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Possibly, similar mechanisms counteracted the expansion of gene-protected cells in the presence of ongoing virus replication in the mouse experiment described here.
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The study protocol MO08M334 "Evaluating vaginal microbicides in mice", which is specific for the mouse experiments described in this study, was approved by the Johns Hopkins University Animal Care and Use Committee (i.e. the Johns Hopkins Animal Ethics Committee) Chaired by Nancy A. Ator.
All mouse experiments described in this study were conducted according to the national (Belgian Law 14/08/1986 and 22/12/2003, Belgian Royal Decree 06/04/2010) and European (EU Directives 2010/63/EU, 86/609/EEG) animal regulations.
The mouse experiments described in this paper have been permitted by the Animal Care Committee of Rhineland-Palatinate (Koblenz, Germany) with the permit No. AZ 23 177-07/G 1231-043.
The growth of poxviruses in embyonated eggs and the mouse experiments described below were approved by the Animal Research Ethics Committee in the Faculty of Health Sciences, University of Cape Town.
To analyse whether mice vaccinated with liposomal vaccine preparations were protected against repeated tumour challenge, mice from the experiment described above that had rejected initial tumour challenge were re-challenged after day 96 by i.v. injection of Renca-lacZ/ErbB2 cells.
Assays were performed on the lungs from mice from the experiment described in Figure 6.
However, we failed to detect tumor cells in the sections of femora and tibiae from either the control or the treated mice in our experiment described in Figure 6.
A reduction in SOD1 activity is not causative for ALS (which is certainly what the mouse data show), however, it may modify disease, as suggested by results from the mouse cross experiments described above.
Although AxCA-IFN effectively suppressed tumour growth as shown in our previous study (Hatanaka et al, 2004) and Figure 1, complete tumour regression was observed in only one of six mice, and in the particular experiment described here, one of the six mice failed to respond to AxCA-IFN.
In contrast to Canault et al., and seemingly at variance with their findings with p55−/− mice, loss of TNF-α did not alter lesion development in female C57/BL6 mice in experiments described by Schreyer et al., while LTα deficiency resulted in a marked 62% reduction in lesion size.
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