Background and Objectives: Although the clinical consequences of advanced heart failure (HF) may be similar across different etiologies of cardiomyopathies, their proteomic expression may show substantial differences in relation to underlying pathophysiology. We aimed to identify myocardial tissue–based proteomic characteristics and the underlying molecular pathophysiology in non-ischemic cardiomyopathy with different etiologies. Methods: Comparative extensive proteomic analysis of the myocardium was performed in nine patients with biopsy-proven non-ischemic cardiomyopathies (3 dilated cardiomyopathy [DCM], 2 hypertrophic cardiomyopathy [HCM], and 4 myocarditis) as well as five controls using tandem mass tags combined with liquid chromatography–mass spectrometry.Differential protein expression analysis, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify proteomic differences and molecular mechanisms in each cardiomyopathy type compared to the control. Proteomic characteristics were further evaluated in accordance with clinical and pathological findings. Results: The principal component analysis score plot showed that the controls, DCM, and HCM clustered well. However, myocarditis samples exhibited scattered distribution. IPA revealed the downregulation of oxidative phosphorylation and upregulation of the sirtuin signaling pathway in both DCM and HCM. Various inflammatory pathways were upregulated in myocarditis with the downregulation of Rho GDP dissociation inhibitors. The molecular pathophysiology identified by extensive proteomic analysis represented the clinical and pathological properties of each cardiomyopathy with abundant proteomes. Conclusions Different etiologies of non-ischemic cardiomyopathies in advanced HF exhibit distinct proteomic expression despite shared pathologic findings. The benefit of tailored management strategies considering the different proteomic expressions in non-ischemic advanced HF requires further investigation.

Background and Objectives: Although the clinical consequences of advanced heart failure (HF) may be similar across different etiologies of cardiomyopathies, their proteomic expression may show substantial differences in relation to underlying pathophysiology. We aimed to identify myocardial tissue–based proteomic characteristics and the underlying molecular pathophysiology in non-ischemic cardiomyopathy with different etiologies. Methods: Comparative extensive proteomic analysis of the myocardium was performed in nine patients with biopsy-proven non-ischemic cardiomyopathies (3 dilated cardiomyopathy [DCM], 2 hypertrophic cardiomyopathy [HCM], and 4 myocarditis) as well as five controls using tandem mass tags combined with liquid chromatography–mass spectrometry.Differential protein expression analysis, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify proteomic differences and molecular mechanisms in each cardiomyopathy type compared to the control. Proteomic characteristics were further evaluated in accordance with clinical and pathological findings. Results: The principal component analysis score plot showed that the controls, DCM, and HCM clustered well. However, myocarditis samples exhibited scattered distribution. IPA revealed the downregulation of oxidative phosphorylation and upregulation of the sirtuin signaling pathway in both DCM and HCM. Various inflammatory pathways were upregulated in myocarditis with the downregulation of Rho GDP dissociation inhibitors. The molecular pathophysiology identified by extensive proteomic analysis represented the clinical and pathological properties of each cardiomyopathy with abundant proteomes. Conclusions Different etiologies of non-ischemic cardiomyopathies in advanced HF exhibit distinct proteomic expression despite shared pathologic findings. The benefit of tailored management strategies considering the different proteomic expressions in non-ischemic advanced HF requires further investigation.

Purpose: This study aimed to compare and evaluate the efficiency and accuracy of computerized adaptive testing (CAT) under 2 stopping rules (standard error of measurement [SEM]=0.3 and 0.25) using both real and simulated data in medical examinations in Korea. Methods: This study employed post-hoc simulation and real data analysis to explore the optimal stopping rule for CAT in medical examinations. The real data were obtained from the responses of 3rd-year medical students during examinations in 2020 at Hallym University College of Medicine. Simulated data were generated using estimated parameters from a real item bank in R. Outcome variables included the number of examinees’ passing or failing with SEM values of 0.25 and 0.30, the number of items administered, and the correlation. The consistency of real CAT result was evaluated by examining consistency of pass or fail based on a cut score of 0.0. The efficiency of all CAT designs was assessed by comparing the average number of items administered under both stopping rules. Results: Both SEM 0.25 and SEM 0.30 provided a good balance between accuracy and efficiency in CAT. The real data showed minimal differences in pass/fail outcomes between the 2 SEM conditions, with a high correlation (r=0.99) between ability estimates. The simulation results confirmed these findings, indicating similar average item numbers between real and simulated data. Conclusion The findings suggest that both SEM 0.25 and 0.30 are effective termination criteria in the context of the Rasch model, balancing accuracy and efficiency in CAT.

Purpose: This study aimed to compare and evaluate the efficiency and accuracy of computerized adaptive testing (CAT) under 2 stopping rules (standard error of measurement [SEM]=0.3 and 0.25) using both real and simulated data in medical examinations in Korea. Methods: This study employed post-hoc simulation and real data analysis to explore the optimal stopping rule for CAT in medical examinations. The real data were obtained from the responses of 3rd-year medical students during examinations in 2020 at Hallym University College of Medicine. Simulated data were generated using estimated parameters from a real item bank in R. Outcome variables included the number of examinees’ passing or failing with SEM values of 0.25 and 0.30, the number of items administered, and the correlation. The consistency of real CAT result was evaluated by examining consistency of pass or fail based on a cut score of 0.0. The efficiency of all CAT designs was assessed by comparing the average number of items administered under both stopping rules. Results: Both SEM 0.25 and SEM 0.30 provided a good balance between accuracy and efficiency in CAT. The real data showed minimal differences in pass/fail outcomes between the 2 SEM conditions, with a high correlation (r=0.99) between ability estimates. The simulation results confirmed these findings, indicating similar average item numbers between real and simulated data. Conclusion The findings suggest that both SEM 0.25 and 0.30 are effective termination criteria in the context of the Rasch model, balancing accuracy and efficiency in CAT.

