154 research outputs found

    Defect-related optical absorption bands in CdSiP2 crystals

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    When used as optical parametric oscillators, CdSiP2 crystals generate tunable output in the mid-infrared. Their performance, however, is often limited by unwanted optical absorption bands that overlap the pump wavelengths. A broad defect-related optical absorption band peaking near 800 nm, with a shoulder near 1 µm, can be photoinduced at room temperature in many CdSiP2 crystals. This absorption band is efficiently produced with 633 nm laser light and decays with a lifetime of ∼0.5 s after removal of the excitation light. The 800 nm band is accompanied by a less intense absorption band peaking near 1.90 µm. Data from eight CdSiP2 crystals grown at different times show that the singly ionized silicon vacancy (VSi− role= presentation style= box-sizing: border-box; display: inline; font-size: 12.880000114440918px; line-height: normal; word-spacing: normal; word-wrap: normal; white-space: nowrap; float: none; direction: ltr; max-width: none; max-height: none; min-width: 0px; min-height: 0px; border: 0px; padding: 0px; margin: 0px; position: relative; \u3e−) is responsible for the photoinduced absorption bands. Electron paramagnetic resonance (EPR) is used to identify and directly monitor these silicon vacancies

    Dual Role of Sb Ions as Electron Traps and Hole Traps in Photorefractive Sn2P2S6 Crystals

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    Doping photorefractive single crystals of Sn2P2S6 with antimony introduces both electron and hole traps. In as-grown crystals, Sb3+ (5s2 ) ions replace Sn2+ ions. These Sb3+ ions are either isolated (with no nearby perturbing defects) or they have a chargecompensating Sn2+ vacancy at a nearest-neighbor Sn site. When illuminated with 633 nm laser light, isolated Sb3+ ions trap electrons and become Sb2+ (5s2 5p1 ) ions. In contrast, Sb3+ ions with an adjacent Sn vacancy trap holes during illumination. The hole is primarily localized on the (P2S6) 4− anionic unit next to the Sb3+ ion and Sn2+ vacancy. These trapped electrons and holes are thermally stable below ∼200 K, and they are observed with electron paramagnetic resonance (EPR) at temperatures below 150 K. Resolved hyperfine interactions with 31P, 121Sb, and 123Sb nuclei are used to establish the defect models

    Ir \u3csup\u3e4+\u3c/sup\u3e Ions in β-Ga\u3csub\u3e2\u3c/sub\u3eO\u3csub\u3e3\u3c/sub\u3e Crystals: An Unintentional Deep Donor

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    Electron paramagnetic resonance (EPR) and infrared absorption are used to detect Ir4+ ions in β-Ga2O3 crystals. Mg and Fe doped crystals are investigated, and concentrations of Ir4+ ions greater than 1 × 1018 cm−3 are observed. The source of the unintentional deep iridium donors is the crucible used to grow the crystal. In the Mg-doped crystals, the Ir4+ ions provide compensation for the singly ionized Mg acceptors and thus contribute to the difficulties in producing p-type behavior. The Ir4+ ions replace Ga3+ ions at the Ga(2) sites, with the six oxygen neighbors forming a distorted octahedron. A large spin-orbit coupling causes these Ir4+ ions to have a low-spin (5d5, S = 1/2) ground state. The EPR spectrum consists of one broad line with a significant angular dependence. Principal values of the g matrix are 2.662, 1.815, and 0.541 (with principal axes near the crystal a, b, and c directions, respectively). Ionizing radiation at 77 K decreases the Ir4+ EPR signal in Mg-doped crystals and increases the signal in Fe-doped crystals. In addition to the EPR spectrum, the Ir4+ ions have an infrared absorption band representing a d-d transition within the t2g orbitals. At room temperature, this band peaks near 5153 cm−1 (1.94 μm) and has a width of 17 cm−1. The band is highly polarized: its intensity is maximum when the electric field E is parallel to the b direction in the crystal and is nearly zero when E is along the c direction

    Circulating cell-free DNA level predicts all-cause mortality independent of other predictors in the Health 2000 survey

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    Increased levels of circulating cell-free DNA (cf-DNA) are associated with and predict poor health outcomes. However, its predictive ability for mortality in population-based samples remains understudied. We analysed the capability of cf-DNA to predict all-cause mortality and assessed whether it adds predictive value on top of the other risk factors in the Health 2000 survey (n = 1,257, 46-76 years of age, 15-years-follow-up, 18% deceased). When analysed in a multivariate model with the other factors that independently predicted mortality in the sample (age, gender, self-rated health, smoking and plasma levels of glucose and adiponectin), increases in cf-DNA levels were associated with increased risk of mortality (hazard ratio [HR] for 0.1 mu g increase in cf-DNA: 1.017, 95% confidence interval [CI] 1.008-1.026, p = 0.0003). Inclusion of cf-DNA in the model improved the model fit and discrimination. Stratifying the analysis by cardiovascular disease (CVD) status indicated that cf-DNA predicted mortality equally well in individuals with (HR 1.018, 95% CI 1.008-1.026, p = 0.002) and without (HR 1.018, 95% CI 1.001-1.035, p = 0.033) CVD. In conclusion, our study indicates that cf-DNA level predicts mortality in middle-aged and older individuals, also among those with established CVD, and adds significant value to mortality prediction. Our results thus underscore the role of cf-DNA as a viable marker of health

    Assessment of the role of transcript for GATA-4 as a marker of unfavorable outcome in human adrenocortical neoplasms

