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6 produkter
6 produkter
1 854 kr
Skickas inom 10-15 vardagar
This is a reference handbook for young researchers exploring gene and cell therapy. Gene therapy could be defined as a set of strategies modifying gene expression or correcting mutant/defective genes through the administration of DNA (or RNA) to cells, in order to treat disease.
1 311 kr
Skickas inom 10-15 vardagar
This is a reference handbook for young researchers exploring gene and cell therapy. Gene therapy could be defined as a set of strategies modifying gene expression or correcting mutant/defective genes through the administration of DNA (or RNA) to cells, in order to treat disease.
1 094 kr
Skickas inom 10-15 vardagar
Obesity is a multi-factorial disease, in which an excess of accumulated body fat can reach levels capable of affecting health. It results from an interplay between environmental factors, eating behavior, genes, epigenetics, and neuronal stimuli. The main aim of this book is to provide a state-of-the-art revision about the molecular mechanisms underpinning the development of obesity, reviewing the current knowledge in areas like monogenic and polygenic obesity forms, but also providing an updated view of the emerging knowledge about epigenetics, nutrigenomics, and neuronal aspects that also contribute to obesity.
1 094 kr
Skickas inom 10-15 vardagar
Obesity is a multi-factorial disease, in which an excess of accumulated body fat can reach levels capable of affecting health. It results from an interplay between environmental factors, eating behavior, genes, epigenetics, and neuronal stimuli. The main aim of this book is to provide a state-of-the-art revision about the molecular mechanisms underpinning the development of obesity, reviewing the current knowledge in areas like monogenic and polygenic obesity forms, but also providing an updated view of the emerging knowledge about epigenetics, nutrigenomics, and neuronal aspects that also contribute to obesity.
1 963 kr
Skickas inom 10-15 vardagar
This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17).The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.
Del 1049 - Advances in Experimental Medicine and Biology
Polyglutamine Disorders
Häftad, Engelska, 2019
1 419 kr
Skickas inom 10-15 vardagar
This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17).The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.