It is well known that benign tumors originate seldom in the trachea. Especially the occurence of neurinoma in the trachea is extrmely rare. The authors reported a large pedunculated neurinoma originated from the 1st and 2nd tracheal ring in a 12 year-old-boy who complained chiefly incereasing dyspnea and cough, sputum and noisy stridor simultaneously. Tracheotomy was done first, and the tumor was exstirpated with forceps through the stoma of tracheotomy successfully. No subsequent complications, and no recurrens fur 1.5 years.
The resistivity of poly-Si1-XGeX (X=0.0, 0.2, 0.4) films was studied in terms of process fluctuation and long-term stability. Experimental results demonstrated that poly-Si0.6Ge0.4 is superior to poly-Si because of its low process fluctuation of less than 3% across a wafer and significant reduction of resistivity-drift. The measured Hall mobility and trapping density reveal that the atomic configuration at the grain boundary of boron-doped poly-Si1-XGeX film differs from that of the conventional poly-Si film. Under hydrogen exposure, the electrical properties of poly-Si1-XGeX films in a wide range of carrier concentration are more stable than those of poly-Si, because of a smaller amount of dangling bonds, stronger bonding energy to hydrogen and more segregation of boron atoms at poly-Si1-XGeX boundaries. These results indicate that the poly-Si1-XGeX resistors are superior to poly-Si ones for obtaining high precision and low power analog circuits.
Abstract Spherical silver nanoparticles (diameter: 7–10 nm) were fabricated through passivation by fullerodendrons (C60(Gn-COOK) (n = 0.5, 1.5, 2.5)), which were synthesized from fullerene and anthracenyl focal poly(amido amine) dendrons with carboxylate terminals and different generations (G). The resultant nanocomposites presented unique luminescence, which was contributed by not only anthracenyl moiety but also poly(amido amine) dendron moiety, although the latter has no traditional fluorophore. Furthermore, fluorescence of C60(G2.5-COOK) was quenched by the silver nanoparticles, indicating that the excitation energy transferred to silver particles.
The CREB-specific coactivator TORC2 (also known as CRTC2) upregulates gluconeogenic gene expression in the liver. Salt-inducible kinase (SIK) family enzymes inactivate TORC2 through phosphorylation and localize it in the cytoplasm. Ser 171 and Ser 275 were found to be phosphorylated in pancreatic β-cells. Calcineurin (Cn) is proposed as the Ser 275 phosphatase, because its inhibitor cyclosporin A (CsA) stabilizes phospho-Ser 275 and retains TORC2 in the cytoplasm. Because the regulation of dephosphorylation at Ser 171 has not been fully clarified, we performed experiments with a range of doses of okadaic acid (OA), an inhibitor of PP2A/PP1, and with overexpression of various phosphatases and found that PP1 functions as an activator for TORC2, whereas PP2A acts as an inhibitor. In further studies using TORC2 mutants, we detected a disassociation between the intracellular distribution and the transcription activity of TORC2. Additional mutant analyses suggested the presence of a third phosphorylation site, Ser 307 . The Ser 307 -disrupted TORC2 was constitutively localized in the nucleus, but its coactivator activity was normally suppressed by SIK1 in COS-7 cells. CsA, but not OA, stabilized the phosphogroup at Ser 307 , suggesting that differential dephosphorylation at Ser 171 and Ser 307 cooperatively regulate TORC2 activity and that the nuclear localization of TORC2 is insufficient to function as a coactivator. Because the COS-7 cell line may not possess signaling cascades for gluconeogenic programs, we next examined the importance of Ser 307 and Ser 171 for TORC2's function in mouse liver. Levels of phosphorylation at Ser 171 and Ser 307 changed in response to fasting or fed conditions and insulin resistance of the mouse liver, which were modified by treatment with CsA/OA and by overexpression of PP1/PP2A/Cn. These results suggest that multiple phosphorylation sites and their phosphatases may play important roles in regulating TORC2/CREB-mediated gluconeogenic programs in the liver.