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    BACKGROUND: Malignant neoplasia of the adrenal cortex is usually associated with very poor prognosis. When adrenocortical neoplasms are diagnosed in the early stages, distinction between carcinoma and adenoma can be very difficult to accomplish, since there is yet no reliable marker to predict tumor recurrence or dissemination. GATA transcription factors play an essential role in the developmental control of cell fate, cell proliferation and differentiation, organ morphogenesis, and tissue-specific gene expression. Normal mouse adrenal cortex expresses GATA-6 while its malignant counterpart only expresses GATA-4. The goal of the present study was to assess whether this reciprocal change in the expression of GATA factors might be relevant for predicting the prognosis of human adrenocortical neoplasms. Since human adrenal cortices express luteinizing hormone (LH/hCG) receptor and the gonadotropins are known to up-regulate GATA-4 in gonadal tumor cell lines, we also studied the expression of LH/hCG receptor. METHODS: We conducted a study on 13 non-metastasizing (NM) and 10 metastasizing/recurrent (MR) tumors obtained from a group of twenty-two adult and pediatric patients. The expression of GATA-4, GATA-6, and LH/hCG receptor (LHR) in normal and tumoral human adrenal cortices was analysed using reverse transcriptase-polymerase chain reaction (RT-PCR) complemented by dot blot hybridization. RESULTS: Messenger RNA for GATA-6 was detected in normal adrenal tissue, as well as in the totality of NM and MR tumors. GATA-4, by its turn, was detected in normal adrenal tissue, in 11 out of 13 NM tumors, and in 9 of the 10 MR tumors, with larger amounts of mRNA found among those presenting aggressive clinical behavior. Transcripts for LH receptor were observed both in normal tissue and neoplasms. A more intense LHR transcript accumulation was observed on those tumors with better clinical outcome. CONCLUSION: Our data suggest that the expression of GATA-6 in human adrenal cortex is not affected by tumorigenesis. GATA-4 expression is more abundant in MR tumors, while NM tumors express more intensely LHR. Further studies with larger cohorts are needed to test whether relative expression levels of LHR or GATA-4 might be used as prognosis predictors

    Obesity accelerates epigenetic aging in middle-aged but not in elderly individuals

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    Background: Human aging is associated with profound changes in one of the major epigenetic mechanisms, DNA methylation. Some of these changes occur in a clock-like fashion, i.e., correlating with the calendar age of an individual, thus providing a new aging biomarker. Some reports have identified factors associated with the acceleration of the epigenetic age. However, it is also important to analyze the temporal changes in the epigenetic age, i.e., the duration of the observed acceleration, and the effects of the possible therapeutic and lifestyle modifications.Methods: To address this issue, we determined the epigenetic age for a cohort of 183 healthy individuals using blood samples derived from two time points that were 25 years apart (between 15-24 and 40-49 years of age). Additionally, we also determined the epigenetic ages of 119 individuals in a cohort consisting of 90-year-old participants (nonagenarians). These were determined by using the Horvath algorithm based on the methylation level of 353 CpG sites. The data are indicated as the deviation of the epigenetic age from the calendar age (calendar age minus epigenetic age = delta age, Delta AGE). As obesity is often associated with accelerating aging and degenerative phenotypes, the correlation of the body mass index (BMI) with the Delta AGE was analyzed in the following three age groups: young adults, middle-aged, and nonagenarian.Results: The data showed that BMI is associated with decreased Delta AGE, i.e., increased epigenetic age, in middle-aged individuals. This effect is also seen during the 25-year period from early adulthood to middle age, in which an increase in the BMI is significantly associated with a decrease in the Delta AGE. We also analyzed the association between BMI and epigenetic age in young and elderly individuals, but these associations were not significant.Conclusion: Taken together, the main finding on this report suggests that association between increased BMI and accelerated epigenetic aging in the blood cells of middle-aged individuals can be observed, and this effect is also detectable if the BMI has increased in adulthood. The fact that the association between BMI and epigenetic age can only be observed in the middle-aged group does not exclude the possibility that this association could be present throughout the human lifespan; it might just be masked by confounding factors in young adults and nonagenarian individuals

    Is telomere length socially patterned? Evidence from the West of Scotland Twenty-07 study

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    Lower socioeconomic status (SES) is strongly associated with an increased risk of morbidity and premature mortality, but it is not known if the same is true for telomere length, a marker often used to assess biological ageing. The West of Scotland Twenty-07 Study was used to investigate this and consists of three cohorts aged approximately 35 (N = 775), 55 (N = 866) and 75 years (N = 544) at the time of telomere length measurement. Four sets of measurements of SES were investigated: those collected contemporaneously with telomere length assessment, educational markers, SES in childhood and SES over the preceding twenty years. We found mixed evidence for an association between SES and telomere length. In 35-year-olds, many of the education and childhood SES measures were associated with telomere length, i.e. those in poorer circumstances had shorter telomeres, as was intergenerational social mobility, but not accumulated disadvantage. A crude estimate showed that, at the same chronological age, social renters, for example, were nine years (biologically) older than home owners. No consistent associations were apparent in those aged 55 or 75. There is evidence of an association between SES and telomere length, but only in younger adults and most strongly using education and childhood SES measures. These results may reflect that childhood is a sensitive period for telomere attrition. The cohort differences are possibly the result of survival bias suppressing the SES-telomere association; cohort effects with regard different experiences of SES; or telomere possibly being a less effective marker of biological ageing at older ages
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