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6H-Pyrrolo[3,2-b:4,5-b 0 ]bis [1,4]benzothiazine (PBBTZ, 1) and its two 6-substituted derivatives (2 and 3) were conveniently synthesized. Their optical properties were studied by UV-vis and fluorescence spectroscopy, and electrochemical properties were investigated by cyclic voltammetry (CV). Good thermal stability was observed by thermogravimetric analysis. X-Ray analysis revealed a coplanar structure and a column stacking in the single crystal of compound 1. OFET measurements showed that 1-3 were p-type semiconductors. The performance of these devices displayed good reproducibility at ambient conditions. When devices containing 1 were fabricated on OTS-treated SiO 2 /Si substrates at 60 C, the best performance was achieved with the average hole mobility as high as 0.34 cm 2 V À1 s À1 and the on/off ratio about 10 6 -10 7 . This performance resulted from the well-ordered molecular packing as revealed by XRD and AFM analysis.Scheme 1 Synthesis of 6-substituted PBBTZ (1-3).

PBBTZ (6H-pyrrolo [3,2-b:4,5-b']bis [1,4]benzothiazine) was a p-type semiconductor with high field-effect transistor (FET) performance that we have just reported. Two trifluoromethyl substituted PBBTZ derivatives 3a and 3b were synthesized from facile one-pot condensation. They were characterized by means of 1 H NMR, IR, HRMS (EI-TOF) and elemental analysis, furthermore, the crystal structure of 3b was described and discussed. Their optical properties were studied by UV-Vis and fluorescence spectroscopy, electrochemical properties were investigated by cyclic voltammetry (CV), and thermal properties were evaluated by thermal gravimetric analysis (TGA). The energy gaps of 3a and 3b, taken directly from spectroscopic measurements, are as broad as 2.45 and 2.48 eV, leading to bluish green and green photoluminescence. The LUMO and HOMO energy levels are -5.73 and -3.28 eV for 3a, -5.67 and -3.19 eV for 3b, respectively. The low energy levels render them well air-stable, and to be promising n-type semiconductor candidates for use in organic electronics.

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Abstract Background Statins are the most widely used drugs in elderly patients, the most common clinical application of statins is in aged hyperlipemia patients. There are few studies on the effects and mechanisms of statins on bone in elderly mice with hyperlipemia. The study is to examine the effects of atorvastatin on bone phenotypes and metabolism in aged apolipoprotein E-deficient (apoE –/– ) mice, and the possible mechanisms involved in these changes. Methods Twenty-four 60-week-old apoE –/– mice were randomly allocated to two groups. Twelve mice were orally gavaged with atorvastatin (10 mg/kg body weight/day) for 12 weeks; the others served as the control group. Bone mass and skeletal microarchitecture were determined using micro-CT. Bone metabolism was assessed by serum analyses, qRT-PCR, and Western blot. Bone marrow-derived mesenchymal stem cells (BMSCs) from apoE –/– mice were differentiated into osteoblasts and treated with atorvastatin and Sirt1 inhibitor EX-527. Results The results showed that long-term administration of atorvastatin increases bone mass and improves bone microarchitecture in trabecular bone but not in cortical bone. Furthermore, the serum bone formation marker osteocalcin (OCN) was ameliorated by atorvastatin, whereas the bone resorption marker tartrate-resistant acid phosphatase 5b (Trap5b) did not appear to be impacted by atorvastatin treatment. The mRNA expression of Sirt1, runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP) and OCN in bone tissue were increased after atorvastatin administration. Western blot showed same trend in Sirt1 and Runx2. The in vitro study showed that when BMSCs from apoE –/– mice were pretreated with EX527, the higher expression of Runx2, ALP and OCN activated by atorvastatin decreased significantly or showed no difference compared with the control. The protein expression of Runx2 showed same trend. Conclusions Accordingly, the current study validates the hypothesis that atorvastatin can increase bone mass and promote osteogenesis in aged apoE −/− mice by regulating the Sirt1–Runx2 axis.