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.

A biosynthetic gene cluster for the bioactive fungal sesterterpenoids variecolin ( 1) and variecolactone ( 2) was identified in Aspergillus aculeatus ATCC 16872. Heterologous production of 1 and 2 was achieved in Aspergillus oryzae by expressing the sesterterpene synthase VrcA and the cytochrome P450 VrcB. Intriguingly, the replacement of VrcB with homologous P450s from other fungal terpenoid pathways yielded three new variecolin analogues ( 5- 7). Analysis of the compounds' anticancer activity in vitro and in vivo revealed that although 5 and 1 had comparable activities, 5 was associated with significantly reduced toxic side effects in cancer-bearing mice, indicating its potentially broader therapeutic window. Our study describes the first tests of variecolin and its analogues in animals and demonstrates the utility of synthetic biology for creating molecules with improved biological activities.

Background: Parathyroid adenoma (PA) is a common endocrine disease linked to multiple complications, but the pathophysiology of the disease remains incompletely understood. The study aimed to identify the key regulator proteins and pathways of PA according to functionality and volume through quantitative proteomic analyses. Methods: We conducted a retrospective study of 15 formalin-fixed, paraffin-embedded PA samples from tertiary hospitals in South Korea. Proteins were extracted, digested, and the resulting peptides were analyzed using liquid chromatography-tandem mass spectrometry. Pearson correlation analysis was employed to identify proteins significantly correlated with clinical variables. Canonical pathways and transcription factors were analyzed using Ingenuity Pathway Analysis. Results: The median age of the participants was 52 years, and 60.0% were female. Among the 8,153 protein groups analyzed, 496 showed significant positive correlations with adenoma volume, while 431 proteins were significantly correlated with parathyroid hormone (PTH) levels. The proteins SLC12A9, LGALS3, and CARM1 were positively correlated with adenoma volume, while HSP90AB2P, HLA-DRA, and SCD5 showed negative correlations. DCPS, IRF2BPL, and FAM98A were the main proteins that exhibited positive correlations with PTH levels, and SLITRK4, LAP3, and AP4E1 had negative correlations. Canonical pathway analysis demonstrated that the RAN and sirtuin signaling pathways were positively correlated with both PTH levels and adenoma volume, while epithelial adherence junction pathways had negative correlations. Conclusion Our study identified pivotal proteins and pathways associated with PA, offering potential therapeutic targets. These findings accentuate the importance of proteomics in understanding disease pathophysiology and the need for further research.

Background: This study aimed to compare the effects of applying a vibrating foam roller before resistance exercise versus after resistance exercise on changes in serum muscle damage markers, muscle stiffness, and range of motion. This study also aimed to provide foundational data for optimizing the timing of vibrating foam roller application to enhance recovery after resistance exercise in practical settings. Methods: Twelve healthy adult males were recruited as participants. Each participant was subjected to three interventions in a random order with a washout period of at least 5 days: vibration foam rolling before resistance exercise, vibration foam rolling after resistance exercise, and resistance exercise without vibration foam rolling. Blood creatine kinase, knee flexion range of motion, and muscle stiffness were measured before, immediately after, 24 hours after, and 48 hours after exercise and foam rolling protocols. Results: Creatine kinase levels in vibration foam rolling after resistance exercise were significantly lower than those in vibration foam rolling before resistance exercise at 24 and 48 hours post-exercise. Muscle stiffness was significantly lower immediately and 24 hours post-exercise in vibration foam rolling after resistance exercise than in vibration foam rolling before resistance exercise and resistance exercise without vibration foam rolling. Knee flexion range of motion was significantly lower in resistance exercise without vibration foam rolling than in vibration foam rolling after resistance exercise at 24 and 48 hours post-exercise. Conclusions The application of vibration foam rolling after resistance exercise was more effective than that before exercise in decreasing muscle damage markers, reducing muscle stiffness, and improving the range of motion.

Background: The purpose of this study was to identify the prevalence of posttraumatic embitterment disorder (PTED) among soldiers, and examine its relation to stress, depression, self-esteem, impulsiveness, and suicidal ideation. Methods: The subjects of this study were 200 soldiers and 197 control subjects, a total of 397 persons. Measurement tools used included the PTED self-rating scale, Stress Response Inventory, Beck Depression Inventory, Rosenberg Self-Esteem Inventory, Barratt Impulsiveness Scale, and Beck Scale of Suicide Ideation.Result: The major findings of the analysis are as follows: first, 11.5% of the soldiers were in the risk group for PTED, and 4% of them had PTED. Second, PTED in the soldiers was significantly associated with a number of variables such as their educational background, stress, depression, self-esteem, impulsiveness, and suicidal ideation, while it was not significantly associated with age. Third, through the hierarchical multiple regression analysis, it was found that academic background, stress, and depression had a statistically significant positive effect on the incidence of PTED in the soldiers. Conclusion In order to prevent and effectively intervene in PTED in soldiers, there is a need for interventional efforts focused on depression and stress related to negative life events.

Background: The relationship between cystitis glandularis (CG) and bladder malignancy remains unclear. Methods: We identified the oncologic significance of CG at the molecular level using liquid chromatography-tandem mass spectrometry-based proteomic analysis of 10 CG, 12 urothelial carcinoma (UC), and nine normal urothelium (NU) specimens. Differentially expressed proteins (DEPs) were identified based on an analysis of variance false discovery rate < 0.05, and their functional enrichment was analyzed using a network model, Gene Set Enrichment Analysis, and Gene Ontology annotation. Results: We identified 9,890 proteins across all samples and 1,139 DEPs among the three entities. A substantial number of DEPs overlapped in CG/NU, distinct from UC. Interestingly, we found that a subset of DEP clusters (n = 53, 5%) was differentially expressed in NU but similarly between CG and UC. This “UC-like signature” was enriched for reactive oxygen species (ROS) and energy metabolism, growth and DNA repair, transport, motility, epithelial-mesenchymal transition, and cell survival. Using the top 10 shortlisted DEPs, including SOD2, PRKCD, CYCS, and HCLS1, we identified functional elements related to ROS metabolism, development, and transport using network analysis. The abundance of these four molecules in UC/CG than in NU was consistent with the oncologic functions in CG. Conclusions Using a proteomic approach, we identified a predominantly non-neoplastic landscape of CG, which was closer to NU than to UC. We also confirmed a small subset of common DEPs in UC and CG, suggesting that altered ROS metabolism might imply potential cancerous risks in CG.