Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

The detrimental effects of hyperlipidemia on the healing of rotator cuff tears are well documented. The proposed underlying mechanisms for these effects include alterations in the extracellular matrix, inflammation, and oxidative stress, which hamper the reparative processes in the affected tendon tissues. Recent therapeutic strategies target these pathways, reflecting a growing body of research dedicated to mitigating these effects and promoting healing. This literature review aims to provide a comprehensive understanding of the pathophysiology underlying rotator cuff tears, examine the interplay between hyperlipidemia and rotator cuff tear healing, synthesize current knowledge on contributing biological mechanisms, and outline potential therapeutic interventions to optimize clinical management and treatment outcomes for patients.

Background: This study aimed to investigate changes after repeated subacromial drug injections in a rat model of normal rotator cuff. Methods: Thirty-nine male Sprague-Dawley rats were divided into groups 1 (no injection, n = 3), 2 (parecoxib, n = 18; 6 subgroups, n = 3 each; 0.5 mg/kg), and 3 (triamcinolone, n = 18; 6 subgroups, n = 3 each; 0.3 mg/kg). Groups 2 and 3 received subacromial injections 1–6 times once weekly for 6 weeks. The supraspinatus and infraspinatus tendons and muscles were used for biomechanical and histological evaluation. The subacromial bursa was used to analyze the prostaglandin E2 (PEG2) level. Results: In the biomechanical test, load-to-failure and ultimate stress decreased in groups 2 and 3 with repeated injections and the values were significantly lower in group 3 than in group 1 only at the sixth injection (p = 0.007 and p = 0.008, respectively). On the Bonar score, the cellularity, ground substance, and total score were significantly different among the 3 groups at the fifth and sixth injections (cellularity: p = 0.028 and p = 0.033, ground substance: p = 0.018 and p = 0.006, and total score: p = 0.029 and p = 0.027, respectively). The myocyte cross-sectional area of the infraspinatus muscle showed a significant difference among the 3 groups at the third and fourth injections (p = 0.031 and p = 0.020, respectively). The PEG2 level in the subacromial bursa was significantly different among the 3 groups at the third, fifth, and sixth injections (p = 0.019, p = 0.004, and p = 0.004, respectively). Conclusions In the rat model of normal rotator cuff, repeated local injections of the cyclooxygenase-2 inhibitor showed fewer negative effects on the biomechanical and histological properties of the normal tendon than triamcinolone.

Background/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

The detrimental effects of hyperlipidemia on the healing of rotator cuff tears are well documented. The proposed underlying mechanisms for these effects include alterations in the extracellular matrix, inflammation, and oxidative stress, which hamper the reparative processes in the affected tendon tissues. Recent therapeutic strategies target these pathways, reflecting a growing body of research dedicated to mitigating these effects and promoting healing. This literature review aims to provide a comprehensive understanding of the pathophysiology underlying rotator cuff tears, examine the interplay between hyperlipidemia and rotator cuff tear healing, synthesize current knowledge on contributing biological mechanisms, and outline potential therapeutic interventions to optimize clinical management and treatment outcomes for patients.

Background: This study aimed to investigate changes after repeated subacromial drug injections in a rat model of normal rotator cuff. Methods: Thirty-nine male Sprague-Dawley rats were divided into groups 1 (no injection, n = 3), 2 (parecoxib, n = 18; 6 subgroups, n = 3 each; 0.5 mg/kg), and 3 (triamcinolone, n = 18; 6 subgroups, n = 3 each; 0.3 mg/kg). Groups 2 and 3 received subacromial injections 1–6 times once weekly for 6 weeks. The supraspinatus and infraspinatus tendons and muscles were used for biomechanical and histological evaluation. The subacromial bursa was used to analyze the prostaglandin E2 (PEG2) level. Results: In the biomechanical test, load-to-failure and ultimate stress decreased in groups 2 and 3 with repeated injections and the values were significantly lower in group 3 than in group 1 only at the sixth injection (p = 0.007 and p = 0.008, respectively). On the Bonar score, the cellularity, ground substance, and total score were significantly different among the 3 groups at the fifth and sixth injections (cellularity: p = 0.028 and p = 0.033, ground substance: p = 0.018 and p = 0.006, and total score: p = 0.029 and p = 0.027, respectively). The myocyte cross-sectional area of the infraspinatus muscle showed a significant difference among the 3 groups at the third and fourth injections (p = 0.031 and p = 0.020, respectively). The PEG2 level in the subacromial bursa was significantly different among the 3 groups at the third, fifth, and sixth injections (p = 0.019, p = 0.004, and p = 0.004, respectively). Conclusions In the rat model of normal rotator cuff, repeated local injections of the cyclooxygenase-2 inhibitor showed fewer negative effects on the biomechanical and histological properties of the normal tendon than triamcinolone.

Background/Aims: This study aimed to evaluate the performance of the Model for End-Stage Liver Disease (MELD) 3.0 for predicting mortality and liver-related complications compared with the Child-Pugh classification, albumin-bilirubin (ALBI) grade, the MELD, and the MELD sodium (MELDNa) score. Methods: We evaluated a multicenter retrospective cohort of incorporated patients with cirrhosis between 2013 and 2019. We conducted comparisons of the area under the receiver operating characteristic curve (AUROC) of the MELD3.0 and other models for predicting 3-month mortality. Additionally, we assessed the risk of cirrhosis-related complications according to the MELD3.0 score. Results: A total of 3,314 patients were included. The mean age was 55.9±11.3 years, and 70.2% of the patients were male. Within the initial 3 months, 220 patients (6.6%) died, and the MELD3.0had the best predictive performance among the tested models, with an AUROC of 0.851, outperforming the Child-Pugh classification, ALBI grade, MELD, and MELDNa. A high MELD3.0score was associated with an increased risk of mortality. Compared with that of the group with a MELD3.0 score <10 points, the adjusted hazard ratio of the group with a score of 10–20 pointswas 2.176, and that for the group with a score of ≥20 points was 4.892. Each 1-point increase inthe MELD3.0 score increased the risk of cirrhosis-related complications by 1.033-fold. The risk of hepatorenal syndrome showed the highest increase, with an adjusted hazard ratio of 1.149, followed by hepatic encephalopathy and ascites. Conclusions The MELD3.0 demonstrated robust prognostic performance in predicting mortality in patients with cirrhosis. Moreover, the MELD3.0 score was linked to cirrhosis-related complications, particularly those involving kidney function, such as hepatorenal syndrome and ascites.

The detrimental effects of hyperlipidemia on the healing of rotator cuff tears are well documented. The proposed underlying mechanisms for these effects include alterations in the extracellular matrix, inflammation, and oxidative stress, which hamper the reparative processes in the affected tendon tissues. Recent therapeutic strategies target these pathways, reflecting a growing body of research dedicated to mitigating these effects and promoting healing. This literature review aims to provide a comprehensive understanding of the pathophysiology underlying rotator cuff tears, examine the interplay between hyperlipidemia and rotator cuff tear healing, synthesize current knowledge on contributing biological mechanisms, and outline potential therapeutic interventions to optimize clinical management and treatment outcomes for patients.