Publications by authors named "A A Zharikova"
Patients with genetically-based hyperlipidemias exhibit a wide phenotypic variability. Investigation of clinical and biochemical features is important for identifying genetically-based hyperlipidemias, determining disease prognosis, and initiating timely treatment. We analyzed genetic data from 3374 samples and compared clinical data, lipid levels (low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, triglycerides, and lipoprotein (a)), frequency, age at onset of coronary heart disease (CHD), and the severity of carotid and femoral atherosclerosis (plaque number, maximum stenosis, total stenosis, maximum plaque height, and plaque score) among patients with familial hypercholesterolemia (FH), familial dysbetalipoproteinemia (FD), polygenic hypercholesterolemia (HCL), severe HCL, and those without lipid disorders (n = 324).
View Article and Find Full Text PDFFamilial dysbetalipoproteinemia (FD) is a highly atherogenic, prevalent genetically based lipid disorder. About 10% of FD patients have rare variants associated with autosomal dominant FD. However, there are insufficient data on the relationship between rare variants and FD.
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- * Among 82 LQTS patients, a 75% diagnostic yield was found in those with high Schwartz scores, while 50% of those with lower scores (<3.5) were diagnosed through broader genetic testing.
- * The findings suggest that the existing LQTS genetic diagnosis framework may not effectively capture cases with lower Schwartz scores, and additional rare variants could indicate more severe disease, pointing towards the need for improved referral criteria.
The ketogenic diet (KD) has been shown to be effective in treating various brain pathologies. In this study, we conducted detailed transcriptomic and metabolomic profiling of rat brains after KD and ischemic stroke in order to investigate the effects of KD and its underlying mechanisms. We evaluated the effect of a two-month KD on gene expression in intact brain tissue and after middle cerebral artery occlusion (MCAO).
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- * The HIV-1 protein Tat, released from infected cells, enters uninfected B cells and alters their gene expression, contributing to this increased lymphoma risk.
- * Research showed that while acute exposure to Tat reduces cell proliferation by downregulating certain genes, chronic exposure restores growth and enhances protective gene expression, suggesting a mechanism of adaptation that may influence lymphoma development in HIV-1 patients.