Winmaximizer 1.6.35 Keygen.rar
Winmaximizer 1.6.35 Keygen.rar
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Winmaximizer 1.6.35 Keygen.rar
Winmaximizer 1.6.35 Keygen.rar (2.1MB)
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Resolved class-path is still included in a jar, but it is automatically unarchived
I have tried to resolve the class-path for a maven JAR file, that includes a couple of other JAR files.
The problem is that the final jar I want to pack has this included, as the final jar with reduced class-path will be treated as a secondary JAR, which is not what I want.
This is what I have tried:
1st step
mvn install
2nd step
mvn install:resolve-only -Dincludes=**\*
3rd step
mvn package
Here is an excerpt of the original jar file
Manifest-Version: 1.0
Created-By: 1.6.0_11 (Sun Microsystems Inc.)
Main-Class: com.example.Main
Class-Path: mypackage1-0.0.0.jar mypackage2-1.0.0.jar mypackage3-0.0.0.jar
Which results in:
[INFO] [INFO] — maven-install-plugin:2.4:install (default-install) @ my-package —
[INFO] Installing C:\Program Files\Java\jdk1.6.0_11\jre\lib\ext\mysql-connector-java-5.0.8-bin.jar to C:\Users\Jonas\tmp\my-package\target\my-package-0.0.0.jar
[INFO] Installing C:\Program Files\Java\jdk1.6.0_11\jre\lib\ext\jdbc-libs.jar to C:\Users\Jonas\tmp\my-package\target\my-package-0.0.0.jar
[INFO] Installing C:\Program Files\Java\jdk1.6.0_11\jre\lib\ext\jrockit-jdk13-v71.jar to C:\Users\Jonas\tmp\my-
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Yes, see:
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Mutation of p34cdc2 is associated with the development of epithelial dysplasia in oral leukoplakia.
Mutations in the p34(cdc2) gene play a significant role in the development of many human cancers. However, the prevalence of p34(cdc2) mutations in oral leukoplakia (OL), a major precancer lesion of the oral cavity, and their role in the carcinogenesis of OL have not yet been investigated. We studied the mutation status of the p34(cdc2) gene using polymerase chain reaction single strand conformation polymorphism and DNA sequencing in 79 oral precancer lesions, including 26 OL. Of these, 14 exhibited complete mutation of the gene. Among these, 11 OL exhibited hyperkeratosis, 13 OL presented with various degrees of dysplasia, and 2 OL showed both clinical and histological features of epithelial dysplasia. Five (38%) cases with epidermal lesions (hyperkeratosis, hyperkeratosis with dysplasia, and dysplasia) had mutations in the p34(cdc2) gene. There was a strong correlation between p34(cdc2) mutation and the increasing severity of epithelial lesions, as well as with the clinical stages of OL. In conclusion, the frequency of p34(cdc
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