No abstract available.
Intussusception* ; Ultrasonography*

No abstract available.
Humans ; Measles*

No abstract available.
Cardiomyopathy, Hypertrophic*

BACKGROUND: Scid.adh is a recently developed murine thymic lymphoma cell line, which has been used as in vitro model for the study of double negative stage III thymocytes. In this study, we compared the expression profile of a number of genes and proteins, which are tightly related to T cell development and apoptosis, in thymic lymphoma cell lines, R1.1, EL-4, and Scid.adh for the developmental staging. METHODS: We examined the expression of development marker genes and proteins in three lymphoma cell lines by flow cytometry and RT-PCR. In addition, the expression of apoptosis-related molecules including bcl-2, bax and Fas was also investigated. RESULTS: As previously reported, Scid.adh cell line expressed CD8 and CD25 but not TCR alpha chain, while R1.1 cells expressed TCR alpha chain and both CD4 and CD8 transcripts. These suggest that R1.1 might be in double positive stage, and low level of CD44 expression and the absence of CD25 support this suggestion. In contrast, EL-4 cells showed high level of TCR alpha chain transcript, and low-level of CD4 expression, suggesting that EL-4 is in more mature stage than R1.1. Further, this suggestion was supported by the lack of mT-20 in EL-4 cells, which is expressed in the immature thymocytes, and Scid.adh and R1.1 cell lines, but not in the terminally differentiated thymocytes and peripheral T cells. Among the apoptosis-related gene, transcripts of bcl-2 gene were detected in both R1.1 and EL-4 but not in Scid.adh cells, while bax was expressed in all cell lines. Fas expression was the highest in EL-4 cells and low in Scid.adh cell line. CONCLUSION: R1.1 cell may represent double positive stage, and EL-4 is more differentiated cell line. In addition, Scid.adh and EL-4 cell lines are suspected to be useful for the study of function of bcl-2 family and Fas during the thymocyte development, respectively.
Apoptosis ; Cell Line* ; Flow Cytometry ; Genes, bcl-2 ; Humans ; Lymphoma* ; T-Lymphocytes ; Thymocytes

BACKGROUND: Recent findings in molecular pathology suggest that genetic translocation and/or overexpression of oncoproteins is important in salivary gland tumorigenesis and diagnosis. We investigated PLAG1, SOX10, and Myb protein expression in various salivary gland neoplasm tissues. METHODS: A total of 113 cases of surgically resected salivary gland neoplasms at the National Cancer Center from January 2007 to March 2017 were identified. Immunohistochemical staining of PLAG1, SOX10, and Myb in tissue samples was performed using tissue microarrays. RESULTS: Among the 113 cases, 82 (72.6%) were benign and 31 (27.4%) were malignant. PLAG1 showed nuclear staining and normal parotid gland was not stained. Among 48 cases of pleomorphic adenoma, 29 (60.4%) were positive for PLAG1. All other benign and malignant salivary gland neoplasms were PLAG1-negative. SOX10 showed nuclear staining. In normal salivary gland tissues SOX10 was expressed in cells of acinus and intercalated ducts. In benign tumors, SOX10 expression was observed in all pleomorphic adenoma (48/48), and basal cell adenoma (3/3), but not in other benign tumors. SOX10 positivity was observed in nine of 31 (29.0%) malignant tumors. Myb showed nuclear staining but was not detected in normal parotid glands. Four of 31 (12.9%) malignant tumors showed Myb positivity: three adenoid cystic carcinomas (AdCC) and one myoepithelial carcinoma with focal AdCC-like histology. CONCLUSIONS: PLAG1 expression is specific to pleomorphic adenoma. SOX10 expression is helpful to rule out excretory duct origin tumor, but its diagnostic value is relatively low. Myb is useful for diagnosing AdCC when histology is unclear in the surgical specimen.
Adenoma ; Adenoma, Pleomorphic ; Antibody-Dependent Cell Cytotoxicity ; Carcinogenesis ; Carcinoma, Adenoid Cystic ; Diagnosis ; Immunohistochemistry ; Oncogene Proteins ; Oncogene Proteins v-myb ; Parotid Gland ; Pathology, Molecular ; Salivary Gland Neoplasms ; Salivary Glands ; SOX Transcription Factors ; Translocation, Genetic

BACKGROUND: Paroxysmal atrial fibrillation (PAF) causes not only severe symptoms and hemodynamic changes, but may progress to chronic atrial fibrillation. Autonomic nervous system or atrial premature beat (APB) has been suggested to contribute to the spontaneous initiation of PAF, but the exact mechanism has been largely unknown. METHODS: One hundred and twenty nine episodes of PAF lasting longer than 5 sec were analyzed in 18 patients (M:F=11:?). Two minutes of normal sinus rhythm before the onset of PAF, and the initial one minute of PAF were printed and analyzed. RESULTS: Most of PAFs were initiated by APBs (38%) or rapid atrial tachycardias (AT, 59%). The frequency of APBs tended to increase immediately before PAF onset (p=0.08). The coupling intervals and coupling indices were not significantly different between PAF-producing APBs and benign APBs. More than half of PAF episodes were initiated by rapid ATs (rate, 357+/-50 bpm). After the onset, they accelerated over several seconds and then degenerated into AF. In some cases, transition from AF to atrial flutter and vice versa were observed. Heart rate, measured at 60-second intervals during 2 minutes before PAF onset, did not change significantly (p=0.44). CONCLUSION: Most of PAFs were initiated by APBs or rapid ATs. Heart rate did not change significantly but the frequency of APBs tended to increase immediately before PAF onset. Rapid ATs frequently accelerated and degenerated into AF. In this regard, Holter monitoring could be useful in identifying patients with PAF triggered by rapid ATs.
Atrial Fibrillation* ; Atrial Flutter ; Autonomic Nervous System ; Cardiac Complexes, Premature ; Electrocardiography, Ambulatory* ; Heart Rate ; Hemodynamics ; Humans ; Tachycardia

CD43 (sialophorin, leukosialin) is a heavily sialylated surface protein expressed on most leukocytes and platelets including T cells. Although CD43 antigen is known to have multiple and complex structure, exact function of CD43 in each cell type is not completely understood. Here we evaluated the role of CD43 in Fas (CD95)-induced cell death in human T lymphoblastoid cell line, Jurkat. Crosslinking CD43 antigen by K06 mAb increased the Fas-mediated Jurkat cell apoptosis and the augmentation was inhibited by treatment with caspase inhibitors. Further, CD43 signaling of Jurkat cells induced Fas oligomerization on the cell surfaces implying that CD43 ligation have effects on early stage of Fas-induced T cell death. These also suggest that CD43 might play an important role in contraction of the immune response by promotion of Fas-induced apoptosis in human T cells.
Receptor Aggregation/immunology ; Jurkat Cells ; Humans ; Caspases/metabolism ; Apoptosis/*immunology ; Antigens, Surface/metabolism ; Antigens, CD95/metabolism/*physiology ; Antigens, CD43/metabolism/*physiology ; Antibodies, Monoclonal/metabolism