Reliability Performance Study of SiC, GaN, and Si Photodetectors Under High-Dose UV Irradiation

Microcrystalline thin metal oxide films for optoelectronic applications

DNA damage in mammalian cells stabilizes the p53 protein which then functions as a cell cycle checkpoint by leading to growth arrest or apoptosis. p53 is a transcription factor and positively regulates the expression of the p21/WAF-1 gene and the mdm2 gene. After high-dose UV irradiation, p53 increases the expression of the p21/WAF-1 gene immediately (2 to 5 hours after irradiation) while the induction of the mdm2 gene is delayed (8 to 12 hours after irradiation). Experiments presented here explore this differential expression of two different p53-regulated genes. IP-Western (protein) and Northern (mRNA) blot experiments are used to follow mdm2 and p21/WAF-1 expression in primary rat or mouse cells after a low-dose (4 J/m2) or a high-dose (20 J/M2) of UV irradiation. Northern blot and nuclear run-on experiments are employed to study mRNA stability as well as transcription rates of selected genes. After high-dose UV irradiation, p53 is rapidly stabilized and the expression of p21/WAF1 is immediately increased. By contrast, both protein and mRNA levels of mdm2 first decrease in a p53-independent manner, and later increase in a p53-dependent manner. The initial decline of mdm2 expression following high-dose UV irradiation is UV-dosage dependent and regulated at the level of transcription. p53 regulates two genes, p21/WAF1 (blocks cell cycle progression) and mdm2 (reverses p53 activity), that mediate opposite actions. This process is regulated in a temporal fashion after high-dose UV irradiation, so that cell cycle progression can be halted while DNA repair continues prior to reversal of p53-mediated arrest by mdm2.

We fabricated GaN and 6H-SiC p-i-n photodetectors and compared their electrical and optical characteristics. The GaN diodes suffered from significant leakage current of 37 /spl mu/A/mm/sup 2/ at -5 V, while the SiC diode leakage current was below the noise level at 10 pA/mm/sup 2/ at -20 V. The built-in potentials and the unintentional "i-layer" doping densities were obtained from capacitance-voltage (C-V) measurements. The SiC detectors exhibited a broad spectral response in contrast to the abrupt cutoff observed in the GaN detectors. The peak responsivities of the GaN and SiC photodetectors corresponded to internal quantum efficiencies of 57% at 3.42 eV and 82% at 4.49 eV, respectively. Furthermore, both detectors exhibited excellent visible rejection ratios which is needed for solar-blind applications. The response times at zero bias were 18 and 102 ns for the GaN and SiC detectors, respectively.

Application of high-dose UV irradiation as nanofiltration pretreatment for drinking water production: Organic fouling mitigation and micropollutant removal

UV or gamma irradiation mediated DNA damage activates p53 and induces cell cycle arrest. Induction of cyclin-dependent kinase inhibitor p21WAF1 by p53 after DNA damage plays an important role in cell cycle arrest after gamma irradiation. The p53 mediated cell cycle arrest has been postulated to allow cells to repair the DNA damage. Repair of UV damaged DNA occurs primarily by the nucleotide excision pathway (NER). It is known that p21WAF1 binds PCNA and inhibits PCNA function in DNA replication. PCNA is also required for repair by NER but there have been conflicting reports on whether p21 can inhibit PCNA function in NER. It has therefore been difficult to integrate the UV induced cell cycle arrest by p21 in the context of repair of UV damaged DNA. A recent study reported that p21WAF1 protein is degraded after low but not high doses of UV irradiation, that cell cycle arrest after UV is p21 independent, and that at low dose UV irradiation p21 degradation is essential for optimal DNA repair. These findings shed new light on the role of p21 in the cellular response to UV and clarify some outstanding issues concerning p21 function.

Prevention of fungal infestation of rainbow trout (Oncorhynchus mykiss) eggs using UV irradiation of the hatching water

UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.

