On-surface synthesis of hydroxy-functionalized graphene nanoribbons through deprotection of methylenedioxy groups

We demonstrate on-surface deprotection of methylenedioxy groups which yielded graphene nanoribbons (GNRs) with edges functionalized by hydroxy groups. While anthracene trimer precursors functionalized with hydroxy groups did not yield GNRs, it was found that hydroxy groups are first protected as methylenedioxy groups and then deprotected during the cyclo-dehydrogenation process to form GNRs with hydroxy groups. The X-ray photoemission spectroscopy and non-contact atomic force microscopy studies revealed that ∼20% of the methylenedioxy turned into hydroxy groups, while the others were hydrogen-terminated. The first-principles density functional theory (DFT) study on the cyclo-dehydrogenation process was performed to investigate the deprotection mechanism, which indicates that hydrogen atoms emerging during the cyclo-dehydrogenation process trigger the deprotection of methylenedioxy groups. The scanning tunneling spectroscopy study and DFT revealed a significant charge transfer from hydroxy to the Au substrate, causing an interface dipole and the HOMO being closer to the Fermi level when compared with hydrogen-terminated GNR/Au(111). This result demonstrates on-surface deprotection and indicates a possible new route to obtain GNRs with desired edge functionalization, which can be a critical component for high-performance devices

Mast Cells and Angiogenesis in Oral Malignant and Premalignant Lesions

Mast cell contribution to neoangiogenesis during tumorigenesis in oral squamous cell carcinoma is not determined yet. Objectives: To associate numerical mast cell density (MCD) to numerical microvessel density (MVD) during the progression of oral leukoplakia without dysplasia and leukoplakia with dysplasia to squamous cell carcinoma (OSCC). Materials and methods: MVD was analysed immunohistochemically (mouse monoclonal anti-human CD34) in 49 paraffin-embedded specimens, 35 OSCCs, 9 leukoplakias and 5 normal oral tissues. Toluidine blue counterstaining revealed mast cells. MCD and MVD were assessed at the same optical field. Results: MVD increased between: normal oral mucosa, dysplasia (p=0.004), OSCC (p=0.001), leukoplakia and OSCC (p=0.041). MCD increased between: normal oral mucosa, dysplasia (p=0.003), OSCC (p=0.000), leukoplakia and OSCC (p=0.007). MVD was found to depend on MCD (p=0.000) in a percent 28.3% (power curve fit model). Conclusions: Mast cells are attracted at the lesion site and may turn on an angiogenic switch during tumorigenesis in OSCC