The Solar Optical Telescope (SOT) aboard the Hinode satellite (formerly called Solar-B) consists of the Optical Telescope Assembly (OTA) and the Focal Plane Package (FPP). The OTA is a 50-cm diffraction-limited Gregorian telescope, and the FPP includes the narrowband filtergraph (NFI) and the broadband filtergraph (BFI), plus the Stokes SpectroPolarimeter (SP). The SOT provides unprecedented high-resolution photometric and vector magnetic images of the photosphere and chromosphere with a very stable point spread function and is equipped with an image-stabilization system with performance better than 0.01 arcsec rms. Together with the other two instruments on Hinode (the X-Ray Telescope M. Otsubo is a former NAOJ staff scientist.

The Solar Optical Telescope (SOT) aboard the Solar-B satellite (Hinode) is designed to perform high-precision photometric and polarimetric observations of the Sun in visible light spectra (388 -668 nm) with a spatial resolution of 0.2 -0.3 arcsec. The SOT consists of two optically separable components: the Optical Telescope Assembly (OTA), consisting of a 50-cm aperture Gregorian with a collimating lens unit and an active tip-tilt mirror, and an accompanying Focal Plane Package (FPP), housing two filtergraphs and a spectro-polarimeter. The optomechanical and optothermal performance of the OTA is crucial to attain unprecedented high-quality solar observations. We describe in detail the instrument design and expected stable diffraction-limited on-orbit performance of the OTA, the largest state-of-the-art solar telescope yet flown in space.

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Background-Mice with cardiac-specific overexpression of signal transducer and activator of transcription 3 (STAT3) are resistant to doxorubicin-induced damage. The STAT3 signal may be involved in the detoxification of reactive oxygen species (ROS). Methods and Results-The effects of leukemia inhibitory factor (LIF) or adenovirus-mediated transfection of constitutively activated STAT3 (caSTAT3) on the intracellular ROS formation induced by hypoxia/reoxygenation (H/R) were examined using rat neonatal cardiomyocytes. Either LIF treatment or caSTAT3 significantly suppressed the increase of H/R-induced ROS evaluated by 2Ј,7Ј-dichlorofluorescin diacetate fluorescence. To assess whether ROS are really involved in H/R-induced cardiomyocyte injury, the amount of creatine phosphokinase in cultured medium was examined. Both LIF treatment and caSTAT3 significantly decreased H/R-induced creatine phosphokinase release. These results indicate that the gp130/STAT3 signal protects H/R-induced cardiomyocyte injury by scavenging ROS generation. To investigate the mechanism of scavenging ROS, the effects of LIF on the induction of antioxidant enzymes were examined. LIF treatment significantly increased the expression of manganese superoxide dismutase (MnSOD) mRNA, whereas the expression of the catalase and glutathione peroxidase genes were unaffected. This induction of MnSOD mRNA expression was completely blocked by adenovirus-mediated transfection of dominant-negative STAT3. Moreover, caSTAT3 augmented MnSOD mRNA and its enzyme activity. In addition, the antisense oligodeoxyribonucleotide to MnSOD significantly inhibited both LIF and caSTAT3-mediated protective effects. Key Words: antioxidants Ⅲ hypoxia Ⅲ signal transduction I n the heart, it has been reported that reactive oxygen species (ROS) contribute to cardiac dysfunction and myocardial damage under a variety of conditions, such as ischemia-reperfusion, congestive heart failure, and doxorubicin-induced cardiomyopathy. 1-3 Recent studies have shown that gp130-mediated signals transduced both cytoprotective and hypertrophic responses in the heart. 4 The signal transducer and activator of transcription-3 (STAT3) is a key molecule downstream of gp130, which is activated under various stressful conditions, such as pressure-overload and myocardial infarction. 4 Transgenic mice with cardiac-specific overexpression of the STAT3 gene are protected against doxorubicin-induced cardiomyopathy. 5 Therefore, the activation of STAT3 might induce a protective effect against oxidative stress-induced cardiomyocyte damage by scavenging ROS. Conclusions-TheIn the present study, we explored whether the gp130/ STAT3 signal has a protective function against hypoxia/reoxygenation (H/R)-induced cardiomyocyte damage. Methods Cell Culture and H/R ExperimentsPrimary cultures of neonatal rat cardiomyocytes were prepared from the ventricles of 1-day-old Sprague-Dawley rats (Kiwa Dobutsu Wakayama, Japan), as previously described. 6 Hypoxia was created by incubating cells in an airtight Plexiglas chamber w...

