Background: Nonalcoholic fatty liver disease, a progressive condition caused by the accumulation of fat in the liver, begins with simple steatosis and can potentially progress to metabolic dysfunction-associated steatohepatitis (MASH) in the presence of inflammation and fibrosis, ultimately leading to cirrhosis or hepatocellular carcinoma. Increasing evidence indicates that sodiumglucose cotransporter 2 (SGLT2) inhibitors effectively alleviate MASH in mouse models. However, there is a lack of research on the effects of enavogliflozin on liver disease. In the present study, we investigated the effects of SGLT2 inhibitors on MASH induced by a high-fat, high-cholesterol (HFHC) diet in mice. Methods: Male C57BL/6 mice were fed a normal chow diet, HFHC diet, or HFHC diet with enavogliflozin for 12 weeks. LX-2 and HepG2 cells were treated with enavogliflozin in the presence of various pathological stimuli. Results: The HFHC diet induced excessive hepatic lipid accumulation, inflammation, and severe fibrosis. Administration of enavogliflozin not only ameliorated hepatic steatosis and fibrotic conditions but also suppressed the production of inflammatory cytokines. Positive outcomes were also observed in in vitro experiments, where enavogliflozin demonstrated the ability to impede the activation of hepatic stellate cells and alleviate lipid accumulation in hepatocytes. The potential pathway through which enavogliflozin attenuated liver fibrosis development may be associated with the transforming growth factor β1/Smad signaling pathway. Conclusion Our results suggest that enavogliflozin is effective in a mouse model of MASH by attenuating hepatic steatosis, suppressing inflammation, and improving liver fibrosis.

Purpose: This study aimed to investigate differences in perceptions of occupational health management and communication between health managers of partner companies and those of main contractors. Methods: Questionnaires were distributed to main contractor health managers and partner company representatives, and the collected data were compared and analyzed using a t-test and a chi-squared test. Results: Partner company representatives generally reported lower perceptions than health managers across most occupational health management items. The largest perception gaps were found in pre-placement health checks, workplace environment measurements and corrective actions, and the establishment of an occupational health management system.For business coordination, face-to-face meetings were most preferred, followed by official letters. Both groups agreed that face-to-face communication was the most effective method for providing health information, with no significant differences. However, for communication with workers, health managers preferred direct meetings, online channels, or individual phone calls, while partner company representatives favored individual phone calls or online group chats. Conclusion Partner companies have characteristics that differ from typical small-scale workplaces, requiring occupational health management and communication methods tailored to these unique features. There is also a need to develop guidelines and policies that partner company representatives can easily understand and implement effectively.

Multiple myeloma (MM), a hematological malignancy, is characterized by malignant plasma cell proliferation in the bone marrow. Recent treatment advances have significantly improved patient outcomes associated with MM.In this study, we aimed to develop comprehensive, evidence-based guidelines for the diagnosis, prognosis, and treat‑ ment of MM. We identified 12 key clinical questions essential for MM management, guiding the extensive literature review and meta-analysis of the study. Our guidelines provide evidence-based recommendations by integrating patient preferences with survey data. These recommendations include current and emerging diagnostic tools, thera‑ peutic agents, and treatment strategies. By prioritizing a patient-centered approach and rigorous data analysis, these guidelines were developed to enhance MM management, both in Korea and globally.

Background: This study aimed to document the patterns, challenges, and opportunities for biobank utilization within the Female Breast and Genital Disease with Microbiome Biobank Network (FDMNet) in South Korea. Annual surveys (2022–2024) assessed researcher awareness, utilization patterns, barriers to access, research requirements, and interest in microbiome research. Methods: Online questionnaires were distributed to staff members at five university hospitals participating in FDMNet. Data from 155 respondents across 3 years were analyzed using descriptive statistics for quantitative data. Qualitative feedback was examined using Uniform Manifold Approximation and Projection and natural language processing to identify the thematic clusters of user challenges. Results: Despite high engagement with biobank resources (76% of the respondents), declining participation rates and interinstitutional collaborations were observed, particularly in 2024, amid the nationwide healthcare crisis. The major barriers to utilization included complex access procedures (31.0%), lack of process knowledge (23.9%), and concerns about Institutional Review Board approval (11.6%). Breast neoplasms (12.3%) and female genital neoplasms (11.0%) were the primary research interests, with blood (24.5%) and tissue (23.9%) samples being the most requested specimens. Most respondents (66.5%) expressed interest in microbiome research but reported insufficient knowledge. Conclusion These findings highlight the need for streamlined access procedures, improved researcher education, enhanced clinical data integration, and stronger governance structures to overcome existing barriers to biobank utilization. These insights can guide strategic improvements in biobank operations and resource allocation to serve the evolving needs of the research community better.

Background: We aimed to examine the prevalence of burnout among imaging cardiologists in Korea and to identify its associated factors. Methods: An online survey of imaging cardiologists affiliated with university hospitals in Korea was conducted using SurveyMonkey ® in November 2023. The validated Korean version of the Maslach Burnout Inventory-Human Service Survey was used to assess burnout across three dimensions: emotional exhaustion, depersonalization, and lack of personal accomplishment. Data on demographics, work environment factors, and job satisfaction were collected using structured questionnaires. Results: A total of 128 imaging cardiologists (46.1% men; 76.6% aged ≤ 50 years) participated in the survey. Regarding workload, 74.2% of the respondents interpreted over 50 echocardiographic examinations daily, and 53.2% allocated > 5 of 10 working sessions per week to echocardiographic laboratory duties. Burnout levels were high, with a significant proportion of participants experiencing emotional exhaustion (28.1%), depersonalization (63.3%), and a lack of personal accomplishment (92.2%). Younger age (< 50 years) was correlated with higher emotional exhaustion risk, while more research time was protective against burnout in the depersonalization domain. Factors, such as being single, living with family, and specific job satisfaction facets, including uncontrollable workload and value mismatch, were associated with varying levels of burnout risk across different dimensions Conclusion Our study underscores the high burnout rates among Korean imaging cardiologists, attributed to factors such as the subjective environment and job satisfaction.Hence, evaluating and supporting cardiologists in terms of individual values and subjective factors are important to effectively prevent burnout..

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Background: Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction. Methods: In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days. Results: In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery. Conclusion Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.