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HIGHLIGHTS OF PRESCRIBING INFORMATION Peripheral vascular disease (4) •
HIGHLIGHTS OF PRESCRIBING INFORMATION Peripheral vascular disease (4) •

... The recommended starting dose of ZOMIG is 1.25 mg or 2.5 mg. The 1.25 mg dose can be achieved by manually breaking the functionally-scored 2.5 mg tablet in half. The maximum recommended single dose of ZOMIG is 5 mg. In controlled clinical trials, a greater proportion of patients had headache respons ...
INTERFERONS, ALPHA - DavisPlus
INTERFERONS, ALPHA - DavisPlus

... 5 days, with recovery 3– 5 days after withdrawal of interferon alpha-2b For malignant melanoma, if granulocyte count ⬎250/mm3 but ⬍500/mm3, discontinue interferon alpha-2b until platelet or granulocyte counts return to normal or baseline levels, then reinstitute at 50% of dose. If granulocyte count ...
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How do you write 23 using only the number 2?

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... exon 7 and 3’ flanking region. Sac II revealed two alleles (A and B) with three different restriction patterns or genotypes (AA, AB and BB) (Fig. 2). The β-LG AB genotype had two restriction sites and generated three bands i.e. 427 bp, 349 bp and 78 bp. The β-LG BB genotype with only one restriction ...
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get PDF - cadisp

... One CAD family carrying a mutation in the COL3A1 gene, usually responsible for vEDS, was reported, but none of the family members had typical clinical features of vEDS (21). Tentative candidate loci were identified on chromosomes 15q24 and 10q26 in another family with inherited dermal connective tis ...
monohybrid cross
monohybrid cross

... meaning single); that is, a cross between organisms that are heterozygous at a single genetic locus, for example, eye colour in blowflies and flower colour in snapdragons. ...
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Pharmacogenomics

Pharmacogenomics (a portmanteau of pharmacology and genomics) is the study of the role of genetics in drug response. It deals with the influence of acquired and inherited genetic variation on drug response in patients by correlating gene expression or single-nucleotide polymorphisms with drug absorption, distribution, metabolism and elimination, as well as drug receptor target effects. The term pharmacogenomics is often used interchangeably with pharmacogenetics. Although both terms relate to drug response based on genetic influences, pharmacogenetics focuses on single drug-gene interactions, while pharmacogenomics encompasses a more genome-wide association approach, incorporating genomics and epigenetics while dealing with the effects of multiple genes on drug response.Pharmacogenomics aims to develop rational means to optimize drug therapy, with respect to the patients' genotype, to ensure maximum efficacy with minimal adverse effects. Through the utilization of pharmacogenomics, it is hoped that drug treatments can deviate from what is dubbed as the “one-dose-fits-all” approach. It attempts to eliminate the trial-and-error method of prescribing, allowing physicians to take into consideration their patient’s genes, the functionality of these genes, and how this may affect the efficacy of the patient’s current and/or future treatments (and where applicable, provide an explanation for the failure of past treatments). Such approaches promise the advent of ""personalized medicine""; in which drugs and drug combinations are optimized for each individual's unique genetic makeup. Whether used to explain a patient’s response or lack thereof to a treatment, or act as a predictive tool, it hopes to achieve better treatment outcomes, greater efficacy, minimization of the occurrence of drug toxicities and adverse drug reactions (ADRs). For patients who have lack of therapeutic response to a treatment, alternative therapies can be prescribed that would best suit their requirements. In order to provide pharmacogenomic-based recommendations for a given drug, two possible types of input can be used: genotyping or exome or whole genome sequencing. Sequencing provides many more data points, including detection of mutations that prematurely terminate the synthesized protein (early stop codon).
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