Heart failure (HF) is a major cause of mortality and morbidity in South Korea, imposing substantial physical, emotional, and financial burdens on patients and society. Despite the high burden of symptom and complex care needs of HF patients, palliative care and hospice services remain underutilized in South Korea due to cultural, institutional, and knowledge-related barriers. This position statement from the Korean Society of Heart Failure emphasizes the need for integrating palliative and hospice care into HF management to improve quality of life and support holistic care for patients and their families. By clarifying the role of palliative care in HF and proposing practical referral criteria, this position statement aims to bridge the gap between HF and palliative care services in South Korea, ultimately improving patient-centered outcomes and aligning treatment with the goals and values of HF patients.

Objective: To analyze the relationship between pelvic organ prolapse (POP) and menopausal hormone therapy (MHT). Methods: This retrospective cohort study used Korean National Health checkup and insurance data from 2002 to 2019. Women who used MHT for more than 6 months between 2002 and 2011 were included in the MHT group; postmenopausal women with no MHT use comprised the non-MHT group. Results: In the non-MHT group, there were 1,001,350 women, while the MHT group had 353,206 women. Tibolone (adjusted hazard ratio [aHR], 0.87; 99% confidence interval [CI], 0.818-0.926) and combined estrogen plus progestin by the manufacturer (CEPM) (aHR, 0.821; 99% CI, 0.758-0.89) were associated with reduced POP risk. The other oral MHT groups and the transdermal estrogen group showed no significant difference in POP risk compared with the non-MHT group (other oral MHT: aHR, 1.045; 99% CI, 0.941-1.161) (transdermal estrogen: aHR, 1.252; 99% CI, 0.731-2.145). Lower body mass index (BMI) (<18.5) was associated with reduced POP risk (aHR, 0.822; 99% CI, 0.698-0.968), while a BMI between 23 and 29.9 was associated with increased risk (BMI 23-24.9: aHR, 1.143; 99% CI, 1.088-1.2) (BMI 25-29.9: aHR, 1.173; 99% CI, 1.12-1.228). All parities had a higher POP risk than parity 1 (parity 0 or no response: aHR, 1.785; 99% CI, 1.589-2.005; parity 2: aHR, 1.434; 99% CI, 1.292-1.592; parity ≥3: aHR, 1.916; 99% CI, 1.712-2.144). Conclusion Tibolone and CEPM use were associated with reduced POP risk in postmenopausal women. Other MHT types showed no significant association with POP.

The 5-hydroxytryptamine type3 (5-HT3 ) receptor, a ligand-gated ion channel, plays a critical role in synaptic transmission. It has been implicated in various neuropsychiatric disorders. This study aimed to elucidate the mechanism by which quetiapine, an atypical antipsychotic, could inhibit 5-HT3 receptor-mediated currents in NCB20 neuroblastoma cells. Whole-cell patch-clamp recordings were used to study effects of quetiapine on receptor ion channel kinetics and its competitive antagonism. Co-application of quetiapine shifted 5-HT concentration-response curve rightward, significantly increasing the EC50 without altering the maximal response (Emax ), suggesting a competitive inhibition. Quetiapine's IC50 varied with 5-HT concentration and treatment condition. The IC50 value of quetiapine was 0.58 μM with 3μM 5-HT and 25.23 μM with 10 μM 5-HT, indicating an inverse relationship between quetiapine efficacy and agonist concentration. Pretreatment of quetiapine significantly enhanced its inhibitory potency, reducing its IC50 from 25.23 μM to 0.20 μM.Interaction kinetics experiments revealed an IC50 of 5.17 μM for an open state of the 5-HT3 receptor, suggesting weaker affinity during receptor activation. Quetiapine also accelerated receptor deactivation and desensitization, suggesting that it could stabilize the receptor in non-conducting states. Additionally, quetiapine significantly prolonged recovery from desensitization without affecting recovery from deactivation, demonstrating its selective impact on receptor kinetics. Inhibition of the 5-HT3 receptor by quetiapine was voltage-independent, and quetiapine exhibited no usedependency, further supporting its role as a competitive antagonist. These findings provide insights into inhibitory mechanism of quetiapine on 5-HT3 receptor and suggest its potential therapeutic implications for modulating serotonergic pathways in neuropsychiatric disorders.

