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  • Book
    Luca Aldrighetti, Francesco Cetta, Gianfranco Ferla, editors ; forewords by Gennaro Nuzzo and Antonio Daniele Pinna ; in collaboration with Francesca Ratti.
    Summary: Diagnosis of benign tumors of the liver is experiencing exponential growth, mainly owing to the diffusion of more accurate imaging techniques. This monograph opens by examining the epidemiology, histopathology, and genetics of these diseases and discussing liver physiopathology. The role of imaging techniques is described, and clear guidance provided on differential diagnosis. The full range of benign liver tumors and conditions is then systematically reviewed, including liver cysts and polycystic liver disease, Caroli disease, hemangiomas, focal nodular hyperplasia, adenomas, hepatic manifestations of systemic diseases, and focal infectious diseases. Surgical indications are accurately analyzed, with a view to assisting in the avoidance of useless interventions. Transplantation, laparoscopic resection, and robotic surgical techniques are described and illustrated, emphasizing the optimization of intra- and postoperative management in order to avoid potential complications and degeneration. In these chapters, attention is drawn to the ways in which the surgical management of benign liver tumors differs from that of malignant tumors. Information is also provided on anesthesia, blood transfusion, the role of interventional radiology in patients with benign liver tumors and fast track programs for liver surgery. This book, in handy format, will prove essential reading for all who are interested in benign liver surgery and will represent an invaluable source of knowledge for general and hepatobiliary surgeons, whether in training or practice.

    Contents:
    Foreword
    Preface
    Part I: General Perspective
    1. Epidemiology and Histopathology of Benign Liver Tumors
    2. Molecular Biology and Genetics of Benign Liver Tumors
    3. Genetic Syndromes and Benign Liver Tumors (Multiple Adenomas in Glycogen Storage Disease)
    4. Liver Physiopathology (Ischemia/Reperfusion, Factors affecting Liver Regeneration)
    Part II: Imaging
    5. Imaging Techniques (Ultrasound, CT, MR) of Benign Liver Tumors
    6. Imaging Morphology in Benign Liver Tumors
    7. Differential Diagnosis of Benign Liver Tumors
    Part III: Systematic Review of Benign Liver Tumors
    8. Cysts and Polycystic Liver Disease
    9. Caroli's Disease: Cystic Bile Duct Dilatations
    10.Hepatolithiasis
    11. Hemangiomas
    12. Focal Nodular Hyperplasia
    13. Hepatocellular Adenoma
    14. Adenoma and Biliary Cystadenoma
    15.Benign Tumors of Bile Ducts and Gallbladder
    16. Liver Focal Localizations of Systemic Diseases
    17. Focal Infectious Diseases
    Part IV: Treatment of Benign Liver Tumors
    18. Transplantation for Benign Liver Lesions
    19. Laparoscopic Liver Surgery in Benign Liver Lesions
    20. Robotic Liver Resection for Benign Tumors
    21. Interventional Radiology in Benign Liver Tumors: Embolization and Ablation
    22. Intraoperative Ultrasound in Liver Surgery for Benign Tumors
    23. Anesthesia and Intraoperative Management in Liver Surgery
    24. Blood and Transfusion Management in Benign Liver Tumors
    25. Fast Track Programs in Benign Liver Tumors.
    Digital Access Springer 2015
  • Article
    Zighelboim J.
    Cancer Res. 1979 Sep;39(9):3357-62.
    Patients with acute myelogenous leukemia in remission have pronounced deficiency in antibody-dependent cellular cytotoxicity (ADCC) and mitogen-induced cellular cytotoxicity. The deficiency in ADCC was partly explained by reduction in the number of circulating effector cells (Fc receptor-bearing cells) demonstrable at a time when white blood cell and platelet counts were normal. These cytotoxic functions, as well as the circulating numbers of T-cells and Fc receptor-bearing cells were further decreased by the administration of monthly cycles of combination chemotherapy with 1-beta-D-arabinofuranosylcytosine and 6-thioguanine. Following each cycle of chemotherapy, progressive recovery of these functions occurs during the third and fourth weeks with occasional increases above base line in patients in whom chemotherapy is withheld for longer than five weeks. In selected patients recovery of one cytotoxic function preceded the other, indicating that these functions are mediated by different effector cells. Administration of a single dose of daunomycin i.v. had no effect in either of these cytotoxic functions or in the circulating numbers of lymphocytes. The decrease in ADCC effector cell function induced by phase cycle-specific agents correlated with the level of reactivity exhibited by patients after achieving bone marrow and clinical remission. Patients showing low levels of reactivity postremission experienced highest degree of depression. In two patients, complete abrogation of ADCC effector function was demonstrated with minimal recovery even six weeks after stopping chemotherapy. These findings indicate that effector cells in ADCC and mitogen-induced cellular cytotoxicity are highly susceptible to phase cycle-specific agents, and their recovery takes longer that of other lymphoid and nonlymphoid populations.
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