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: 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: 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: 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: 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.

By investigating the characteristics and prognosis of breast cancer (BC) patients who have undergone hormone replacement therapy (HRT), this study addresses a gap in the existing literature. A total of 17,355 postmenopausal patients with BC were analyzed using data from the Korea Breast Cancer Society database (2000–2014). Among them, 3,585 (20.7%) had a history of HRT before BC diagnosis (HRT group), while 13,770 (79.3%) never received HRT (non-HRT group). The HRT group exhibited an earlier pathologic stage, lower histologic and nuclear grades, and a higher rate of breast conservation surgery compared to the non-HRT group. Furthermore, this group had a higher rate of screening participation and a greater proportion of patients with a normal or overweight body mass index (BMI). The prognosis of the HRT group was better than that of the non-HRT group, with a 5-year overall survival rate of 93.9% versus 91.7% (p < 0.001). The hazard ratio for the HRT group was 0.7 (95% confidence interval, 0.608–0.805; p < 0.001). Increased screening participation, longer HRT duration, and a normal or overweight BMI were associated with a better prognosis in the HRT group. Patients with BC who underwent HRT showed better clinicopathological characteristics and prognosis than those who did not receive HRT. The results highlighted significant differences in patients who underwent screening and those with a normal or overweight BMI. Furthermore, a longer HRT duration was associated with a better prognosis.

A 55-year-old male with hemophilia A came to the outpatient clinic with chest pain for several days after overdose injection of coagulation factor. He was a heavy smoker and a chronic alcoholic. An electrocardiogram (ECG) showed no specific change. A coronary computed tomography showed moderate stenosis with soft plaque at the distal segment of right coronary artery. His pain was improved with antianginal and reflux medications. Twenty days later, he ran to the emergency room complaining of squeezing chest pain. ECG showed mild ST segment elevation in inferior territories. Invasive coronary angiography via right radial artery revealed severe thrombotic occlusion at the same lesion. A bare metal stent was deployed and dual antiplatelet therapy including aspirin and clopidogrel had been maintained for 6 months under the conventional hemophilia management. The patient did not develop any coronary events just with single clopidogrel therapy for 5 years until he passed away from pancreatic cancer. Our case implicates that the invasive coronary intervention and post-procedural management could be safely performed with conventional standards of care while maintaining the usual dose of coagulation factors in a hemophilia patient with acute coronary syndrome.

Background: and Purpose In young patients (aged 18–60 years) with patent foramen ovale (PFO)- associated stroke, percutaneous closure has been found to be useful for preventing recurrent ischemic stroke or transient ischemic attack (TIA). However, it remains unknown whether PFO closure is also beneficial in older patients. Methods: Patients aged ≥60 years who had a cryptogenic stroke and PFO from ten hospitals in South Korea were included. The effect of PFO closure plus medical therapy over medical therapy alone was assessed by a propensity-score matching method in the overall cohort and in those with a high-risk PFO, characterized by the presence of an atrial septal aneurysm or a large shunt. Results: Out of the 437 patients (mean age, 68.1), 303 (69%) had a high-risk PFO and 161 (37%) patients underwent PFO closure. Over a median follow-up of 3.9 years, recurrent ischemic stroke or TIA developed in 64 (14.6%) patients. In the propensity score-matched cohort of the overall patients (130 pairs), PFO closure was associated with a significantly lower risk of a composite of ischemic stroke or TIA (hazard ratio [HR]: 0.45; 95% confidence interval [CI]: 0.24–0.84; P=0.012), but not for ischemic stroke. In a subgroup analysis of confined to the high-risk PFO patients (116 pairs), PFO closure was associated with significantly lower risks of both the composite of ischemic stroke or TIA (HR: 0.40; 95% CI: 0.21–0.77; P=0.006) and ischemic stroke (HR: 0.47; 95% CI: 0.23–0.95; P=0.035). Conclusion Elderly patients with cryptogenic stroke and PFO have a high recurrence rate of ischemic stroke or TIA, which may be significantly reduced by device closure.

Objective: Emergency department-based interventions are known to be effective at reducing the risk of repeat suicide attempts among patients admitted to emergency departments after attempting suicide. However, the factors that influence loss to follow-up after emergency department-based interventions are not well known. Methods: This study investigated suicide attempt patients who registered with an emergency department-based intervention and received counseling at least once from January 2019 to December 2020. Patients were allocated to a follow-up group or a loss-to-follow-up group depending on whether emergency department-based interventions had been performed more than three times. Clinical factors and socioeconomic status were considered independent variables. Logistic regression analysis was performed to identify factors that influenced loss to emergency department-based interventions. Results: Of 339 patients enrolled, 210 (61.9%) were lost to follow-up. Time taken to initiation of intervention after discharge (adjusted odds ratio [aOR]=2.42; 95% confidence interval [CI], 1.38-4.30) and suicide attempt associated with physical illness (aOR=0.31; 95% CI, 0.14-0.68) independently influenced loss to emergency department-based interventions. Conclusion Initiation of intervention after discharge significantly influenced emergency department-based intervention follow-up loss of suicide attempt patients. The study suggests initiation of intervention prior to discharge might reduce the risk of repeat suicide attempts.

A 55-year-old male with hemophilia A came to the outpatient clinic with chest pain for several days after overdose injection of coagulation factor. He was a heavy smoker and a chronic alcoholic. An electrocardiogram (ECG) showed no specific change. A coronary computed tomography showed moderate stenosis with soft plaque at the distal segment of right coronary artery. His pain was improved with antianginal and reflux medications. Twenty days later, he ran to the emergency room complaining of squeezing chest pain. ECG showed mild ST segment elevation in inferior territories. Invasive coronary angiography via right radial artery revealed severe thrombotic occlusion at the same lesion. A bare metal stent was deployed and dual antiplatelet therapy including aspirin and clopidogrel had been maintained for 6 months under the conventional hemophilia management. The patient did not develop any coronary events just with single clopidogrel therapy for 5 years until he passed away from pancreatic cancer. Our case implicates that the invasive coronary intervention and post-procedural management could be safely performed with conventional standards of care while maintaining the usual dose of coagulation factors in a hemophilia patient with acute coronary syndrome.