Background: To investigate the clinicopathologic pattern of prostate cancer (PCa) in elderly patients compared with their younger counterparts with a prostate-specific antigen (PSA) level below the low-risk threshold (< 10 ng/mL), which is often a deciding factor for biopsy. Methods: A nationwide database of PCa at the time of biopsy from 2010 to 2020 was constructed from 39 hospitals. Patients were categorized into age groups of < 64 years, 65–69 years, 70–74 years, and ≥ 75 years considering guidelines that recommend PSA testing only for those aged 55–69 years during the study period, the average age of Korean PCa registrants of 70.3 years (2010–2020), and the average life expectancy of Korean males of 80.3 years (2020). Results: The mean ± standard deviation age was 70.3 ± 8.2 years, which was normally distributed (kurtosis = 0.095). Among 14,548 subjects, 54.1%, 39.5%, and 6.4% of them had high-risk disease, intermediate-risk disease, and low-risk disease, respectively. Based on three risk parameters, a marked increase in high-risk cancer was observed in the oldest age group (linear combination, P < 0.001). The same pattern was observed among patients with low-risk disease (PSA < 10 ng/mL), who were divided into PSA tiers as follows: 4–5 ng/mL (P < 0.001), 5–6 ng/mL (P < 0.001), 6–7 ng/mL (P < 0.001), 7–8 ng/mL (P < 0.001), 8–9 ng/mL (P = 0.009), and 9–10 ng/mL (P < 0.001). In all PSA tiers between 4 and 10 ng/mL, multivariate analysis demonstrated a significantly higher prevalence of high-risk cancer in the oldest age group than in the youngest age group. In the lowest tier (4–5 ng/mL), 35.2% of those aged over 75 years had high-risk PCa. Conclusion The older the patient, the more aggressive the PCa. Moreover, there was an increase in high-risk PCa in older males compared with younger males even with a PSA level below the low-risk threshold of 10 ng/mL, suggesting the need to strengthen cancer screening policies in the older population.

Background: The increasing incidence and mortality rates of tuberculosis among older individuals who suffer from multiple morbidities and are vulnerable to malnutrition are major obstacles to efforts to eradicate tuberculosis in the Republic of Korea. Herein, we identified the factors associated with mortality during anti-tuberculosis treatment in patients with pulmonary tuberculosis. Methods: We conducted a case-control study and extracted data from the database of a multi-center prospective observational cohort study in Korea. Among the participants with rifampicin-susceptible pulmonary tuberculosis, the survival group was defined as those who successfully completed treatment within one year, whereas the mortality group was defined as those who died during treatment. Univariable and multivariable logistic regression analyses were performed to identify factors associated with TB mortality. Results: Among 1,119 participants with pulmonary TB registered between 2019 and 2021, 799 and 59 were grouped in the survival and mortality groups, respectively. Age, positive smear results, alarming symptoms, nutrition risk score, Charlson comorbidity index score, and initial standard treatment regimen were significant based on univariable analysis and were selected for the multivariable logistic regression model. Nutrition risk score (adjusted odds ratio, 2.44; 95% confidence interval, 1.72–3.48) and Charlson comorbidity index score (adjusted odds ratio, 1.62; 95% confidence interval, 1.35–1.94) remained statistically significant in the multivariate analysis. Conclusion Nutritional status and comorbidities at baseline were identified as important factors associated with mortality in patients with pulmonary tuberculosis.

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: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

Background: Post-transplantation cyclophosphamide (PTCy) and anti-thymocyte globulin (ATG) are common pro‑ phylactic strategies for graft-versus-host disease (GVHD) after haploidentical hematopoietic stem cell transplantation (haplo-HSCT). Interleukin (IL)-6 is a surrogate marker for cytokine release syndrome (CRS) and acute GVHD.Method The clinical outcomes and complications of haplo-HSCT with PTCy plus ATG versus PTCy monotherapy were compared according to serum IL-6 levels at Chungnam National University Hospital (Daejeon, South Korea) from Jan‑ uary 2019 to February 2023. Results: Forty patients who underwent haplo-HSCT were analyzed. A significant difference in IL-6 levels was observed between the PTCy plus ATG and PTCy alone groups (7.47 ± 10.55 vs. 117.65 ± 127.67; p = 0.003). More patients in the PTCy plus ATG group had a CRS grade of 0 than in the PTCy alone group (p < 0.001). Serum IL-6 levels were associated with grades II–IV acute GVHD (r = 0.547, p < 0.001). The cumulative incidence (CI) of grades II–IV acute GVHD was significantly higher in the PTCy alone group (67.9% vs. 4.8%; p < 0.001). No significant difference in the CI for chronic GVHD was detected between the PTCy plus ATG and PTCy alone groups (72.1% vs. 82.0%; p = 0.730). The CI of 1-year non-relapse mortality was significantly higher in the PTCy alone group than in the PTCy plus ATG group (42.2% vs. 15.9%; p = 0.022). The 1-year overall survival (OS) was significantly better in the PTCy plus ATG group (75.9% vs. 35.3%; p = 0.011). The 1-year GVHD-free, relapse-free survival rate was 29.4% in the PTCy alone group and 54.0% in the PTCy plus ATG group (p = 0.038). Conclusion Serum IL-6 levels were higher in the PTCy alone group than in the PTCy plus ATG group. The addition of ATG before stem cell infusion affected IL-6 levels and reduced the incidences of CRS and grade II–IV acute GVHD in haplo-HSCT patients. This study suggests that PTCy plus ATG as GVHD prophylaxis in haplo-HSCT is beneficial in terms of clinical outcomes and complications of HSCT.

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: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

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: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

Background: To investigate the clinicopathologic pattern of prostate cancer (PCa) in elderly patients compared with their younger counterparts with a prostate-specific antigen (PSA) level below the low-risk threshold (< 10 ng/mL), which is often a deciding factor for biopsy. Methods: A nationwide database of PCa at the time of biopsy from 2010 to 2020 was constructed from 39 hospitals. Patients were categorized into age groups of < 64 years, 65–69 years, 70–74 years, and ≥ 75 years considering guidelines that recommend PSA testing only for those aged 55–69 years during the study period, the average age of Korean PCa registrants of 70.3 years (2010–2020), and the average life expectancy of Korean males of 80.3 years (2020). Results: The mean ± standard deviation age was 70.3 ± 8.2 years, which was normally distributed (kurtosis = 0.095). Among 14,548 subjects, 54.1%, 39.5%, and 6.4% of them had high-risk disease, intermediate-risk disease, and low-risk disease, respectively. Based on three risk parameters, a marked increase in high-risk cancer was observed in the oldest age group (linear combination, P < 0.001). The same pattern was observed among patients with low-risk disease (PSA < 10 ng/mL), who were divided into PSA tiers as follows: 4–5 ng/mL (P < 0.001), 5–6 ng/mL (P < 0.001), 6–7 ng/mL (P < 0.001), 7–8 ng/mL (P < 0.001), 8–9 ng/mL (P = 0.009), and 9–10 ng/mL (P < 0.001). In all PSA tiers between 4 and 10 ng/mL, multivariate analysis demonstrated a significantly higher prevalence of high-risk cancer in the oldest age group than in the youngest age group. In the lowest tier (4–5 ng/mL), 35.2% of those aged over 75 years had high-risk PCa. Conclusion The older the patient, the more aggressive the PCa. Moreover, there was an increase in high-risk PCa in older males compared with younger males even with a PSA level below the low-risk threshold of 10 ng/mL, suggesting the need to strengthen cancer screening policies in the older population.