After Yeungnam University's College of Medicine was established in 1979, the curriculum for a preclinical medical education course was developed and implemented. Several modifications have since been made to the curriculum which was driven by changes in national policies and in the medical education environment. In recent years, it has become necessary to complement the weaknesses or shortcomings in the curriculum that were discovered during the basic medical education assessment process of the medical college. Since 2009, Yeungnam University has run two medical courses: a 6-year college of medicine course and a 4-year medical school course. However, as a result of changes in national policy, Yeungnam University decided to offer only the 6-year college of medicine course with an entirely new curriculum which will be implemented in 2017. The new curriculum for the preclinical medical education course consists of 36 credits of cultural essentials courses, 44 credits of major required courses, and 2 credits of major elective courses. The curriculum development requires the support of the university and/or college, the ensured independence of the curriculum development organization, and the cooperation and attention of fellow professors. Continuous efforts are needed to check, evaluate, and improve the curriculum.
Complement System Proteins ; Curriculum ; Education, Medical ; Schools, Medical

Medical education research subjects are incredibly diverse and have changed over time. This work in particular aims to compare and analyze research trends in medical education through the words used in the titles of these research papers. Academic Medicine (the journal of the Association of American Medical Colleges), Medical Teacher (the journal of the Association of Medical Education in Europe), the Korean Journal of Medical Education (KJME), and Korean Medical Education Review (KMER) were selected and analyzed for the purposes of this research. From 2009 to 2018, Academic Medicine and Medical Teacher published approximately 10 to 20 times more papers than the KJME and KMER. Frequently used words in these titles include “medical,” “student,” “education,” and “learning”. The words “clinical” and “learning” were used relatively often (7.80% to 13.66%) in Korean journals and Medical Teacher, but Academic Medicine used these phrases relatively less often (6.47% and 4.41%, respectively). Concern with such various topics as problem-based learning, team-based learning, program evaluations, burnout, e-learning, and digital indicates that Medical Teacher seems to primarily deal with teaching and learning methodologies, and Academic Medicine handles all aspects of medical education. The KJME and KMER did not cover all subjects, as they publish smaller papers. However, it is anticipated that research on new subjects, such as artificial intelligence in medical education, will occur in the near future.
Artificial Intelligence ; Education, Medical ; Humans ; Learning ; Problem-Based Learning ; Program Evaluation ; Research Subjects

Medical education research subjects are incredibly diverse and have changed over time. This work in particular aims to compare and analyze research trends in medical education through the words used in the titles of these research papers. Academic Medicine (the journal of the Association of American Medical Colleges), Medical Teacher (the journal of the Association of Medical Education in Europe), the Korean Journal of Medical Education (KJME), and Korean Medical Education Review (KMER) were selected and analyzed for the purposes of this research. From 2009 to 2018, Academic Medicine and Medical Teacher published approximately 10 to 20 times more papers than the KJME and KMER. Frequently used words in these titles include “medical,”“student,”“education,” and “learning”. The words “clinical” and “learning” were used relatively often (7.80% to 13.66%) in Korean journals and Medical Teacher, but Academic Medicine used these phrases relatively less often (6.47% and 4.41%, respectively). Concern with such various topics as problem-based learning, team-based learning, program evaluations, burnout, e-learning, and digital indicates that Medical Teacher seems to primarily deal with teaching and learning methodologies, and Academic Medicine handles all aspects of medical education. The KJME and KMER did not cover all subjects, as they publish smaller papers. However, it is anticipated that research on new subjects, such as artificial intelligence in medical education, will occur in the near future.

