FULL Jeppesen FliteStar V941 JeppView V361 FliteDeck Chart Training
A:
It seems like Jeppesen have migrated their content to the new Jeppesen Learning Platform – which means if you have any Jeppesen Learning products (e.g. Jeppesen or Jeppesen Student) the content is now located at If you have any questions, feel free to contact us at techsupport@jeppesen.com
A:
I have checked in “Jeppesen Standard Airway Manual” and it’s not possible to download the file.
You are better of printing out the whole manual and print it yourself.
Migrating genomic mutations in acute and chronic myeloid leukemia: relation to chronic phase relapse.
Several genes that are involved in the regulation of growth and survival of normal hematopoietic cells, such as BCR-ABL, MYC, KIT, and MLLT1 have been shown to be involved in the pathogenesis of chronic myeloid leukemia (CML). We have evaluated the role of genes involved in the regulation of cellular growth and apoptosis (RARA, FOS, PIM1, ERG, ARNT, MPL, CCAAT/enhancer binding protein alpha, STAT1, and STAT3) in 54 patients with de novo CML and in 8 patients with CML in evolution towards blast crisis (BC). All the patients were either in chronic phase (CP) or in CP relapsed after initial treatment. DNA from each patient was studied by Southern blot hybridization for the presence of mutations in TEL and other genes which have been identified as relevant in CML. Results showed that 63.0% of CML in CP and 75.0% of CML in CP relapsed after initial treatment had a mutation in a gene not involved in the regulation of apoptosis and/or growth (p=0.7). The study of the mutation patterns showed a significantly higher number of mutations in BCR-ABL, PIM1, and MPL genes in CML in CP relapsed after initial treatment. Whereas mutations in genes involved in the regulation of growth and apoptosis were detected in all patients studied, additional mutations were found in genes not implicated in the regulation of the growth and/or survival of hematopoietic cells (TEL, MPL, CCAAT/enhancer binding protein alpha, RARA, STAT1, and STAT
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