Tae W.S.,Kangwon National University |
Kim S.S.,Kangwon National University |
Kim S.S.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species |
Lee K.U.,Kangwon National University |
And 3 more authors.
American Journal of Neuroradiology | Year: 2011
BACKGROUND AND PURPOSE: The hippocampal atrophy of MDD has been known, but the region shape contractions of the hippocampus in MDD were inconsistent. Spheric harmonic shape analysis was applied to the hippocampus in female patients with unremitting MDD to evaluate morphometric changes of the hippocampus. MATERIALS AND METHODS: Shape analysis was performed by using T1-weighted MR imaging in 21 female patients with MDD and 21 age- and sex-matched healthy controls. Manually segmented hippocampi were parameterized, and the point-to-point - based group difference was compared by using the Hotelling T-squared test. The partial correlation analyses were tested between clinical variables and shape changes. RESULTS: Both hippocampal volumes were small in patients with MDD compared with healthy controls, and the right hippocampal volume was negatively correlated with the number of episodes at marginal significance. Regional shape contractions were found in the ambient gyrus, basal hippocampal head, posterior subiculum, and dorsal hippocampus of the left hemisphere. The right hippocampus showed a similar pattern but was less atrophic compared with the left hippocampus. A negative correlation was found between the HDRS and shape deformation in the CA3, ambient gyrus, posterior subiculum, and gyrus fasciolaris of the left hippocampus. CONCLUSIONS: We showed atrophy and regional shape contractions in the hippocampi of patients with MDD, which were more dominant on the left side. The causes of hippocampal damage could be the hypersecretion of glucocorticoids contributing to neuronal death or the failing of adult neurogenesis in the dentate gyrus. Copyright © 2011 by the American Society of Neuroradiology.
Won K.Y.,Kyung Hee University |
Kalil R.K.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species |
Kalil R.K.,A+ Network |
Kim Y.W.,Kyung Hee University |
Park Y.-K.,Kyung Hee University
Pathology | Year: 2011
Aims: The interactions between the receptor activator of NFkB (RANK), its ligand (RANKL), and the decoy receptor for RANKL, osteoprotegerin (OPG), play a pivotal role in promoting osteoclast differentiation and activation leading to bone resorption. Giant cell tumours, chondroblastomas, and aneurysmal bone cysts harbour osteolytic lesions containing osteoclast-like giant cells. We investigated the characteristics of the RANKL signalling pathway in each of these bone lesions. Methods: We evaluated 44 cases of giant cell tumour, 12 cases of chondroblastoma, six cases of aneurysmal bone cyst, and five cases of metastatic giant cell tumour (including paired primary giant cell tumours). We assessed RANK, RANKL, and OPG expression in chondroblastomas, giant cell tumours, and aneurysmal bone cysts using immunohistochemical methods. Results: Our findings revealed that RANK, RANKL, and OPG expression differed significantly among disease types. Giant cells of chondroblastomas showed significantly higher RANK expression than the giant cells of giant cell tumours and aneurysmal bone cysts; similarly, stromal cells of chondroblastomas showed significantly higher OPG expression than the stromal cells of giant cell tumours and aneurysmal bone cysts. Furthermore, giant cells of giant cell tumours expressed significantly more RANK than the giant cells of aneurysmal bone cysts. Conclusions: The expression of RANK, RANKL, and OPG in osteoclast-like giant cells differs significantly by disease; OPG expression differs significantly between giant cell tumours and chondroblastomas. © 2011 Royal College of Pathologists of Australasia.
Kim S.-M.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species |
Kim J.-Y.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species |
Lee S.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species |
Park J.-H.,Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species
FEBS Letters | Year: 2010
Adrenomedullin (ADM) functions as a survival factor against hypoxic cell death. However, molecular mechanisms underlying the cell survival pathway remain largely unknown. In this report, we showed that ADM suppressed reactive oxygen species (ROS) increase by inhibiting reduction of glutathione (GSH) level in hypoxia/reoxygenation (H/R) injury, and increased the activities of glutathione peroxidase and reductase. In addition, ADM maintained total and active reduced thioredoxin (Trx) levels against H/R. We also found that ADM blocked nuclear translocation of Trx induced by H/R. The results of the present study show that ADM regulates cellular ROS levels via the GSH and Trx system. © 2009 Federation of European Biochemical Societies.