Fused Filament Fabrication is a promising manufacturing technology for the circularity of space missions. Potential scenarios include in‐orbit applications to maximize mission life and to support long‐term exploration missions with in situ manufacturing and recycling. However, its adoption is restricted by the availability of engineering polymers displaying mechanical performance combined with resistance to space conditions. Here, a thermotropic Liquid Crystal Polymer (LCP) is reported as a candidate material with extrusion 3D printing. To expand its scope of applicability to structural parts for space applications, four different exposure conditions are studied: thermal cycling under vacuum, atomic oxygen, UV, and electron irradiations. While 1 MeV‐electron irradiation leads to a green coloration due to annealable color centers, the mechanical performance is only slightly decreased in dynamic mode. It is also found that increased printing temperature improves transverse strength and resistance to thermal cycling with the trade‐off of tensile stiffness and strength. Samples exposed to thermal cycling and the highest irradiation dose at lower printing temperatures still display a Young's modulus of 30 GPa and 503 MPa of tensile strength which is exceptionally high for a 3D‐printed polymer. For the types of exposure studied, overall, the results indicate that LCP 3D‐printed parts are well suited for space applications.

It was previously reported that low doses, but not high doses, of UV trigger the Skp2-mediated proteasomal degradation of the cyclin-dependent kinase inhibitor p21 in mammalian cells. Here we show that both UV-C and UV-B lead to decrease of p21 protein, but not mRNA, level in a dose-dependent fashion in all of six human cell lines and five mouse cell lines tested. Also, high doses of UV reduce the half-life of p21. High doses, but not low doses, of UV induced p21 degradation in both skp2-proficient and -deficient murine embryonic fibroblast cells. UV-induced p21 reduction was rescued by proteasome inhibitors in all human and mouse cell lines tested. Neither a caspase inhibitor nor small interfering RNA against skp2 had an effect on the UV-induced p21 decrease, suggesting that this p21 degradation pathway may not involve caspases, or Skp2. Finally, UV did not induce p21 ubiquitination but still induced its degradation when the E1-activating enzyme was inactivated in an E1 temperature-sensitive mouse embryonic fibroblast cell line. Altogether, these results demonstrate that UV induces p21 degradation through an Skp2 and ubiquitin-independent pathway.

ABSTRACTUltraviolet (UV) irradiation at 254 run and doses of 300 mWs/cm2 from a photochemical reactor (16.6 min at 300 μW/cm2) or 4.8 Ws/cm2 from a high intensity UV‐C lamp (40 sec at 120–180 mW/cm2 reduced surface microbial count on mackerel by two to three log cycles. UV treated mackerel wrapped in 1 mil polyethylene and packed in ‐1°C ice had at least a 7 day longer shelf life than conventional ice‐packed untreated controls. Spray washing with water containing 10 ppm chlorine by itself or in combination with UV irradiation was necessary to reduce surface counts on rough surfaced fish to the same extent as that on smooth surfaced fish. When UV irradiated and packed in 0°C ice, surface microbial counts on vacuum packaged mackerel lagged by 4 days those on mackerel wrapped in 1 mil polyethylene.

