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Biology subjects

Baek, Y.

Publications and source records attributed to Baek, Y..

4 recordsLinked to original sources

10,239 whole genomes with multiomic and clinical health information as the Korean population multiomic reference dataset

We present Korea10K, the largest genomic dataset of the Korean population, comprising 10,239 high-coverage whole genomes (mean depth 30x) with matched multiomic profiles and phenotype data. Korea10K achieves complete and near-complete discovery of very rare and ultra-rare alleles, respectively, at 9,000 Korean genomes. This dataset provides the high-quality population-specific imputation panel, enabling accurate inference of low-frequency variants. Admixture analyses confirm the genetic homogeneity of the Korean population, despite its diverse Y-chromosomal, mitochondrial, and HLA repertoires. This pattern reflects a long and continuous lineage history characterized by persistent internal admixture and genomic homogenization over thousands of years on the Korean peninsula. We also identified 16.8 million genomic variants that directly modify CG sites by creating or abolishing CG dinucleotides, providing the population-scale evidence of coordinated genomic-epigenomic regulatory mechanism in Koreans.

genomics↗

Impact of Membrane Fluidity on α-syn Fibril Structures and Neuronal Pathology

Conformational variations in -syn fibrils are thought to underlie the distinct clinical features of synucleinopathies, including Lewy body dementia (LBD), Parkinsonss disease (PD), and multiple system atrophy (MSA), suggesting that distinct fibril structures act as molecular fingerprints linked to disease phenotype. While the origins of these conformational variations remain unclear, increasing evidence points to membranes as key modulators of fibrils conformations. In this study, we investigated how age-related alterations in membrane composition and fluidity influence -syn fibril formation and cellular outcomes. Using complex mixture membranes that mimic normal neuronal membranes and their age-related modifications in fatty acid chains, we found that -syn fibrils grown with these membranes displayed distinct 2D ssNMR spectral patterns compared to lipid-free -syn fibrils, reflecting differences in rigid fibril cores. Moreover, fibrils grown with age-related membranes exhibited weaker membrane association than those grown with normal neuronal membranes. These membrane-associated fibrils induce stronger neuronal pathologies than lipid-free fibrils, though the severity differed in intraneuronal aggregation and inflammation responses. Overall, our findings provide new insights into how age-related changes in membrane composition shape -syn fibril structure and pathogenicity, strengthening the link between membrane dynamics and amyloid-driven neurodegeneration.

molecular biology↗

Microphysiological engineering of the capillary interface of substantia nigra dopaminergic neurons to study vascular alterations in Parkinson's Disease

Parkinsons Disease (PD) is primarily characterized by -synuclein pathology, which manifests as intraneuronal inclusions, neuroinflammation, and neurodegeneration. However, emerging evidence also points to significant vascular impairments as a critical aspect of PD pathology, which remains largely underexplored due to the inability of traditional in vitro models to recapitulate such vascular changes. To address this unmet need, here we combine the human organ-on-a-chip technology with the principle of vasculogenic self-assembly to engineer the capillary interface of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. In our proof-of-concept demonstration, we successfully recreated critical neuronal pathology in PD, including -synuclein aggregation, inflammatory responses, and progressive neuronal degeneration, by exposing our model to specially generated PD-associated -synuclein preformed fibrils. Importantly, this engineering approach also enables the investigation of progressive vascular changes characteristic of PD, such as endothelial dysfunction, barrier disruption, and vascular regression. Our sophisticated PD model establishes a novel platform for exploring the multifaceted nature of the disease and understanding the complex interplay between neurodegeneration and vascular pathology, offering a unique tool for developing innovative therapeutic strategies that address both the neuronal and vascular components of PD pathology.

bioengineering↗

Rapid antimicrobial susceptibility test using spatiotemporal analysis of laser speckle dynamics of bacterial colonies

Antimicrobial susceptibility testing (AST) is crucial for providing appropriate choices and doses of antibiotics to patients. However, standard ASTs require a time-consuming incubation of about 16-20 h for visual accumulation of bacteria, limiting the use of AST for an early prescription. In this study, we propose a rapid AST based on laser speckle formation (LSF) that enables rapid detection of bacterial growth, with the same sample preparation protocol as in solid-based ASTs. The proposed method exploits the phenomenon that well-grown bacterial colonies serve as optical diffusers, which convert a plane-wave laser beam into speckles. The generation of speckle patterns indicates bacterial growth at given antibiotic concentrations. Speckle formation is evaluated by calculating the spatial autocorrelation of speckle images, and bacterial growth is determined by tracking the autocorrelation value over time. We demonstrated the performance of the proposed method for several combinations of bacterial species and antibiotics to achieve the AST in 2-4.5 hours. Furthermore, we also demonstrated the sensitivity of the technique for low bacterial density. The proposed method can be a powerful tool for rapid, simple, and low-cost AST. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/853168v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@8ee314org.highwire.dtl.DTLVardef@de47c5org.highwire.dtl.DTLVardef@13a0103org.highwire.dtl.DTLVardef@118ad36_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