Purpose: To investigate whether a new phospholipid-releasing soft contact lens can improve symptoms of dry eyes. Methods: The study used 2.5-3.0 kg New Zealand rabbits including both normal non-dry eye rabbits and dry eye rabbits, the latter having undergone electrocauterization of the meibomian glands to block the gland orifices. Each rabbit wore a control contact lens on one eye and a phospholipid-releasing contact lens on the other eye daily. Phospholipid-releasing and control contact lenses were provided by NEOVISION Co., Ltd. The parameters assessed included tear film break-up time, tear osmolarity, ocular surface staining, and central corneal thickness. After the experiment, the rabbits were euthanized and their conjunctival tissue was stained with Periodic Acid Schiff (PAS) to observe conjunctival goblet cells. Results: In both dry eye and normal non-dry eye rabbits, tear film break-up time was longer and tear osmolarity was lower when using the phospholipid-releasing contact lens compared to the control contact lens. The ocular surface remained unstained in normal non-dry eye rabbits while staining was observed in dry eye rabbits. There was no significant difference in central corneal thickness between the control and phospholipid-releasing contact lenses in either group. PAS staining showed no difference in conjunctival goblet cell density between the two lens types in normal non-dry eye rabbits. However, in dry eye rabbits, the conjunctival goblet cell density tended to be slightly higher with the phospholipid-releasing contact lens compared to the control lens. Conclusions Phospholipid-releasing contact lenses may help reduce dry eye symptoms and minimize contact lens-related complications by stabilizing the tear film and lowering tear osmolarity.

Objective: Cardiac arrest and cardiopulmonary resuscitation (CA/R) lead to whole-body ischemia and reperfusion (IR) injury, causing multiple organ dysfunction, including ischemic spinal cord injury. The thoracic spinal cord levels are crucial for maintaining the sympathetic functions vital for life. This study examined blood-spinal cord barrier (BSCB) leakage and astrocyte endfeet (AEF) disruption and their effects on survival, physiological variables, and neuronal damage/death in the intermediate zone (IMZ) at the seventh thoracic spinal cord level after asphyxial CA/R in rats. Methods: The rats underwent whole-body IR injury by asphyxial CA/R. Kaplan-Meier analysis was conducted to assess the cumulative survival post-CA/R. The histological changes post-CA/R were evaluated using immunohistochemistry, histofluorescence, and double histofluorescence. Results: No significant differences in body weight, mean arterial pressure, and heart rate were found between the sham and CA/R groups post-CA/R. The survival rates in the CA/R group at 12, 24, and 48 hours were 62.58%, 36.37%, and 7.8%, respectively. Neuronal loss and BSCB leakage began 12 hours post-CA/R, increasing with time. Reactive astrogliosis appeared at 12 hours and increased, while AEF disruption around blood vessels was evident at 48 hours. Conclusion The survival rate declined significantly by 48 hours post-CA/R. Neuronal loss and BSCB leakage in the thoracic spinal cord IMZ was evident at 12 hours and significant by 48 hours, aligning with AEF disruption. Neuronal loss in the thoracic spinal cord IMZ post-CA/R may be related to BSCB leakage and AEF disruption.

Background: This study aimed to evaluate the degree of glenoid concavity restoration and its effect on surgical failure after arthroscopic bony Bankart repair for recurrent anterior shoulder instability with a bony Bankart lesion. Methods: Forty-one patients who underwent arthroscopic bony Bankart repair for recurrent anterior shoulder instability with a bony Bankart lesion were retrospectively evaluated. All patients underwent 3-dimensional computed tomography (3D-CT) preoperatively to evaluate the glenoid concavity using the bony shoulder stability ratio (BSSR). Bony fragments were incorporated to the anterior glenoid during arthroscopic stabilization procedure. All patients were reevaluated by 3D-CT at postoperative 1 year to assess the changes in the BSSR and the final glenoid bone defect size after bony Bankart repair. Clinical outcomes including surgical failure were evaluated at least 2 years after surgery. Results: The BSSR significantly increased after surgery (26.0% ± 14.0% preoperatively and 35.5% ± 13.2% postoperatively, p < 0.001). Preoperative glenoid bone defect size was 16.2% ± 8.1%, and bony Bankart fragment size was 11.3% ± 7.2%. Four patients (9.8%) had recurrent instability requiring revision surgery. In patients with surgical failure, the BSSR was not improved after surgery (18.2% ± 13.3% preoperatively and 23.1% ± 17.3% postoperatively, p = 0.24). In contrast, patients without surgical failure showed significantly improved BSSR after surgery (26.9% ± 14.0% preoperatively and 36.9% ± 12.2% postoperatively, p < 0.001).No significant differences were found in the final glenoid bone defect size (6.6% ± 5.9% in patients with surgical failure vs. 6.2% ± 5.7% in patients without surgical failure, p = 0.92) and bony Bankart fragment nonunion rate (0% in patients with surgical failure vs. 5.4% in patients without surgical failure, p = 0.99) between patients with and without surgical failure. Conclusions Glenoid concavity, as represented by the BSSR, improved after arthroscopic bony Bankart repair, and satisfactory restoration of the glenoid concavity led to successful clinical outcomes without surgical failure. The BSSR could be considered an important factor for predicting clinical outcomes after arthroscopic bony Bankart repair. However, further research including more contributing factors is needed to better analyze the impact of the BSSR on clinical outcomes.

Purpose: This multicenter, open-label, phase II trial evaluated the efficacy and safety of bortezomib combined with dexamethasone for the treatment of relapsed/refractory cutaneous T-cell lymphoma (CTCL) in previously treated patients across 14 institutions in South Korea. Materials and Methods: Between September 2017 and July 2020, 29 patients with histologically confirmed CTCL received treatment, consisting of eight 4-week cycles of induction therapy followed by maintenance therapy, contingent upon response, for up to one year. The primary endpoint was the proportion of patients achieving an objective global response. Results: Thirteen of the 29 patients (44.8%) achieved an objective global response, including two complete responses. The median progression-free survival (PFS) was 5.8 months, with responders showing a median PFS of 14.0 months. Treatment-emergent adverse events were generally mild, with a low incidence of peripheral neuropathy and hematologic toxicities. Despite the trend toward shorter PFS in patients with higher mutation burdens, genomic profiling before and after treatment showed no significant emergence of new mutations indicative of disease progression. Conclusion This study supports the use of bortezomib and dexamethasone as a viable and safe treatment option for previously treated CTCL, demonstrating substantial efficacy and manageability in adverse effects. Further research with a larger cohort is suggested to validate these findings and explore the prognostic value of mutation profiles.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

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.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

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.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

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.