Examples of using Genetic polymorphism in English and their translations into Bulgarian
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What is Genetic polymorphism.
The metabolism is subject to genetic polymorphism.
Key words: genetic polymorphisms, glutathione S-transferases.
This enzyme exhibits genetic polymorphism.
Key words: genetic polymorphisms, drug-metabolizing enzymes, drug transporters.
CYP 2D6 is subject to genetic polymorphism.
Patients with genetic polymorphisms affecting CYP3A4 and CYP3A5.
Both UGT1A9 andUGT2B4 are subject to genetic polymorphism.
Key words: cytokines, genetic polymorphisms, bipolar disorder.
Immune responses to the vaccine have not been studied in the context of genetic polymorphism.
Key words: cytokines, genetic polymorphisms, schizophrenia.
The expression of CYP3A and CYP3A4 may vary by as much as 40 fold due to genetic polymorphism.
The metabolism is subject to genetic polymorphism(CYP2D6 and CYP2C19)(see section 4.2).
Genetic polymorphisms of drug targets and disease-modifying genetic polymorphisms.
Not all inherited variants of haemoglobin are detrimental,a concept known as genetic polymorphism.
Key words: genetic polymorphisms, glutathione S-transferases, multifactorial diseases.
Not all the variants of the mutated hemoglobin are detrimental,a concept known as genetic polymorphism.
Confounding factors and genetic polymorphism in the evaluation of individual steroid profiling.
Dose adjustment is not considered necessary in subjects with reduced UGT1A1 activity due to genetic polymorphism.
CYP2D6 genetic polymorphism has minimal impact on the mean plasma exposure to mirabegron(see section 5.2).
Codeine is converted into morphine in the body by cytochrome P450 2D6(CYP2D6),an enzyme which shows genetic polymorphism.
Genetic polymorphisms of glutathione S-transferases in human population and association with multifactorial diseases.
UGT1A1 activity is reduced in individuals with genetic polymorphisms that lead to reduced enzyme activity such as the UGT1A1*28 polymorphism. .
In terms of other patient characteristics,a study in CYP2D6 poor metabolisers showed no evidence of a clinically significant effect of CYP2D6 genetic polymorphism on systemic exposure to umeclidinium.
Due to genetic polymorphism, slow and extensive metabolisers exist for this enzyme which could result in markedly increased plasma levels of lornoxicam in slow metabolisers.
A study in CYP2D6 poor metabolisers showed no evidence of a clinically significant effect of CYP2D6 genetic polymorphism on systemic exposure to umeclidinium bromide.
Inhibition of these enzymes or genetic polymorphisms(e.g. CYP2D6, CYP2C9 or CYP2C19) are not expected to result in clinically significant effects on cladribine pharmacokinetics or exposure.
The extent of metabolism of levocetirizine in humans is less than 14% of the dose andtherefore differences resulting from genetic polymorphism or concomitant intake of enzyme inhibitors are expected to be negligible.
Around 10% of patients are at higher risk of haematological complications(cytopoenia, or a decrease in white blood cells, red blood cells or platelets)due to a possible genetic defect(partial thiopurine methyltransferase- TPMT- deficiency also known as genetic polymorphism).
Cytochrome P450 2C9 activity is reduced in individuals with genetic polymorphisms that lead to reduced enzyme activity, such as those homozygous for the CYP2C9*3 polymorphism. .