968 resultados para Marshall, Wendy
Resumo:
In survival analysis, the response is usually the time until the occurrence of an event of interest, called failure time. The main characteristic of survival data is the presence of censoring which is a partial observation of response. Associated with this information, some models occupy an important position by properly fit several practical situations, among which we can mention the Weibull model. Marshall-Olkin extended form distributions other a basic generalization that enables greater exibility in adjusting lifetime data. This paper presents a simulation study that compares the gradient test and the likelihood ratio test using the Marshall-Olkin extended form Weibull distribution. As a result, there is only a small advantage for the likelihood ratio test
Resumo:
Incluye Bibliografía
Resumo:
Pós-graduação em Agronomia (Entomologia Agrícola) - FCAV
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
The Marshall Family Papers includes originals and photocopies of two letters written by Fred D. Marshall of Rock Hill. The first is from Camp Thomas in Chickamauga, Georgia and the second was from Camp Cuba Libre in Jacksonville, FL. while he was a soldier during the Spanish American War to his parents, Capt and Mrs. John Wilson Marshall of Rock Hill Also included is a letter by W.W. Byre to Capt. John Wilson Marshall while a missionary in Mexico. Fred D. Marshall served as mayor of Columbia from 1941 to 1946 and W.W. Byre became Dean of Erskine Theological Seminary at Due West, SC.
Resumo:
Marshall's (1970) lemma is an analytical result which implies root-n-consistency of the distribution function corresponding to the Grenander (1956) estimator of a non-decreasing probability density. The present paper derives analogous results for the setting of convex densities on [0,\infty).
Resumo:
BACKGROUND: The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. RESULTS: Here we report genes regulated either directly or indirectly by RUNX1 based on the study of gene expression profiles generated from 3 different human and mouse platforms. The platforms used were global gene expression profiling of: 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFbeta, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays. We observe that our datasets (lists of differentially expressed genes) significantly correlate with published microarray data from sporadic AML patients with mutations in either RUNX1 or its cofactor, CBFbeta. A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability. In addition, analysis of the regulatory regions of the differentially expressed genes has for the first time systematically identified numerous potential novel RUNX1 target genes. CONCLUSION: This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia. The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications.
Resumo:
von Augustin Krämer, Hans Nevermann
Resumo:
E. G. F.
Resumo:
von H. Linckens