Haloperidol is a typical antipsychotic drug effective in alleviating positive symptoms of schizophrenia by blocking dopamine receptor 2 (DR2). However, it is also known to produce neuropsychiatric effects by acting on various targets other than DR. In this study, we investigated effect of haloperidol on function of 5-hydroxytryptamine (5-HT) 3 receptor, a ligand-gated ion channel belonging to the serotonin receptor family using the whole-cell voltage clamp technique and NCB20 neuroblastoma cells. When co-applied with 5-HT, haloperidol inhibited 5-HT3 receptormediated currents in a concentration-dependent manner. A reduction in maximal effect (E max ) and an increase in EC 50 observed during co-application indicated that haloperidol could act as a non-competitive antagonist of 5-HT3 receptors. Haloperidol inhibited the activation of 5-HT3 receptor, while also accelerating their deactivation and desensitization. The inhibitory effect of haloperidol showed no significant difference between pre- and co-application. Haloperidol did not alter the reversal potential of 5-HT3 receptor currents. Furthermore, haloperidol did not affect recovery from deactivation or desensitization of 5-HT3 receptors. It did not show a use-dependent inhibition either. These findings suggest that haloperidol can exert its inhibitory effect on 5-HT3 receptors by allosterically preventing opening of ion channels. This mechanistic insight enhances our understanding of relationships between 5-HT3 receptors and pharmacological actions of antipsychotics.

The 5-hydroxytryptamine type3 (5-HT3 ) receptor, a ligand-gated ion channel, plays a critical role in synaptic transmission. It has been implicated in various neuropsychiatric disorders. This study aimed to elucidate the mechanism by which quetiapine, an atypical antipsychotic, could inhibit 5-HT3 receptor-mediated currents in NCB20 neuroblastoma cells. Whole-cell patch-clamp recordings were used to study effects of quetiapine on receptor ion channel kinetics and its competitive antagonism. Co-application of quetiapine shifted 5-HT concentration-response curve rightward, significantly increasing the EC50 without altering the maximal response (Emax ), suggesting a competitive inhibition. Quetiapine's IC50 varied with 5-HT concentration and treatment condition. The IC50 value of quetiapine was 0.58 μM with 3μM 5-HT and 25.23 μM with 10 μM 5-HT, indicating an inverse relationship between quetiapine efficacy and agonist concentration. Pretreatment of quetiapine significantly enhanced its inhibitory potency, reducing its IC50 from 25.23 μM to 0.20 μM.Interaction kinetics experiments revealed an IC50 of 5.17 μM for an open state of the 5-HT3 receptor, suggesting weaker affinity during receptor activation. Quetiapine also accelerated receptor deactivation and desensitization, suggesting that it could stabilize the receptor in non-conducting states. Additionally, quetiapine significantly prolonged recovery from desensitization without affecting recovery from deactivation, demonstrating its selective impact on receptor kinetics. Inhibition of the 5-HT3 receptor by quetiapine was voltage-independent, and quetiapine exhibited no usedependency, further supporting its role as a competitive antagonist. These findings provide insights into inhibitory mechanism of quetiapine on 5-HT3 receptor and suggest its potential therapeutic implications for modulating serotonergic pathways in neuropsychiatric disorders.

Haloperidol is a typical antipsychotic drug effective in alleviating positive symptoms of schizophrenia by blocking dopamine receptor 2 (DR2). However, it is also known to produce neuropsychiatric effects by acting on various targets other than DR. In this study, we investigated effect of haloperidol on function of 5-hydroxytryptamine (5-HT) 3 receptor, a ligand-gated ion channel belonging to the serotonin receptor family using the whole-cell voltage clamp technique and NCB20 neuroblastoma cells. When co-applied with 5-HT, haloperidol inhibited 5-HT3 receptormediated currents in a concentration-dependent manner. A reduction in maximal effect (E max ) and an increase in EC 50 observed during co-application indicated that haloperidol could act as a non-competitive antagonist of 5-HT3 receptors. Haloperidol inhibited the activation of 5-HT3 receptor, while also accelerating their deactivation and desensitization. The inhibitory effect of haloperidol showed no significant difference between pre- and co-application. Haloperidol did not alter the reversal potential of 5-HT3 receptor currents. Furthermore, haloperidol did not affect recovery from deactivation or desensitization of 5-HT3 receptors. It did not show a use-dependent inhibition either. These findings suggest that haloperidol can exert its inhibitory effect on 5-HT3 receptors by allosterically preventing opening of ion channels. This mechanistic insight enhances our understanding of relationships between 5-HT3 receptors and pharmacological actions of antipsychotics.

Objective: To analyze the relationship between pelvic organ prolapse (POP) and menopausal hormone therapy (MHT). Methods: This retrospective cohort study used Korean National Health checkup and insurance data from 2002 to 2019. Women who used MHT for more than 6 months between 2002 and 2011 were included in the MHT group; postmenopausal women with no MHT use comprised the non-MHT group. Results: In the non-MHT group, there were 1,001,350 women, while the MHT group had 353,206 women. Tibolone (adjusted hazard ratio [aHR], 0.87; 99% confidence interval [CI], 0.818-0.926) and combined estrogen plus progestin by the manufacturer (CEPM) (aHR, 0.821; 99% CI, 0.758-0.89) were associated with reduced POP risk. The other oral MHT groups and the transdermal estrogen group showed no significant difference in POP risk compared with the non-MHT group (other oral MHT: aHR, 1.045; 99% CI, 0.941-1.161) (transdermal estrogen: aHR, 1.252; 99% CI, 0.731-2.145). Lower body mass index (BMI) (<18.5) was associated with reduced POP risk (aHR, 0.822; 99% CI, 0.698-0.968), while a BMI between 23 and 29.9 was associated with increased risk (BMI 23-24.9: aHR, 1.143; 99% CI, 1.088-1.2) (BMI 25-29.9: aHR, 1.173; 99% CI, 1.12-1.228). All parities had a higher POP risk than parity 1 (parity 0 or no response: aHR, 1.785; 99% CI, 1.589-2.005; parity 2: aHR, 1.434; 99% CI, 1.292-1.592; parity ≥3: aHR, 1.916; 99% CI, 1.712-2.144). Conclusion Tibolone and CEPM use were associated with reduced POP risk in postmenopausal women. Other MHT types showed no significant association with POP.

