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.

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.

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.

Background and Objectives: Ultimaster™, a third-generation sirolimus-eluting stent using biodegradable polymer, has been introduced to overcome long term adverse vascular events, such as restenosis or stent thrombosis. In the present study, we aimed to evaluate the 12-month clinical outcomes of Ultimaster™ stents in Korean patients with coronary artery disease. Methods: This study is a multicenter, prospective, observational registry across 12 hospitals. To reflect real-world clinical evidence, non-selective subtypes of patients and lesions were included in this study. The study end point was target lesion failure (TLF) (the composite of cardiac death, target vessel myocardial infarction [MI], and target lesion revascularization [TLR]) at 12-month clinical follow up. Results: A total of 576 patients were enrolled between November 2016 and May 2021. Most of the patients were male (76.5%), with a mean age of 66.0±11.2 years. Among the included patients, 40.1% had diabetes mellitus (DM) and 67.9% had acute coronary syndrome (ACS).At 12 months, the incidence of TLF was 4.1%. The incidence of cardiac death was 1.5%, MI was 1.0%, TLR was 2.7%, and stent thrombosis was 0.6%. In subgroup analysis based on the presence of ACS, DM, hypertension, dyslipidemia, or bifurcation, there were no major differences in the incidence of the primary endpoint. Conclusions The present registry shows that Ultimaster™ stent is safe and effective for routine real-world clinical practice in non-selective Korean patients, having a low rate of adverse events at least up to 12 months.

Objectives: Patients undergoing oral surgery exhibit high anxiety, which may elevate their cortisol levels and affect postoperative recovery. Overweight patients are often encountered in the dental clinic due to the increasing prevalence of overweight. We aimed to investigate the relationships between preoperatively assessed body mass index (BMI), serum cortisol and high-sensitivity C-reactive protein (hs-CRP) levels, and visual analog scale (VAS) scores and preoperative anxiety in patients undergoing mandibular third molar (MM3) extraction and to identify predictors of postoperative complications. Patients and Methods: We analyzed 43 patients (age, 20-42 years) undergoing MM3 extraction. At the first visit, patients completed the Modified Dental Anxiety Scale (MDAS) and Amsterdam Preoperative Anxiety and Information Scale (APAIS) questionnaires. Their BMI and VAS scores were also calculated. The participants underwent blood tests 1 hour before MM3 extraction. On the first postoperative day, the participants’ VAS scores and serum hs-CRP levels were reevaluated. Results: We found that BMI was significantly correlated with preoperative VAS scores. Further, BMI and preoperative hs-CRP levels were significantly correlated among women and patients undergoing extractions of fully impacted MM3s. No correlations were found between serum cortisol and other variables. The preoperative MDAS and VAS scores were significantly positively correlated, especially among patients undergoing extractions of fully impacted MM3s. Multiple linear regression showed that BMI and the eruption status of the MM3 were significant predictors of postoperative hsCRP levels and VAS scores, respectively. Conclusion In MM3 removals, patients with higher BMI showed elevated hs-CRP and higher VAS scores before surgery. Patients with higher anxiety among those undergoing extractions of fully impacted MM3s showed higher preoperative VAS scores. The two main predictors of postoperative complications were BMI and MM3 eruption status.

Mucopolysaccharidoses are rare lysosomal storage diseases resulting from defects in lysosomal enzymes involved in degradation of glycosaminoglycans. Different mucopolysaccharidoses are caused by different enzyme deficiencies The anesthetic complications are related to the organs involved. Patients with mucopolysaccharidoses are rare, and few anesthetists encounter such patients. We experienced a case of mucopolysaccharidoses type II. Several endotracheal intubation attempts were tried, but we experienced failed endotracheal intubation. And we decided to proceed with surgery under bag-mask ventilation because of the short operation time. There’s no desaturation time. And the patient’s spontaneous ventilation was recovered and awakened. We have also briefly discussed the pathophysiology, clinical features, and possible airway management options for patients with mucopolysaccharidoses type II.

Background: Plasmodium vivax is a major pathogen that causes malaria in South Korea.Several genetic polymorphisms in dihydrofolate reductase (pvdhfr), P. vivax multidrug resistance protein 1 (pvmdr1 ), and P. vivax hydroxymethylpterin pyrophosphokinasedihydropteroate synthetase (pvdhps) genes are known to be associated with drug resistance in P. vivax. The objective of this study was to profile the known polymorphisms of P. vivax resistance genes in patients at a secondary hospital in South Korea. Methods: A total of 12 patients with confirmed P. vivax infections were enrolled for this study. Sanger sequencing was performed for the pvdhfr, pvmdr1, and pvdhps genes to detect polymorphisms of these drug resistance genes. Results: Each specimen had single or double polymorphism in pvdhfr. One specimen had a polymorphism in pvdhps. However, no specimen had any polymorphisms in pvmdr1. There was no strain with multi-polymorphisms exceeding double polymorphisms, which reported the geographic location of treatment failure. Conclusion No specimen showed chloroquine-resistance polymorphism in pvmdr1.Treatment with first-line therapy was successful. The prevalence of F57L in pvdhfr was higher than that reported previously. This change must be confirmed by further monitoring and surveillance of the strains with multi-polymorphisms.