Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Objective: Deficits in social cognition (mentalization) and other cognitive deficits have been reported in patients with major depressive disorder (MDD) and may influence treatment response. This study examined the impact of cognitive function on treatment response of patients with MDD after 8 weeks of medication and whether the impact was mediated by mentalization. Methods: Cognitive function (memory, attention, executive function, processing speed) and mentalization were measured in 28 patients with MDD at baseline using neuropsychological tests and self-report scales. The treatment response was defined as the rate of improvement in symptom severity and global function. Results: Multiple regression analyses, controlling for mentalization and cognitive function, separately revealed that delayed recall was a negative predictor of functional improvement after 8 weeks of treatment, while mentalization was a positive predictor. A single mediation model using PROCESS macro showed that delayed recall and Digit Span backward indirectly affected functional improvement, mediated by mentalization. When age at onset was controlled for as a covariate, the mediating effect lost significance, and the direct effect of delayed recall on functional improvement was still significant. Conclusion Despite the small sample size, our results provide evidence that patients with MDD and low memory (delayed recall) at baseline may benefit more from short-term pharmacological treatments.

Background: Complete revascularization has demonstrated better outcomes in patients with acute myocardial infarction (AMI) and multivessel disease. However, in the case of left main (LM) culprit lesion AMI with multivessel disease, there is limited evidence to suggest that complete revascularization is better. Methods: We reviewed 16,831 patients in the Korea Acute Myocardial Infarction Registry who were treated from July 2016 to June 2020, and 399 patients were enrolled with LM culprit lesion AMI treated with percutaneous coronary intervention. We categorized the patients as those treated with complete revascularization (n=295) or incomplete revascularization (n=104). The study endpoint was major adverse cardiac and cerebrovascular events (MACCE), a composite of all-cause death, myocardial infarction, ischemia-driven revascularization, stent thrombosis, and stroke. We performed propensity score matching (PSM) and analyzed the incidence of MACCE at 1 year. Results: After PSM, the two groups were well balanced. There was no significant difference between the two groups in MACCE at 1 year (12.1% vs. 15.2%; hazard ratio, 1.28; 95% confidence interval, 0.60–2.74; p=0.524) after PSM. The components of MACCE and major bleeding were also not significantly different. Conclusion There was no significant difference in clinical outcomes between the groups treated with complete or incomplete revascularization for LM culprit lesion AMI with multivessel disease.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Objective: Deficits in social cognition (mentalization) and other cognitive deficits have been reported in patients with major depressive disorder (MDD) and may influence treatment response. This study examined the impact of cognitive function on treatment response of patients with MDD after 8 weeks of medication and whether the impact was mediated by mentalization. Methods: Cognitive function (memory, attention, executive function, processing speed) and mentalization were measured in 28 patients with MDD at baseline using neuropsychological tests and self-report scales. The treatment response was defined as the rate of improvement in symptom severity and global function. Results: Multiple regression analyses, controlling for mentalization and cognitive function, separately revealed that delayed recall was a negative predictor of functional improvement after 8 weeks of treatment, while mentalization was a positive predictor. A single mediation model using PROCESS macro showed that delayed recall and Digit Span backward indirectly affected functional improvement, mediated by mentalization. When age at onset was controlled for as a covariate, the mediating effect lost significance, and the direct effect of delayed recall on functional improvement was still significant. Conclusion Despite the small sample size, our results provide evidence that patients with MDD and low memory (delayed recall) at baseline may benefit more from short-term pharmacological treatments.

Objective: Deficits in social cognition (mentalization) and other cognitive deficits have been reported in patients with major depressive disorder (MDD) and may influence treatment response. This study examined the impact of cognitive function on treatment response of patients with MDD after 8 weeks of medication and whether the impact was mediated by mentalization. Methods: Cognitive function (memory, attention, executive function, processing speed) and mentalization were measured in 28 patients with MDD at baseline using neuropsychological tests and self-report scales. The treatment response was defined as the rate of improvement in symptom severity and global function. Results: Multiple regression analyses, controlling for mentalization and cognitive function, separately revealed that delayed recall was a negative predictor of functional improvement after 8 weeks of treatment, while mentalization was a positive predictor. A single mediation model using PROCESS macro showed that delayed recall and Digit Span backward indirectly affected functional improvement, mediated by mentalization. When age at onset was controlled for as a covariate, the mediating effect lost significance, and the direct effect of delayed recall on functional improvement was still significant. Conclusion Despite the small sample size, our results provide evidence that patients with MDD and low memory (delayed recall) at baseline may benefit more from short-term pharmacological treatments.

