No abstract available.
Ear* ; Fascia* ; Temporal Muscle* ; Transplants*

BACKGROUND: Breast cancer is the one of the commonly diagnosed female cancer in Korea. Numerous factors have been noted to be associated with risk of breast cancer: body mass index, menarche, menopause, family history, pregnancy and delivery, breastfeeding, alcohol use, smoking habits, diet, education and use of oral contraceptives. Little is known about hair minerals in breast cancer patient and about correlation between hair minerals and body mass index. METHODS: We compared hair mineral analysis data of 37 breast cancer subject with age and body mass index-matched normal control data (N = 144) by cross-sectional analysis. All breast cancer patients were newly diagnosed at one Breast Cancer Center in Ajou University and had their hair cut before anti-cancer chemotherapy, and the normal controls (without breast cancer) also had their hair cut for various reasons in out-patient clinics of the Department of Family Practice and Community Health. RESULTS: Breast cancer patients had low calcium, magnesium, and zinc, whereas they had high arsenic, sodium, and potassium compared with the normal controls. Only hair zinc level had significant negative correlation with body mass index (r = -0.705, P < 0.001) in breast cancer patients, not in normal controls. CONCLUSION: We observed the difference of hair mineral patterns in newly diagnosed breast cancer patients compared to normal controls and the correlation between these minerals and body mass index in breast cancer patient. Especially hair zinc concentration was significantly reduced and had significant negative correlation with body mass index in breast cancer patients.
Arsenic ; Body Mass Index ; Breast ; Breast Feeding ; Breast Neoplasms ; Calcium ; Contraceptives, Oral ; Cross-Sectional Studies ; Family Practice ; Female ; Food Habits ; Hair ; Humans ; Korea ; Magnesium ; Menarche ; Menopause ; Minerals ; Outpatients ; Potassium ; Reproductive History ; Smoke ; Smoking ; Sodium ; Zinc

Inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) have been known to be involved in various pathophysiological processes such as inflammation. This study was performed to determine the regulatory function of superoxide dismutase (SOD) on the LPS-induced expression of iNOS, and COX-2 in RAW 264.7 cells. When a cell-permeable SOD, Tat-SOD, was added to the culture medium of RAW 264.7 cells, it rapidly entered the cells in a dose-dependent manner. Treatment of RAW 264.7 cells with Tat-SOD led to decrease in LPS-induced ROS generation. Pretreatment with Tat-SOD significantly inhibited LPS-induced expression of iNOS and NO production but had no effect on the expression of COX-2 and PGE2 production in RAW 264.7 cells. Tat-SOD inhibited LPS-induced NF-kappaB DNA binding activity, IkappaBalpha degradation and activation of MAP kinases. These data suggest that SOD differentially regulate expression of iNOS and COX-2 in LPS-stimulated RAW 264.7 cells.
Animals ; Cell Line ; Cyclooxygenase 2/*genetics/metabolism ; Cytokines/immunology ; *Gene Expression Regulation ; Lipopolysaccharides/immunology/metabolism ; Mice ; Mitogen-Activated Protein Kinase Kinases/metabolism ; NF-kappa B/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/*genetics/metabolism ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/*metabolism

HIV-1 Tat is considered to be one of key players to facilitate monocyte entry into the CNS, which is characteristic feature of AIDS-related encephalitis and dementia. This study was performed to determine the regulatory function of superoxide dismutase (SOD) on the HIV-1 Tat-induced signaling pathways leading to NF-kappaB activation, expression of adhesion molecules, and monocyte adhesion in CRT-MG human astroglioma cells by using cell-permeable SOD. When cell-permeable SOD was added to the culture medium of CRT-MG cells, it rapidly entered the cells in dose- and time-dependent manners. Treatment of astrocytes with cell-permeable SOD led to decrease in Tat-induced ROS generation as well as NF-kappaB activation. Cell-permeable SOD inhibited the activation of MAP kinases including ERK, JNK and p38 by HIV-1 Tat. Treatment of CRT-MG cells with cell-permeable SOD significantly inhibited protein and mRNA levels of ICAM-1 and VCAM-1 up-regulated by HIV-1 Tat, as measured by Western blot analysis and RT-PCR. Furthermore, enhanced adhesiveness of monocyte to astrocyte by HIV-1 Tat was significantly abrogated by pretreatment with cell-permeable SOD fusion proteins. These data indicate that SOD has a regulatory function for HIV-1 Tat-induced NF-kappaB activation in astrocytes and suggest that cell-permeable SOD can be used as a feasible therapeutic agent for regulation of ROS-related neurological diseases.
Astrocytes/*enzymology ; Cell Adhesion/*physiology ; Cell Membrane Permeability ; Gene Products, tat/*pharmacology ; HIV Infections/metabolism ; HIV-1/*chemistry ; Humans ; Monocytes/cytology/*drug effects ; Signal Transduction ; Superoxide Dismutase/genetics/*physiology

