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김성민,이종인,조용준,황형식,송준호,임대현,안무업,안명수,황장회 대한외상학회 2001 大韓外傷學會誌 Vol.14 No.1
Background: Extradural post-traumatic posterior fossa hematoma is a rare condition estimated to complicate about 0.3% of all craniocerebral injuries and represents 1.2% to 15% of the entire group of extradural hematomas. Clinical progress is silent and slow, but the deterioration is sudden and quick to become fetal if not promptly treated. The recommended treatment for a posterior fossa extradural hematoma is surgical evacuation soon after the diagnosis. However, conservative management under close clinical and radiological supervision can be applied in patients without mass effect. Materials and Methods: In our study, a review of 52 cases with posterior fossa extradural hematomas among a total number of 367 patients with extradural hematoma is presented. In this series, 20 patients were treated conservatively (Group Ⅰ) while 32 required surgery (Group Ⅱ). We evaluated the common clinical manifestations, the treatment methods and results, the complications, and the outcomes. Hospital data were obtained from medical records and radiological data. The x2-test and the Fisher-test were used for statistics, and p<0.05 was taken as the measure of statistical significance. Result: Hematomas commonly occurred in the younger age groups and with a clear male predominance. The most common cause of injury was falls (40.3%). A fracture of the occipital bone was seen in 43 cases (82.7%). Thirty-three patients (63.4%) had other lesions of the brain, mainly cerebral contusions and subdural hematomas. Nineteen cases among Group Ⅰand 25 among Group Ⅱ(84.6% of total cases) showed excellent recovery, 2 patients had a severe disability, I patient was in a vegetative state, and 2 patients died (mortality rate of 3.8%). The significant factors related to outcome were the initial Glasgow coma scale, pupil response, brain stem compression signs, and cerebellar compression signs. Conclusion: The signs and the symptoms are usually nonspecific for an extradural post-traumatic posterior fossa hematoma. Because an early diagnosis is mandatory for a favorable outcome, an aggressive use of computed tomography scanning and careful physical neurological examinations for all patients should be carried out during the acute phase.
Dual Gate Single-Electron Transistors with a Recessed Channel and Underlapped Source/Drain Structure
Lee, Joung-Eob,Kim, Garam,Yun, Jang-Gn,Kang, Kwon-Chil,Lee, Jung-Han,Kim, Dae-Hwan,Lee, Jong-Ho,Shin, Hyungcheol,Park, Byung-Gook IOP Publishing 2010 Japanese journal of applied physics Vol.49 No.r11
Eun-Kyoung Choi,Dae-Eob Kim,Won-Mann Oh,Yun-Woong Paek,In-Chol Kang KOREAN ACADAMY OF ORAL BIOLOGY 2010 International Journal of Oral Biology Vol.35 No.2
Enterococcus faecalis, a gram-positive bacterium, has been implicated in endodontic infections, particularly in chronic apical periodontitis. Proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), are involved in the pathogenesis of these apical lesions. E. faecalis has been reported to stimulate macrophages to produce TNF-α. The present study investigated the mechanisms involved in TNF-α production by a murine macrophage cell line, RAW 264.7 in response to exposure to E. faecalis. Both live and heat-killed E. faecalis induced high levels of gene expression and protein release of TNF-α. Treatment of RAW 264.7 cells with cytochalasin D, an inhibitor of endocytosis, prevented the mRNA up-regulation of TNF-α by E. faecalis. In addition, antioxidant treatment reduced TNF-α production to baseline levels. Inhibition of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinase also significantly attenuated E. faecalis-induced TNF-α expression by RAW 264.7 cells. Furthermore, activation of NF-κB and AP-1 in RAW 264.7 cells was also stimulated by E. faecalis. These results suggest that the phagocytic uptake of bacteria is necessary for the induction of TNF-α in E. faecalis-stimulated macrophages, and that the underlying intracellular signaling pathways involve reactive oxygen species, ERK, p38 MAP kinase, NF-κB, and AP-1.