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  • Book
    Sudip Paul, editor.
    Summary: This book focuses on interdisciplinary research in the field of biomedical engineering and neuroscience. Biomedical engineering is a vast field, ranging from bioengineering to brain-computer interfaces. The book explores the system-level function and dysfunction of the nervous system from scientific and engineering perspectives. The initial sections introduce readers to the physiology of the brain, and to the biomedical tools needed for diagnostics and effective therapies for various neurodegenerative and regenerative disorders. In turn, the book summarizes the biomedical interventions that are used to understand the neural mechanisms underlying empathy disorders, and reviews recent advances in biomedical engineering for rehabilitation in connection with neurodevelopmental disorders and brain injuries. Lastly, the book discusses innovations in machine learning and artificial intelligence for computer-aided disease diagnosis and treatment, as well as applications of nanotechnology in therapeutic neurology.

    Contents:
    Module 1_ Introduction to Human Physiology
    Module 2_ Neural engineering
    Module 3_ Introduction to Neurodegenerative and regenerative Disorders
    Module 4_ Brain images and it`s classifications
    Module 5_ EEG, EOG and their significance
    Module 6_ Artificial Intelligence and Computer Aided diagnosis
    Module 7_ Nanomaterials involved in therapeutic strategy
    Module 8_ Emotion, Stress and other Neurological dysfunctions
    Module 9_ Emotion, Stress and other Neurological dysfunctions.
    Digital Access Springer 2019
  • Article
    Pine MJ.
    Antimicrob Agents Chemother. 1978 Apr;13(4):676-85.
    The relative toxicities of several incorporated analogs of phenylalanine, methionine, arginine, and proline were assessed by a variety of criteria in a derivative of Escherichia coli 15 requiring the antagonized amino acids. Toxicity of the analog-substituted cell protein was most consistently indicated by its insolubility at graded temperatures, its increased breakdown, the relative suppression of further cell growth, and lethality. The relative toxicity of poorly utilized analogs could be judged clearly only by the first two criteria. Toxicity generally increased as follows: selenomethionine < 2,5-dihydrophenylalanine and m-fluorophenylalanine < o-fluorophenylalanine and norleucine < ethionine < p-fluorophenylalanine < azetidine-2-carboxylate < canavanine. The overall perturbation of cell protein structure indicated by the toxicity of the methionine and phenylalanine analogs correlated with their alteration of charge and bulk and was greatly modified by minor positional modifications of fluorine. Among the more specific functional impairments, the activity and heat stability of beta-galactosidase were lowered in parallel by substitutions of phenylalanine and methionine analogs, but not in the usual order of toxicity. Flagella were transiently motile with p-fluorophenylalanine, moderately motile with m-fluorophenylalanine, and fully motile with all methionine analogs. Usually the analog incorporations were no more than bacteriostatic in E. coli strains, canavanine killing only the E. coli 15 substrain extensively in minimal media. Selenomethionine supported indefinite growth of procaryotes such as Bacillus subtilis and certain E. coli strains, but only upon supplementation, at least initially, with many nonessential metabolites.
    Digital Access Access Options