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Our current studies, designed to determine the role of VP-16 independently of CsA in this effect show that increased dose intensity of VP-16, in the absence of CsA, improves the frequency of 60 day survival of treated mice but impairs the ability of 60 day surviving mice to reject L1210 leukemia challenge.
Radiosurgery can obliterate 80-90% of small arteriovenous malformations, but no information exists on the survival of treated compared with untreated patients.
We observed increased survival of treated mice in all three survival endpoint studies: the AM5512 model (Fig. 4a), the AM7577 model (Fig. 4b), and the AM8096 model (Fig. 4c).
We have previously shown that immune tolerance induced by the anti-DNA Ig peptide pCons in (NZB × NZW F1 (NZB/W) lupus mice prolonged survival of treated animals and delayed the appearance of autoantibodies and glomerulonephritis.
The utilization of in-house engineered nano-formulation was also successful in significantly up-regulating Bax and down-regulating bcl-2 gene expression eventually helping in better survival of treated mice.
At the end of the experiments there was no incidence for toxicity comparing the survival of treated animals with the untreated controls.
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T, mean survival time of treated diabetic group; C, mean survival time of untreated diabetic group.
The survival rate of treated mice was 8/8 in the PM4 group, compared to 3/8 in the paclitaxel group.
The survival rate of treated seedlings decreased with increase of colchicine concentration.
OD was expressed as percentage cell survival (absorbance of treated wells/absorbance of control wells × 100).
The survival fractions of treated cells were determined using the ratio of the number of colonies formed/number of cells seeded × plating efficiency.
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