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Böcker av Badrul Hisham Yahaya

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  • av Badrul Hisham Yahaya
    1 736 - 2 000,-

    Organoid Technology for Disease Modelling and Personalised Treatment provides a comprehensive overview of current knowledge of the organoid as a human-organ-in-a-dish, a powerful new technology for studying fundamental aspects of human organ development and disease progression in the search for drugs for personalised treatment. This preclinical tool is extensively being utilised as a model for studying human diseases in a dish, which is critical for accurate predictive modelling in precision medicine. The chapters in this book introduces readers to the numerous applications of organoids in various fields of study, as well as ethical considerations associated with organoids. In stem cell biology and regenerative medicine, where chimaera research, biomaterials for tissue vascularisation, gene-editing technologies, and their use in clinical procedures especially issues related to ethical concern over the use of human organoids have gotten much attention. Organoid Technology for Disease Modelling and Personalised Treatment is an excellent resource for in-depth research on one of the most interesting and significant topics in stem cell and regenerative medicine. This book's chapter collection covers a fresh viewpoint on organoid technology that scholars will require reading.

  • av Rosline Hassan, Badrul Hisham Yahaya & Narazah Yusoff
    936,-

    The most frequent single nucleotide polymorphisms (SNPs) of MDR1 gene (in exons 12, 21 and 26) were reported to contribute to the drug resistance in many tumors. The main objectives of this study were to establish the feasible tools for screening of these three most frequent polymorphisms and to investigate the distribution of these polymorphisms in Malay leukemic patients. DNA samples were collected from Malay patients diagnosed as leukemia was subjected to dHPLC and RFLP analyses. From the results, 25 (25.7%) of the patients showed heterozygous mutation, 7 (6.7%) wild type, while 2 (1.9%) showed homozygous mutation. There was a significant difference in the distribution of polymorphisms between exons 21 and 26 (p

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