KEYWORDS: Accelerated life testing, Semiconductor lasers, High power lasers, Data modeling, Failure analysis, Lithium, Continuous wave operation, Analytical research, Defense and security, Optoelectronic devices
High power semiconductor laser is widely used because of its high transformation efficiency, good working stability, compact volume and simple driving requirements. Laser’s lifetime is very long, but tests at high levels of stress can speed up the failure process and shorten the times to failure significantly. So accelerated life test is used here for forecasting the lifetime of 808nm CW GaAs/AlGaAs high power semiconductor laser that has an output power of 1W under 1.04A. Accelerated life test of constant current stress based on the Inverse Power Law Relationship was designed. Tests were conducted under 1.3A, 1.6A and 1.9A at room temperature. It is the first time that this method is used in the domestic research of laser’s lifetime prediction. Applying Weibull Distribution to describe the lifetime distribution and analyzing the data of times to failure, characteristics lifetime’s functional relationship model with current is achieved. Then the characteristics lifetime under normal current is extrapolated, which is 9473h. Besides, to confirm the validity of the functional relationship model, we conduct an additional accelerated life test under 1.75A. Based on this experimental data we calculated the characteristics lifetime corresponding to 1.75A that is 171h, while the extrapolated characteristics lifetime from the former functional relationship model is 162h. The two results shows 5% deviation that is very low and acceptable, which indicates that the test design is reasonable and authentic.
Our previous study has shown that Ultraviolet-A (UVA) irradiation induces heme oxygenase 1 (HO-1) expression in
cultured human primary skin fibroblasts FEK4. In the present study, we demonstrate a coordinated induction of HO-1
and NF-E2-related factor 2 (Nrf2) following UVA irradiation or hemin treatment. The induction of HO-1 by either UVA
irradiation or hemin treatment was largely abolished by down-regulation of Nrf2 with its targeted short interfering RNA
(siNrf2). The study further reveals that knockdown of Nrf2 protein increased UVA-induced cell death measured by MTS
assay. These findings together indicate that Nrf2-mediated induction of HO-1 expression may provide a cytoprotection
for human skin cells from oxidative damage.
Ultraviolet A (UVA) radiation is an oxidizing agent that strongly induces the heme oxygenase 1(HO-1) expression in
cultured human skin fibroblasts, but weakly induces it in skin keratinocytes. Here, we report that low basal levels of HO-
1 and much higher basal levels of HO-2 protein were observed in keratinocytes compared with fibroblasts. Silencing of
Bach1 strongly increased HO-1 levels in HaCaT transformed keratinocytes and these HO-1 levels were not further
increased by either UVA irradiation or silencing of HO-2. This is consistent with the conclusion that high constitutive
levels of HO-2 expression in keratinocytes are responsible for the resistance of these cells to HO-1 induction by UVA
radiation and that Bach1 plays a predominant role in influencing the lack of HO-1 expression in keratinocytes. Bach1
inhibition reduced the 500 kJ/m2 UVA-induced cell damage by LDH membrane integrity and MTS viability assays.
These results suggest that Bach1 inhibition protect against high dose of UVA irradiation induced damage in
keratinocytes.
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