Jae Kyeom Kim

Fragrant olive (Osmanthus fragrans var. aurantiacus (O. fragrans)) extract is known to influence neurophysiological responses through inhalation, yet research on concentration-dependent effects and sex-specific variations remains insufficient. This study utilized an electronic nose (E-nose), electroencephalography (EEG), and standardized low-resolution electromagnetic tomography (sLORETA) to characterize the volatile profiles and neurophysiological impacts of O. fragrans at 3% and 5% concentrations. E-nose analysis identified 48 volatile compounds, with chemometric modeling (PCA, HCA) showing clear discrimination between concentrations. EEG results demonstrated that inhalation induced significant concentration-dependent changes—specifically increasing sedation-related alpha waves and decreasing tension-related gamma waves—with 5% O. fragrans eliciting more widespread cortical responses than the 3% concentration. Notably, no significant sex-related differences were observed in general EEG patterns; however, sLORETA revealed that 5% inhalation specifically suppressed high beta and gamma activities in male participants within Brodmann areas 13, 21, 22, and 44, regions associated with emotional and multisensory processing. In conclusion, this study successfully quantified the relationship between volatile profiles and human brain responses using an integrated biomimetic and neurophysiological approach. These findings provide objective evidence that O. fragrans inhalation, particularly at 5%, modulates neural oscillations toward a relaxed state, offering valuable data for olfactory perception and potential applications as functional volatile compounds.

Buds are continuously renewed sensory organs in which development, adult maintenance, and repair share overlapping molecular circuitry. During embryogenesis, WNT/β-catenin signaling promotes taste placode formation and placodal Shh expression, while SHH refines papilla spacing and restricts neighboring papilla formation. SOX2 functions as a taste-competence and progenitor maintenance factor. In adults, LGR5/LGR6–RSPO–WNT signaling sustains progenitor activity, and gustatory neurons are an important source of RSPO2; available genetic evidence is consistent with a neuron-derived contribution to the LGR5/LGR6 niche, and AAV-Cre-mediated neuron-specific ablation of Rspo2 in the petrosal ganglion led to near-complete loss of circumvallate taste buds. HH signaling from epithelial and neuronal sources further supports SOX2-dependent progenitor homeostasis. Lineage allocation is governed by transcriptional programs that include POU2F3/SKN-1a for sweet, umami, and bitter type II taste receptor cells, and ASCL1 with posterior-field NKX2-2 for type III presynaptic/sour cells. After denervation or irradiation, regeneration depends primarily on LGR5⁺/KRT14⁺ progenitors and may be supplemented, in specific injury contexts, by plasticity of a subset of K8-lineage taste receptor cells that acquire KRT14/SOX2/PCNA progenitor-like features. Key unresolved questions include the direct chromatin targets of taste lineage regulators (which remain to be defined by ChIP-seq in native taste progenitors), the identity of the type I cell selector, the contribution of dedifferentiation across injury models, and the degree to which mouse-derived networks are conserved in human taste biology.

Taste buds are continuously renewed sensory organs in which development, adult maintenance, and repair share overlapping molecular circuitry. During embryogenesis, WNT/β-catenin signaling promotes taste placode formation and placodal Shh expression, whereas SHH refines papilla spacing and restricts neighboring papilla formation. SOX2 functions as a taste-competence and progenitor-maintenance factor. In adults, LGR5/LGR6-RSPO-WNT signaling sustains progenitor activity, and gustatory neurons provide RSPO2 as a niche signal that maintains epithelial renewal. HH signaling from epithelial and neuronal sources further supports SOX2-dependent progenitor homeostasis. Lineage allocation is controlled by transcriptional programs that include POU2F3/SKN-1a for sweet, umami, and bitter type II taste receptor cells and ASCL1 with posterior-field NKX2-2 for type III presynaptic/sour cells. After denervation or irradiation, regeneration depends primarily on LGR5+/KRT14+ progenitors and may be supplemented, in specific injury contexts, by plasticity of a subset of K8-lineage taste receptor cells that acquire KRT14/SOX2/PCNA progenitor-like features. Key unresolved issues include the direct chromatin targets of taste lineage regulators (which remain to be defined by ChIP-seq in native taste progenitors), the identity of the type I cell selector, the contribution of dedifferentiation across injury models, and the extent to which mouse-derived networks are conserved in human taste biology.