Background: Complete revascularization has demonstrated better outcomes in patients with acute myocardial infarction (AMI) and multivessel disease. However, in the case of left main (LM) culprit lesion AMI with multivessel disease, there is limited evidence to suggest that complete revascularization is better. Methods: We reviewed 16,831 patients in the Korea Acute Myocardial Infarction Registry who were treated from July 2016 to June 2020, and 399 patients were enrolled with LM culprit lesion AMI treated with percutaneous coronary intervention. We categorized the patients as those treated with complete revascularization (n=295) or incomplete revascularization (n=104). The study endpoint was major adverse cardiac and cerebrovascular events (MACCE), a composite of all-cause death, myocardial infarction, ischemia-driven revascularization, stent thrombosis, and stroke. We performed propensity score matching (PSM) and analyzed the incidence of MACCE at 1 year. Results: After PSM, the two groups were well balanced. There was no significant difference between the two groups in MACCE at 1 year (12.1% vs. 15.2%; hazard ratio, 1.28; 95% confidence interval, 0.60–2.74; p=0.524) after PSM. The components of MACCE and major bleeding were also not significantly different. Conclusion There was no significant difference in clinical outcomes between the groups treated with complete or incomplete revascularization for LM culprit lesion AMI with multivessel disease.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Background: Complete revascularization has demonstrated better outcomes in patients with acute myocardial infarction (AMI) and multivessel disease. However, in the case of left main (LM) culprit lesion AMI with multivessel disease, there is limited evidence to suggest that complete revascularization is better. Methods: We reviewed 16,831 patients in the Korea Acute Myocardial Infarction Registry who were treated from July 2016 to June 2020, and 399 patients were enrolled with LM culprit lesion AMI treated with percutaneous coronary intervention. We categorized the patients as those treated with complete revascularization (n=295) or incomplete revascularization (n=104). The study endpoint was major adverse cardiac and cerebrovascular events (MACCE), a composite of all-cause death, myocardial infarction, ischemia-driven revascularization, stent thrombosis, and stroke. We performed propensity score matching (PSM) and analyzed the incidence of MACCE at 1 year. Results: After PSM, the two groups were well balanced. There was no significant difference between the two groups in MACCE at 1 year (12.1% vs. 15.2%; hazard ratio, 1.28; 95% confidence interval, 0.60–2.74; p=0.524) after PSM. The components of MACCE and major bleeding were also not significantly different. Conclusion There was no significant difference in clinical outcomes between the groups treated with complete or incomplete revascularization for LM culprit lesion AMI with multivessel disease.

Objective: Deficits in social cognition (mentalization) and other cognitive deficits have been reported in patients with major depressive disorder (MDD) and may influence treatment response. This study examined the impact of cognitive function on treatment response of patients with MDD after 8 weeks of medication and whether the impact was mediated by mentalization. Methods: Cognitive function (memory, attention, executive function, processing speed) and mentalization were measured in 28 patients with MDD at baseline using neuropsychological tests and self-report scales. The treatment response was defined as the rate of improvement in symptom severity and global function. Results: Multiple regression analyses, controlling for mentalization and cognitive function, separately revealed that delayed recall was a negative predictor of functional improvement after 8 weeks of treatment, while mentalization was a positive predictor. A single mediation model using PROCESS macro showed that delayed recall and Digit Span backward indirectly affected functional improvement, mediated by mentalization. When age at onset was controlled for as a covariate, the mediating effect lost significance, and the direct effect of delayed recall on functional improvement was still significant. Conclusion Despite the small sample size, our results provide evidence that patients with MDD and low memory (delayed recall) at baseline may benefit more from short-term pharmacological treatments.