Interactions of electrophoretically silent hemoglobin Hekinan II [HBA1:c.84G>T] with various forms of alpha-thalassemias and other hemoglobinopathies: novel insights into the molecular and hematological characteristics and genetic origins.
Distinct pattern and prevalence of Plasmodium falciparum dihydropteroate synthase gene mutations in children with sickle cell anaemia and haemoglobin AA in Benin City Nigeria: the impact of HbAA.
Choice of HbA1c threshold for identifying individuals at high risk of type 2 diabetes and implications for diabetes prevention programmes: a cohort study.
Investigating the changes in the levels of HbA1c blood fat and insulin sensitivity in elder patients with type II diabetes mellitus due to combined medication of pioglitazone and melbine and single-use of pioglitazone.
alpha-Thalassemia Intermedia Results from Interactions of Unstable Hb Prato [alpha31(B12)Arg-->Ser (HBA1 or HBA2 c.96G>T or C)] with the alpha-Thalassemia-1 [- -(SEA) (Southeast Asian)] Deletion in Thailand.
Relationship between glycated hemoglobin level and duration of hypoglycemia in type 2 diabetes patients treated with sulfonylureas: A multicenter cross-sectional study.
The clinical consequences of the Hb Milano variant differ based on the genotype: according to our study the hematological parameters range from a marked microcythemia with mild anemia if the variant is coinherited with an alpha gene deletion to mild microcytosis when the variant is not associated with alpha gene deletions.
Fasting glucose (FG) and glycated hemoglobin A1c (HbA1c) perform sub-optimally in people of African origin especially in individuals with sickle-cell trait (SCT). This study compared the relationships between HbA1c FG and fructosamine in individuals from Senegal with and without SCT.
The study concluded that HbA1c value correlate well with lipid profile in-diabetes patients. So HbA1c can be used as a predictor of dyslipidemia in type 2 diabetes.
In this new nonsense mutation short genetic products may suffer nonsense-mediated degradation whereas the abnormal protein will be eliminated through the proteolytic pathway mediated by ubiquitin
The frequency of the alpha-globin triplication was 1.7% and phenotype aggravation was observed in alpha-globin triplication Iranian patients who were carriers of beta-thalassemia.
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