Alzheimer's disease (AD) is characterized by multifactorial pathological processes, including cholinergic dysfunction and oxidative stress, highlighting the need for safer, multi‐target interventions beyond current synthetic acetylcholinesterase (AChE) inhibitors. In the present study, we screened ethanolic extracts from various edible and medicinal plants to identify natural sources with cholinesterase‐modulating activity and found that Sparassis crispa ( S. crispa ) extract exhibited robust AChE inhibitory activity. The extract also demonstrated significant antioxidant capacity and protected rat pheochromocytoma cells against oxidative stress–induced cytotoxicity. Chemical characterization using gas chromatography–mass spectrometry identified ergosterol as a major bioactive constituent of S. crispa extract. Ergosterol directly inhibited AChE activity in vitro and was subsequently evaluated in vivo using a trimethyltin chloride (TMT)–induced mouse model of cognitive impairment. Dietary supplementation with S. crispa extract significantly improved spatial working memory and attenuated TMT‐induced elevation of brain AChE activity. Notably, ergosterol supplementation produced dose‐dependent improvements in both spatial working memory and aversive learning, accompanied by restoration of cholinergic function and reduction of lipid peroxidation in brain tissues. No signs of hepatic toxicity were observed following ergosterol administration. Collectively, these findings demonstrate that S. crispa extract exerts cognitive benefits through combined modulation of cholinergic dysfunction and oxidative stress, and identify ergosterol as a key bioactive contributor to these effects. This study provides mechanistic insight into the neuroprotective potential of S. crispa and supports its development, together with ergosterol, as functional food–derived candidates for the prevention or mitigation of cognitive decline.

Unique skin microbial communities have been shaped by the harsh climatic conditions in high-altitude areas, such as intense ultraviolet radiation and low oxygen concentration. However, it is unknown whether high altitude contributes to shaping common microbiota inhabiting the skin across different mammals. The skin microbial communities of humans and horses living in high-altitude (Tibetan) and low-altitude areas were analyzed using full-length 16S rRNA sequencing technology. Alpha diversity differed between high- and low-altitude groups (p < 0.01). Skin microbial community composition also differed between high- and low-altitude areas (p < 0.05). Some of the common taxa present in the skin of humans and horses in high-altitude areas were identified as extreme microorganisms capable of adapting to the harsh high-altitude environment. Five bacterial taxa, including the genera Sphingomonas, Brevundimonas, and Kocuria, as well as the species Acinetobacter guillouiae and Arboricoccus pini, were significantly enriched (p < 0.01) on the skin of both humans and horses in high-altitude areas. Meanwhile, some taxa enriched on the skin surface at the same altitude showed preferences for mammalian species. Acinetobacter johnsonii, Anaerococcus nagyae, and Anaerococcus octavius were significantly enriched (p < 0.05) in the skin of humans at both high and low altitudes, whereas Acinetobacter pseudolwoffii and Armatimonas rosea, Archangium gephyra and Acinetobacter lwoffii were significantly enriched (p < 0.05) in the skin of horses at both high and low altitudes. In the network analyses, a positive correlation (p < 0.01) was shown between the skin taxa enriched in high-altitude areas and each other, while a negative correlation (p < 0.01) was found between the skin microorganisms enriched in high-altitude areas and those enriched in low-altitude areas. Overall, our findings indicate that high-altitude extreme environments drive convergent evolution of skin microbiota across mammals, reflecting the joint effects of environmental selection and host-related filtering on community assembly. This cross-species comparison provides a framework for understanding skin microbiome responses to extreme environments in plateau mammals.

Recent epidemiological studies have shown that dietary fructose intake is associated with an increased risk of colorectal cancer, yet its specific molecular mechanisms in colon carcinogenesis remain underexplored. Here we investigate the molecular mechanisms by which dietary fructose contributes to colon carcinogenesis, focusing on the role of mitochondrial NADP ⁺ -dependent isocitrate dehydrogenase 2 (IDH2). Using an unbiased multiomics approach (transcriptomics and proteomics), liver and colon tissues from fructose-fed wild-type mice were analyzed to identify key genes involved in cancer-related pathways. In addition, human liver transcriptomic data (GSE256398) were analyzed to confirm alterations in aryl hydrocarbon receptor (AhR) signaling and the sirtuin (SIRT)3–IDH2 axis. IDH2-knockout mice were exposed to a dietary carcinogen, 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP), to validate IDH2’s role in colon cancer development. In vitro, fructose’s effects on SIRT3 expression and IDH2 activity were assessed. Fructose-fed wild-type mice exhibited suppressed AhR signaling, increased oxidative stress and mitochondrial dysfunction via the SIRT3–IDH2 axis. In human liver datasets, AhR-associated genes and SIRT3–IDH2 expression were reduced in metabolic dysfunction-associated steatotic liver disease and cirrhosis. The IDH2-knockout mice showed heightened DNA damage, colonic tumorigenesis and mitochondrial and glutathione-mediated detoxification disruptions following PhIP exposure. In vitro, fructose reduced SIRT3 expression and IDH2 activity, further supporting its role in promoting colon carcinogenesis. Fructose promotes colon carcinogenesis by disrupting mitochondrial function and impairing DNA damage response mechanisms, particularly through SIRT3–IDH2 axis suppression. These findings highlight the critical role of mitochondrial dysfunction in fructose-induced carcinogenesis and suggest the SIRT3–IDH2 axis as a potential therapeutic target.