CD10 is a cell surface neutral endopeptidase that is not consistently expressed in the stromal cells of the normal breast. Expression of CD10 is sometimes observed in the stromal cells of invasive ductal carcinoma, but its clinical significance has never been studied. Immunohistochemical examination of CD10 was performed in 123 cases of breast cancer. The median follow-up period of all patients was 8.0 years, and univariate and multivariate analyses were performed to evaluate the prognostic significance of stromal CD10 expression. There was no staining in the stromal cells of 13 non-invasive ductal carcinomas or normal breast tissue. Of 110 invasive ductal carcinomas, 20 cases (18%) in which more than 10% of the stromal cells stained positive throughout the cancer tissue were judged "positive". The frequency of positive stromal staining was significantly higher in the cases with axillary lymph-node metastasis ( P=0.038), but there were no correlations between stromal CD10 expression and age, tumor size, histologic grade, or clinical stage. The patients whose tumors contained CD10-positive stromal cells had a shorter metastasis-free interval ( P=0.0008). Univariate analysis demonstrated that patients with lymph-node metastasis also had a significantly shorter metastasis-free interval (metastasis vs no metastasis; P=0.0318). In the multivariate analysis, only CD10 remained a significant predictor for time to recurrence ( P=0.0059), and CD10 was the single significant prognostic factor for overall survival in the univariate analysis ( P=0.0021). These results suggest that stromal expression of CD10 in breast cancer is an important novel prognostic factor.

Superconducting technology applications in electric machines have long been pursued due to their significant advantages of higher efficiency and power density over conventional technology. However, in spite of many successful technology demonstrations, commercial adoption has been slow, presumably because the threshold for value versus cost and technology risk has not yet been crossed. One likely path for disruptive superconducting technology in commercial products could be in applications where its advantages become key enablers for systems which are not practical with conventional technology. To help systems engineers assess the viability of such future solutions, we present a technology roadmap for superconducting machines. The timeline considered was ten years to attain a Technology Readiness Level of 6+, with systems demonstrated in a relevant environment. Future projections, by definition, are based on the judgment of specialists, and can be subjective. Attempts have been made to obtain input from a broad set of organizations for an inclusive opinion. This document was generated

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Activation of glycoprotein (gp) 130 transduces hypertrophic and cytoprotective signals in cardiac myocytes.In the present study, we have demonstrated that signals through gp130 increase the expression of vascular endothelial growth factor (VEGF) in cardiac myocytes via the signal transducer and activator of transcription (STAT) 3 pathway. After activation of gp130 with leukemia inhibitory factor (LIF), expression of VEGF mRNA rapidly increased with a peak at 3 h in cultured cardiac myocytes. Cardiotrophin-1 also enhanced VEGF mRNA expression in a dose-dependent manner. VEGF protein production and secretion to the medium were also enhanced by LIF and cardiotrophin-1 but not by interleukin-6. Adenovirus transfer of the dominant-negative form of STAT3 to cultured cardiac myocytes inhibited induction of VEGF expression induced by LIF, but neither PD98059 nor wortmannin was affected. In murine hearts, intravenous administration of LIF augmented expression of VEGF mRNA; however, the hearts of transgenic mice overexpressing dominant-negative STAT3 showed reduced expression of VEGF mRNA that was not induced after LIF stimulation. These data provide the first evidence that a STAT family protein functions as a regulator of angiogenic growth factors and suggest that gp130/STAT signaling in cardiac myocytes can control vessel growth during cardiac remodeling.