By Ma Li Wong, Julio Licinio, Ma-Li Wong
This paintings represents the 1st finished ebook within the leading edge box of pharmacogenomics, a box that's set to revolutionize pharmaceutical learn. as well as well known editors, the record of members is a "who-is-who" within the box. vast assurance of all points of pharmacogenomics with a whole presentation of functions to ailment stipulations is featured. someone excited about pharmaceutical study and drug improvement wishes this ebook to maintain with this new and progressive technique
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Additional info for Pharmacogenomics: The Search for Individualized Therapies
Sample text
The black dots denote the site of termination of the sodium channel. 2. XXXV XXXVI Color Plates Fig. 2 Chronic lithium and valproate robustly increase bcl-2 immunoreactive neurons in the frontal cortex. p. injections for four weeks. Rats brains were cut at 30 lm; serial sections were cut coronally through the anterior portion of the brain, mounted on gelatincoated glass slides and were stained with thionin. 3% Triton X-100 (Sigma, St. Louis, MO). Subsequently, the immunoreaction product was visualized according to the avidin-biotin complex method.
3 Pharmacogenomics – Hope or Hype? At present, genetic testing is restricted to a limited number of patients or volunteers in academic institutions and clinical drug trials, although evidence is accumulating that prospective testing could be of major benefit to many patients [11]. The lack of large prospective studies to evaluate the impact of genetic variation on drug therapy is one reason for the slow acceptance of these principles. Phenotyping tests require the administration of a specific marker drug or test drug, collection of urine, blood, or saliva for analysis of drug and metabolite concentrations.
The multidrug resistance gene MDR1, are subject to genetic variation. Adverse drug reactions in individual subjects and members of their families often were the clinical events that revealed genetic variants of these and other drug-metabolizing enzymes or drug targets (reviewed in [5–8]). All these observations dealt with variations of specific genes or polymorphisms. Genetic polymorphisms are monogenic variations that exist in the normal population in a frequency of more than 1% [9]. One reason for the pre-occupation of pharmacogenetics with single genes is that they were easier to study with the classical genetic techniques and many of them were clinically important.