Tofu, a traditional food made from soybeans, has been widely consumed in the world but tofu production generates significant by-products such as tofu whey, and other residues. In the present study, Aquaforte, derived from tofu whey, was investigated for its antioxidative and anti-inflammatory properties in combating oxidative stress-induced damage in human keratinocytes (HaCaT). Antioxidant capacities were assessed through antioxidant properties were evaluated through DPPH and ABTS assays in which the Aquaforte samples demonstrated superior efficacy. In AAPH induced oxidative stress model, Aquaforte significantly suppressed intracellular reactive oxygen species levels, enhanced cell viability, and accelerated cellular migration in the wound healing assay, suggesting its potential in tissue regeneration. Furthermore, Aquaforte reduced the formation of senescence-associated heterochromatin foci. Additionally, quantitative real-time PCR analysis showed that Aquaforte decreased interlukin-6 expression and upregulated nuclear factor erythroid 2-related factor 2. This research contributes to sustainable upcycling by valorizing tofu whey by-products into beneficial bioactive compounds.

Researchers have long focused on the accumulation of amyloid beta (Aβ) peptides in the brain as a primary pathological hallmark driving cognitive decline. This study investigated the neuroprotective effects of Rosa rugosa (RR) root extract and its key bioactive constituent, oleamide, against amyloid beta (Aβ)-induced neurotoxicity. Initially, an ethanolic extract of RR root was screened via in vitro assays to assess antioxidant and cytoprotective potential in rat pheochromocytoma cells. Subsequent fractionation, open-column chromatography, and preparatory thin-layer chromatography led to the isolation of oleamide, confirmed by gas chromatography–mass spectrometry and ¹H/¹³C nuclear magnetic resonance analyses. In vivo experiments using intracerebroventricularly injected Aβ in male mice demonstrated that both RR root extract and oleamide significantly improved cognitive performance in the Y-maze and passive avoidance tests. Additionally, oleamide restored acetylcholine levels and reduced malondialdehyde concentrations in brain tissue, indicating mitigation of oxidative stress and support of cholinergic function. No significant toxicity was observed, as evidenced by stable serum transaminase levels and unaltered body or brain weights. These findings highlight oleamide’s potential to protect against Aβ-driven pathology through multiple mechanisms, including reduced lipid peroxidation and improved neurotransmission. Further investigations into oleamide’s molecular targets and synergy with existing therapies may advance its development as a novel candidate for Alzheimer’s disease prevention or adjunct treatment.

Introduction The potential roles of fructose in colon cancer are growing concerns. Fructose consumption has been linked to oxidative stress and mitochondrial dysfunction, yet its specific molecular mechanisms in colon carcinogenesis remain underexplored. Objectives This study aimed to investigate the molecular mechanisms by which dietary fructose contributes to colon carcinogenesis, focusing on the role of mitochondrial NADP ⁺ -dependent isocitrate dehydrogenase (IDH2). Methods Using an unbiased multi-omics approach (transcriptomics and proteomics), liver and colon tissues from fructose-fed wild-type (WT) mice were analyzed to identify key genes involved in cancer-related pathways. Human liver transcriptomic data (GSE256398) was analyzed to confirm alterations in aryl hydrocarbon receptor (AhR) signaling and the SIRT3-IDH2 axis. IDH2 knockout (KO) mice were exposed to a dietary carcinogen, 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP), to validate IDH2's role in colon cancer development. In vitro, fructose’s effects on SIRT3 expression and IDH2 activity were assessed. Results Fructose-fed WT mice exhibited suppressed AhR signaling, increased oxidative stress, and mitochondrial dysfunction via the SIRT3-IDH2 axis. In human liver datasets, AhR-associated genes and SIRT3-IDH2 expression were reduced in MASLD and cirrhosis. IDH2 KO mice showed heightened DNA damage, colonic tumorigenesis, and mitochondrial and GSH-mediated detoxification disruptions following PhIP exposure. In vitro, fructose reduced SIRT3 expression and IDH2 activity, further supporting its role in promoting colon carcinogenesis. Conclusion Fructose promotes colon carcinogenesis by disrupting mitochondrial function and impairing DNA damage response mechanisms, particularly through SIRT3-IDH2 axis suppression. These findings highlight the critical role of mitochondrial dysfunction in fructose-induced carcinogenesis and suggest the SIRT3-IDH2 axis as a potential therapeutic target.