The 5-hydroxytryptamine type3 (5-HT3 ) receptor, a ligand-gated ion channel, plays a critical role in synaptic transmission. It has been implicated in various neuropsychiatric disorders. This study aimed to elucidate the mechanism by which quetiapine, an atypical antipsychotic, could inhibit 5-HT3 receptor-mediated currents in NCB20 neuroblastoma cells. Whole-cell patch-clamp recordings were used to study effects of quetiapine on receptor ion channel kinetics and its competitive antagonism. Co-application of quetiapine shifted 5-HT concentration-response curve rightward, significantly increasing the EC50 without altering the maximal response (Emax ), suggesting a competitive inhibition. Quetiapine's IC50 varied with 5-HT concentration and treatment condition. The IC50 value of quetiapine was 0.58 μM with 3μM 5-HT and 25.23 μM with 10 μM 5-HT, indicating an inverse relationship between quetiapine efficacy and agonist concentration. Pretreatment of quetiapine significantly enhanced its inhibitory potency, reducing its IC50 from 25.23 μM to 0.20 μM.Interaction kinetics experiments revealed an IC50 of 5.17 μM for an open state of the 5-HT3 receptor, suggesting weaker affinity during receptor activation. Quetiapine also accelerated receptor deactivation and desensitization, suggesting that it could stabilize the receptor in non-conducting states. Additionally, quetiapine significantly prolonged recovery from desensitization without affecting recovery from deactivation, demonstrating its selective impact on receptor kinetics. Inhibition of the 5-HT3 receptor by quetiapine was voltage-independent, and quetiapine exhibited no usedependency, further supporting its role as a competitive antagonist. These findings provide insights into inhibitory mechanism of quetiapine on 5-HT3 receptor and suggest its potential therapeutic implications for modulating serotonergic pathways in neuropsychiatric disorders.

Haloperidol is a typical antipsychotic drug effective in alleviating positive symptoms of schizophrenia by blocking dopamine receptor 2 (DR2). However, it is also known to produce neuropsychiatric effects by acting on various targets other than DR. In this study, we investigated effect of haloperidol on function of 5-hydroxytryptamine (5-HT) 3 receptor, a ligand-gated ion channel belonging to the serotonin receptor family using the whole-cell voltage clamp technique and NCB20 neuroblastoma cells. When co-applied with 5-HT, haloperidol inhibited 5-HT3 receptormediated currents in a concentration-dependent manner. A reduction in maximal effect (E max ) and an increase in EC 50 observed during co-application indicated that haloperidol could act as a non-competitive antagonist of 5-HT3 receptors. Haloperidol inhibited the activation of 5-HT3 receptor, while also accelerating their deactivation and desensitization. The inhibitory effect of haloperidol showed no significant difference between pre- and co-application. Haloperidol did not alter the reversal potential of 5-HT3 receptor currents. Furthermore, haloperidol did not affect recovery from deactivation or desensitization of 5-HT3 receptors. It did not show a use-dependent inhibition either. These findings suggest that haloperidol can exert its inhibitory effect on 5-HT3 receptors by allosterically preventing opening of ion channels. This mechanistic insight enhances our understanding of relationships between 5-HT3 receptors and pharmacological actions of antipsychotics.

Lecanemab and donanemab have received full U.S. Food and Drug Administration (FDA) approval, and subsequently, lecanemab has been approved by the Korean FDA and it has recently entered commercial use in Korea. This has increased interest in anti-amyloid immunotherapy for Alzheimer’s disease. Anti-amyloid immunotherapy has shown potential to modify the progression of the disease by specifically binding to amyloid β, a key pathological product in Alzheimer’s disease, and eliminating accumulated amyloid plaques in the brain. However, this treatment can be accompanied by a side-effect, amyloid-related imaging abnormalities (ARIA), which requires periodic monitoring by MRI. It is crucial to detect ARIA and accurately assess the severity by radiology. The role of the radiologist is important in this context, requiring proficiency in basic knowledge of ARIA, and in diagnosing/evaluating ARIA. This review aims to comprehensively cover aspects of ARIA, including its definition, pathophysiology, incidence, risk factors, assessment of severity by radiology, differential diagnosis, and management.