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MAF?26Mo2
MAF?26Mo2

... clarify that the product is only for maintenanceof cholesterol levels that are already within the normal range. The sameprinciple applies to your claim about healthy sugar balance; that is, a claim that does not establish that the claim is about blood sugar that is already within normal limits impli ...
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Mersyndol (with codeine)

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issue highlights

... of suppressed recombination in the fungus Neurospora tetrasperma. They discover a series of three inversions within the nonrecombining region, formulate a model for its evolution, and examine the consequences of suppressed recombination for the genes residing within it. Quantification of inbreeding ...
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Non-selective CNS depressants ©2010 Mark Tuttle Non
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to our crestor information package

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Biotech drugs: biological therapeutic agents

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... Alterations in the VKORC1 gene can affect the ability of warfarin to impair the activity of the vitamin K-dependent factors and, therefore, alter response to therapy.9 VKORC1 variants (polymorphisms) are thought to ac­count for as much as 25% of the interindividual variation in re­quired warfarin do ...
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Nós médicos seguimos o lema: “Deixar de aprender é omitir socorro”

... ibuprofen (20.3%) was lower than for acetaminophen with codeine (31.0%), though not statistically significant (difference=10.7%; 95% confidence interval -0.2 to 21.6). The proportion of children who had any function (play, sleep, eating, school) affected by pain when pain was analyzed by day after i ...
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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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