Modelo de regressao Weibull discreto com fracao de cura em dados de sobrevivencia

This paper presents a regression model for discrete time data with cure fraction. For this purpose, we considered a mixture model, in which times are modeled through the discrete Weibull distribution and the cure probability modeled with covariates by using the logit link function. Considering that the model is a mixture, the estimation of the parameters was performed by EM algorithm. The behavior of the estimating algorithm was tested with Monte Carlo simulation experiments and an application for real data was added.Este trabalho apresenta a formulacao de um modelo de regressao para dados de tempo discretos com fracao de cura. Para tanto, foi considerado um modelo de mistura, no qual os tempos sao modelados através da distribuicao Weibull discreta e a probabilidade de cura é modelada a partir de covariáveis utilizando a funcao de ligacao logito. Por se tratar de um modelo de mistura a estimacao dos parametros do modelo é feita via o algoritmo EM. O comportamento do algoritmo de estimacao é testado com vários experimentos de simulacao Monte Carlo e uma aplicacao em dados reais foi adicionada

Procedure for short-lived particle detection in the OPERA experiment and its application to charm decays

The OPERA experiment, designed to perform the first observation of $\nu_\mu \rightarrow \nu_\tau$ oscillations in appearance mode through the detection of the $\tau$ leptons produced in $\nu_\tau$ charged current interactions, has collected data from 2008 to 2012. In the present paper, the procedure developed to detect $\tau$ particle decays, occurring over distances of the order of 1 mm from the neutrino interaction point, is described in detail. The results of its application to the search for charmed hadrons are then presented as a validation of the methods for $\nu_\tau$ appearance detection

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Active Pin1 is a key target of all-trans retinoic acid in acute promyelocytic leukemia and breast cancer

A common key regulator of oncogenic signaling pathways in multiple tumor types is the unique isomerase Pin1. However, available Pin1 inhibitors lack the required specificity and potency. Using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but its drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site. ATRA-induced Pin1 ablation degrades the fusion oncogene PML-RARα and treats APL in cell and animal models and human patients. ATRA-induced Pin1 ablation also inhibits triple negative breast cancer cell growth in human cells and in animal models by acting on many Pin1 substrate oncogenes and tumor suppressors. Thus, ATRA simultaneously blocks multiple Pin1-regulated cancer-driving pathways, an attractive property for treating aggressive and drug-resistant tumors