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High-temperature superconducting (HTS) cable systems are expected to be a solution for improvement of the power grid and three demonstration projects in the real grid are underway in the United States. One of these is the Albany, NY HTS Cable Project, involving the installation and operation of a 350 meter HTS cable system with a capacity of 34.5 kV, 800 A, installed between two substations in National Grid's electric utility system. A 320 meter and a 30 meter cable are installed in an underground conduit and connected together by a joint, or splice in a vault. In Phase I of this project, the cables were fabricated with DI-BSCCO wire in a 3-core-in-one cryostat structure. After the installation of the HTS cable system, the in.grid operation began on July 20, 2006 and operated successfully in unattended condition through May 1, 2007. In Phase II, the 30 meter section was replaced by a 2G (YBCO) cable. The 2G cable was fabricated with SuperPower's YBCO coated conductors in a 3 core-in-one cryostat. After replacement of the 30 meter section, the joint and one termination were reassembled and the commissioning tests that included initial cooling, critical current measurement and DC withstand voltage test were completed successfully. After the commissioning tests, the HTS cable system with a 30 meter YBCO cable and a 320 meter DI-BSCCO cable was re-energized on January 8, 2008 and started again to operate in a live utility network. This paper describes the latest status of the Albany HTS cable project. [ABSTRACT FROM AUTHOR]

The Albany Cable Project team (BOC, National Grid, Sumitomo Electric, SuperPower) have built and tested a 350-m long HTS cable and cryogenic system rated at 48 MVA (800 Arms, 34.5-kV). The cable system included the world's first demonstration of an HTS cable-to-cable joint (or splice) as well as some novel design aspects in both the cryogenic refrigeration system and the terminations. The cable was installed and began operation in July 2006. This paper will summarize the testing and operational aspects of the HTS cable system and its integration into the existing National Grid 34.5-kV network. [ABSTRACT FROM AUTHOR]

High temperature superconducting transformers offer many economic, operational, and environmental benefits over conventional power transformers for utility applications. To establish the technical and economic feasibility and benefits of HTS transformers of medium-to-large (>10 MVA) ratings, a team that includes Waukesha Electric Systems (transformer manufacturer), SuperPower, Inc. (HTS systems manufacturer), Oak Ridge National Lab, and Energy East has designed, built and tested a prototype 5/10 MVA superconducting transformer. The transformer's 4.5-ton cold mass has been successfully maintained at temperatures of 30-50 K for several months, without full-lime operator attendance. The transformer has reached its full three-phase operating current, and has been tested to 1.4 limes operating current (limited by available power supplies) in single-phase mode. It is now undergoing long-term tests at various current levels, high-voltage tests, and transient overcurrent tests at the Waukesha site. This paper summarizes the manufacturing, cooldown, and the test results achieved to date. [ABSTRACT FROM AUTHOR]

A team consisting of SuperPower, Inc. (HTS systems manufacturer), The BOC Group (global industrial gases company), Sumitomo Electric Industries (cable manufacturer), and Niagara Mohawk (electric utility) is developing a 34.5 kV HTS cable for installation in the distribution network in downtown Albany, NY. Energization is projected for the winter of 2005. The cable will be rated for 800 Arms, with all three electrical phases in one cryostat. The 350 m long cable will be pulled through a duct that includes a 90° bend. A field installed underground cable joint will allow for the replacement of a 30 m section of the original first generation HIS cable with a section manufactured utilizing second generation superconductor, in 2006. This paper will summarize the progress made to date and outline future development work. [ABSTRACT FROM AUTHOR]

1. The Ca(2+) sensitivity of smooth muscle contractility is modulated via regulation of phosphatase activity. Protein phosphatase inhibitor-1 (I-1) is the classic type-1 phosphatase inhibitor, but its presence and role in cAMP-dependent protein kinase (PKA) modulation of smooth muscle is unclear. To address the relevance of I-1 in vivo, we investigated smooth muscle function in a mouse model lacking the I-1 protein (I-1((-/-)) mice). 2. Significant amounts of I-1 protein were detected in the wild-type (WT) mouse aorta and could be phosphorylated by PKA, as indicated by (32)P-labelled aortic extracts from WT mice. 3. Despite the significant presence of I-1 in WT aorta, phenylephrine and KCl concentration- isometric force relations in the presence or absence of the PKA pathway activator isoproterenol (isoprenaline) were unchanged compared to I-1((-/-)) aorta. cGMP-dependent protein kinase (PKG) relaxation pathways were also not different. Consistent with these findings, dephosphorylation rates of the 20 kDa myosin light chains (MLC(20)), measured in aortic extracts, were nearly identical between WT and I-1((-/-)) mice. 4. In the portal vein, I-1 protein ablation was associated with a significant (P < 0.05) rightward shift in the EC(50) of isoproterenol relaxation (EC(50) = 10.4 +/- 1.4 nM) compared to the WT value (EC(50) = 3.5 +/- 0.2 nM). Contraction in response to acetylcholine as well as Ca(2+) sensitivity were similar between WT and I-1((-/-)) aorta. 5. Despite the prevalence of I-1 and its activation by PKA in the aorta, I-1 does not appear to play a significant role in contractile or relaxant responses to any pharmacomechanical or electromechanical agonists used. I-1 may play a role as a fine-tuning mechanism involved in regulating portal vein responsiveness to beta-adrenergic agonists.