Dexamethasone converts pluripotent pancreatic AR42J cells into exocrine cells expressing digestive enzymes. In order to address molecular mechanism of this differentiation, we have investigated the role of mitogen-activated protein (MAP) kinase pathway and gene expressions of p21(waf1/cip1)and nuclear oncogenes (c-fos and c-myc) during AR42J cell differentiation. Dexamethasone markedly increased the intracellular and secreted amylase contents as well as its mRNA level. However, cell growth and DNA content were significantly decreased. With these phenotypic changes, AR42J cells induced transient mRNA expression of p21(waf1/cip1)gene, which reached maximal level by 6 h and then declined gradually toward basal state. In contrast to p21(waf1/cip1), c-fos gene expression was transiently inhibited by 6 h and then recovered to basal level by 24 h. Increased c-myc expression detected after 3 h, peaked by 12 h, and remained elevated during the rest of observation. Dexamethasone inhibited epidermal growth factor-induced phosphorylation of extracellular signal regulated kinase. Inhibition of MAP kinase pathway by PD98059 resulted in further elevation of the dexamethasone-induced amylase mRNA and p21(waf1/cip1)gene expression. These results suggest that p21(waf1/cip1)and nuclear oncogenes are involved in dexamethasone-induced differentiation and inhibition of MAP kinase pathway accelerates the conversion of undifferentiated AR42J cells into amylase-secreting exocrine cells.
Amylases/genetics ; Animals ; Cell Differentiation/*drug effects ; Cell Division/drug effects ; Cell Line, Tumor ; Cyclins/genetics/*metabolism ; Dexamethasone/*pharmacology ; Gene Expression Regulation/drug effects ; Genes, fos/genetics ; Genes, myc/genetics ; MAP Kinase Signaling System/*drug effects ; Mitogen-Activated Protein Kinases/*metabolism ; Pancreas/cytology/*drug effects/enzymology/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Support, Non-U.S. Gov't

Left ventricular pseudoaneurysm, in which a ventricular free wall rupture is locally contained by adherent pericardium, is a rare complication of myocardial infarction. Compared w'th a true left ventricular aneunsm, a pseudoaneurysm has a greater propensity to sudden rupture, with catastrophic sequelae. Pseudoaneurysm may be surgically curable, a prompt and accurate diagnosis is thus essential. Transthoracic echocardiography has been the procedure of choice in the diagnosis of pseu- doaneurysm. Transesophageal echocardiography can provide more accurate information than transthoracic echocardiography for the evaluation of ventricular pseudoaneurysm located in posterior and inferior wall. We experienced a case of pseudoaneurysm of left ventricle in a 75-year-old female who presented with dyspnea. A large pseudoaneurysm of left ventricle vith narrow neck was de- tected by transesophageal echocardiography.
Aged ; Aneurysm, False* ; Diagnosis ; Dyspnea ; Echocardiography ; Echocardiography, Transesophageal* ; Female ; Heart Rupture ; Heart Ventricles ; Humans ; Myocardial Infarction ; Neck ; Pericardium ; Rupture

Fungi produce various secondary metabolites that have beneficial and harmful effects on other organisms. Those bioactive metabolites have been explored as potential medicinal and antimicrobial resources. However, the activities of the culture filtrate (CF) and metabolites of white-rot fungus (Schizophyllum commune) have been underexplored. In this study, we assayed the antimicrobial activities of CF obtained from white-rot fungus against various plant pathogens and evaluated its efficacy for controlling anthracnose and gray mold in pepper plants. The CF inhibited the mycelial growth of various fungal plant pathogens, but not of bacterial pathogens. Diluted concentrations of CF significantly suppressed the severity of anthracnose and gray mold in pepper fruits. Furthermore, the incidence of anthracnose in field conditions was reduced by treatment with a 12.5% dilution of CF. The active compound responsible for the antifungal and disease control activity was identified and verified as schizostatin. Our results indicate that the CF of white-rot fungus can be used as an eco-friendly natural product against fungal plant pathogens. Moreover, the compound, schizostatin could be used as a biochemical resource or precursor for development as a pesticide. To the best of our knowledge, this is the first report on the control of plant diseases using CF and active compound from white-rot fungus. We discussed the controversial antagonistic activity of schizostatin and believe that the CF of white-rot fungus or its active compound, schizostatin, could be used as a biochemical pesticide against fungal diseases such as anthracnose and gray mold in many vegetables.
Agaricales ; Fruit ; Fungi ; Incidence ; Plant Diseases ; Plants ; Vegetables

Primary venous thrombosis caused by deficiency or qualitative abnormality of antithrombin III, protein C and protein S is usually inherited as an autosomal dominant trait. Usually, deep vein thrombosis or pulmonary thromboembolism is developed by such abnormalities, however, mesenteric vein thrombosis is rarely reported. A 27-year-old man with previous history of deep vein thrombosis underwent segmental resection of jejunum due to mesenteric vein thrombosis complicated by necrosis of jejunum. Postoperative investigation disclosed combined deficiency of antithrombin III and protein C. His son also showed deficiency of antithrombin III. Postoperatively, he is on life-long warfarin therapy without experiencing recurrence of venous thrombosis.
Adult ; Antithrombin III* ; Humans ; Jejunum ; Mesenteric Veins ; Necrosis ; Protein C* ; Protein S ; Pulmonary Embolism ; Recurrence ; Thrombosis ; Venous Thrombosis* ; Warfarin