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  • Book
    Raul Delgado-Morales, editor.
    Summary: This book looks at where stem cell technology is presently and how it is instrumental in advancing the field of disease modeling and cell transplantation. By focusing on major human disorders such as Alzheimer's disease, cancer, and heart disorders, the book summarizes the major findings in the field of human stem cells and dissect the current limitations on our understanding of stem cells biology. The chapters focus on the genetics, genomics, epigenetics and physiology of stem cells models, together with technological advances on molecular biology such as CRISPR/Cas9 or epigenetic editing, that will be instrumental in the future of human disease modeling and treatment. In base of the limitations of current disease models and in front of the unmet necessity of finding therapeutical interventions for human disorders, the availability of stem cell technology has opened new doors for several fields. The unlimited self-renewal capacity and more extensive differentiation potential of stem cells offers a theoretically inexhaustible and replenishable source of any cell subtype. Since Professor Shinya Yamanaka described it, 10 years ago in his seminal paper, that somatic cells could be reprogrammed to inducible stem cells (iPSC) just by expressing four transcription factors, the field of has exploded, especially its applications in biomedical research.

    Contents:
    Part I: Stem cells for brain disorders
    Chapter 1: Human induced pluripotent stem cell-derived neurons to model and gain insights into Alzheimer's disease pathogenesis
    Chapter 2: Modeling schizophrenia with human stem cells
    Chapter 3: Rett Syndrome and Stem Cell research
    Chapter 4: Stem Cell Applications in Spinal Cord Injury: A Primer
    Chapter 5: Cell-Based Therapy for Retinal Degenerative Disease
    Chapter 6: Past, present and future of cell based-therapy in progressive multiple sclerosis
    Part II: Stem cells for cardiovascular diseases
    Chapter 7: Cardiac Stem Cells: a plethora of potential therapies for myocardial regeneration within reach
    Chapter 8: Human Induced Pluripotent Stem Cell-derived Cardiomyocytes in the Evaluation of Cardiotoxic Potential of Drugs
    Part III: Stem cells for general medicine
    Chapter 9: Regenerative medicine for diabetes treatment: new cell sources
    Chapter 10: Dental pulp stem cells promote wound healing and muscle regeneration
    Chapter 11: From bench to bedside of mesenchymal Stem Cells use for Rheumatoid Arthritis treatment
    Chapter 12: Stem Cells and Cancer
    Chapter 13: The relevance of induced pluripotent stem cells for the study of physiological and premature aging
    Part IV: Technical challenges and future
    Chapter 14: Pluripotent stem cell banks
    Chapter 15: Genetic and Epigenetic engineering: the CRISPR/Cas9 era.
    Digital Access Springer 2018
  • Article
    Bullock WE, Carlson EM, Gershon RK.
    J Immunol. 1978 May;120(5):1709-16.
    Immunosuppressor activity of considerable potency and complexity was generated during the course of chronic, progressive infection of C3H/Anf mice by Mycobacterium lepraemurium. From the 5th through 10th week after inoculation, spleen cells from infected mice mildly but reproducibly suppressed the direct plaque-forming cell response of normal spleen cell cultures to sheep erythrocytes. Suppression at this stage of infection was mediated by cells with macrophage-like characteristics. A marked increase in splenic suppressor activity at 10 to 11 weeks was associated with the appearance of a second suppressor cell subpopulation composed of T lymphocytes. The appearance of these cells was closely related in time to the onset of rapid splenic enlargement and a loss of cutaneous delayed type hypersensitivity to antigens of M. lepraemurium in mice at 10 to 11 weeks of infection. Suppressor cells were not present in peripheral lymph nodes until terminal infection at 22 to 25 weeks. Suppressor spleen cells depressed the T-dependent antibody response most severely, but there was also a direct effect upon B cells as shown by moderate suppression of responses to TNP-LPS and DNP-Ficoll. Spleen cells from 14-week-infected mice generated a soluble suppressor factor(s) that induces depression of moderate severity, however, the immunosuppression by intact cells was far greater.
    Digital Access Access Options