PRISMΔDB

Analyze how specific documents activate the features of the SAE. Select a dataset, a run and a document to begin.

Active Features

1502

0.0
Details List
#690 Feature 690
2.8
#1863 Feature 1863
2.5
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2.4
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2.3
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2.3
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2.2
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2.2
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2.1
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2.0
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1.9
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1.9
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1.9
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1.9
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1.9
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1.8
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1.8
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1.8
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1.8
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1.8
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1.8
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1.8
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1.8
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1.7
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1.7
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1.7
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1.7
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1.6
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1.6
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1.6
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1.6
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1.6
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1.5
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1.5
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1.5
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1.5
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1.5
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1.5
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1.5
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1.5
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1.5
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
#708 Drug Resistance Mechanisms in Cancer
0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.7
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0.7
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Document Content

Mycophenolate mofetil and daclizumab targeting T lymphocytes in bleomycin-induced experimental scleroderma.
T lymphocytes induce the transformation of fibroblasts into myofibroblasts, the main mediators of fibrogenesis. The inosine 5'-monophosphate dehydrogenase inhibitor mycophenolate mofetil (MMF) and the anti-CD25 monoclonal antibody daclizumab (DCZ) have been reported to suppress the proliferation of T lymphocytes. To evaluate the preventive effects of MMF and DCZ in early stages of bleomycin (BLM)-induced scleroderma. This study involved five groups of Balb/c mice (n = 10 per group). Mice in four of the groups were injected subcutaneously (SC) with BLM [100 μg/day in 100 μL phosphate-buffered saline (PBS)] for 4 weeks; the remaining (control) group received only 100 μL PBS. Three of the BLM-treated groups also received either intraperitoneal MMF 50 or 150 mg/kg/day, or SC DCZ 100 μg/week. At the end of the fourth week, all mice were killed, and blood and tissue samples were obtained for further analysis. In the BLM-treated group, increases were seen in inflammatory-cell infiltration, α-smooth muscle actin-positive (α-SMA+) fibroblastic cell count, tissue hydroxyproline content, and dermal thickness. Dermal fibrosis was histopathologically prominent. In BLM-treated mice also given MMF or DCZ, inflammatory-cell infiltration, tissue hydroxyproline content and dermal thickness were decreased. In the MMF groups, decreases were also noted in α-SMA+ fibroblastic cell count. In this BLM-induced dermal fibrosis model, MMF and DCZ treatments prevented the development of dermal fibrosis. Further studies are needed to evaluate whether targeting T lymphocytes is effective in resolving pre-existing fibrosis in human scleroderma.