Since the capacity for DNA repair relative to other cellular processes should be an important parameter of mutagenesis, carcinogenesis, and also aging, this capacity should preferably be studied in intact animals. Thus, we developed autoradiographic techniques for measuring DNA repair directly in vivo. By these methods unscheduled DNA synthesis (UDS) was detected quantitatively as silver grains on epithelial cells of mouse skin after treatment with chemical carcinogens or UV irradiation, and on cerebral ganglion cells of aquarium fish after treatment with various chemical carcinogens. Several interesting findings so far obtained are presented. Possible age-related change in the UDS response was examined by the skin technique with mice of 2 and 18 months old. Similar dose-dependent induction of UDS was observed in mice of both ages after treatment with 4-hydroxyaminoquinoline 1-oxide; their levels of UDS at each dose were not significantly different. The dose-response curves for young and aged animals after UV irradiation showed similar increases to a plateau at low doses, but their responses to high doses were very different: in aged mice the UDS level decreased markedly with increase in the dose, whereas in young mice it remained at the same level. This suggests that in aged animals, high doses of UV irradiation cause deterioration of DNA repair systems, and that aged animals cannot repair extensive DNA damage efficiently. It is generally thought that DNA has a stable structure and a much slower turnover than other cellular components. Although the effect of DNA repair on DNA turnover may be insignificant, accumulation of repaired DNA in cells should result in detectable DNA turnover. Therefore, we investigated DNA turnover in postmitotic ganglion cells of rat retina. However, careful autoradiographic studies on pairs of eyes showed no detectable DNA turnover up to nearly their median life span (2 years). This result suggests that the DNA of post-mitotic cells, which are not replaced throughout the life span of the animal, is very stable and is possibly protected in some special way.

Damage-specific DNA binding protein 1 (DDB1) is involved in ubiquitin-mediated proteolysis of p27Kip1 in response to UV irradiation

A case-control study of 232 cases of cutaneous malignant melanoma and 232 matched controls was performed to assess the association of the disease with nonmelanotic skin tumors--basal cell carcinomas, squamous cell carcinomas, and solar keratoses. There was a fourfold increase in risk of melanoma of all types when actinic tumors were present on the face. The risk was not restricted to the lentigo malignant melanoma class as might be expected but was significantly raised for superficial spreading melanoma and nodular melanoma as well (relative risk, 2.8; 95% confidence interval, 1.1-7.2). This relationship with lesions known to be associated with high-dose solar UV irradiation was supported by quantitative evidence that heavy sun exposure was associated with an increased risk of malignant melanoma.

The induction of Lambda prophages in lysogenic Escherichia coli cells is started after inactivation of repressor molecules coded for by the prophage genome itself. All agents known to inhibit bacterial DNA synthesis are able to initiate a set of processes resulting in the inactivation of these repressors. In the case of UV light as an inducing agent it is suggested that the UV mediated damages within the bacterial DNA diminish the replication velocity leading through a set of intermediate processes to the inactivation of phage repressors by accumulation of repressor inactivating precursors of DNA synthesis. The analytical function for the dose effect curve is obtained from the product of the probability PI of cells containing I UV damages multiplied by the number I of UV damages after summing up all possible numbers of I. The probability of PI is calculated on the basis of the radiation kinetic model of RONTOet al. (1972). The theoretical dose effect curve, obtained shows a shoulder with an extrapolation number of 1.2 and a linear part at high irradiation doses in semilogarithmic plot. The experimental data obtained with UV induction of E. coli K12 (λ) are consistent with the model and show that only a few UV damages smaller than 10 per bacterial chromosome are sufficient for induction.

The induction of Lambda prophages in lysogenic Escherichia coli cells is started after inactivation of repressor molecules coded for by the prophage genome itself. All agents known to inhibit bacterial DNA synthesis are able to initiate a set of processes resulting in the inactivation of these repressors. In the case of UV light as an inducing agent it is suggested that the UV mediated damages within the bacterial DNA diminish the replication velocity leading through a set of intermediate processes to the inactivation of phage repressors by accumulation of repressor inactivating precursors of DNA synthesis. The analytical function for the dose effect curve is obtained from the product of the probability PI of cells containing I UV damages multiplied by the number I of UV damages after summing up all possible numbers of I. The probability of PI is calculated on the basis of the radiation kinetic model of RONTÓ et al. (1972). The theoretical dose effect curve, obtained shows a shoulder with an extrapolation number of 1.2 and a linear part at high irradiation doses in semilogarithmic plot. The experimental data obtained with UV induction of E. coli K12 (λ) are consistent with the model and show that only a few UV damages smaller than 10 per bacterial chromosome are sufficient for induction.