https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/287 Fri, 03 Jul 2026 08:25:27 GMT 2026-07-03T08:25:27Z https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/210987 Title: Toward a better measure of functional laterality: Comparing and refining laterality indices in resting-state functional connectivity Authors: Lee, Taeyoung; Kim, Kyung Hwan; Ha, Seo Yeong; Jo, Hang Joon Abstract: Systematic investigations into the lateralized human brain have revealed a bivariate functional architecture that underpins distinct cognitive processes. This architecture manifests through inter- and intra-hemispheric lateralization, captured respectively by neural integration and segregation. In this study, we conducted a comprehensive evaluation of multiple quantitative laterality metrics in resting-state fMRI connectivity, using conceptual models to illustrate how inter- and intra-hemispheric correlations shape functional lateralization. We further highlight the critical influence of factors such as correlation sign, correlation coefficient distribution, and statistical thresholding methodology on the interpretation of functional connectivity-based laterality indices. Our findings show that, in our dataset, laterality metrics based on positive-only functional connectivity with a lenient connection-level threshold most consistently capture established relationships between functional brain lateralization and performance in language and visuospatial domains. Sun, 01 Mar 2026 00:00:00 GMT https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/210987 2026-03-01T00:00:00Z https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/211881 Title: Hippocalcin Regulates NMDA Receptor Function and Neuronal Activity Through Elavl3 in Mouse Hippocampal Neural Precursor Cells Authors: Kang, Min-Jeong; Jung, Sung Jun; Son, Hyeon; Han, Joong-Soo; Park, Shin-Young Abstract: Hippocalcin (HPCA), a neuron-enriched calcium-binding protein, plays a critical role in brain function, but its role in neural precursor cells remains unclear. N-methyl-D-aspartate (NMDA) receptors are calcium-permeable glutamate receptors essential for neurodevelopment and synaptic plasticity, and their function has been implicated in neurological conditions. In this study, we investigated the role of HPCA in regulating NMDA receptor expression and function in mouse hippocampal neural precursor cells (mHNPCs). HPCA knockdown significantly reduced the expression of NMDA receptor-related genes, including Grin2C, Shank1, Serpine2, and selectively attenuated NMDA-induced calcium signaling. Transcriptomic analysis identified ELAV-like RNA-binding protein 3 (Elavl3), a neuron-enriched factor associated with neuronal activity, as a downstream candidate affected by HPCA knockdown. Consistently, Elavl3 suppression phenocopied HPCA deficiency, resulting in impaired NMDA receptor activity and reduced neuronal differentiation. Furthermore, hippocampal HPCA knockdown in vivo led to alterations in locomotor activity, contextual memory, and affective behaviors. Taken together, these findings demonstrate that HPCA supports NMDA receptor function and neuronal development, in part through Elavl3-associated pathways, and highlight HPCA as an important regulator of hippocampal function. Sun, 01 Mar 2026 00:00:00 GMT https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/211881 2026-03-01T00:00:00Z https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/209423 Title: Biologically calibrated and quantitative spiciness measurement based on a TRPV1-Responsive biosensing platform Authors: Yu, Seungwon; Kim, Minwoo; Han, Yiseul; Kim, Hyunsoo; Yeom, Kyung Tae; Jung, Sung Jun; Jang, Yongwoo Abstract: The Scoville Heat Unit (SHU) scale has long been regarded as the standard for measuring pungency. However, its reliance on subjective human sensory panels inherently limits its accuracy and reproducibility. To overcome this limitation, we developed a biologically grounded spiciness assessment platform based on the activation of the transient receptor potential vanilloid 1 (TRPV1) channel, a key pain receptor triggered by capsaicinoids and mediates the burning sensation associated with pungency. To establish a physiologically relevant spiciness index, we investigated the quantitative correlation between TRPV1-mediated calcium influx in primary sensory neurons and nocifensive behavior in mice, following exposure to both pure capsaicin and chili pepper extracts. By analyzing patterns in the conversion factor, we