Modified polyvinyl alcohol layer with hydrophobic surface for the passivation of pentacene thin-film transistor.

We modified the surface of a polyvinyl alcohol (PVA) layer by self assembly monolayer technique using a fluorine substituted silane compound (1H,1H,2H,2H-perfluorooctyl-trichlorosilane: FTS) to protect a pentacene thin-film transistor (TFT) from O2 and H2O. Surface modified PVA showed very low surface energy with water contact angle of 106.2 degrees. Surface treatment of PVA layer on pentacene TFT device was done in toluene solvent and we did not observe any damage to the PVA layer or pentacene TFT devices during surface modification process. Pentacene TFT with surface modified PVA passivation layer exhibited very stable TFT operation with almost no field effect mobility drop or threshold voltage shift up to 400 hrs. The performance of unpassivated OTFTs exponentially degraded and almost failed in 290 hrs. We propose that modified PVA layer can be used as a good passivation layer for oxygen and water in OTFT.

Type I collagen is the autoantigen in experimental autoimmune anterior uveitis.

This study was undertaken to identify and characterize the Ag responsible for the induction of experimental autoimmune anterior uveitis (EAAU). Melanin-associated Ag isolated from bovine iris and ciliary body was digested with the proteolytic enzyme V8 protease to solubilize the proteins and the pathogenic protein was purified to homogeneity. Lewis rats were sensitized to various fractions and investigated for the development of anterior uveitis and an immune response to the purified Ag. The uveitogenic Ag had a mass of 22 kDa (SDS-PAGE) and an isoelectric point of 6.75. The N-terminal amino acid sequence of this protein demonstrated 100% homology with the bovine type I collagen alpha-2 chain starting from amino acid 385 and will be referred to as CI-alpha2 (22 kDa). Animals immunized with bovine CI-alpha2 (22 kDa) developed both cellular and humoral immunity to the Ag. They developed anterior uveitis only if the CI-alpha2 chain underwent proteolysis and if the bound carbohydrates were intact. EAAU induced by CI-alpha2 (22 kDa) can be adoptively transferred to naive syngenic rats by primed CD4(+) T cells. EAAU could not be induced by the adoptive transfer of sera obtained from animals immunized with CI-alpha2 (22 kDa). The alpha-1 and alpha-2 chains (intact or proteolytically cleaved) of type I collagen from calfskin were not pathogenic. Although human anterior uveitis has been historically characterized as a collagen disease, this is first time collagen has been directly identified as the target autoantigen in uveitis.

Tolerance is dependent on complement C3 fragment iC3b binding to antigen-presenting cells.

Systemic tolerance can be induced by the introduction of antigen into an immune-privileged site. Here we investigated the role of complement in the induction of tolerance after intraocular injection. We found that the development of antigen-specific tolerance is dependent on a complement activation product. The ligation of the complement C3 activation product iC3b to complement receptor type 3 (the iC3b receptor) on antigen-presenting cells resulted in the sequential production of transforming growth factor-beta2 and interleukin-10, which is essential for the induction of tolerance. These observations may extend to the development of both neonatal tolerance and other forms of acquired tolerance.