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  • 1
    Electronic Resource
    Electronic Resource
    Reciprocal effects of chronic diazepam and melatonin on brain melatonin and benzodiazepine binding sites (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 20 (1996), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Recent reports indicate that benzodiazepines can suppress melatonin levels and that melatonin can increase brain benzodiazepine binding. We have studied the possibility of reciprocal effects of chronic diazepam and melatonin on brain melatonin and benzodiazepine binding sites. Daily injections (3 weeks) of diazepam markedly reduced 125I-melatonin binding site density in the medulla-pons but not cortex of male rats, whereas benzodiazepine binding was not significantly affected. Melatonin, administered via the drinking water, significantly enhanced benzodiazepine (3H-RO 15-1788) binding in the medulla-pons and slightly reduced it in the cortex, but did not affect 125I-melatonin binding. Diazepam and melatonin combination reversed the suppression by diazepam of 125I-melatonin binding in the medulla-pons and the suppression by melatonin of benzodiazepine (3H-RO 15-1788 and 3H-flunitrazepam) binding in the cerebral cortex. These results indicate benzodiazepine-mediated suppression of brain melatonin binding sites that can be abrogated by melatonin administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-079X.1996.tb00241.x
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  • 2
    Electronic Resource
    Electronic Resource
    Ataxia-telangiectasia: Linkage analysis in highly inbred Arab and Druze families and differentiation from an ataxia-microcephaly-cataract syndrome (1992)
    Springer
    Human genetics 〈Berlin〉 88 (1992), S. 619-626 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Ataxia-telangiectasia (A-T) is a progressive autosomal recessive disease featuring neurodegeneration, immunodeficiency, chromosomal instability, radiation sensitivity and a highly increased proneness to cancer. A-T is ethnically widespread and genetically heterogeneous, as indicated by the existence of four complementation groups in this disease. Several “A-T-like” genetic diseases share various clinical and cellular characteristics with A-T. By using linkage analysis to study North American and Turkish A-O families, the ATA (A-T, complementation group A) gene has been mapped to chromosome 11q23. A number of Israeli Arab A-T patients coming from large, highly inbred families were assigned to group A In one of these families, an additional autosomal recessive disease was identified, characterized by ataxia, hypotonia, microcephaly and bilateral congenital cataracts. In two patients with this syndrome, normal levels of serum immunoglobulins and alpha-fetoprotein, chromosomal stability in peripheral blood lymphocytes and skin fibroblasts, and normal cellular response to treatments with X-rays and the radiomimetic drug neocarzinostatin indicated that this disease does not share, with A-T, any additional features other than ataxia. These tests also showed that another patient in this family, who is also mentally retarded, is affected with both disorders. This conclusion was further supported by linkage analysis with 11q23 markers. Lod scores between A-O and these markers, cumulated over three large Arab families, were significant and confirmed the localization of the ATA gene to aq23. However, another Druze family unassigned to a specific complementation group, showed several recombinants between A-T and the same markers, leaving the localization of the A-T gene in this family open.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02265285
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  • 3
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    Development of APE1 enzymatic DNA repair assays: low APE1 activity is associated with increase lung cancer risk (2015)
    Oxford University Press
    Details
    Publication Date: 2015-08-29
    Description: The key role of DNA repair in removing DNA damage and minimizing mutations makes it an attractive target for cancer risk assessment and prevention. Here we describe the development of a robust assay for apurinic/apyrimidinic (AP) endonuclease 1 (APE1; APEX1), an essential enzyme involved in the repair of oxidative DNA damage. APE1 DNA repair enzymatic activity was measured in peripheral blood mononuclear cell protein extracts using a radioactivity-based assay, and its association with lung cancer was determined using conditional logistic regression with specimens from a population-based case–control study with 96 lung cancer cases and 96 matched control subjects. The mean APE1 enzyme activity in case patients was 691 [95% confidence interval (CI) = 655–727] units/ng protein, significantly lower than in control subjects (mean = 793, 95% CI = 751–834 units/ng protein, P = 0.0006). The adjusted odds ratio for lung cancer associated with 1 SD (211 units) decrease in APE1 activity was 2.0 (95% CI = 1.3–3.1; P = 0.002). Comparison of radioactivity- and fluorescence-based assays showed that the two are equivalent, indicating no interference by the fluorescent tag. The APE1Asp148Glu SNP was associated neither with APE1 enzyme activity nor with lung cancer risk. Taken together, our results indicate that low APE1 activity is associated with lung cancer risk, consistent with the hypothesis that ‘bad DNA repair’, rather than ‘bad luck’, is involved in cancer etiology. Such assays may be useful, along with additional DNA repair biomarkers, for risk assessment of lung cancer and perhaps other cancers, and for selecting individuals to undergo early detection techniques such as low-dose CT.
