The Effect of Additional Follow-up and Accrual on Survival Time Data

Biometrics ◽  
1985 ◽  
Vol 41 (1) ◽  
pp. 129 ◽  
Author(s):  
Ron Brookmeyer ◽  
Steven G. Self
Keyword(s):  
Survival Time ◽  
Time Data ◽  
Survival Time Data

Development and validation of a prognostic model for survival time data: application to prognosis of HIV positive patients treated with antiretroviral therapy

2004 ◽  
Vol 23 (15) ◽  
pp. 2375-2398 ◽  
Author(s):  
Margaret May ◽  
Patrick Royston ◽  
Matthias Egger ◽  
Amy C. Justice ◽  
Jonathan AC Sterne ◽  
...  
Keyword(s):  
Antiretroviral Therapy ◽  
Survival Time ◽  
Prognostic Model ◽  
Hiv Positive ◽  
Time Data ◽  
Data Application ◽  
Development And Validation ◽  
Survival Time Data

Interactions of increased pO2 and pCO2 effects in producing convulsions and death in mice

1961 ◽  
Vol 16 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John R. Marshall ◽  
Christian J. Lambertsen
Keyword(s):  
Carbon Dioxide ◽  
High Pressure ◽  
Blood Flow ◽  
Latent Period ◽  
Survival Time ◽  
Brain Blood Flow ◽  
Time Data ◽  
Cortical Depression ◽  
Survival Time Data ◽  
Very High

In 379 mice subjected to from 1 to 11 atm. of pO2 and 0 to 304 mm Hg of pCO2 for 90 minutes, oxygen was convulsigenic at pressures greater than 3 atm. and lethal at greater than 4 atm. Carbon dioxide in 1 atm. of O2 was not convulsigenic but was lethal at very high tensions. In the presence of O2 at high pressure (OHP) small elevations of CO2 tension shortened the preconvulsive latent period, whereas CO2 tensions greater than 120 mm Hg inhibited convulsions. Survival time in OHP was shortened by the addition of CO2. An interaction between OHP and CO2 effects is suggested by both the preconvulsive latent period and survival time data. The effects of CO2 on OHP and electroshock convulsions are compared and possible reasons for differences are discussed in light of the previously demonstrated general cortical depression and inhibition of convulsions by CO2. The potentiation of OHP convulsions by low CO2 tensions is probably due to effects on brain blood flow. Although death can occur without convulsions there is a tendency for animals susceptible to convulsions to be also susceptible to the lethal properties of OHP with CO2. Submitted on July 28, 1960

Correlated gamma frailty models for bivariate survival time data

2018 ◽  
Vol 28 (10-11) ◽  
pp. 3437-3450
Author(s):  
Adelino Martins ◽  
Marc Aerts ◽  
Niel Hens ◽  
Andreas Wienke ◽  
Steven Abrams
Keyword(s):  
Survival Time ◽  
Frailty Models ◽  
Current Status Data ◽  
Current Status ◽  
Mortality Data ◽  
Time Data ◽  
Additive Decomposition ◽  
Bivariate Survival ◽  
Gamma Frailty ◽  
Survival Time Data

Frailty models have been developed to quantify both heterogeneity as well as association in multivariate time-to-event data. In recent years, numerous shared and correlated frailty models have been proposed in the survival literature allowing for different association structures and frailty distributions. A bivariate correlated gamma frailty model with an additive decomposition of the frailty variables into a sum of independent gamma components was introduced before. Although this model has a very convenient closed-form representation for the bivariate survival function, the correlation among event- or subject-specific frailties is bounded above which becomes a severe limitation when the values of the two frailty variances differ substantially. In this article, we review existing correlated gamma frailty models and propose novel ones based on bivariate gamma frailty distributions. Such models are found to be useful for the analysis of bivariate survival time data regardless of the censoring type involved. The frailty methodology was applied to right-censored and left-truncated Danish twins mortality data and serological survey current status data on varicella zoster virus and parvovirus B19 infections in Belgium. From our analyses, it has been shown that fitting more flexible correlated gamma frailty models in terms of the imposed association and correlation structure outperforms existing frailty models including the one with an additive decomposition.

scholarly journals Reversal of Resistance to Methotrexate in L1210 Murine Leukemia by Uracil

Blood ◽  
1971 ◽  
Vol 38 (5) ◽  
pp. 648-656
Author(s):  
HARRY WALLERSTEIN ◽  
LEWIS M. SLATER ◽  
BEN ENG ◽  
NEIL CALMAN
Keyword(s):  
Survival Time ◽  
Dihydrofolate Reductase ◽  
Thymidine Incorporation ◽  
Tritiated Thymidine ◽  
L1210 Leukemia ◽  
Time Data ◽  
Multiple Generations ◽  
Methotrexate Resistance ◽  
Survival Time Data

Abstract BDF1 mice bearing L1210 leukemia, when treated with a regimen of uracil and methotrexate, show an increase in survival time greater than when treated with methotrexate alone. The uracil and methotrexate regimen also delays the development of methotrexate resistance as L1210 leukemia is transferred with therapy through multiple generations of mice. When uracil is applied to multiple generations of mice bearing tumor resistant to methotrexate, there is a return to sensitivity to methotrexate. It is also noted that uracil blocks the responsiveness of L1210 leukemia to 6-mercaptopurine. The responsiveness of these tumor lines to the addition of uracil in their regimens was monitored by in vitro tritiated thymidine incorporation into DNA and by dihydrofolate reductase activities. These data, when integrated with survival time data, suggest that in part, the reported results are mediated by a uracil-induced reduction in the availability of dihydrofolate reductase and phosphoribosylpyrophosphate.

Joint Modelling of Repeated Measures and Survival Time Data

2003 ◽  
Vol 45 (6) ◽  
pp. 647-658 ◽  
Author(s):  
Il Do Ha ◽  
Taesung Park ◽  
Youngjo Lee
Keyword(s):  
Survival Time ◽  
Repeated Measures ◽  
Time Data ◽  
Joint Modelling ◽  
Survival Time Data
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