Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Purpose: Incidental prostate cancer (IPCa) is frequently discovered during radical cystectomy (RC) for bladder cancer. While small-scale Korean studies have reported IPCa in 36%–50% of cases and clinically significant prostate cancer (sPCa) in up to 20%, large-scale data assessing its oncologic impact remain scarce. Materials and Methods: We retrospectively analyzed 1,358 male patients who underwent RC between June 1996 and January 2024. IPCa was histologically confirmed and classified per the International Society of Urological Pathology (ISUP) system. sPCa was defined as ISUP grade group (GG) ≥2. Kaplan-Meier analyses were conducted to evaluate survival outcomes. Results: IPCa was identified in 240 patients (17.7%), among whom 7.51% had sPCa. The distribution of ISUP GG was: GG1, 53.8%; GG2, 27.9%; GG3, 9.6%; GG4, 2.5%; and GG5, 1.7%. The proportion of sPCa remained stable across 3 time periods (p=0.281). Mean preoperative prostate-specific antigen (PSA) levels significantly differed among GG1, GG2, and GG3+ groups (2.14±2.37, 4.31±6.69, and 5.86±7.66 ng/mL, respectively; p<0.001). Mean patient age also varied significantly (67.99±8.39, 71.54±8.60, and 72.97±5.53 years; p<0.001). After a median follow-up of 44 months, deaths were unrelated to IPCa. Biochemical recurrence (BCR), defined as PSA ≥0.2 ng/mL, occurred in 11 patients (4.58%), with rates of 3.10%, 4.48%, and 12.12% in GG1, GG2, and GG3+ groups, respectively. Overall mortality rates across GG groups were similar (33.3%, 34.3%, and 33.3%; p=0.99). Compared to GG1, hazard ratios for overall survival were 1.03 (GG2, p=0.92), 0.87 (GG3, p=0.76), and 1.05 (GG4–5, p=0.89). Conclusion In this large Korean cohort, IPCa and sPCa were frequently detected at rates similar to global reports. Bladder cancer remained the primary determinant of survival. For older patients with elevated PSA, radical cystoprostatectomy may offer added benefit by treating undiagnosed high-risk IPCa.

PURPOSE: This purpose of this study was to identify both good teaching and desirable teaching behaviors perceived by nursing students.METHODS: A cross-sectional descriptive design was used. A convenience sample of 324 nursing students was selected and they completed self-reported questionnaires from November 1 to December 30, 2015.RESULTS: Among 4 perspectives of good teaching (traditional, systemic, interaction, and constructionism), the traditional perspective was perceived as the highest form of good teaching, while the systemic perspective was perceived as the lowest. Meanwhile, disclosure and clarity were perceived as the highest desirable teaching behaviors. Regardless of students' perspective of good teaching, all 4 perspectives of good teaching were positively related with clarity, enthusiasm, interaction, organization, and disclosure as desirable teaching behaviors independently.CONCLUSIONS: Nursing students perceived that the highest perspective of good teaching was the traditional perspective. Meanwhile, they perceived that clarity, enthusiasm, interaction, organization, and disclosure were desirable teaching behaviors regardless of their perspective of good teaching. Further study will be needed to perceive nursing faculty's awareness of good teaching and desirable teaching behaviors to identify the difference of awareness between nursing students and faculty.
Disclosure ; Education, Nursing ; Humans ; Nursing ; Students, Nursing

OBJECTIVE: Enhanced technology in computer and internet has driven scale and quality of data to be improved in various areas including healthcare sectors. Machine Learning (ML) has played a pivotal role in efficiently analyzing those big data, but a general misunderstanding of ML algorithms still exists in applying them (e.g., ML techniques can settle a problem of small sample size, or deep learning is the ML algorithm). This paper reviewed the research of diagnosing mental illness using ML algorithm and suggests how ML techniques can be employed and worked in practice. METHODS: Researches about mental illness diagnostic using ML techniques were carefully reviewed. Five traditional ML algorithms-Support Vector Machines (SVM), Gradient Boosting Machine (GBM), Random Forest, Naïve Bayes, and K-Nearest Neighborhood (KNN)-frequently used for mental health area researches were systematically organized and summarized. RESULTS: Based on literature review, it turned out that Support Vector Machines (SVM), Gradient Boosting Machine (GBM), Random Forest, Naïve Bayes, and K-Nearest Neighborhood (KNN) were frequently employed in mental health area, but many researchers did not clarify the reason for using their ML algorithm though every ML algorithm has its own advantages. In addition, there were several studies to apply ML algorithms without fully understanding the data characteristics. CONCLUSION: Researchers using ML algorithms should be aware of the properties of their ML algorithms and the limitation of the results they obtained under restricted data conditions. This paper provides useful information of the properties and limitation of each ML algorithm in the practice of mental health.
Bays ; Forests ; Health Care Sector ; Internet ; Learning ; Machine Learning ; Mental Health ; Residence Characteristics ; Sample Size ; Support Vector Machine