    Print ISSN: 0143-3334
    Electronic ISSN: 1460-2180
    Topics: Medicine
    Published by Oxford University Press
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  • 4
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    N-Methylpurine DNA Glycosylase and OGG1 DNA Repair Activities: Opposite Associations With Lung Cancer Risk (2012)
    Oxford University Press
    Details
    Publication Date: 2012-11-21
    Description: Only a minority of smokers develop lung cancer, possibly due to genetic predisposition, including DNA repair deficiencies. To examine whether inter-individual variations in DNA repair activity of N-methylpurine DNA glycosylase (MPG) are associated with lung cancer, we conducted a blinded, population-based, case–control study with 100 lung cancer case patients and 100 matched control subjects and analyzed the data with conditional logistic regression. All statistical tests were two-sided. MPG enzyme activity in peripheral blood mononuclear cells from case patients was higher than in control subjects, results opposite that of 8-oxoguanine DNA glycosylase (OGG1) DNA repair enzyme activity. For lung cancer associated with one standard deviation increase in MPG activity, the adjusted odds ratio was 1.8 (95% confidence interval [CI] = 1.2 to 2.6; P = .006). A combined MPG and OGG1 activities score was more strongly associated with lung cancer risk than either activity alone, with an odds ratio of 2.3 (95% CI = 1.4 to 3.6; P 〈 .001). These results form a basis for a future panel of risk biomarkers for lung cancer risk assessment and prevention.
    Electronic ISSN: 1460-2105
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Enzymatic MPG DNA repair assays for two different oxidative DNA lesions reveal associations with increased lung cancer risk (2014)
    Oxford University Press
    Details
    Publication Date: 2014-11-30
    Description: DNA repair is a major mechanism for minimizing mutations and reducing cancer risk. Here, we present the development of reproducible and specific enzymatic assays for methylpurine DNA glycosylase (MPG) repairing the oxidative lesions 1,N6-ethenoadenine (A) and hypoxanthine (Hx) in peripheral blood mononuclear cells protein extracts. Association of these DNA repair activities with lung cancer was determined using conditional logistic regression with specimens from a population-based case–control study with 96 lung cancer cases and 96 matched control subjects. The mean MPG-A in case patients was 15.8 units/μg protein (95% CI 15.3–16.3), significantly higher than in control subjects—15.1 (14.6–15.5), * P = 0.011. The adjusted odds ratio for lung cancer associated with a one SD increase in MPG-A activity (2.48 units) was significantly bigger than 1 (OR = 1.6, 95% CI = 1.1–2.4; * P = 0.013). When activity of OGG1, a different DNA repair enzyme for oxidative damage, was included in the model, the estimated odds ratio/SD for a combined MPG-A-OGG1 score was 2.6 (95% CI 1.6–4.2) * P = 0.0001, higher than the odds ratio for each single assay. The MPG enzyme activity assays described provide robust functional risk biomarkers, with increased MPG-A activity being associated with increased lung cancer risk, similar to the behavior of MPG-Hx. This underscores the notion that imbalances in DNA repair, including high DNA repair, usually perceived as beneficial, can cause cancer risk. Such DNA repair risk biomarkers may be useful for risk assessment of lung cancer and perhaps other cancer types, and for early detection techniques such as low-dose CT.
    Print ISSN: 0143-3334
    Electronic ISSN: 1460-2180
    Topics: Medicine
    Published by Oxford University Press
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  • 6
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    Minority carrier recombination of ordered Ga0.51In0.49P at high temperatures (2016)
    American Institute of Physics (AIP)
    Details
    Publication Date: 2016-12-03
    Description: The minority carrier lifetime of high-quality ordered GaInP lattice matched to GaAs and the surface recombination velocity at its interface to AlInP were measured using time-resolved photo-luminescence in the temperature range of 77 – 500   K . The surface recombination velocity was found to be relatively low (under   500   cm / s ) over the measured temperature range. The effective lifetime increased with a temperature up to around     300   K , and then decreased in the 300 – 500   K range. The variations in the effective lifetime, caused by the variations in the bulk lifetime, are explained by considering the separate contributions of radiative and non-radiative recombination and their respective temperature dependencies.
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
    Published by American Institute of Physics (AIP)
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