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"Hans, D."
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Catalytic disconnection of C–O bonds in epoxy resins and composites
Fibre-reinforced epoxy composites are well established in regard to load-bearing applications in the aerospace, automotive and wind power industries, owing to their light weight and high durability. These composites are based on thermoset resins embedding glass or carbon fibres
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. In lieu of viable recycling strategies, end-of-use composite-based structures such as wind turbine blades are commonly landfilled
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–
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. Because of the negative environmental impact of plastic waste
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,
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, the need for circular economies of plastics has become more pressing
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,
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. However, recycling thermoset plastics is no trivial matter
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–
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. Here we report a transition-metal-catalysed protocol for recovery of the polymer building block bisphenol A and intact fibres from epoxy composites. A Ru-catalysed, dehydrogenation/bond, cleavage/reduction cascade disconnects the C(alkyl)–O bonds of the most common linkages of the polymer. We showcase the application of this methodology to relevant unmodified amine-cured epoxy resins as well as commercial composites, including the shell of a wind turbine blade. Our results demonstrate that chemical recycling approaches for thermoset epoxy resins and composites are achievable.
The authors report a transition-metal-catalysed protocol for recovery of polymer building block bisphenol A and intact fibres from epoxy composites, demonstrating that chemical recycling approaches for thermoset epoxy resins and composites are achievable.
Journal Article
Accuracy of Predicting the Genetic Risk of Disease Using a Genome-Wide Approach
The prediction of the genetic disease risk of an individual is a powerful public health tool. While predicting risk has been successful in diseases which follow simple Mendelian inheritance, it has proven challenging in complex diseases for which a large number of loci contribute to the genetic variance. The large numbers of single nucleotide polymorphisms now available provide new opportunities for predicting genetic risk of complex diseases with high accuracy.
We have derived simple deterministic formulae to predict the accuracy of predicted genetic risk from population or case control studies using a genome-wide approach and assuming a dichotomous disease phenotype with an underlying continuous liability. We show that the prediction equations are special cases of the more general problem of predicting the accuracy of estimates of genetic values of a continuous phenotype. Our predictive equations are responsive to all parameters that affect accuracy and they are independent of allele frequency and effect distributions. Deterministic prediction errors when tested by simulation were generally small. The common link among the expressions for accuracy is that they are best summarized as the product of the ratio of number of phenotypic records per number of risk loci and the observed heritability.
This study advances the understanding of the relative power of case control and population studies of disease. The predictions represent an upper bound of accuracy which may be achievable with improved effect estimation methods. The formulae derived will help researchers determine an appropriate sample size to attain a certain accuracy when predicting genetic risk.
Journal Article
كيمياء الغذاء
بقي هذا الكتاب، لأكثر من عقدين من الزمن، الكتاب المتقدم والرائد، والمرجع سهل الاستعمال في كيمياء الغذاء وتقنياته. وقد أعيدت كتابة طبعته حيث غطت المواضيع المتنوعة مثل التقصي عن الأكريلاميد. وعالجت بعمق مواضيع التحسس الغذائي (الأرجية الغذائية)، والمشروبات الكحولية، والستيرولات النباتية. وتمت المحافظة على السمات الثابتة في الطبعات السابقة إذ : تضمن الكتاب ما يزيد عن 600 جدول، و500 شكل توضيحي وما يقارب 1100 صيغة بنيوية للمكونات الغذائية. تم ترتيب الكتاب منطقيا حسب مركبات الغذاء وسلعه. ألحق بالكتاب فهرس موسع وشامل. تزود هذه الميزات الطالب والباحث في علوم الغذاء وتقانات الأغذية والكيمياء الزراعية والتغذية بنظرة ثاقبة في كيمياء الغذاء وتقنياته. تجعل هذه السمات مجتمعة هذا الكتاب مرجعا علميا نفيسا للكيميائيين، وكيميائيي الغذاء، وتقنيي ومهندسي الغذاء، والكيميائيين الحيويين، والتغذويين، ومحللي الغذاء الكيميائيين، والعاملين في البحوث الزراعية، والصناعات الغذائية، والتغذية، ومختبرات الرقابة الغذائية.
BOOK
Long-Term Outcomes of Imatinib Treatment for Chronic Myeloid Leukemia
After nearly 11 years of follow-up, long-term administration of imatinib was shown to be associated with prolonged control of chronic myeloid leukemia and no cumulative or late toxic effects have emerged.
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm that is characterized by the Philadelphia (Ph) chromosome and driven by its product, the BCR-ABL1 tyrosine kinase.
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In 2001, imatinib was introduced as a BCR-ABL1 tyrosine kinase inhibitor and was approved for the treatment of CML on the basis of a high level of activity in phase 2 studies.
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Early results from the phase 3 International Randomized Study of Interferon and STI571 (IRIS) showed that imatinib at a dose of 400 mg once daily was more active and was associated with fewer side effects than interferon alfa plus cytarabine in patients with . . .
Journal Article