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- BookRoberto N. Miranda, Joseph D. Khoury, L. Jeffrey Medeiros.Summary: Atlas of Lymph Node Pathology reviews the histopathology of nodal diseases, illustrating the use of ancillary studies and includes concise discussions of pathogenesis, clinical settings and clinical significance of the pathologic diagnosis. The atlas features an overview of the benign reactive processes secondary to infectious, environmental or unknown insults, as well as relevant illustrations of virtually all primary and secondary neoplasms involving lymph nodes. The atlas also includes macroscopic images of some disorders, tables that help readers understand and comprehend diseases that look alike, and diagnostic algorithms for certain groups of diseases. Authored by highly experienced pathologists, Atlas of Lymph Node Pathology is a valuable resource that illustrates the vast majority of diseases practicing pathologists, clinicians and oncologists are likely to encounter in daily practice.
Contents:
Normal Lymph Node Architecture and Function
Reactive Follicular Hyperplasia
Reactive Paracortical Hyperplasia
Bacterial (Suppurative) Lymphadenitis
Chronic Granulomatous Lymphadenitis
Mycobacterium Tuberculosis Lymphadenitis
Atypical Mycobacterial Lymphadenitis
Mycobacterial Spindle Cell Pseudotumor
Cat-Scratch Lymphadenitis
Bacillary Angiomatosis of Lymph Nodes
Lymphogranuloma Venereum Lymphadenitis
Whipple Disease Lymphadenitis
Syphilitic Lymphadenitis
Brucellosis Lymphadenitis
Toxoplasma Lymphadenitis
Fungal Lymphadenitis: Histoplasma, Cryptococcus, and Coccidioides
Infectious Mononucleosis
Herpes Simplex Virus and Varicella-Herpes Zoster Lymphadenitis
Cytomegalovirus Lymphadenitis
Human Immunodeficiency Virus Lymphadenitis
Inflammatory Pseudotumor of Lymph Nodes
Progressive Transformation of Germinal Centers
Kikuchi-Fujimoto Disease
Rosai Dorfman Disease
Kimura Lymphadenopathy
Unicentric Castleman Disease
Multicentric Castleman Disease
Rheumatoid Arthritis-Related Lymphadenopathy
Systemic Lupus Erythematosus Lymphadenopathy
Sarcoidosis Lymphadenopathy
Dermatopathic Lymphadenopathy
Hemophagocytic Lymphohistiocytosis/Hemophagocytic Syndromes
Lymph Node Infarction
Silicone-Induced Lymphadenopathy
Lymphadenopathy Associated with Joint Prostheses
Lymphadenopathy in IgG4-Related Disease
Lymphadenopathy Secondary to Drug-Induced Hypersensitivity Syndrome
Amyloidosis Lymphadenopathy
B-Lymphoblastic Lymphoma/Leukemia
T-Lymphoblastic Lymphoma/Leukemia
Lymphomas Associated with FGFR1 Abnormalities
Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma
Richter Syndrome
Nodal Marginal Zone Lymphoma
Extranodal Marginal Zone Lymphoma of Mucosa-Associated Lymphoid Tissue (MALT Lymphoma)
Splenic B-cell Marginal Zone Lymphoma in Lymph Node
Lymphoplasmacytic Lymphoma and Waldenstrom Macroglobulinemia
Solitary Plasmacytoma of Lymph Node
Follicular Lymphoma
Mantle Cell Lymphoma
Diffuse Large B-cell Lymphoma, Not Otherwise Specified
T cell/Histiocyte-Rich Large B-cell Lymphoma
ALK-Positive Diffuse Large B-cell Lymphoma
Epstein-Barr Virus-Positive Diffuse Large B-Cell Lymphoma of the Elderly
Primary Mediastinal (Thymic) Large B-cell Lymphoma
Plasmablastic Lymphoma
Large B-cell Lymphoma Arising in HHV8-Positive Multicentric Castleman Disease
B-cell Lymphoma, Unclassifiable, with Features Intermediate Between Diffuse Large B-cell Lymphoma and Burkitt Lymphoma
B-cell Lymphoma, Unclassifiable, with Features Intermediate Between DLBCL and Burkitt Lymphoma
B-cell Lymphoma, Unclassifiable, With Features Intermediate Between Diffuse Large B-cell Lymphoma and Classical Hodgkin Lymphoma
Peripheral T-cell Lymphoma, Not Otherwise Specified
Angioimmunoblastic T-cell Lymphoma
ALK-Positive Anaplastic Large Cell Lymphoma
ALK-Negative Anaplastic Large Cell Lymphoma
Cutaneous Anaplastic Large Cell Lymphoma with Dissemination to Lymph Nodes and Other Sites
Mycosis Fungoides
T-Cell Prolymphocytic Leukemia Involving Lymph Nodes and Other Tissues
Adult T-cell Leukemia/Lymphoma
Extranodal NK/T-cell Lymphoma, Nasal Type
Nodular Lymphocyte-Predominant Hodgkin Lymphoma
Nodular Sclerosis Hodgkin Lymphoma
Lymphocyte-Rich Classical Hodgkin Lymphoma
Mixed Cellularity Hodgkin Lymphoma
Lymphocyte-Depleted Hodgkin Lymphoma
Lymphoproliferative Diseases Associated with Primary Immune Disorders
Autoimmune Lymphoproliferative Syndrome
Immunomodulating Agent-Associated Lymphoproliferative Disorders
Post-Transplant Lymphoproliferative Disorder: Early and Polymorphic Lesions
Monomorphic B-cell (Including Plasmacytic) Post-transplant Lymphoproliferative Disorder
Post-transplant Lymphoproliferative Disorder, Monomorphic T/NK-cell Type, and Classical Hodgkin Lymphoma
Lymphomas Associated with HIV Infection
Blastic Plasmacytoid Dendritic Cell Neoplasm
Langerhans Cell Histiocytosis
Langerhans Cell Sarcoma
Interdigitating Dendritic Cell Sarcoma
Follicular Dendritic Cell Sarcoma
Histiocytic Sarcoma
Granulocytic Sarcoma
Monocytic Sarcoma
Mast Cell Disease
Extramedullary Hematopoiesis in Lymph Nodes
Epithelial Inclusions in Lymph Node
Nevus Cell Inclusions
Vascular Transformation of Lymph Node Sinuses
Angiomyomatous Hamartoma
Palisaded Myofibroblastoma
Metastatic Kaposi Sarcoma
Metastases to Lymph Nodes.Digital Access Springer 2013 - ArticleOkamoto M, Mayer MM.J Immunol. 1978 Jan;120(1):279-85.In the previous paper it was suggested that the primary action of guinea pig lymphotoxin (LT) involved creation of ionic imbalances within the target L cells. The nature of these ionic disturbances is explored in this paper. The exogenous addition of CaCl2, but not KCl or NaCl, inhibited the cytotoxic action of LT. Cellular uptake rates of 45Ca++, but not 86Rb+, increased in LT-damaged L cells. The factor responsible for increasing the 45Ca++ uptake rate cochromatographed on a hydroxyapatite column with the cytotoxic activity of LT. Ouabain prevented the LT-mediated lysis and, concomitantly, depressed the LT-induced increase of 45Ca++ uptake rate. The LT-damaged L cells excluded trypan blue to the same extent as the normal cells. The addition of LT to and LT-resistant L cell mutant affected neither the 45Ca++ uptake rate nor the viability. From these observations, damage to the calcium transport system in the L cell plasma membrane is proposed as a mechanism of LT action.