Purpose: To evaluate leptin and leptin receptor (OB-R) expression in human breast cancer and determine whether it could be effective for the prevention and treatment of breast cancer.Experimental Design: Immunohistochemical staining using specific antibodies was used to evaluate the protein expression of leptin and OB-R in 76 invasive ductal carcinomas and 32 samples of corresponding normal mammary gland, and the relationship between the expression of OB-R and leptin and clinicopathological features was analyzed.Results: Normal mammary epithelial cells did not express a significant level of Ob-R, whereas carcinoma cells showed positive staining for OB-R in 63 (83%) cases. Both normal epithelial cells and carcinoma cells expressed a significant level of leptin. However, overexpression of leptin, as determined by staining intensity, was observed in 70 cancers (92%) but in no normal epithelium. The expression of OB-R showed a significant correlation with the level of leptin expression. Interestingly, distant metastasis was detected in 21 (34%) of 61 OB-R-positive tumors with leptin overexpression, but in none of the 15 tumors that lacked OB-R expression or leptin overexpression (P < 0.05). Consequently, patients with the former tumors showed significantly lower survival than those with the latter.Conclusions: Leptin may have a promoting effect on the carcinogenesis and metastasis of breast cancer, possibly in an autocrine manner. Functional inhibition of leptin may be effective for the prevention and treatment of breast cancer.

Evaluation for JENDL-3.3 has been performed by considering the accumulated feedback information and various benchmark tests of the previous library JENDL-3.2. The major problems of the JENDL-3.2 data were solved by the new library: overestimation of criticality values for thermal fission reactors was improved by the modifications of fission cross sections and fission neutron spectra for 235 U; incorrect energy distributions of secondary neutrons from important heavy nuclides were replaced with statistical model calculations; the inconsistency between elemental and isotopic evaluations was removed for medium-heavy nuclides. Moreover, covariance data were provided for 20 nuclides. The reliability of JENDL-3.3 was investigated by the benchmark analyses on reactor and shielding performances. The results of the analyses indicate that JENDL-3.3 predicts various reactor and shielding characteristics better than JENDL-3.2.

The revision work of JENDL-3 has been made by considering feedback information of various benchmark test,s. The main revised quantities are the resonance parameters, capture and inelastic scattering cross sections, and fission spectra of main actinide nuclides, the total and inelastic scattering cross sections of structural materials, the resonance parameters the capture and inelastic scattering cross sections of fission products, and the y-ray production data. The revised data were released as JENDG3.2 in June 1994. The preliminary benchmark tests indicate thar JENDG3.2 predicts various reactor characteristics more successfully than the previous versioli of JENDL-3.1.

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Rationale Electrogram-based catheter ablation, targeting complex fractionated atrial electrograms (CFAEs), is empirically known to be effective in halting persistent/permanent atrial fibrillation (AF). However, the mechanisms underlying CFAEs and electrogram-based ablation remain unclear. Objective Because atrial fibrosis is associated with persistent/permanent AF, we hypothesized that electrotonic interactions between atrial myocytes and fibroblasts play an important role in CFAE genesis and electrogram-based catheter ablation. Methods and Results We used a human atrial tissue model in heart failure and simulated propagation and spiral wave reentry with and without regionally proliferated fibroblasts. Coupling of fibroblasts to atrial myocytes resulted in shorter action potential duration, slower conduction velocity, and lower excitability. Consequently, heterogeneous fibroblast proliferation in the myocardial sheet resulted in frequent spiral wave breakups, and the bipolar electrograms recorded at the fibroblast proliferation area exhibited CFAEs. The simulations demonstrated that ablation targeting such fibroblast-derived CFAEs terminated AF, resulting from the ablation site transiently pinning the spiral wave and then pushing it out of the fibroblast proliferation area. CFAEs could not be attributed to collagen accumulation alone. Conclusions Fibroblast proliferation in atria might be responsible for the genesis of CFAEs during persistent/ permanent AF. Our findings could contribute to better understanding of the mechanisms underlying CFAE-targeted AF ablation.