Loss-of-Mains Detection by Internet Based ROCOF

This paper considers the enhancement of loss-of-mains detection by use of a differential rate-of-change-of-frequency relay to reduce nuisance tripping and improve sensitivity to small excursions in frequency. The telecommunications media which might carry the differential ROCOF signal are reviewed with a focus on channel latency, bandwidth and security.

Disruption of the langerin/CD207 Gene Abolishes Birbeck Granules without a Marked Loss of Langerhans Cell Function

Langerin is a C-type lectin expressed by a subset of dendritic leukocytes, the Langerhans cells (LC). Langerin is a cell surface receptor that induces the formation of an LC-specific organelle, the Birbeck granule (BG). We generated a langerin(-/-) mouse on a C57BL/6 background which did not display any macroscopic aberrant development. In the absence of langerin, LC were detected in normal numbers in the epidermis but the cells lacked BG. LC of langerin(-/-) mice did not present other phenotypic alterations compared to wild-type littermates. Functionally, the langerin(-/-) LC were able to capture antigen, to migrate towards skin draining lymph nodes, and to undergo phenotypic maturation. In addition, langerin(-/-) mice were not impaired in their capacity to process native OVA protein for I-A(b)-restricted presentation to CD4(+) T lymphocytes or for H-2K(b)-restricted cross-presentation to CD8(+) T lymphocytes. langerin(-/-) mice inoculated with mannosylated or skin-tropic microorganisms did not display an altered pathogen susceptibility. Finally, chemical mutagenesis resulted in a similar rate of skin tumor development in langerin(-/-) and wild-type mice. Overall, our data indicate that langerin and BG are dispensable for a number of LC functions. The langerin(-/-) C57BL/6 mouse should be a valuable model for further functional exploration of langerin and the role of BG.

Induction of tetraploidy through loss of p53 and upregulation of Plk1 by Human Papillomavirus type-16 E6

Cancer cells are insensitive to many signals that inhibit growth of untransformed cells. Here, we show that primary human epithelial cells expressing human papillomavirus (HPV) type-16 E6/E7 bypass arrest caused by the DNA-damaging drug adriamycin and become tetraploid. To determine the contribution of E6 in the context of E7 to the resistance of arrest and induction of tetraploidy, we used an E6 mutant unable to degrade p53 or RNAi targeting p53 for knockdown. The E6 mutant fails to generate tetraploidy; however, the presence of E7 is sufficient to bypass arrest while the p53 RNAi permits both arrest insensitivity and tetraploidy. We published previously that polo-like kinase 1 (Plk1) is upregulated in E6/E7-expressing cells. We observe here that abnormal expression of Plk1 protein correlates with tetraploidy. Using the p53 binding-defective mutant of E6 and p53 RNAi, we show that p53 represses Plk1, suggesting that loss of p53 results in tetraploidy through upregulation of Plk1. Consistent with this hypothesis, overexpression of Plk1 in cells generates tetraploidy but does not confer resistance to arrest. These results support a model for transformation caused by HPV-16 where bypass of arrest and tetraploidy are separable consequences of p53 loss with Plk1 required only for the latter effect.

Progressive loss of ferroelectricity under bipolar pulsed fields and experimental determination of non-switchable polarization in Au/Ba0.5Sr0.5TiO3/SrRuO3 thin-film capacitors

175 nm-thick Ba0.5Sr0.5TiO3 (BST) thin film fabricated by pulsed laser deposition (PLD) technique is found to be a mixture of two distributions of material. We discuss whether these two components are nano-regions of paraelectric and ferroelectric phases, or a bimodal grain-size distribution, or an effect of oxygen vacancy gradient from the electrode interface. The fraction of switchable ferroelectric phase decreases under bipolar pulsed fields, but it recovers after removal of the external fields. The plot of capacitance in decreasing dc voltage (C(Vdown arrow) versus that in increasing dc 61 voltage C(Vup arrow) is a superposition of overlapping of two triangles, in contrast to one well-defined triangle for typical ferroelectric SrBi2Ta2O9 thin films.

Special issue on design and programming of signal processors for multimedia communication:Special issue on design and programming of signal processors for multimedia communication

The technical challenges in the design and programming of signal processors for multimedia communication are discussed. The development of terminal equipment to meet such demand presents a significant technical challenge, considering that it is highly desirable that the equipment be cost effective, power efficient, versatile, and extensible for future upgrades. The main challenges in the design and programming of signal processors for multimedia communication are, general-purpose signal processor design, application-specific signal processor design, operating systems and programming support and application programming. The size of FFT is programmable so that it can be used for various OFDM-based communication systems, such as digital audio broadcasting (DAB), digital video broadcasting-terrestrial (DVB-T) and digital video broadcasting-handheld (DVB-H). The clustered architecture design and distributed ping-pong register files in the PAC DSP raise new challenges of code generation.

Limpet grazing and loss of Ascophyllum nodosum canopies on decadal time scales

The role of limpet grazing in preventing the development of algal canopies is a recurrent theme in intertidal ecology. Less is known about interactions of limpets with the long-term dynamics of established canopies. Aerial photographs indicate that intertidal canopy cover has declined over the past 44 yr in Strangford Lough, Northern Ireland. There has been a loss of the previously continuous cover of Ascophyllum nodosum (L.) Le Jolis in the mid-shore. A barnacles dominated assemblage now fills gaps in the A. nodosum canopy. The rates at which barnacle patches become established and grow have increased since 1990. Changes in canopy cover have been accompanied by increases in limpet densities since the 1980s. Measurements between 2003 and 2004 showed no increase in length of A. nodosum fronds when limpets Patella vulgata had access to the algal holdfasts. In contrast, when limpets were experimentally excluded from the holdfasts, there was net frond growth. In the Isle of Man, which is climatically similar to Strangford Lough but has fewer limpets, growth occurred regardless of limpet grazing. The breaking force for A. nodosum declined with increasing local densities of limpets. A. nodosum is a sheltered shore species, potentially vulnerable to changes in wave exposure. There is no evidence, however, that Strangford Lough has become windier over the past 3 decades. Variation in wave exposure among locations within the lough was not related to rates of barnacle patch creation or expansion, Limpet population density has increased following a series of mild winters. Climate change may have a role in causing canopy loss, not by direct effects on the limpet populations.

Loss of the LAT adaptor converts antigen-responsive T cells into pathogenic effectors that function independently of the T cell receptor.

Despite compromised T cell antigen receptor (TCR) signaling, mice in which tyrosine 136 of the adaptor linker for activation of T cells (LAT) was constitutively mutated (Lat(Y136F) mice) accumulate CD4(+) T cells that trigger autoimmunity and inflammation. Here we show that equipping postthymic CD4(+) T cells with LATY136F molecules or rendering them deficient in LAT molecules triggers a lymphoproliferative disorder dependent on prior TCR engagement. Therefore, such disorders required neither faulty thymic T cell maturation nor LATY136F molecules. Unexpectedly, in CD4(+) T cells recently deprived of LAT, the proximal triggering module of the TCR induced a spectrum of protein tyrosine phosphorylation that largely overlapped the one observed in the presence of LAT. The fact that such LAT-independent signals result in lymphoproliferative disorders with excessive cytokine production demonstrates that LAT constitutes a key negative regulator of the triggering module and of the LAT-independent branches of the TCR signaling cassette.