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  • Book
    Oscar H. Del Brutto, Héctor H. García.
    Summary: Neurocysticercosis (neural infection by larvae of Taenia solium) occurs when humans become intermediate hosts of the tapeworm Taenia solium after ingesting its eggs, usually directly from a Taenia carrier. Nowadays, the disease is the most common helminthic infection of the nervous system in humans, and a major cause of acquired epilepsy. It has long been endemic in developing countries of Latin America, sub-Saharan Africa, the Indian subcontinent, and Southeast Asia. Recently, however, mass migration from endemic to non-endemic areas and growth in overseas travel have resulted in an increase in the prevalence of cysticercosis in countries where it was formerly considered exotic. The introduction of modern neuroimaging and serologic techniques has improved the diagnosis of neurocysticercosis, and the development of potent cysticidal drugs has changed the prognosis of most affected patients. Nevertheless, much remains to be learned about this parasitic disease. This book provides a comprehensive and up-to-date review of the various aspects of cysticercosis of the nervous system that will be of interest to all who are involved in the care of patients with the disease. Epidemiology, neuropathology, immunopathogenesis, clinical manifestations, diagnosis, and management are all thoroughly discussed based on current evidence and practice.

    Contents:
    1 Foreword
    2 History of taeniasis and cysticercosis
    3 Epidemiology of human cysticercosis:
    Cysticercosis in endemic regions
    Cysticercosis in travelers and non-endemic regions
    4 Life cycle and biological characteristics of Taenia solium
    5 Neuropathology of cysticercosis and evolutive stages of cysticerci
    6 Immunopathogenesis of cysticercosis
    7 Clinical manifestations of Parenchymal neurocysticercosis:
    Epilepsy
    Focal neurological deficits
    Cognitive decline and psychiatric alterations
    Increased intracranial pressure
    8 Clinical manifestations of Extraparenchymal neurocysticercosis:
    Intraventricular NCC
    Cysticercosis of the Sylvian fissure and basal CSF cisterns
    Subarachnoid NCC of the convexity
    9 Diagnosis of cysticercosis (and Taeniasis):
    Neuroimaging
    Immunological diagnosis
    Other exams
    Diagnosis of taeniasis
    Diagnostic criteria for neurocysticercosis
    10 Management of neurocysticercosis:
    Cysticidal drugs (albendazole and praziquantel) Surgery
    11 Control and perspectives for elimination. .
    Digital Access Springer 2014
  • Article
    Nathan DG, Chess L, Hillman DG, Clarke B, Breard J, Merler E, Housman DE.
    J Exp Med. 1978 Feb 01;147(2):324-39.
    Human mononuclear leukocytes were fractionated into populations of null, T and B cells by immunoabsorbent column chromatography followed by E-rosette formation and purification of T cells by differential centrifugation and osmotic lysis. The unfractionated and fractionated cell populations were first separately cultured for 14 days in plasma clots in the presence of two international units erythropoietin. Typical erythroid burst-forming unit (BFU-E)-derived colonies grew in the unfractionated cell cultures but not from T- or B-cell cultures. BFU-E colonies grew in null cell cultures but most of the colonies were small and variably hemoglobinized with less than three subcolonies. When intact T cells were added to null cells and cocultured, many typical large BFU-E colonies with more than 10 well homogenized subcolonies appeared. Increasing numbers of large BFU-E colonies in null cell cultures were induced by stepwise addition of T cells but not by the addition of B cells. A conditioned medium in which T cells had been induced to divide by tetanus toxoid substituted for intact T cells in this T-cell-dependent BFU-E colony formation observed in null cells. These findings demonstrate that the BFU-E, a committeded erythroid stem cell, resides in the null cell fraction of peripheral blood, but its proliferative capacity and differentiation in vitro requires a soluble product of T cells. Such experiments now permit a new approach to the assessment of various disorders of erythropoiesis. Erythroid hypoplasia in a particular case may be due to dysfunction of the committed precursor cell or to a failure of a helper effect induced by T cells.
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