No abstract available.
Rhabdomyosarcoma* ; Urinary Bladder*

PURPOSE: The purpose of this study is to describe characteristic contrast enhanced MR mammographic findings of ductal carcinoma in situ (DCIS) and also DCIS with microinvasion. MATERIALS AND METHODS: From January 2000 to July 2005, 32 women with 33 lesions affected by DCIS or DCIS with microinvasion underwent contrast enhanced MRI, and they were then retrospectively evaluated. All the patients had previously undergone mammography and ultrasonography. All the findings of mammography, ultrasonography (US), and MRI were analyzed by using an ACR BI-RADS lexicon. RESULTS: All 33 cases were enhanced on the enhanced MR images. A smooth margined homogeneous enhanced mass was seen in the two (2/33) cases, and nonmass enhancement was seen in 31 (31/33) cases. Among the non-mass enhancement, focal enhancement (7/31), ductal enhancement (5/31), segmental enhancement (9/31), and regional enhancement (10/31) were observed. On the kinetic study, a wash-out pattern (10/33), a plateau pattern (20/33), and a persistent pattern (3/33) were demonstrated. No significant differences were noted between the pure and microinvasive DCIS. CONCLUSION: There is no significant difference between pure and microinvasive DCIS. However, contrast enhanced MR images can demonstrate occult foci, multifocal lesion and the tumor extent of DCIS on mammogram or ultrasonogram.
Breast Neoplasms ; Carcinoma, Ductal* ; Carcinoma, Intraductal, Noninfiltrating* ; Female ; Humans ; Magnetic Resonance Imaging* ; Mammography ; Retrospective Studies ; Ultrasonography

BACKGROUND AND OBJECTIVES: The 5-HT2A receptor is one of the main mediators of a serotonin-evoked coronary artery contraction. This is because vasoconstriction is selectively blocked by the 5-HT2 receptor antagonist, with the 5-HT2A receptor gene mRNA being detected in spastic coronary arteries. The relationship between the T102C polymorphism of the 5-HT2A receptor gene and the response to the 5-HT2A antagonist (clozapine) has recently been established, suggestive of a functional implication. Previous studies have observed an association between low cholesterol levels and mental disorders, but the underlying cause has not been determined. It has been established that the T102C polymorphism of the 5-HT2A serotonin receptor gene and a variety of psychological problems are related, but the relationship between the serum lipid level and this genetic polymorphism has not been reported. We investigated the influence of this polymorphism on coronary artery disease, including vasospastic angina and the clinical parameters, such as the lipid profile. SUBJECTS AND METHODS: After a diagnostic angiography was performed, the genotype was identified from the genomic DNA extracted from the peripheral blood of 646 patients without specific psychiatric diseases. RESULTS: There were no differences in the genotype frequencies between coronary artery disease, coronary artery disease with vasospasm, and the normal control groups, even from a subgroup analysis of the clinical parameters. Contrary to previous reports, the genotype distribution was not related to a myocardial infarction or hypertension. The lipid profile analysis showed significantly lower total cholesterol (193.5 vs. 202.1mg/dL, p=0.016) and HDL-cholesterol (42.7 vs. 46.2mg/dL, p=0.003) levels in the CC genotype than the other genotypes, and the frequencies of CC genotype showed a significantly decreasing trend between the HDL-cholesterol (p=0.003) and total cholesterol (p=0.003) quartiles. From a multivariate analysis, only the HDL-cholesterol level was significantly associated with a lower frequency of the CC genotype (p=0.006). CONCLUSION: The T102C polymorphism is not related to coronary artery disease, including vasospasm of the coronary artery, but the CC genotype of this polymorphism is related to low HDL-cholesterol. We identified a novel genetic polymorphism of the serotonin receptor, which affects the HDL-cholesterol level. Because previous observational studies have shown an association between low cholesterol levels and mental disorders, our data should be considered when analyzing the serum lipid levels and serotonin receptor function in humans.
Angiography ; Cholesterol ; Coronary Artery Disease* ; Coronary Vessels* ; DNA ; Genotype ; Humans ; Hypertension ; Mental Disorders ; Multivariate Analysis ; Muscle Spasticity ; Myocardial Infarction ; Polymorphism, Genetic ; Receptor, Serotonin, 5-HT2A* ; RNA, Messenger ; Serotonin ; Serotonin 5-HT2 Receptor Antagonists ; Vasoconstriction

NF-kappa B promotes cell survival against external stress such as radiation. We examined whether NF-kappa B decoy transfection enhances the antiproliferative effects of radiation on vascular smooth muscle cells (VSMCs) in vitro. The irradiation induced activation or nuclear translocation of NF-kappa B p65 in VSMCs was confirmed by immunofluorescence. NF-kB decoy transfection resulted in inhibition of the radiation-induced NF-kB activation in VSMCs and the subsequent reduction of transcription and translocation of ICAM, iNOS, and TNF-alpha, downstream molecules under the control of NF-kappa B. By using MTT assay, NF-kappa B decoy augmented the antiproliferative effects of radiation, where the effect of low dose radiation (2 and 8-Gy) of the cells transfected with NF-kappa B decoy was equivalent to the high dose (16-Gy) irradiated non-transfected cells at 48 h after irradiation: 1.06+/-0.16, 1.11+/-0.22, 1.20+/-0.25, respectively. The decrease in proliferation and survival of the radiation treated cells by flow cytometry analysis showed that NF-kappa B inhibition did not show any additive effects on the cell cycle of the irradiated VSMCs, while apoptosis was significantly increased after NF-kappa B decoy transfection in the irradiated VSMCs (apoptosis fraction: 13.33+/-2.08% vs. 26.29+/-7.43%, for radiation only vs. radiation+NF-kappa B decoy transfection, P < 0.05). In addition, at 48 h, NF-kappa B decoy transfection dose dependently (10 mM vs. 20 mM) inhibited proliferation of 16Gy-irradiated VSMCs, and showed greater antiproliferative efficacy than 100 mM sulfasalazine, a specific NF-kappa B inhibitor. These results indicate that NF-kappa B inhibition reduces proliferation and survival of irradiated VSMCs, likely by increased apoptosis rather than additive cell cycle arrest and suggest the possibility of adjunctive gene therapy using NF-kappa B decoy to improve efficacy and to decrease the adverse effects of intracoronary radiation therapy.
Animals ; Aorta/cytology/radiation effects ; *Apoptosis ; Cell Cycle/physiology/radiation effects ; Cell Proliferation/radiation effects ; Cells, Cultured ; Gamma Rays ; Intercellular Adhesion Molecule-1/metabolism ; Male ; Muscle, Smooth, Vascular/cytology/physiology/*radiation effects ; Myocytes, Smooth Muscle/cytology/radiation effects ; NF-kappa B/*antagonists & inhibitors/metabolism ; Nitric-Oxide Synthase/metabolism ; Protein Transport ; Rats ; Rats, Sprague-Dawley ; Research Support, Non-U.S. Gov't ; Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/metabolism