defined five biologically relevant spiciness ranges: undetectable, minimal response, transitional range, pungent, and oversaturation. To implement this index, we engineered a label-free, live cell-free biosensor by incorporating nanovesicles (NVs) containing functional TRPV1 receptors into an electrode. This sensor detected capsaicin-induced ionic flux through TRPV1 channels, producing voltage shifts with femtomolar sensitivity and high molecular specificity. Notably, the biosensor showed a strong correlation with cellular and behavioral assays and enabled the quantitative classification of chili extracts into five spiciness categories. Integration with a portable electronic reader enabled real-time, on-site classification of spiciness, offering an objective alternative to the subjective SHU scale. This study establishes a reproducible and physiologically relevant framework for quantifying spiciness based on receptor-level molecular recognition, offering alternative to traditional sensory and analytical methods with broad applications in food science, quality control, and consumer product development. Sun, 01 Feb 2026 00:00:00 GMT https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/209423 2026-02-01T00:00:00Z https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/210249 Title: Azelastine Inhibits Triple-Negative Breast Cancer Cell Viability via an ARF1-Dependent Mechanism Authors: Park, Seon Uk; Jung, Gi Ung; Paik, Eun Kyung; Lee, Jeong-Yeon; Cho, Dong Charn; Chung, Heekyoung; Jo, Hang Joon; Jung, Sung Jun Abstract: Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by a lack of targetable receptors, leading to limited treatment options and a critical need for novel therapeutic strategies. This study aimed to evaluate the potential of azelastine, a clinically approved H1-antihistamine, for drug repositioning against TNBC and to elucidate its underlying HRH1-independent mechanism of action. Cell viability assays (CCK-8) were performed on TNBC cell lines (MDA-MB-231 and BT-549) following treatment with azelastine and its major metabolite, desmethyl azelastine. After observing ambiguous clinical associations between HRH1 expression and patient prognosis, HRH1 dependency was assessed through histamine stimulation and HRH1 knockdown (siRNA). Subsequently, the role of ADP-ribosylation factor 1 (ARF1), found to be overexpressed in TNBC and linked to poor prognosis, was investigated using ARF1 knockdown (siRNA), co-treatment with the Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1 (GBF1) inhibitor golgicide A (GCA), and co-treatment with the Drp1 inhibitor M-divi 1. Azelastine and desmethyl azelastine potently reduced MDA-MB-231 cell viability in a dose- and time-dependent manner, achieving cell survivals of 61.3 ± 6.1% (30 µM) and 34.9 ± 3.7% (50 µM) for azelastine, and 52.4 ± 12.5% (30 µM) for desmethyl azelastine, respectively, after 72 h, with an IC50 of 35.93 µM determined for azelastine in MDA-MB-231 cells. Additionally, azelastine significantly reduced the viability of BT-549 cells. Bioinformatic analysis of clinical datasets revealed HRH1 downregulation in tumors and, functionally, neither histamine stimulation nor HRH1 knockdown mediated azelastine cytotoxicity in cell culture. Importantly, ARF1 expression was significantly upregulated in TNBC and associated with poor prognosis. Co-treatment with GCA, preventing ARF1 activation, restored viability to near-control levels, supporting dependence on the GBF1–ARF1 activation axis of azelastine, whereas the Dynamic-related protein 1 (Drp1) inhibitor M-divi 1 not only partially rescued CCK-8-based cell viability but also normalized azelastine-induced loss of MitoTracker™ Red CMXRos signal and partially preserved (4′,6-diamidino-2-phenylindole) DAPI-based cell density, indicating Drp1-dependent mitochondrial dysfunction. Furthermore, azelastine selectively reduced p-ERK phosphorylation in the cell signaling pathway. Azelastine exerts potent anticancer effects in TNBC cells via an HRH1-independent, ARF1-dependent mechanism that attenuates the Extracellular signal-regulated kinase (ERK)–Drp1 axis, and induces Drp1-dependent mitochondrial dysfunction, independent of its canonical HRH1 receptor function. This ARF1-dependent mechanism provides strong scientific rationale for the drug repositioning of azelastine as an effective therapeutic agent for ARF1-driven TNBC. Mon, 01 Dec 2025 00:00:00 GMT https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/210249 2025-12-01T00:00:00Z