A LiF-buffered silver cathode has been used in organic light-emitting devices (OLEDs) with structure indium–tin–oxide/N,N′-bis-(1-naphthl)-diphenyl-1,1′-biphenyl-4,4′-diamine (50 nm)/Alq3 (100 nm)/cathode. The efficiency of electron injection from the cathode is strongly dependent on the thickness of the LiF buffer layer. While a LiF layer thinner than 1.0 nm leads to higher turn-on voltage and decreased electroluminescent (EL) efficiency, a LiF layer of 3.0 nm significantly enhances the electron injection and results in lower turn-on voltage and increased EL efficiency. A brightness of 16 000 cd/m2 and EL efficiency of 4.8 cd/A can be achieved with an Ag/LiF cathode. This dependence of electron injection on the LiF thickness is quite different from that reported for OLEDs with a Al/LiF cathode, but can be well understood using the tunneling model.
The IFIH1 gene is a key factor connecting environmental and genetic factors in the pathogenesis of immune-related diseases. We aimed to investigate whether it has effects on psoriasis, chronic periodontitis and skin test-positive penicillin allergy and to confirm whether these diseases have shared molecular mechanisms originating from shared genetics. Two common variants in IFIH1 were genotyped in 561 patients with psoriasis, 421 patients with chronic periodontitis, 175 patients with skin test-positive penicillin allergy and 1100 shared controls. Then, case-control study was used to analyse the association between IFIH1 and the three diseases. The allele distributions of rs1990760 and rs3747517 in the Chinese population are much different from the European population. The A allele of rs1990760 (OR = 1.30, P = 5.4 × 10(-3)) and A-G (rs1990760/rs3747517) haplotype (OR = 1.31, P = 3.8 × 10(-3)) were highly associated with the risk of psoriasis. However, the A allele of rs1990760 (OR = 0.73, P = 7.8 × 10(-3)) and A-G haplotype (OR = 0.71, P = 4.5 × 10(-3)) were identified as protective factors for chronic periodontitis. IFIH1 affects several immune-related diseases, including psoriasis and chronic periodontitis, and provides a molecular link between genetic susceptibility, viral infections and immune-related diseases. Moreover, we also confirm the hypothesis that shared molecular mechanisms from common genetic variants contribute to a spectrum of immune-related diseases.
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