Andong National University

Considering that bat ecology alterations may be linked with pathogen spillover, research on bat coronaviruses, particularly on the infection and transmission pattern among bats in relation with their ecology, is essential. We captured bats distributed in Korea from 2021 to 2022, examined coronaviruses in oral swabs, feces, urine, and ectoparasites, and were able to detect alphacoronavirus. We investigated coronaviruses, but noted no substantial differences in the body condition index in the coronavirus-positive bats. Binary logistic regression analysis revealed that bat ecological factors that were significantly associated with coronavirus-positive were roost type, sample type, and bat species. Coronavirus-positive ectoparasite cases suggested additional study on the potential role of them as the viral transmission vectors or fomites. Reinfection of a different coronavirus in recaptured bats was evident, suggesting the possibility that coronavirus circulation can evade the potential protective immunity acquired from previous coronavirus infections. The present findings provide comprehensive information on the coronaviruses transmission dynamics within bat populations linked with bat ecology.

We have extended the d. functional approach proposed by Kim et al. (2011) for the higher-order perturbative contributions to study the structural and interfacial properties of hard-core Yukawa and Jagla fluids with the repulsive and attractive potentials.The higher-order perturbative contributions have been estimated by using the weighted-d. approximation and the bulk pressure of model fluids.The new functional has been utilized to compute the particle d. distribution, compressibility factor, and phase coexistence curve within the nanopores.The calculated results illustrate that for the hard-core Yukawa (HCY) fluid, the present theory provides a significant improvement over other approximations proposed by Kim et al. (2011) and based on the second-order perturbative term even for the low temperatures and predicts a surface-induced liquid-vapor phase transition within the nanopore.The present theory predicts the interfacial properties of the Jagla fluid characterized by the repulsive ramp and attractive ramp potentials well, and provides better results than the two-reference model proposed by Gussmann et al. (2020).However, the accuracy between the theory and simulation results for the Jagla fluid slightly deteriorates at low bulk d. due to the relatively strong repulsive interaction between particles.

Sarcopenia, characterized by the progressive loss of skeletal muscle mass, strength, and physical performance, is traditionally associated with aging. However, chronic conditions such as type 2 diabetes mellitus (T2DM) have been recognized as key accelerators of its progression. In this study, we investigated the therapeutic effects of umbelliferone on diabetes-induced muscle atrophy using C2C12 myoblasts and a db/db diabetic mouse model.

This study aims to provide scientific evidence supporting the potential of umbelliferone, a naturally occurring compound widely found in food, in alleviating diabetes-induced muscle dysfunction and preventing muscle atrophy. Specifically, we evaluated its effectiveness in mitigating diabetic sarcopenia. This study is the first to elucidate the molecular mechanisms by which umbelliferone improves mitochondrial quality control and suppresses proteolysis under hyperglycemic conditions, providing novel insights into its role in preserving muscle homeostasis in diabetes.

C2C12 myoblasts were cultured in DMEM supplemented with 10 % fetal bovine serum (FBS) under normal conditions. Myogenic differentiation was induced by switching to DMEM containing 2 % horse serum (HS) for six days. After differentiation, the cells were exposed to high-glucose (50 mM) medium with or without 10-20 μM umbelliferone before sample collection. Myotube formation was confirmed via microscopy, and protein expression levels of muscle differentiation markers, mitochondrial biogenesis-related factors, and components of the ubiquitin-proteasome system associated with muscle atrophy were analyzed using Western blotting. Additionally, an in vivo study was conducted using db/db mice, a well-established type 2 diabetic model. Umbelliferone was administered orally at a dose of 10 mg/kg daily for eight weeks. Baseline metabolic and physiological parameters were assessed. Muscle tissues were collected for protein expression analysis and histological staining to evaluate morphological and functional changes in muscle structure.

Our findings demonstrated that umbelliferone effectively attenuated muscle atrophy and improved muscle function in diabetes. Umbelliferone significantly upregulated key myogenic markers, including MyoD, myogenin, Myh2, and skeletal muscle myosin, thereby promoting myoblast differentiation into myotubes. In diabetic mice, umbelliferone treatment enhanced grip strength and lean mass, highlighting its potential to restore overall muscle function. Furthermore, umbelliferone improved mitochondrial quality control by modulating the expression of proteins involved in mitochondrial biogenesis (SIRT1, p-AMPK, PGC-1α), fusion (MFN1, OPA1), and fission (FIS1, DRP1). Additionally, umbelliferone suppressed hyperglycemia-induced activation of the ubiquitin-proteasome system, which plays a crucial role in muscle protein degradation. Specifically, it inhibited the upregulation of muscle atrophy-associated proteins, including muscle ring-finger protein-1 (MuRF-1), forkhead box class O3a (FoxO3a), and Atrogin-1.

Importantly, this is the first study to comprehensively demonstrate the dual action of umbelliferone in enhancing mitochondrial dynamics and inhibiting muscle protein degradation in both cellular and diabetic animal models, Theses findings offer a new mechanism perspective on how dietary phytochemicals may combat diabetic sarcopenia. These findings highlight the therapeutic potential of umbelliferone in alleviating diabetes-related muscle atrophy and suggest its potential as a promising intervention for diabetic muscle complications.