Mouse Anti-Human Alpha-Fetoprotein monoclonal antibody, clone JID621

We propose an electro-optic approach for transparent optical networking, in which frequency channels are actively transformed into any desired mapping in a wavelength-multiplexed environment. Based on electro-optic phase modulators and Fourier-transform pulse shapers, our all-optical frequency processor (AFP) is examined numerically for the specific operations of frequency channel hopping and broadcasting, and found capable of implementing these transformations with favorable component requirements. Extending our analysis via a mutual-information-based metric for system optimization, we show how to optimize transformation performance under limited resources in a classical context, contrasting the results with those found using metrics motivated by quantum information, such as fidelity and success probability. Given its compatibility with on-chip implementation, as well as elimination of optical-to-electrical conversion in frequency channel switching, the AFP looks to offer valuable potential in silicon photonic network design, as well as the realization of high-dimensional frequency-bin gates.

The hypomethylation of the Cyclin D1 (CCND1) promoter induced by excess oxidative stress likely promotes the development of hepatitis B virus-associated hepatocellular carcinoma (HBV-HCC). We aimed to evaluate methylation status of theCCND1promoter as a new plasma marker for the detection of HBV-HCC. We consecutively recruited 191 participants, including 105 patients with HBV-HCC, 54 patients with chronic hepatitis B (CHB), and 32 healthy controls (HCs). Using methylation-specific polymerase chain reaction, we identified the methylation status of theCCND1promoter in plasma samples. We analyzed the expression levels of theCCND1mRNA in peripheral blood mononuclear cells by using quantitative real-time PCR. We assessed the plasma levels of superoxide dismutase, 8-hydroxydeoxyguanosine and malondialdehyde by using enzyme-linked immunosorbent assays. Patients with HBV-HCC (23.81%) presented a reduced methylation frequency compared with patients with CHB (64.81%) or HCs (78.13%) (P < .001). When receiver operating characteristic curves were plotted for patients with HBV-HCC versus CHB, the methylation status of theCCND1promoter yielded diagnostic parameter values for the area under the curve of 0.705, sensitivity of 76.19%, and specificity of 64.81%, thus outperforming serum alpha-fetoprotein (AFP), which had an area under the curve of 0.531, sensitivity of 36.19%, and specificity of 90.74%. Methylation of theCCND1promoter represents a prospective diagnostic marker for patients with AFP-negative HBV-HCC and AFP-positive CHB. The expression levels ofCCND1mRNA was increased in patients with HBV-HCC compared with patients with CHB (Z = -4.946,P < .001) and HCs (Z = -6.819,P < .001). Both the extent of oxidative injury and antioxidant capacity indicated by the superoxide dismutase, 8-hydroxydeoxyguanosine and malondialdehyde levels were increased in patients with HBV-HCC. Clinical follow up of patients with HBV-HCC revealed a worse overall survival (P = .012, log-rank test) and a decreased progression-free survival (HR = 0.109, 95%CI: 0.031-0.384) for the unmethylatedCCND1group than methylatedCCND1group. Our study confirms that oxidative stress appears to correlate with plasma levels ofCCND1promoter methylation, and the methylation status of theCCND1promoter represents a prospective biomarker with better diagnostic performance than serum AFP levels.