Retinoids play an important role in growth, reproduction and differentiation. Recently, retinoids have been used to both protect and treat from various animal models of carcinogenesis. In this study the effect of N-(4-hydroxyphenyl) retinamide (fenretinide) on viability of human neuroblastoma cell lines were evaluated. For the evaluation of apoptosis of human neuroblastoma cell lines by fenretinide. MTT assay, cytoplasmic DNA fragmentation, TUNEL stain, and Western blot analysis were performed. In MTT assay, fenretinide inhibited the proliferation of CHP134, IMR32 and SH-SY5Y but not in PC12 cells. Cytoplasmic DNA fragmentation was induced by treament of fenretinide (10 micrometer) for 48 h in IMR32 cells. PARP cleavage was detected by Western blot analysis after 16 h of treatment of fenretinide in CHP134, IMR32 and SH-SY5Y. These fenretinide effects on growth inhibition and increased apoptosis followed to the time dependent manner. The fenretinide treatment did not affect the phosphorylation of MAP kinases (ERK, JNK, p38). There was no change of Bcl-x and Bad expression after treatment of fenretinide (1 micrometer) in neroblastoma cell lines. Pretreatement of PD98059, SB203580, LY294002, or genistein also did not affect fenretinide-induced PARP cleavage in neuroblastoma cell lines. From these results, the fenretinide-induced apoptosis is due to the PARP cleavage which occured MAP kinase signal cascades independently.
Animals ; Apoptosis* ; Blotting, Western ; Carcinogenesis ; Cell Line* ; Cytoplasm ; DNA Fragmentation ; Fenretinide* ; Genistein ; Humans* ; In Situ Nick-End Labeling ; Models, Animal ; Neuroblastoma* ; PC12 Cells ; Phosphorylation ; Phosphotransferases ; Reproduction ; Retinoids

During the treatment of cancers, especially with anticancer drugs, the recurrence of cancer is the most important factor for survival rate. The most common cause of the recurrence is the resistance of cells to anticancer drugs. To explore and analyze the changes of gene expression during the induction of resistance by anticancer drugs in human osteogenic cancer cell line Saos-2. The drug resistance was induced with adriamycin, cisplatin or vincristine at 10(-7) M concentration of each and cDNA microarray was performed. Total RNA was purified from Saos-2, adriamycin-resistant (Saos-2AdR), cisplatin-resistant (Saos-2CpR) and vincristine-resistant (Saos-2VcR) and expressed genes were investigated with a Affymetrix Human HG-U133Plus2.0 GeneChip(TM). The genes of anticancer drug resistant cells that showed more than 2.5 fold expression change than Saos-2 were selected for differential expression. Four hundred seventeen genes were selected for Saos-2 vs Saos-2AdR. Two thousand five hundred thirty six genes were selected for Saos-2 vs Saos-2CpR. Two hundred twenty five genes were selected for Saos-2 vs Saos-2VcR. Eighty seven genes were selected for common differential expression. The results showed that many genes were changed in expression during the acquiring of resistance to anticancer drugs but most of genes were not in common among the three anticancer durg-resistant Saos-2. This means the different anticancer drug takes the different mechanism for acquiring resistance to anticancer drug even we use same cells.
Cell Line ; Cisplatin ; Doxorubicin ; Drug Resistance ; Gene Expression* ; Humans ; Oligonucleotide Array Sequence Analysis ; Recurrence ; RNA ; Survival Rate ; Vincristine

BACKGROUND: General anesthetics were known to induce expression of immediate early genes (IEGs), including c-fos and c-jun. However, mechanisms of IEG induction by general anesthetics were not fully understood. METHODS: IEG induction by propofol, a kind of intravenous anesthetics, and signal transduction pathways for propofol-induced IEG expression were investigated in human neuroblastoma cell line IMR32 and CHP134 with Northern and Western blot analysis. RESULTS: Cell viability was significantly decreased in IMR32 and CHP134 treated with increasing concentrations of propofol. IMR32 was more sensitive to propofol-induced cytotoxicity than CHP134. Propofol did not affect the cell cycle profile of IMR32. Expression of cyclin A, cyclin B1, CDK4 and CDK6 was increased in IMR32 by propofol treatment in a time-dependent manner. However, expression of cyclin A and CDK4 was decreased in CHP134. Proliferating cell nuclear antigen (PCNA) was increased in both IMR32 and CHP134 treated with propofol from 6 h to 24 h. c-fos and c-jun were induced by propofol treatment in both cells. Propofol also induced extracellular signal-regulated kinase (ERK) phosphorylation in both cells. Pretreatment of PD98059, an MEK inhibitor, blocked propofol-induced c-fos and c-jun expression.Propofol treatment was decreased nuclear transcription factor-kappa B (NF-kappa B) expression in IMR32, but not in CHP134. CONCLUSIONS: Propofol-induced c-fos expression might be mediated through ERK phosphorylation in both IMR32 and CHP134. Propofol-induced cytotoxicity, changes in expressions of cell cycle regulatory proteins, expression of IEGs, ERK phosphorylation, and NF-kappa B expression were different between IMR32 and CHP134.
Anesthetics, General ; Anesthetics, Intravenous ; Blotting, Western ; Cell Cycle ; Cell Cycle Proteins ; Cell Line ; Cell Survival ; Cyclin A ; Cyclin B1 ; Cyclins ; Flavonoids ; Gene Expression ; Genes, Immediate-Early ; Humans ; Neuroblastoma ; NF-kappa B ; Phosphorylation ; Phosphotransferases ; Proliferating Cell Nuclear Antigen ; Propofol ; Signal Transduction

