On stochastic properties between some ordered random variables

A great number of articles have dealt with stochastic comparisons of ordered random variables in the last decades. In particular, distributional and stochastic properties of ordinary order statistics have been studied extensively in the literature. Sequential order statistics are proposed as an extension of ordinary order statistics. Since sequential order statistics models unify various models of ordered random variables, it is interesting to study their distributional and stochastic properties. In this work, we consider the problem of comparing sequential order statistics according to magnitude and location orders.Stochastic orderings, Reliability, Order statistics

On the Conjecture of Kochar and Korwar

In this paper, we solve for some cases a conjecture by Kochar and Korwar (1996) in relation with the normalized spacings of the order statistics related to a sample of independent exponential random variables with different scale parameter. In the case of a sample of size n=3, they proved the ordering of the normalized spacings and conjectured that result holds for all n. We give the proof of this conjecture for n=4 and for both spacing and normalized spacings. We also generalize some results to n>4Heterogeneous exponential distribution, Hazard rate order, Normalized

New isometry of Krall-Laguerre orthogonal polynomials in martingale spaces

In this paper we study how an inner product derived from an Uvarov transformation of the Laguerre weight function is used in the orthogonalization procedure of a sequence of martingales related to a Levy process. The orthogonalization is done by isometry. The resulting set of pairwise strongly orthogonal martingales involved are used as integrators in the so-called chaotic representation propertyEdmundo J. Huertas is supported by a grant from Ministerio de Ciencia e Innovación (MTM 2009-12740-C03-01), and by Fundação para a Ciência e Tecnologia (FCT), ref. SFRH/BPD/91841/2012, Portugal. Nuria Torrado is supported by Fundação para a Ciência e Tecnologia (FCT), ref. SFRH/BPD/91832/2012, Portugal. The research of Fabrizio Leisen has been partially supported by the Spanish Ministry of Science and Innovation through grant ECO2011-2570

Validação de 3 Equipamentos de TDR (Reflectometria no Domínio do Tempo) para a Medida da Umidade de Solos.

bitstream/CNPDIA/10455/1/CT61_2004.pd

Distomatosis bovina y ovina

Es una enfermedad parasitaria cuyo agente etiológico se denomina Fasciola hepática, nombre con el que la ciencia distingue a un verme chato, no segmentado, perteneciente a la clase de los trematodes y que se localiza en los canales biliares de los bovinos y ovinos. La enfermedad puede presentarse en forma aguda, con muerte rápida del sujeto, aunque no es lo frecuente. En la generalidad de los casos, sigue un curso lento, presentando una sintomatología sub-clínica que se traduce por disminución de la vivacidad y del apetito, enflaquecimiento. anemia, edema entre las mandíbulas y diarrea. basándonos en su forma de evolución, deducimos que la lucha contra esta enfermedad se deberá orientar en un doble sentido: 1) Profiláctico. Destruyendo las formas libres del parásito y el hospedador intermediario por medio de sustancias molusquicidas. Esta forma de lucha es muy difícil de realizar en nuestro país por tratarse de grandes extensiones de territorio; 2) Terapéutico. Tratando los animales parasitados.Academia Nacional de Agronomía y Veterinari

Distomatosis bovina y ovina

Es una enfermedad parasitaria cuyo agente etiológico se denomina Fasciola hepática, nombre con el que la ciencia distingue a un verme chato, no segmentado, perteneciente a la clase de los trematodes y que se localiza en los canales biliares de los bovinos y ovinos. La enfermedad puede presentarse en forma aguda, con muerte rápida del sujeto, aunque no es lo frecuente. En la generalidad de los casos, sigue un curso lento, presentando una sintomatología sub-clínica que se traduce por disminución de la vivacidad y del apetito, enflaquecimiento. anemia, edema entre las mandíbulas y diarrea. basándonos en su forma de evolución, deducimos que la lucha contra esta enfermedad se deberá orientar en un doble sentido: 1) Profiláctico. Destruyendo las formas libres del parásito y el hospedador intermediario por medio de sustancias molusquicidas. Esta forma de lucha es muy difícil de realizar en nuestro país por tratarse de grandes extensiones de territorio; 2) Terapéutico. Tratando los animales parasitados.Academia Nacional de Agronomía y Veterinari

Microbiological, histological, immunological, and toxin response to antibiotic treatment in the mouse model of Mycobacterium ulcerans disease.

Mycobacterium ulcerans infection causes a neglected tropical disease known as Buruli ulcer that is now found in poor rural areas of West Africa in numbers that sometimes exceed those reported for another significant mycobacterial disease, leprosy, caused by M. leprae. Unique among mycobacterial diseases, M. ulcerans produces a plasmid-encoded toxin called mycolactone (ML), which is the principal virulence factor and destroys fat cells in subcutaneous tissue. Disease is typically first manifested by the appearance of a nodule that eventually ulcerates and the lesions may continue to spread over limbs or occasionally the trunk. The current standard treatment is 8 weeks of daily rifampin and injections of streptomycin (RS). The treatment kills bacilli and wounds gradually heal. Whether RS treatment actually stops mycolactone production before killing bacilli has been suggested by histopathological analyses of patient lesions. Using a mouse footpad model of M. ulcerans infection where the time of infection and development of lesions can be followed in a controlled manner before and after antibiotic treatment, we have evaluated the progress of infection by assessing bacterial numbers, mycolactone production, the immune response, and lesion histopathology at regular intervals after infection and after antibiotic therapy. We found that RS treatment rapidly reduced gross lesions, bacterial numbers, and ML production as assessed by cytotoxicity assays and mass spectrometric analysis. Histopathological analysis revealed that RS treatment maintained the association of the bacilli with (or within) host cells where they were destroyed whereas lack of treatment resulted in extracellular infection, destruction of host cells, and ultimately lesion ulceration. We propose that RS treatment promotes healing in the host by blocking mycolactone production, which favors the survival of host cells, and by killing M. ulcerans bacilli