A new method for calculating loss coefficients [of power systems]

A method is proposed which avoids many limitations associated with traditional B-coefficient loss coefficient calculation. The proposed method, unlike the traditional B-coefficient method, is very fast and can handle line outages. The method utilizes network sensitivity factors which are established from DC load flow solutions, Line outage distribution factors (ODFs) are formulated using changes in network power generations to simulate the outaged line from the network. The method avoids the use of complicated reference frame transformations based upon Kron's tenser analysis. The necessity of data normalization used in least squares and the evaluation of the slope of &thetas;_j versus PG_n is not necessary with the proposed method. Using IEEE standard 14-bus and 30-bus systems, the method's results are compared against results obtained from an AC load flow program (LFED). The method's solution speed is compared to that of the LFED method, the base case database method and the conventional B-coefficient method based on A_jn-factor. The proposed method is easy to implement and, when compared to other methods, has exhibited good accuracy and rapid execution times. The method is well suited to online dispatch applications     

Quantitative analysis of the peripheral blood cytotoxic T lymphocyte response in patients with chronic hepatitis C virus infection

Hepatitis C virus (HCV)-specific cytotoxic T lymphocytes (CTL) are present in the peripheral blood and liver of chronically infected patients. The current study was performed to study the relationship between the strength of the CTL response, liver disease severity, and viral load. The results may be summarized as follows: first, using CTL precursor frequency (CTLpf) analysis to quantitate the peripheral blood CTL response, chronically infected patients were less strongly sensitized to a panel of well-defined HCV epitopes than they were to an epitope within the influenza matrix protein. Second, HCV-specific CTLpf did not correlate with disease activity or viral load in the majority of patients on a cross-sectional basis, although it did increase in three patients concomitant with sharp increases in liver disease. Finally, interferon therapy did not enhance the CTLpf against the HCV epitopes studied in these patients, indicating that its antiviral effect is independent of the CTL response. Since the HCV-specific CTLpf in the blood is actually quite low, the CTL may contribute to ongoing liver disease in these patients while being quantitatively inadequate to destroy all of the infected hepatocytes, thereby facilitating HCV persistence and contributing to chronic liver disease.     

Optimization of a schottky barrier mixer diode in the submillimeter wave region

We have designed a mixer Schottky barrier diode (SBD) for use in the submillimeter wave region with a structure optimized for minimum noise temperature. The dependence of mixer noise temperature upon thickness and doping density of the epitaxial layer and diode diameter of SBDs was simulated within the framework of existing theories. Special care was taken to formulate the SBD current-voltage and capacitance-voltage relations in a way that correctly describes the behavior of real SBDs.     

Inhibition of NFkappaB activity through maintenance of IkappaBalpha levels contributes to dihydrotestosterone-mediated repression of the interleukin-6 promoter

Androgens repress expression of many genes, yet the mechanism of this activity has remained elusive. The cytokine, interleukin-6, is active in a variety of biological systems, and its expression is repressed by androgens. Accordingly we dissected the mechanism of androgen's ability to inhibit interleukin-6 expression at the molecular level. In a series of co-transfection assays, we found that 5alpha-dihydrotestosterone, through the androgen receptor, repressed activation of the interleukin-6 promoter, in part, by inhibiting NFkappaB activity. It did not appear that 5alpha-dihydrotestosterone inhibited NFkappaB by activating the androgen receptor to compete for the NFkappaB response element as we could not detect androgen receptor binding to the IL-6 promoter by DNase I footprinting assay. However, by electrophoretic mobility shift assay we found that 5alpha-dihydrotestosterone repressed formation of NFkappaB middle dotNFkappaB response element complex formation. In LNCaP prostate carcinoma cells, 5alpha-dihydrotestosterone achieved this effect through maintenance of IkappaBalpha protein levels in the face of phorbol ester, a stimulus that results in IkappaBalpha degradation. Finally, we confirmed that IkappaBalpha inhibits NFkappaB-mediated activation of the interleukin-6 promoter. These data suggest that maintenance of IkappaBalpha levels may represent the first identified mechanism for androgen-mediated repression of a natural androgen-regulated gene.