Background: The concept of work-life balance (WLB) has become an important issue in workers' health and safety. This study aims to investigate the relationship between WLB and occupational injury and work-related musculoskeletal pain.Method: The study included 27,383 workers who participated in the Fifth Korean Working Conditions Survey. Participants were divided into good WLB and poor WLB groups based on their responses to the five question items which comprised two dimensions: workon-life conflict (items, 1–3) and life-on-work conflict (items 4 and 5). Occupational injury and musculoskeletal pain were also assessed using the question items. The χ 2 test and multivariate logistic regression analyses were performed to examine the relationship of WLB to occupational injury and musculoskeletal pain while considering socio-demographic and occupational characteristics and ergonomic and psychological risk factors. Results: Of the 27,383 participants, 252 (0.9%) had experienced an occupational injury and 6,408 (23.4%) had musculoskeletal pain. The poor WLB group had higher injury rates for both men (1.7%) and women (0.9%) than the good WLB group (1.1% and 0.4%, respectively).Additionally, the prevalence of musculoskeletal pain was higher for both men and women in the poor WLB group (25.2% and 28.0%, respectively) than for men and women in the good WLB group (18.7% and 23.6%, respectively). In the logistic regression analysis, the adjusted odds ratio of WLB for occupational injury was 1.37 (95% confidence interval [CI]: 1.06–1.78), and that for musculoskeletal pain was 1.14 (95% CI: 1.07–1.21), showing positive associations of WLB with both occupational injury and musculoskeletal pain. Conclusions Poor WLB causes an increase in occupational injury and musculoskeletal pain.Therefore, an improvement in WLB may reduce the incidence of occupational injury and musculoskeletal pain among workers. Social and policy-related initiatives are needed to improve workers' WLB to reduce occupational injury and musculoskeletal pain.

Background: The concept of work-life balance (WLB) has become an important issue in workers' health and safety. This study aims to investigate the relationship between WLB and occupational injury and work-related musculoskeletal pain.Method: The study included 27,383 workers who participated in the Fifth Korean Working Conditions Survey. Participants were divided into good WLB and poor WLB groups based on their responses to the five question items which comprised two dimensions: workon-life conflict (items, 1–3) and life-on-work conflict (items 4 and 5). Occupational injury and musculoskeletal pain were also assessed using the question items. The χ 2 test and multivariate logistic regression analyses were performed to examine the relationship of WLB to occupational injury and musculoskeletal pain while considering socio-demographic and occupational characteristics and ergonomic and psychological risk factors. Results: Of the 27,383 participants, 252 (0.9%) had experienced an occupational injury and 6,408 (23.4%) had musculoskeletal pain. The poor WLB group had higher injury rates for both men (1.7%) and women (0.9%) than the good WLB group (1.1% and 0.4%, respectively).Additionally, the prevalence of musculoskeletal pain was higher for both men and women in the poor WLB group (25.2% and 28.0%, respectively) than for men and women in the good WLB group (18.7% and 23.6%, respectively). In the logistic regression analysis, the adjusted odds ratio of WLB for occupational injury was 1.37 (95% confidence interval [CI]: 1.06–1.78), and that for musculoskeletal pain was 1.14 (95% CI: 1.07–1.21), showing positive associations of WLB with both occupational injury and musculoskeletal pain. Conclusions Poor WLB causes an increase in occupational injury and musculoskeletal pain.Therefore, an improvement in WLB may reduce the incidence of occupational injury and musculoskeletal pain among workers. Social and policy-related initiatives are needed to improve workers' WLB to reduce occupational injury and musculoskeletal pain.

