Purpose: Lupus nephritis (LN) can be caused by the complement activation. This study aimed to investigate the differences and clinical implications of the activation pattern of the complement system for pediatric and adult LN patients. Methods: We retrospectively reviewed the medical records of 40 patients (14 pediatric and 26 adult patients) diagnosed with LN through kidney biopsy. Results: The mean ages at diagnosis of pediatric and adult patients were 11.7±2.92 and 37.3±13.5 years, respectively. At the first LN diagnosis, compared with adult patients, pediatric patients had a higher estimated glomerular filtration rate and milder proteinuria; however, there was no statistical significance. The age-adjusted mean serum complement 3 value was significantly lower in the pediatric group (33.0±11.3 mg/dL) than in the adult group (50.8±25.2 mg/dL) (P<0.01). Based on the findings of kidney biopsy, no significant differences were observed in the severity of pathologic classification and the positive rate of complements between adults and children. However, the chronicity index score of adult patients was significantly higher than that of pediatric patients and in the case of complement 4d, despite a similar positive rate, the intensity was significantly stronger for adults (2.35±0.83 vs. 1.54±0.52, (P=0.04). Conclusions The activation pattern of the complement system in LN differs clinicopathologically between pediatric and adult patients and these differences might play an important role in the age-dependent prognosis of LN.

Purpose: Lupus nephritis (LN) can be caused by the complement activation. This study aimed to investigate the differences and clinical implications of the activation pattern of the complement system for pediatric and adult LN patients. Methods: We retrospectively reviewed the medical records of 40 patients (14 pediatric and 26 adult patients) diagnosed with LN through kidney biopsy. Results: The mean ages at diagnosis of pediatric and adult patients were 11.7±2.92 and 37.3±13.5 years, respectively. At the first LN diagnosis, compared with adult patients, pediatric patients had a higher estimated glomerular filtration rate and milder proteinuria; however, there was no statistical significance. The age-adjusted mean serum complement 3 value was significantly lower in the pediatric group (33.0±11.3 mg/dL) than in the adult group (50.8±25.2 mg/dL) (P<0.01). Based on the findings of kidney biopsy, no significant differences were observed in the severity of pathologic classification and the positive rate of complements between adults and children. However, the chronicity index score of adult patients was significantly higher than that of pediatric patients and in the case of complement 4d, despite a similar positive rate, the intensity was significantly stronger for adults (2.35±0.83 vs. 1.54±0.52, (P=0.04). Conclusions The activation pattern of the complement system in LN differs clinicopathologically between pediatric and adult patients and these differences might play an important role in the age-dependent prognosis of LN.

Purpose: Lupus nephritis (LN) can be caused by the complement activation. This study aimed to investigate the differences and clinical implications of the activation pattern of the complement system for pediatric and adult LN patients. Methods: We retrospectively reviewed the medical records of 40 patients (14 pediatric and 26 adult patients) diagnosed with LN through kidney biopsy. Results: The mean ages at diagnosis of pediatric and adult patients were 11.7±2.92 and 37.3±13.5 years, respectively. At the first LN diagnosis, compared with adult patients, pediatric patients had a higher estimated glomerular filtration rate and milder proteinuria; however, there was no statistical significance. The age-adjusted mean serum complement 3 value was significantly lower in the pediatric group (33.0±11.3 mg/dL) than in the adult group (50.8±25.2 mg/dL) (P<0.01). Based on the findings of kidney biopsy, no significant differences were observed in the severity of pathologic classification and the positive rate of complements between adults and children. However, the chronicity index score of adult patients was significantly higher than that of pediatric patients and in the case of complement 4d, despite a similar positive rate, the intensity was significantly stronger for adults (2.35±0.83 vs. 1.54±0.52, (P=0.04). Conclusions The activation pattern of the complement system in LN differs clinicopathologically between pediatric and adult patients and these differences might play an important role in the age-dependent prognosis of LN.

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.

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.

Objective: The Scales for Outcomes in Parkinson’s Disease–Cognition (SCOPA-Cog) was developed to assess cognition in patients with Parkinson’s disease (PD). In this study, we aimed to evaluate the validity and reliability of the Korean version of the SCOPACog (K-SCOPA-Cog). Methods: We enrolled 129 PD patients with movement disorders from 31 clinics in South Korea. The original version of the SCOPA-Cog was translated into Korean using the translation-retranslation method. The test–retest method with an intraclass correlation coefficient (ICC) and Cronbach’s alpha coefficient were used to assess reliability. Spearman’s rank correlation analysis with the Montreal Cognitive Assessment-Korean version (MOCA-K) and the Korean Mini-Mental State Examination (K-MMSE) were used to assess concurrent validity. Results: The Cronbach’s alpha coefficient was 0.797, and the ICC was 0.887. Spearman’s rank correlation analysis revealed a significant correlation with the K-MMSE and MOCA-K scores (r = 0.546 and r = 0.683, respectively). Conclusion Our results demonstrate that the K-SCOPA-Cog has good reliability and validity.

Background: Angiolipoma is a disorder characterized by the development of distinct, encapsulated subcutaneous tumors. Unlike lipoma, angiolipoma is distinctively accompanied by tenderness, which does not respond to general painkillers. Additionally, the reason for the pain has not been elucidated yet. Objective: This study aims to investigate platelet aggregation as the potential cause of tenderness in angiolipoma. Methods: Twenty-three patients diagnosed with angiolipoma and lipoma were enrolled. Platelet aggregation was visualized by CD61 immunohistochemical staining. The area of platelet aggregation and vessel lumen in a high power field were measured with the QuPath software. The ratio between the area of platelet aggregation and vessel lumen (p/v ratio) was calculated from the captured images. Results: Eleven of 46 patients complained of tenderness (9/23 angiolipoma [39.1%], 2/23 lipoma [8.7%]).Angiolipoma demonstrated a higher p/v ratio than that observed in lipoma (0.27 vs. 0.09, p＜0.001). Furthermore, the mean p/v ratio was high in patients with tenderness (0.44 vs. 0.09, p＜0.01). Patients were divided into three groups according to the aggregation pattern, highly clustered, mixed, and particulated. Nine patients with angiolipoma presented a highly clustered pattern, meanwhile, only three patients with lipoma exhibited a highly clustered pattern. Moreover, the number of patients with tenderness was significant in the highly clustered group (63.6%). Additionally, among the highly clustered group, the mean p/v ratio was higher in patients with tenderness (0.52 vs. 0.24, p＜0.01). Conclusion As clustered platelet aggregation with a high p/v ratio demonstrated relevance to tenderness, medications inhibiting platelet aggregation could mitigate tenderness in patients with angiolipoma.