Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

This guideline aims to promote the prudent use of antibacterial agents for managing carbapenem-resistant Enterobacterales (CRE) infections in clinical practice in Korea. The general section encompasses recommendations for the management of common CRE infections and diagnostics, whereas each specific section is structured with key questions that are focused on antibacterial agents and disease-specific approaches. This guideline covers both currently available and upcoming antibacterial agents in Korea.

This guideline aims to promote the prudent use of antibacterial agents for managing carbapenem-resistant Enterobacterales (CRE) infections in clinical practice in Korea. The general section encompasses recommendations for the management of common CRE infections and diagnostics, whereas each specific section is structured with key questions that are focused on antibacterial agents and disease-specific approaches. This guideline covers both currently available and upcoming antibacterial agents in Korea.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

This guideline aims to promote the prudent use of antibacterial agents for managing carbapenem-resistant Enterobacterales (CRE) infections in clinical practice in Korea. The general section encompasses recommendations for the management of common CRE infections and diagnostics, whereas each specific section is structured with key questions that are focused on antibacterial agents and disease-specific approaches. This guideline covers both currently available and upcoming antibacterial agents in Korea.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Purpose: Moderate-intensity continuous training (MICT) improves exercise capacity with vascular benefits, but time constraints hinder consistent adherence. High-intensity interval training (HIIT) has emerged as a time-efficient alternative, with repeated sprint training (RST) being the shortest format. We hypothesized that RST would be as effective as MICT in improving vascular function and exercise capacity in young adults. Methods: Twenty-three adults (mean age, 26.2±3.8 years) were randomly assigned to either RST or MICT. RST involved 20 sets of 4-second cycling sprints followed by 30-second active recovery, totaling 11 minutes. MICT consisted of 30-minute cycling at 50% to 60% of heart rate reserve. Vascular function evaluated via brachial artery flow-mediated dilation. Exercise capacity (maximum oxygen uptake, total exercise load test time) and anaerobic capacity (maximum power, anaerobic threshold) were measured using maximum exercise tests. These variables were measured befre and after a 6-week training. Results: Both groups showed comparable improvements in flow-mediated dilation (p＜ 0.05). Maximum oxygen intake slightly improved, while total exercise time significantly increased for both (p＜ 0.05). Anaerobic threshold unchanged, while maximum power improved (p＜ 0.05). Conclusion These findings underscore that RST is a time-efficient exercise strategy, which improves vascular function and exercise capacity as effectively as MICT in young adults.

Purpose: Isometric handgrip exercise (IHE) has a favorable cardiovascular effect and improves hemodynamic responses. Whether IHE attenuates stress-related hemodynamic reactivity assessed during a sympathetic challenge remains unexplored. We tested the hypothesis that an acute bout of IHE would improve carotid arterial function and attenuate cardiovascular vasoreactivity response to sympathetic stress in healthy adults. Methods: In a randomized cross-over design, sixteen healthy adults (aged 21.8±3.1 years) were enrolled. Participants completed two testing sessions, separated by 1 week. Trials were either a control trial or performed IHE for two sets of 2 minutes at 30% of maximal voluntary contraction for each hand. The participant’s hand was immersed in an ice water bath (4 ℃ ) up to the wrist for 2 minutes. Carotid artery diameter, β-stiffness index, and compliance using ultrasound machine and brachial blood pressure (BP), heart rate (HR) were measured as indices of vasoreactivity at baseline, during, and recovery from cold pressor testing (CPT). Results: The BP, HR, carotid artery diameter, and β-stiffness index increased similarly during CPT in both trials (p＜ 0.001), without any interaction effect. Compared with the IHE trial, arterial compliance decreased in the control groups at 120 seconds during recovery with a significant interaction effect (p=0.02). Conclusion These findings suggest that an acute IHE did not attenuate BP, HR, carotid artery diameter and β-stiffness index vasoreactivity, but improved carotid artery compliance to sympathetic activation in healthy young adults.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.

Background: Diabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models. Results: Protein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis. Conclusions NET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.