Insulin-like growth factor I (IGF-I) has been postulated to function as a vasodilator. We explored the vasoactive effects of chronic elevations of arterial IGF-I levels in SMP8-IGF-I mice, in which IGF-I is overexpressed in smooth muscle (SM) by means of a SM alpha-actin promoter. Denuded aortas from SMP8-IGF-I mice generated increased force in response to KCl or phenylephrine and had greater sensitivity to KCl depolarization. This is not due to desensitization of a SM NO pathway, as pretreatment with n-omega-nitro-L-arginine affected both wild-type and SMP8-IGF-I aortas to a similar degree. The increased contractility ex vivo is not associated with changes in heart rate or blood pressure. Total smooth muscle myosin heavy chain (SMHC) messenger RNA (mRNA) was greater in SMP8-IGF-I aortas, with preferential expression of SMHC-A. Reciprocal effects on contractility and SMHC mRNA were observed in SMP8-IGFBP-4 animals, in which IGF-binding protein-4 was overexpressed through the same promoter. Also, SM alpha-actin mRNA was increased in the aortas from SMP8-IGF-I mice. In summary, chronic arterial overexpression of IGF-I is associated with increased contractility. These effects differ from those seen after acute exposure to the growth factor and may relate to IGF-mediated changes in expression and relative isoform abundance of critical contractile proteins.

The cell adhesion molecule melonoma cell adhesion molecule (MCAM)/MUC18/CD146 is specifically up-regulated on tumors of neuroectodermal origin and in animal models confers metastatic capacity to human melanoma cells. To identify critical regions regulating MCAM expression in melanomas, 1 kilobase of the MCAM 5' region was analyzed for promoter activity and transcription factor binding in 1 glioma, 1 carcinoma, and 4 melanoma cell lines. The minimal MCAM promoter (-106/+22 base pair (bp)) consists of 4 Sp-1 sites, two AP-2 elements, one cAMP responsive element, and the initiator surrounding the transcriptional start site. Analysis of mutated constructs indicated that the cAMP-responsive element is a major transcriptional activator in the majority of cell lines. Site-directed mutagenesis revealed that, in AP-2 expressing cells, the AP-2 site within the core promoter (-23 bp) has an inhibitory influence on MCAM expression while the AP-2 sites at -131 and -302 bp are activating. Functional AP-2 was observed in both MCAM positive and MCAM negative melanoma cell lines indicating that expression of MCAM does not require loss of this transcription factor. Furthermore, all MCAM constructs were strongly expressed in MCAM negative as well as MCAM positive cells, indicating that the expression of this gene is not controlled solely by the presence of transactivating factors binding to the investigated region.

PTH-related peptide is produced in vascular smooth muscle and is believed to participate in the local control of vascular tone. The recent identification of mid-region PTHrP peptides, as well as the discovery of multiple receptors in blood vessels, raises new questions concerning the mechanisms by which PTHrP relaxes the vasculature. In this study, we examined these mechanisms in two vascular beds of the mouse. PTHrP-(1-34) and PTH-(1-34), but not PTHrP-(38-64) or PTHrP-(38-94), caused concentration-dependent relaxation of pre-contracted aortas and reduced the spontaneous phasic activity of the portal vein. PTHrP and PTH-induced aortic relaxations were largely endothelium dependent, whereas an intact endothelium was not necessary for maximal portal vein relaxation. The endothelium-dependent component of PTHrP and PTH-induced aortic relaxations were unaffected by pretreatment with either L-NNA or indomethacin but were abolished by pretreatment with tetrabutyl ammonium. These results demonstrate that the N-terminal portions of PTHrP and PTH are required for their vasorelaxant activity in the mouse. In addition, maximal relaxant activity of PTHrP and PTH in murine aorta is dependent on the endothelium, which appears to involve the generation of an endothelium-derived hyperpolarizing factor.