A Self-Ordered Nanostructured Transparent Electrode of High Structural Quality and Corresponding Functional Performance.

The preparation of a highly ordered nanostructured transparent electrode based on a combination of nanosphere lithography and anodization is presented. The size of perfectly ordered pore domains is improved by an order of magnitude with respect to the state of the art. The concomitantly reduced density of defect pores increases the fraction of pores that are in good electrical contact with the underlying transparent conductive substrate. This improvement in structural quality translates directly and linearly into an improved performance of energy conversion devices built from such electrodes in a linear manner.

Interval exercise training in cystic fibrosis -- effects on exercise capacity in severely affected adults.

The aims of the present study were to investigate the effects of IT on lung function power (P) and oxygen uptake (VO2) at peak performance (peak) and ventilatory anaerobic threshold (VAT) in CF patients who were unable to participate in a standard exercise program (SEP) and to compare these IT responses with corresponding effects in CF patients performing SEP. 20 patients (FEV1 25.5 ± 7.5%; pred; SpO2 < 90% at rest or P lower than 0.3 W/kg) who were unable to participate in SEP were allocated to IT (5 × 20 min weekly). 23 patients (FEV1 31.6 ± 4.2%; p < 0.05) did 5 × 45 min per week of SEP. Lung function remained unchanged in both groups. VO2peak and PVAT increased in both groups (p < 0.05). However, only after the SEP an increase in Ppeak (p < 0.05) and only after IT a higher VO2VAT (p < 0.05) were found. Compared to SEP, IT improved submaximal exercise capacity to a greater extent whereas responsiveness on peak performance was higher in SEP. This seems to indicate a specific potential of IT for positive peripheral muscular adaptations in spite of diminishing potential of pulmonary improvement. IT represents an alternative, effective and safe training regimen with patients with CF and severe lung disease, with a greater potential than SEP.

Inactivation of Patched1 in mice leads to development of gastrointestinal stromal-like tumors that express Pdgfrα but not kit.

BACKGROUND & AIMS: A fraction of gastrointestinal stromal tumor (GIST) cells overexpress the platelet-derived growth factor receptor (PDGFR)A, although most overexpress KIT. It is not known if this is because these receptor tyrosine kinases have complementary oncogenic potential, or because of heterogeneity in the cellular origin of GIST. Little also is known about why Hedgehog (HH) signaling is activated in some GIST. HH binds to and inactivates the receptor protein patched homolog (PTCH). METHODS: Ptch was conditionally inactivated in mice (to achieve constitutive HH signaling) using a Cre recombinase regulated by the lysozyme M promoter. Cre-expressing cells were traced using R26R-LacZ reporter mice. Tumors were characterized by in situ hybridization, immunohistochemistry, immunoblot, and quantitative reverse-transcriptase polymerase chain reaction analyses. Cell transformation was assessed by soft agar assay. RESULTS: Loss of Ptch from lysozyme M-expressing cells resulted in the development of tumors of GIST-like localization and histology; these were reduced when mice were given imatinib, a drug that targets KIT and PDGFRA. The Hh signaling pathway was activated in the tumor cells, and Pdgfrα, but not Kit, was overexpressed and activated. Lineage tracing revealed that Cre-expressing intestinal cells were Kit-negative. These cells sometimes expressed Pdgfrα and were located near Kit-positive interstitial cells of Cajal. In contrast to KIT, activation of PDGFRA increased anchorage-independent proliferation and was required for tumor formation in mice by cells with activated HH signaling. CONCLUSIONS: Inactivation of Ptch in mice leads to formation of GIST-like tumors that express Pdgfrα, but not Kit. Activation of Pdgfrα signaling appears to facilitate tumorigenesis.