The mechanism of electroconvulsive therapy (ECT) in schizophrenia remains unclear, with limited research available. Previous studies have reported ECT-induced changes in protein markers, including neurotrophic factors, inflammatory markers, and signaling proteins, but findings have been inconsistent. This study reviews existing literature on protein changes associated with ECT and explores potential molecular mechanisms underlying its effects. Additionally, we present pilot findings from 34 patients with schizophrenia or schizoaffective disorder who underwent ECT at Seoul National University Hospital. Blood samples collected before and after ECT were analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins (DEPs), with Pearson’s correlation analysis examining their association with symptom changes. Talin 2 emerged as a potential biomarker linked to clinical improvement. However, given the small sample size, these findings require cautious interpretation. Further research is needed to clarify the molecular mechanisms underlying ECT’s therapeutic effects in schizophrenia.

The mechanism of electroconvulsive therapy (ECT) in schizophrenia remains unclear, with limited research available. Previous studies have reported ECT-induced changes in protein markers, including neurotrophic factors, inflammatory markers, and signaling proteins, but findings have been inconsistent. This study reviews existing literature on protein changes associated with ECT and explores potential molecular mechanisms underlying its effects. Additionally, we present pilot findings from 34 patients with schizophrenia or schizoaffective disorder who underwent ECT at Seoul National University Hospital. Blood samples collected before and after ECT were analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins (DEPs), with Pearson’s correlation analysis examining their association with symptom changes. Talin 2 emerged as a potential biomarker linked to clinical improvement. However, given the small sample size, these findings require cautious interpretation. Further research is needed to clarify the molecular mechanisms underlying ECT’s therapeutic effects in schizophrenia.

The mechanism of electroconvulsive therapy (ECT) in schizophrenia remains unclear, with limited research available. Previous studies have reported ECT-induced changes in protein markers, including neurotrophic factors, inflammatory markers, and signaling proteins, but findings have been inconsistent. This study reviews existing literature on protein changes associated with ECT and explores potential molecular mechanisms underlying its effects. Additionally, we present pilot findings from 34 patients with schizophrenia or schizoaffective disorder who underwent ECT at Seoul National University Hospital. Blood samples collected before and after ECT were analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins (DEPs), with Pearson’s correlation analysis examining their association with symptom changes. Talin 2 emerged as a potential biomarker linked to clinical improvement. However, given the small sample size, these findings require cautious interpretation. Further research is needed to clarify the molecular mechanisms underlying ECT’s therapeutic effects in schizophrenia.

The mechanism of electroconvulsive therapy (ECT) in schizophrenia remains unclear, with limited research available. Previous studies have reported ECT-induced changes in protein markers, including neurotrophic factors, inflammatory markers, and signaling proteins, but findings have been inconsistent. This study reviews existing literature on protein changes associated with ECT and explores potential molecular mechanisms underlying its effects. Additionally, we present pilot findings from 34 patients with schizophrenia or schizoaffective disorder who underwent ECT at Seoul National University Hospital. Blood samples collected before and after ECT were analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins (DEPs), with Pearson’s correlation analysis examining their association with symptom changes. Talin 2 emerged as a potential biomarker linked to clinical improvement. However, given the small sample size, these findings require cautious interpretation. Further research is needed to clarify the molecular mechanisms underlying ECT’s therapeutic effects in schizophrenia.

The mechanism of electroconvulsive therapy (ECT) in schizophrenia remains unclear, with limited research available. Previous studies have reported ECT-induced changes in protein markers, including neurotrophic factors, inflammatory markers, and signaling proteins, but findings have been inconsistent. This study reviews existing literature on protein changes associated with ECT and explores potential molecular mechanisms underlying its effects. Additionally, we present pilot findings from 34 patients with schizophrenia or schizoaffective disorder who underwent ECT at Seoul National University Hospital. Blood samples collected before and after ECT were analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins (DEPs), with Pearson’s correlation analysis examining their association with symptom changes. Talin 2 emerged as a potential biomarker linked to clinical improvement. However, given the small sample size, these findings require cautious interpretation. Further research is needed to clarify the molecular mechanisms underlying ECT’s therapeutic effects in schizophrenia.

Background: Gallbladder cancer (GBC) is usually detected in advanced stages with a low 5-year survival rate. Delta-like ligand 4 (DLL4), vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-2alpha (HIF2α) have been studied for their role in tumorigenesis and potential for therapeutic target, and multiple clinical trials of the agents targeting them are ongoing. We investigated the expression of these markers in surgically resected GBC and tried to reveal their association with the clinicopathologic features, mutual correlation of their expression, and prognosis of the GBC patients by their expression. Methods: We constructed the tissue microarray blocks of 99 surgically resected GBC specimens and performed immunohistochemistry of DLL4, VEGF, and HIF2α. We used the quantitative digital image analysis to evaluate DLL4 and VEGF expression, while the expression of HIF2α was scored manually. Results: The expression of VEGF and HIF2α showed a significant trend with tumor differentiation (p= .028 and p= .006, respectively). We found that the high DLL4 and VEGF expression were significantly correlated with lymph node metastasis (p= .047, both). The expression of VEGF and HIF2α were significantly correlated (p < .001). The GBC patients with low HIF2α expression showed shorter recurrence-free survival than those with high HIF2α expression. Conclusions This study suggested the possibility of the usage of DLL4 and VEGF to predict the lymph node metastasis and the possibility of VEGF and HIF2α to predict the expression level mutually. Further studies may be needed to validate our study results and eventually accelerate the introduction of the targeted therapy in GBC.