BACKGROUND: The sectioned images of a cadaver head made from the Visible Korean project have been used for research and educational purposes. However, the image resolution is insufficient to observe detailed structures suitable for experts. In this study, advanced sectioned images with higher resolution were produced for the identification of more detailed structures. METHODS: The head of a donated female cadaver was scanned for 3 Tesla magnetic resonance images and diffusion tensor images (DTIs). After the head was frozen, the head was sectioned serially at 0.04-mm intervals and photographed repeatedly using a digital camera. RESULTS: On the resulting 4,000 sectioned images (intervals and pixel size, 0.04 mm³; color depth, 48 bits color; a file size, 288 Mbytes), minute brain structures, which can be observed not on previous sectioned images but on microscopic slides, were observed. The voxel size of this study (0.04 mm³) was very minute compared to our previous study (0.1 mm³; resolution, 4,368 × 2,912) and Visible Human Project of the USA (0.33 mm³; resolution, 2,048 × 2,048). Furthermore, the sectioned images were combined with tractography of the DTIs to elucidate the white matter with high resolution and the actual color of the tissue. CONCLUSION: The sectioned images will be used for diverse research, including the applications for the cross sectional anatomy and three-dimensional models for virtual experiments.
Anatomy, Cross-Sectional ; Brain ; Cadaver ; Diffusion ; Diffusion Tensor Imaging ; Female ; Head ; Humans ; White Matter

PURPOSE: Apoptosis of vascular endothelial cells is a type of endothelial damage that is associated with the pathogenesis of cardiovascular diseases such as atherosclerosis. Heterotrimeric GTP-binding proteins (G proteins), including the alpha 12 subunit of G protein (Galpha12), have been found to modulate cellular proliferation, differentiation, and apoptosis of numerous cell types. However, the role of Galpha12 in the regulation of apoptosis of vascular cells has not been elucidated. We investigated the role of Galpha12 in serum withdrawal-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and its underlying mechanisms. MATERIALS AND METHODS: HUVECs were transfected with Galpha12 small-interfering RNA (siRNA) to knockdown the endogenous Galpha12 expression and were serum-deprived for 6 h to induce apoptosis. The apoptosis of HUVECs were assessed by Western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of microRNAs were analyzed by quantitative real-time PCR. RESULTS: Knockdown of Galpha12 with siRNA augmented the serum withdrawal-induced apoptosis of HUVECs and markedly repressed the expression of microRNA-155 (miR-155). Serum withdrawal-induced apoptosis of HUVECs was inhibited by the overexpression of miR-155 and increased significantly due to the inhibition of miR-155. Notably, the elevation of miR-155 expression prevented increased apoptosis of Galpha12-deficient HUVECs. CONCLUSION: From these results, we conclude that Galpha12 protects HUVECs from serum withdrawal-induced apoptosis by retaining miR-155 expression. This suggests that Galpha12 might play a protective role in vascular endothelial cells by regulating the expression of microRNAs.
*Apoptosis ; Atherosclerosis/*blood/genetics/immunology ; Cell Proliferation ; Endothelial Cells/*metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/*genetics ; Gene Expression Profiling ; Gene Expression Regulation ; Human Umbilical Vein Endothelial Cells/cytology ; Humans ; MicroRNAs/*metabolism ; Protective Agents ; *RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; *Transfection

High blood pressure is an important determinant of the incidence of coronary heart disease, stroke, congestive heart failure, renal failure, and peripheral vascular disease. Recommendations for control of high blood pressure emphasize lifestyle modification, including weight control, reduced sodium intake, increased physical activity. Subjects who were normotensive (n = 19, 47.2 +/- 9.0 y, BP 116/81 mmHg), treatment hypertensive (n = 33, 54.2 +/- 6.9 y, BP 132/85 mmHg) and non-treatment hypertensive (n = 14, 50.1 +/- 11.0 y, 149/94 mmHg) recruited. Anthropometric assessment (height, weight, waist circumference, hip circumference, fat %, fat mass, and lean body mass) and dietary assessments (using 3-days food records, daily nutrient intakes were analysed by CAN PRO 2.0 were carried out. Blood and 24-hour urine were collected). Test of recognition for salt taste threshold were performed. In non-treatment hypertensive male subjects, weight, %IBW, BMI, and waist circumference were significantly higher than those of normotensive and treatment hypertensive subjects (p < 0.05). Food habits were not significantly different among the three groups. Intakes of vitamin A, vitamin B1, and vitamin B2 were significantly higher in normotensive group (p < 0.05). Intakes of sodium and salt taste recognition threshold were the highest in normotensive group and the lowest in treatment hypertensive group (p < 0.05). Blood levels of lipids and minerals were not significantly different among the three groups. Urinary calcium level of normotensive group were significantly higher than that of treatment hypertensive and non-treatment hypertensive groups (p < 0.05). These results indicate that continuous management of hypertension by drug and non-drug treatment affects salt taste recognition threshold and reduced the consumption of sodium. However, dietary sodium intake exceed recommended sodium intake to prevent and treat hypertension. It is necessary to develop the lifestyle modification program that may have beneficial effects on hypertension treatment.
Calcium ; Coronary Disease ; Food Habits ; Heart Failure ; Hip ; Humans ; Hypertension* ; Incidence ; Life Style ; Male ; Minerals ; Motor Activity ; Peripheral Vascular Diseases ; Renal Insufficiency ; Riboflavin ; Sodium ; Sodium, Dietary ; Stroke ; Taste Threshold ; Thiamine ; Vitamin A ; Waist Circumference

