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Finally, we review state-of-the-art genomics and new techniques such as high-throughput sequencing and genome-wide chromatin assays, rapidly evolving techniques which have allowed epigenetic changes to be characterized at the genome level.
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These results suggest that the regulation of the initiation process at the origin might indeed be dependent on the growth rate and that these changes still remain to be characterized quantitatively before they can be included in a theoretical model.
Although we have consistently shown that acute administration of various doses of METH can cause substantial alterations in gene expression [ 14- 16, 47], the epigenetic events involved in these changes have yet to be characterized.
In two of the families, the copy number change was the second mutation to be characterized.
In both families, the copy number change was the second mutation to be characterized and shown to have been inherited from one of the healthy carrier parents.
Each of these myocardial tissue changes can be characterized using different magnetic resonance imaging (MRI) approaches.
In addition, the molecular changes can be characterized as intermediate endpoints of response.
Some of these changes have been characterized to provide a clear contribution to the development and/or progression of the cancer and include overexpression of HER2/neu in about 20% of breast cancer [1], and hereditary mutations in BRCA1 or BRCA2 in approximately 5% of breast cancers [2].
Baseline and changes to organ failure were characterized by the Sequential Organ Failure Assessment (SOFA) score[ 25].
The Te and Ne response to solar activity changes is characterized by a linear dependence.
Preventive medication changes were characterized to identify patients who stopped, decreased dose, remained off, or added/increased doses of preventive medications.
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