Background and Objectives: Although the clinical consequences of advanced heart failure (HF) may be similar across different etiologies of cardiomyopathies, their proteomic expression may show substantial differences in relation to underlying pathophysiology. We aimed to identify myocardial tissue–based proteomic characteristics and the underlying molecular pathophysiology in non-ischemic cardiomyopathy with different etiologies. Methods: Comparative extensive proteomic analysis of the myocardium was performed in nine patients with biopsy-proven non-ischemic cardiomyopathies (3 dilated cardiomyopathy [DCM], 2 hypertrophic cardiomyopathy [HCM], and 4 myocarditis) as well as five controls using tandem mass tags combined with liquid chromatography–mass spectrometry.Differential protein expression analysis, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify proteomic differences and molecular mechanisms in each cardiomyopathy type compared to the control. Proteomic characteristics were further evaluated in accordance with clinical and pathological findings. Results: The principal component analysis score plot showed that the controls, DCM, and HCM clustered well. However, myocarditis samples exhibited scattered distribution. IPA revealed the downregulation of oxidative phosphorylation and upregulation of the sirtuin signaling pathway in both DCM and HCM. Various inflammatory pathways were upregulated in myocarditis with the downregulation of Rho GDP dissociation inhibitors. The molecular pathophysiology identified by extensive proteomic analysis represented the clinical and pathological properties of each cardiomyopathy with abundant proteomes. Conclusions Different etiologies of non-ischemic cardiomyopathies in advanced HF exhibit distinct proteomic expression despite shared pathologic findings. The benefit of tailored management strategies considering the different proteomic expressions in non-ischemic advanced HF requires further investigation.

Purpose: This study aimed to compare and evaluate the efficiency and accuracy of computerized adaptive testing (CAT) under 2 stopping rules (standard error of measurement [SEM]=0.3 and 0.25) using both real and simulated data in medical examinations in Korea. Methods: This study employed post-hoc simulation and real data analysis to explore the optimal stopping rule for CAT in medical examinations. The real data were obtained from the responses of 3rd-year medical students during examinations in 2020 at Hallym University College of Medicine. Simulated data were generated using estimated parameters from a real item bank in R. Outcome variables included the number of examinees’ passing or failing with SEM values of 0.25 and 0.30, the number of items administered, and the correlation. The consistency of real CAT result was evaluated by examining consistency of pass or fail based on a cut score of 0.0. The efficiency of all CAT designs was assessed by comparing the average number of items administered under both stopping rules. Results: Both SEM 0.25 and SEM 0.30 provided a good balance between accuracy and efficiency in CAT. The real data showed minimal differences in pass/fail outcomes between the 2 SEM conditions, with a high correlation (r=0.99) between ability estimates. The simulation results confirmed these findings, indicating similar average item numbers between real and simulated data. Conclusion The findings suggest that both SEM 0.25 and 0.30 are effective termination criteria in the context of the Rasch model, balancing accuracy and efficiency in CAT.

Background and Objectives: Although the clinical consequences of advanced heart failure (HF) may be similar across different etiologies of cardiomyopathies, their proteomic expression may show substantial differences in relation to underlying pathophysiology. We aimed to identify myocardial tissue–based proteomic characteristics and the underlying molecular pathophysiology in non-ischemic cardiomyopathy with different etiologies. Methods: Comparative extensive proteomic analysis of the myocardium was performed in nine patients with biopsy-proven non-ischemic cardiomyopathies (3 dilated cardiomyopathy [DCM], 2 hypertrophic cardiomyopathy [HCM], and 4 myocarditis) as well as five controls using tandem mass tags combined with liquid chromatography–mass spectrometry.Differential protein expression analysis, Gene Ontology (GO) analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify proteomic differences and molecular mechanisms in each cardiomyopathy type compared to the control. Proteomic characteristics were further evaluated in accordance with clinical and pathological findings. Results: The principal component analysis score plot showed that the controls, DCM, and HCM clustered well. However, myocarditis samples exhibited scattered distribution. IPA revealed the downregulation of oxidative phosphorylation and upregulation of the sirtuin signaling pathway in both DCM and HCM. Various inflammatory pathways were upregulated in myocarditis with the downregulation of Rho GDP dissociation inhibitors. The molecular pathophysiology identified by extensive proteomic analysis represented the clinical and pathological properties of each cardiomyopathy with abundant proteomes. Conclusions Different etiologies of non-ischemic cardiomyopathies in advanced HF exhibit distinct proteomic expression despite shared pathologic findings. The benefit of tailored management strategies considering the different proteomic expressions in non-ischemic advanced HF requires further investigation.