Heterotrimeric GTP-binding proteins (G proteins) transduce extracellular signals into intracellular signals by activating effector molecules including adenylate cyclases that catalyze cAMP formation, and thus regulate various cellular responses such as metabolism, proliferation, and apoptosis. cAMP signaling pathways have been reported to protect cells from ionizing radiation-induced apoptosis, but however, the protective mechanism is not clear. Therefore, this study aimed to investigate the signaling molecules and the mechanism mediating the anti-apoptotic action of cAMP signaling system in radiation-induced apoptosis. Stable expression of a constitutively active mutant of G alpha s (G alpha sQL) protected gamma ray-induced apoptosis which was assessed by analysis of the cleavages of PARP, caspase-9, and caspase-3 and cytochrome C release in SH-SY5Y human neuroblastoma cells. G alpha sQL repressed the gamma ray-induced down-regulation of Bcl-xL protein, but transfection of Bcl-xL siRNA increased the gamma ray-induced apoptosis and abolished the anti-apoptotic effect of G alpha sQL. G alpha sQL decreased the degradation rate of Bcl-xL protein, and it also restrained the decrease in Bcl-xL mRNA by increasing the stability following ionizing irradiation. Furthermore, prostaglandin E2 that activates G alpha s was found to protect gamma ray-induced apoptosis, and the protective effect was abolished by treatment with prostanoid receptor antagonist specific to EP2/4R subtype. Moreover, specific agonists for adenosine A1 receptor that inhibits cAMP signaling pathway augmented gamma ray-induced apoptosis. From this study, it is concluded that Galphas-cAMP signaling system can protect SH-SY5Y cells from gamma ray-induced apoptosis partly by restraining down-regulation of Bcl-xL expression, suggesting that radiation-induced apoptosis can be modulated by GPCR ligands to improve the efficiency of radiation therapy.
Apoptosis/*physiology/*radiation effects ; Base Sequence ; Cell Line, Tumor ; Cyclic AMP/metabolism ; DNA Primers/genetics ; Down-Regulation/radiation effects ; GTP-Binding Protein alpha Subunits, Gs/*metabolism ; Gamma Rays ; Humans ; Neuroblastoma/genetics/metabolism/pathology ; RNA, Small Interfering/genetics ; Signal Transduction ; bcl-X Protein/genetics/*metabolism

Purpose: Current faculty development (FD) programs are mostly limited to medical education and often lack a comprehensive and systematic structure. Therefore, the present study aimed to explore the current status and needs of FD programs in medical schools to provide a basis for establishing FD strategies. Methods: We conducted an online survey of medical school FD staff and professors regarding FD. Frequency, regression, and qualitative content analyses were conducted. FD programs were categorized into the classification frameworks. Results: A total of 17 FD staff and 256 professors at 37 medical schools participated. There are gaps between the internal and external FD programs offered by medical schools and their needs, and there are gaps between the programs the professors participated in and their needs. Recent internal and external FD programs in medical schools have focused on educational methods, student assessment, and education in general. Medical schools have a high need for leadership and self-development, and student assessment. Furthermore, professors have a high need for leadership and self-development, and research. The number of participants, topics, and needs of FD programs varied depending on the characteristics of individual professors. Conclusion Medical schools should expand their FD programs to meet the needs of individuals and the changing demands of modern medical education. The focus should be on comprehensive and responsive programs that cover various topics, levels, and methods. Tailored programs that consider professors’ professional roles, career stages, and personal interests are essential for effective FD.

OBJECTIVE: The interaction between MK-801, a model of psychosis and KCl-induced depolarization or electroconvulsive shock (ECS), a therapeutic model of electroconvulsive therapy (ECT), was investigated in SH-SY5Y cells and the rat frontal cortex. METHODS: SH-SY5Y cells were pretreated with 1 microM MK-801 for 15 min, followed by cotreatment with 100 mM KCl for 5 min. MK-801 was reintroduced after the KCl was washed out, and the samples were incubated before harvesting. For the experiments in rats, male Sprague-Dawley rats were treated with MK-801 followed by ECS. Immunoblot analyses of glycogen synthase kinase 3beta (GSK3beta) (Ser9), AKT (Ser473) and extracellular legulated kinase (ERK)1/2 in SH-SY5Y cells and the rat frontal cortex were performed. RESULTS: KCl-induced neuronal depolarization resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), followed by increased phosphorylation of the enzymes in SH-SY5Y cells. Cotreatment with MK-801 and KCl inhibited the initial dephosphorylation of AKT and GSK3beta produced by KCl-induced neuronal depolarization. Similarly, ECS resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), whereas cotreatment with MK-801 inhibited the initial dephosphorylation of AKT (Ser473) and GSK3beta (Ser9) produced by ECS in the rat frontal cortex. No significant interaction was observed between MK-801 and KCl in the dephosphorylation of ERK1/2. CONCLUSION: These results suggest that an antagonistic interplay between MK-801 and neuronal depolarization by KCl or ECS is involved the regulation of AKT (Ser473) and GSK3beta (Ser9) phosphorylation.
Animals ; Dizocilpine Maleate* ; Electroconvulsive Therapy ; Electroshock ; Glycogen Synthase Kinases ; Humans ; Male ; Neurons* ; Phosphorylation ; Phosphotransferases ; Psychotic Disorders ; Rats* ; Rats, Sprague-Dawley