BACKGROUND: Alzheimer's disease is a neurodegenerative disorder characterized by the extracellular deposition of beta-amyloid peptide(Abeta) in the brain, presumed to play a pathogenic role. However, the precise molecular mechanisms of its neurotoxicity are not fully understood. METHODS: Abeta-mediated cytotoxicity in neuronal cell lines (PC12, SH-SY5Y, IMR32, and U87) was measured by an MTT assay. NF-kappaB activation by Abetawas examined by a luciferase assay and apoptosis induced by Abetawas measured by cytoplasmic DNA fragmentations. RESULTS: Abetacytotoxicity in the tested cell lines was more prominent in the absence of serum than in the presence of serum in culture media. PC12 cells showed the highest sensitivity to Abetacytotoxicity among the cell lines. The Abeta(25-35) cytotoxicity in PC12 cells was increased in a dose-dependent manner. For convincing oxidative stress involved in Abetacytotoxicity, antioxidants such as DTT, GSH, vitamin C, or NAC were pretreated. GSH protected PC12 cells from Abetacytotoxicity, but DTT or NAC did not. Abeta (25-35) treatment to PC12 cells increased the NF-kappaB activity in a dose-dependent manner. Cytoplasmic DNA fragmentations, one of the apoptotic indicators, were increased at lower concentrations of Abeta(25-35) from 0.01 to 0.1 microM, however, dose-dependent increments of DNA fragmentations were not observed at higher concentrations from 1 to 10 microM. CONCLUSIONS: From these results, Abeta-induced cytotoxicity in PC12 cells might be mediated by oxidative stress.
Alzheimer Disease ; Amyloid beta-Peptides ; Animals ; Antioxidants ; Apoptosis ; Ascorbic Acid ; Brain ; Cell Line ; Culture Media ; Cytoplasm ; DNA ; Luciferases ; Neurodegenerative Diseases ; Neurons ; NF-kappa B ; Oxidative Stress* ; PC12 Cells*

Amyloid beta-peptide (Abeta), a causative molecule in the pathogenesis of Alzheimer's disease and the main component of senile plaques, is known to be neurotoxic in vitro and in vivo. The mechanisms involved in this Ab-mediated neurotoxicity are not fully understood, although there is evidence to suggest the involvement of oxidative stress, alterations in calcium homeostasis, and/or of CDK activators. Many studies have suggested that Ab may exert its toxic effect via the activation of transcription factors. Therefore, we investigated Ab- responsive genes in human neuroblastoma CHP134 cells using 3.1K human DNA microarrays. Among the several genes overexpressed or repressed by Ab, RTP801, Hi95/sestrin 2, and stanniocalcin 2 were confirmed to be Ab-mediated overexpression in the cells by semiquantitative RT-PCR. Transient expression of the sense RTP801 gene in CHP134 cells increased sensitivity to Abeta cytotoxicity and the expression of the antisense RTP801 gene protected the cells from the Abeta toxicity. These results suggest that RTP801 might play important roles in Abeta toxicity and the pathogenesis of Alzheimer's disease.
Alzheimer Disease/genetics/pathology ; Amyloid beta-Protein/analysis/*toxicity ; Base Sequence ; Cell Line, Tumor ; DNA, Complementary/analysis/genetics ; *Gene Expression Profiling ; Gene Expression Regulation/*drug effects ; Glycoproteins/genetics ; Human ; Molecular Sequence Data ; Nuclear Proteins/genetics ; *Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Support, Non-U.S. Gov't ; Transcription Factors/*genetics/*metabolism