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: Poor outcomes after acute ischemic stroke (AIS) revascularization are anticipated in patients with dementia due to advanced age, comorbidities, and reduced disease awareness. This study investigated clinical characteristics and short-term outcomes of AIS revascularization in patients undergoing dementia treatment. Methods: We retrospectively reviewed patients who underwent AIS revascularization therapy at eight centers of the Catholic University of Korea. Patients receiving anti-dementia medication for cognitive impairment before stroke onset were analyzed. Clinical characteristics and outcomes, including the modified Rankin Scale (mRS) score, hemorrhagic transformation, and mortality, were collected. Results: Among 1,379 patients who received AIS revascularization over 5 years, 13 (0.94%; mean age 83 years; 8 females) had a preexisting diagnosis of dementia (Alzheimer’s disease in 11, mild cognitive impairment in 2) and were on anti-dementia medication. Two patients underwent intravenous thrombolysis combined with endovascular therapy, whereas 11 underwent endovascular therapy alone. Most patients (11/13, 84.6%) presented with an unclear onset time. Stroke lesions were located in the right middle cerebral artery (MCA) in seven cases, left MCA in three, bilateral MCAs in one, and posterior circulation in two. Hemorrhagic transformation occurred in six patients (46%), of whom three (23%) were symptomatic. The mRS scores at discharge were 6 in two patients, 5 in one patient, 4 in nine patients, and 3 in one patient. Four patients died within 3 months of stroke onset. Conclusion The proportion of patients with cognitive impairment receiving anti-dementia medication among those undergoing stroke revascularization therapy was very small. The rates of hemorrhagic transformation and mortality were high. None of the patients achieved favorable outcomes at discharge.

Purpose: Various materials and techniques have been explored to prevent anastomotic leakage (AL). Polyglycolic acid (PGA) sheets and cyanoacrylate (CA) glue have been investigated for their potential in wound healing and fistula closure. This study aims to assess the feasibility of PGA-CA complex (PCC) to prevent AL by developing a major leakage model in rats. Methods: After the creation of the major leakage model in the jejunum of rat, the leakage site was treated with each material individually and in combination. Rats were categorized into the control, CA, PGA, and PCC groups. Results: A total of 40 rats were included, with one animal from the CA and PGA groups having expired. Gross intraabdominal conditions showed no significant difference between the groups. Median intraluminal bursting pressure was 120.0 (range, 102.5–138.0) in the CA group and 138.0 (range, 127.0–147.0) in the PCC group (P = 0.286). Pathologic evaluation revealed fibroblast activation was significantly different in the PCC group (P = 0.025). Conclusion No significant differences were observed in the macroscopic intra-abdominal findings or intraluminal bursting pressure between the groups. The only difference in PCC group was enhanced fibroblast activation at moderate levels compare to the control group. Further research is warranted to optimize material combinations and validate efficacy in larger preclinical and clinical settings.

Background/Aims: The optimal duration and interval of follow-up for cystic lesions of the pancreas (CLPs) is not well established. This study was performed to investigate the optimal duration and interval of follow-up for CLPs in clinical practice. Methods: Patients with CLPs without worrisome features or high-risk stigmata underwent followup with computed tomography at 6, 12, 18, and 24 months and then every 12 months thereafter. A retrospective analysis of prospectively collected data was performed. Results: A total of 227 patients with CLPs detected from 2000 to 2008 (mean initial diameter, 1.3±0.6 cm) underwent follow-up for a median of 120 months. Twenty-two patients (9.7%) underwent surgery after a median of 47.5 months. Malignancies developed in four patients (1.8%), one within 5 years and three within 10 years. One hundred and fourteen patients (50.2%) were followed up for more than 10 years. No malignancy developed after 10 years of follow-up. During surveillance, 37 patients (16.3%) experienced progression to surgical indication. In patients with CLPs less than 2 cm in diameter, development of surgical indications did not occur within 24 months of follow-up. Conclusions CLPs should be continuously monitored after 5 years because of the persistent potential for malignant transformation of CLPs. An interval of 24 months for initial follow-up might be enough for CLPs with initial size of less than 2 cm in clinical practice.

Background/Aims: Reports on the association between sarcopenic visceral obesity and nonalcoholic fatty liver disease (NAFLD)-associated morbidities remain scarce. We investigated the association between sarcopenia and visceral obesity, and the influence of this association on hepatic and coronary comorbidities. Methods: The appendicular skeletal muscle mass to visceral fat area ratio (SV ratio) was evaluated using bioelectric impedance analysis. NAFLD and significant liver fibrosis were assessed using transient elastography, and high atherosclerotic cardiovascular disease (ASCVD) risk was defined as a 10-year ASCVD risk score >10%. Sarcopenia was defined as appendicular skeletal muscle mass adjusted by body mass index (<0.789 for men and <0.512 for women). Results: In total, 82.0% (n=1,205) of the entire study population had NAFLD, and 14.6% of these individuals (n=176) exhibited significant liver fibrosis. Individuals with the lowest SV ratio had a significantly increased risk of NAFLD, significant liver fibrosis, and high ASCVD risk (all p<0.05). Individuals with both the lowest SV ratio and sarcopenia had the highest risk of developing NAFLD (odds ratio [OR]=3.11), significant liver fibrosis (OR=2.03), and high ASCVD risk (OR=4.15), compared with those with a higher SV ratio and without sarcopenia (all p<0.05). Conclusions Low SV ratio combined with sarcopenia was significantly associated with an increased risk of NAFLD, significant liver fibrosis, and high ASCVD risk among individuals with a high risk of NAFLD.

Objectives: This study aimed to assess the clinical burden, a critical determinant of medication adherence in patients with schizophrenia, after the administration of Aripiprazole once-monthly (AOM). Methods: This study was a retrospective, non-interventional, multicenter, naturalistic observational study conducted through the analysis of participants’ electronic medical records. Study participants were recruited from eight sites. Data were collected at baseline, defined as the time of AOM administration, and at 1, 3, 6, 9, and 12 months thereafter. The primary outcome measure was the change in the Clinical Global Impression-Clinical Benefit (CGI-CB) score over 12 months, and the secondary outcome measure was the change in the Clinical Global Impression-Improvement (CGI-I) score. Results: The data of 139 participants were analyzed, revealing a statistically significant decrease of 26.8% in CGI-CB scores and 13.4% in CGI-I scores over 12 months. Upon comparison between adjacent visit intervals, significant reductions were observed for both measures between month 3 and month 6. Conclusions This study is the first multicenter investigation to simultaneously evaluate the clinical efficacy and tolerability of transitioning to AOM in the context of polypharmacy. The study suggested that AOM may contribute to reducing the clinical burden, thereby improving the quality of life for patients with schizophrenia.