Biomedical subjects

Kyung Min Lee

Publications and source records attributed to Kyung Min Lee.

3 recordsLinked to original sources

PubMed2025

Comparisons of Methods for Mucus Sampling and Mucin Semi-Quantification on Barramundi (Lates calcarifer) and Atlantic Salmon (Salmo salar) Epithelial Sites.

Fish epithelial surfaces are covered by a mucus layer. The highly glycosylated proteins called mucins are a main component of the mucus, which also contains a range of antibacterial enzymes, proteins, and peptides of importance for its protective properties. Here, we compared the practicality and yield of mucus harvesting from barramundi and Atlantic salmon epithelial sites using glass slide, swab, Super·SAL™ and whole tissue extract. We also compared the feasibility of using the orcinol assay, a glycan-on-membrane assay, and absorbance at 230 nm in combination with standard curves of pig gastric mucin to estimate the mucin concentration. Glycomics demonstrated that non-amine hexose content differed more between fish and tissues than terminal monosaccharides with cis-hydroxy groups, and that non-mucin molecules had a major impact on the A230-based results, making the glycan-on-membrane assay the most versatile method for estimating mucin concentration. We conclude that the most versatile tool for mucus harvesting was swabs, allowing for sufficient amounts of sample to be harvested with relative ease and low levels of contamination from the oral cavity, gill, skin, and intestine. Furthermore, the glycan-on-membrane assay was useful for measuring mucus concentration, and it was beneficial to estimate both sample concentration and purity by comparing samples at relatively similar concentrations.

Animals↗

PubMed2025

Germline Variants Influence Chronic Liver Disease Progression through Distinct Pathways.

Cirrhosis and hepatocellular carcinoma (HCC) are long-term complications of chronic liver disease (CLD). In this large multi-ancestry genome-wide association study of all-cause cirrhosis (35,481 cases, 2.36M controls) and HCC (6,680 cases, 1.76M controls), we identified 27 loci associated with cirrhosis (10 novel) and 11 with HCC (three novel). Three novel cirrhosis loci were replicated in independent cohorts (e.g. FGF21, RPTOR, and IFNL3/4). Fifteen cirrhosis loci exhibited differential effects on cirrhosis risk via underlying etiologies, and six HCC loci influenced HCC risk indirectly via cirrhosis. In a gene-burden analysis of rare variants from whole-genome sequencing data in the VA Million Veteran Program (n=102,677), we identified GSTA5 as a novel cirrhosis-associated gene, while APOB and ATP9B were associated with and replicated for HCC. A high genetic risk score for cirrhosis was associated with a nearly doubled risk of CLD progressing to cirrhosis (HR=1.94, P=2×10-68) and of cirrhosis progressing to HCC (HR=1.65, P=7×10-08). Finally, among individuals with chronic hepatitis C who underwent antiviral therapy, cirrhosis risk was modified by variants in PNPLA3, IFNL3/4, and CD81 following pegylated interferon-α therapy, and by APOE lead variant following direct-acting antiviral therapy. These findings provide new insights into the complex genetic architecture of CLD progression with potential clinical and therapeutic implications.

Journal Article↗

PubMed2025

Genomics-informed drug-repurposing strategy identifies two therapeutic targets for preventing liver disease associated with metabolic dysfunction.

Identification of drug-repurposing targets with genetic and biological support is an economically and temporally efficient strategy for improving the treatment of diseases. We employed a cross-disciplinary approach to identify potential therapeutics for the prevention of metabolic-dysfunction-associated steatotic liver disease (MASLD) in at-risk individuals by using humans as a model organism. We identified 212 putative candidate genes associated with MASLD by using data from a large multi-ancestry genetic association study, of which 158 (74.5%) were previously unreported. From this set, we identified 57 genes that encode for druggable protein targets and for which the effects of increasing genetically predicted gene expression on MASLD risk align with the function of that drug on the protein target. We then used We then evaluated these potential targets for evidence of efficacy by using Mendelian randomization, pathway analysis, and protein structural modeling. Through these approaches, we present compelling evidence to suggest that the activation of FADS1 by icosapent ethyl, as well as S1PR2 by fingolimod, could be a promising therapeutic strategy for MASLD prevention.

Humans↗