A quantitative study of the dynamics of threshold-voltage shifts with time in gallium-indium zinc oxide amorphous thin-film transistors is presented using standard analysis based on the stretched exponential relaxation. For devices using thermal silicon oxide as gate dielectric, the relaxation time is 3 ϫ 10 5 s at room temperature with activation energy of 0.68 eV. These transistors approach the stability of the amorphous silicon transistors. The threshold voltage shift is faster after water vapor exposure suggesting that the origin of this instability is charge trapping at residual-water-related trap sites. © 2009 American Institute of Physics. ͓DOI: 10.1063/1.3187532͔ Amorphous gallium-indium zinc oxide ͑GIZO͒ thin-film transistors ͑TFTs͒ have attracted attention for their possible applications to flat, flexible, and transparent displays, 1-4 especially when processed at low temperatures. However, like the other TFTs' technologies, they also suffer from a stability phenomena known as gate-bias stress. 5,6 This effect manifests itself as a continuous increase in threshold voltage ͑V th ͒ when the gate bias is kept constant over time. This limits the application of these TFTs in demanding applications, such as active matrix organic light emitting displays. The increase in V th lowers the luminance of individual pixels over time, causing display nonuniformity. 7 As an example, using current technologies several driving transistors per pixel are necessary to compensate for the V th shift. Hence, a proper understanding of the stressing mechanism is of paramount importance.Gate-bias stress effects are commonly reported in the literature for a variety of transistors, a-Si TFTs, 8 organic transistors, 9-11 and recently also in amorphous oxide semiconductors TFTs. [12][13][14][15] The effect has been explained as a slow trapping of charge carriers in defects of unknown origin located at the semiconductor/dielectric interface. 13 It is known that the current degradation is faster when the devices are exposed to atmosphere 15,16 and that the stability improves after annealing. 1 Also, it has been reported that the effects can be reduced by the insertion of a passivation layer, either between the dielectric and the semiconductor 17 or on top of the semiconductor in bottom-gate structures. 16 This work provides a quantitative study of the gate-bias stress instability as a function of temperature and environment conditions. The results allow a comparison with competing TFTs technologies. Furthermore, it also provides evidences that water vapor contamination enhances this instability. Therefore, there is no conceptual limitation for the stability of GIZO based TFTs. This is in contrast to hydrogenated amorphous silicon TFTs where the instability is caused by the creation of intrinsic defects, unsaturated valence states into which electrons are trapped.The device fabrication process has been described in detail elsewhere. 18 Briefly, the TFTs were produced with a staggered bottom gate configuration on silicon wafers, which a...

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The damage profile produced by the reaction of singlet molecular oxygen with cellular DNA was determined using the comet assay associated with DNA repair enzymes. Singlet oxygen was produced intracellularly by thermal decomposition of a water-soluble endoperoxide of a naphthalene derivative which is able to penetrate through the membrane into mammalian cells. We found that the DNA modifications produced by singlet oxygen were almost exclusively oxidised purines recognised by the formamidopyrimidine DNA N-glycosylase. In contrast, significant amounts of direct strand breaks and alkali-labile sites or oxidised pyrimidines, detectable by the bacterial endonuclease III, were not produced.

Acetaldehyde is an environmentally widespread genotoxic aldehyde present in tobacco smoke, vehicle exhaust and several food products. Endogenously, acetaldehyde is produced by the metabolic oxidation of ethanol by hepatic NAD-dependent alcohol dehydrogenase and during threonine catabolism. The formation of DNA adducts has been regarded as a critical factor in the mechanisms of acetaldehyde mutagenicity and carcinogenesis. Acetaldehyde reacts with 2'-deoxyguanosine in DNA to form primarily N(2)-ethylidene-2'-deoxyguanosine. The subsequent reaction of N(2)-ethylidenedGuo with another molecule of acetaldehyde gives rise to 1,N(2)-propano-2'-deoxyguanosine (1,N(2)-propanodGuo), an adduct also found as a product of the crotonaldehyde reaction with dGuo. However, adducts resulting from the reaction of more than one molecule of acetaldehyde in vivo are still controversial. In this study, the unequivocal formation of 1,N(2)-propanodGuo by acetaldehyde was assessed in human cells via treatment with [(13)C(2)]-acetaldehyde. Detection of labeled 1,N(2)-propanodGuo was performed by HPLC/MS/MS. Upon acetaldehyde exposure (703 μM), increased levels of both 1,N(2)-etheno-2'-deoxyguanosine (1,N(2)-εdGuo), which is produced from α,β-unsaturated aldehydes formed during the lipid peroxidation process, and 1,N(2)-propanodGuo were observed. The unequivocal formation of 1,N(2)-propanodGuo in cells exposed to this aldehyde can be used to elucidate the mechanisms associated with acetaldehyde exposure and cancer risk.

