High quantum efficiency long-/long-wave dual-color type-Ⅱ InAs/GaSb infrared detector

A long-/long-wave dual-color detector with N-M-π-B-π-M-N structure was developed based on a type-Ⅱ InAs/GaSb superlattice. The saturated responsivity was achieved under low bias voltage for both channels. The device could be operated as a single detector for sequential detection and showed high quantum efficiencies. The peak quantum efficiencies of long-wavelength infrared band-1(blue channel) and long-wavelength infrared band-2(red channel) were 44% at 6.3 μm under 20 mV and 57% at 9.1 μm under-60 mV, respectively. The optical performance for each channel was achieved using a 2 μm thickness absorber. Due to the high QE, the specific detectivities of the blue and red channels reached5.0×10^(11) cm·Hz^(1/2)/W at 6.8 μm and 3.1×10^(11) cm·Hz1^(1/2)/W at 9.1 μm, respectively, at 77 K.

Inhibitory effects of safranal on laser-induced choroidal neovascularization and human choroidal microvascular endothelial cells and related pathways analyzed with transcriptome sequencing

AIM:To determine the effects of safranal on choroidal neovascularization(CNV)and oxidative stress damage of human choroidal microvascular endothelial cells(HCVECs)and its possible mechanisms.METHODS:Forty-five rats were used as a laser-induced CNV model for testing the efficacy and safety of safranal(0.5 mg/kg·d,intraperitoneally)on CNV.CNV leakage on fluorescein angiography(FA)and CNV thickness on histology was compared.HCVECs were used for a H_(2)O_(2)-induced oxidative stress model to test the effect of safranal in vitro.MTT essay was carried to test the inhibition rate of safranal on cell viability at different concentrations.Tube formation was used to test protective effect of safranal on angiogenesis at different concentrations.mRNA transcriptome sequencing was performed to find the possible signal pathway.The expressions of different molecules and their phosphorylation level were validated by Western blotting.RESULTS:On FA,the average CNV leakage area was 0.73±0.49 and 0.31±0.11 mm^(2)(P=0.012)in the control and safranal-treated group respectively.The average CNV thickness was 127.4±18.75 and 100.6±17.34μm(P=0.001)in control and safranal-treated group.Under the condition of oxidative stress,cell proliferation was inhibited by safranal and inhibition rates were 7.4%-35.4%at the different concentrations.For tube formation study,the number of new branches was 364 in control group and 35,42,and 17 in 20,40,and 80μg/mL safranal groups respectively(P<0.01).From the KEGG pathway bubble graph,the PI3K-AKT signaling pathway showed a high gene ratio.The protein expression was elevated of insulin receptor substrate(IRS)and the phosphorylation level of PI3K,phosphoinositide-dependent protein kinase 1/2(PDK1/2),AKT and Bcl-2 associated death promoter(BAD)was also elevated under oxidative stress condition but inhibited by safranal.CONCLUSION:Safranal can inhibit CNV both in vivo and in vitro,and the IRS-PI3K-PDK1/2-AKT-BAD signaling pathway is involved in the pathogenesis of CNV.