investigate the interactions of macrophages with chronic ischaemia (as reflected by the presence of necrosis) and angiogenesis in breast tumours, we quantified the levels of these three biological parameters in a series of 109 consecutive invasive breast carcinomas. We found that the degree of tumour necrosis was correlated with both microphage infiltration (Mann–Whitney U, P-value = 0.0009; chi-square, P-value = 0.01) and angiogenesis (Mann–Whitney U P-value = 0.0008, chi square P-value = 0.03). It was also observed that necrosis was a feature of tumours possessing an aggressive phenotype, i.e. high tumour grade (chi-square, P-value < 0.001), larger size (Mann–Whitney U, P-value = 0.003) and low oestrogen receptor status (Mann–Whitney U, P-value = 0.008; chi-square, P-value < 0.008). We suggest, therefore, that aggressive tumours rapidly outgrow their vascular supply in certain areas, leading to areas of prolonged hypoxia within the tumour and, subsequently, to necrosis. This, in turn, may attract macrophages into the tumour, which then contribute to the angiogenic process, giving rise to an association between high levels of angiogenesis and extensive necrosis. © 1999 Cancer Research Campaig
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