trans,trans-2,4-Decadienal (DDE) is a widespread alpha, beta-unsaturated aldehyde found, for example, in food, water, and environmental pollutants. DDE is also endogenously generated as a breakdown product of lipid peroxidation in cell membranes. In the work presented here, the reaction of DDE with 2'-deoxyadenosine (dAdo) was investigated in an effort to assess its possible DNA damage potential. Besides 1,N(6)-etheno-2'-deoxyadenosine and two products, namely, 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)-3H-imidazo[2, 1-i]purin-7-yl]-1,2,3-octanetriol (adduct I) and 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)-3H-imidazo[2, 1-i]purin-7-yl]-1,2-heptanediol (adduct II), previously described by our group, two novel etheno adducts were identified. Thus, 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)-3H-imidazo[2, 1-i]purin-7-yl]-1-hexanol (adduct III) and 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)-3H-imidazo[2, 1-i]purin-7-yl]-2,3-epoxy-1-octanol (adduct IV) were isolated by reverse-phase high-performance liquid chromatography and characterized on the basis of extensive spectroscopic measurements. The formation of the adducts is likely to involve initial DDE oxidation followed by generation of reactive intermediates such as diepoxides, epoxides, and/or hydroperoxides. The subsequent reaction of the latter oxidation products with dAdo will give rise to the four described adducts. We also demonstrated here that upon oxidation, DDE reacts with calf thymus DNA, producing the four dAdo adducts. Interestingly, two of them are the expected products arising from the reaction of dAdo with 4-hydroxy-trans-2-nonenal (HNE) and trans-2-octenal, two other important breakdown lipid peroxidation products. The reactivity of DDE with DNA is lower than that of the latter aldehydes. However, DDE produced a wider variety of adducts. The characterization of the different DNA-etheno adducts and the determination of the mechanism of formation are of great importance for a better understanding of the deleterious biological effects associated with this class of compounds.

Distinguishing between gay venues may provide important information to better understand patterns of environmental influence and HIV/STI behavioral risk among MSM. Massachusetts MSM accessing State Health Department mobile van services (n = 214) at Gay Pride events, bars/clubs, and private safer sex parties completed a one-time, cross-sectional survey via ACASI. In the past 12 months, private safer sex party attendees reported a higher mean number of anonymous partners, were more likely to report meeting sex partners via the Internet, and were more likely to report sex while drunk; in logistic regression analyses, they were less likely to report both unprotected insertive and receptive anal sex in the past year relative to men from other venues. Private safer sex parties may represent a strategy used by some MSM to reduce HIV/STI risk. Differentiating risk behavior by venue type provides valuable information with which to effectively target interventions to reach MSM at greatest risk.

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The heme precursor 5-aminolevulinic acid (ALA) accumulates under pathological conditions, namely, acute intermittent porphyria (AIP) and tyrosinosis, two diseases that are associated with increased liver cancer incidence. This has been previously linked to an enhanced production of reactive oxygen species generated by a metal-catalyzed ALA oxidation process, which was shown to cause DNA single-strand breaks and guanine oxidation within both isolated and cellular DNA. In the present work, we established that the final oxidation product of ALA, 4,5-dioxovaleric acid (DOVA), is an efficient alkylating agent of the guanine moieties within both nucleoside and isolated DNA. Adducts were produced through the formation of a Schiff base involving the N2-amino group of 2'-deoxyguanosine (dGuo) and the ketone function of DOVA, respectively. The modified dGuo nucleosides were characterized, following reduction into stable secondary amines, by extensive NMR, infrared, and mass spectrometry analyses. A method, based on the use of HPLC with electrochemical detection, was then developed for the sensitive measurement of the DOVA-dGuo adducts. Using this assay, we showed that the guanine moieties of isolated DNA can undergo the same reaction as the free nucleoside. The present data provide additional information on the genotoxic potential of ALA and reinforce the hypothesis that AIP may be involved in the induction of primary liver cell carcinoma.