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[null,"1.","Record Nr.",null,"UNISALENTO991000703079707536"]
[null,null,"Autore",null,"Modesti, Giovanni"]
[null,null,"Titolo",null,"Puglia anni '50 : cronache / Giovanni Modesti"]
[null,null,"Pubbl/distr/stampa",null,"Bari : [s.n.], 1984"]
[null,null,"Descrizione fisica",null,"100 p. ; 20 cm"]
[null,null,"Collana",null,"L'Arneide vicenda salentina"]
[null,null,"Lingua di pubblicazione",null,"Italiano"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,"2.","Record Nr.",null,"UNISALENTO991001249109707536"]
[null,null,"Autore",null,"Beaulieux, Charles <1872- >"]
[null,null,"Titolo",null,"Formation de l'orthographe des origines au milieu du 16. siècle / Charles Beaulieux"]
[null,null,"Pubbl/distr/stampa",null,"Paris : Librairie Honoré Champion, 1967"]
[null,null,"Descrizione fisica",null,"366 p. ; 23 cm"]
[null,null,"Collana",null,"Histoire de l'orthographe française ; 1"]
[null,null,"Lingua di pubblicazione",null,"Francese"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,"3.","Record Nr.",null,"UNINA9910495203303321"]
[null,null,"Titolo",null,"Resistance to targeted therapies in multiple myeloma / / Silvia Cw Ling, Steven Trieu, editors"]
[null,null,"Pubbl/distr/stampa",null,"Cham, Switzerland : , : Springer, , [2021]"]
[{"$nulls":4},"©2021"]
[null,null,"ISBN",null,"3-030-73440-4"]
[null,null,"Descrizione fisica",null,"1 online resource (161 pages)"]
[null,null,"Collana",null,"Resistance to Targeted Anti-Cancer Therapeutics ; ; Volume 22"]
[null,null,"Disciplina",null,"616.994061"]
[null,null,"Soggetti",null,"Drug resistance in cancer cells"]
[{"$nulls":4},"Multiple myeloma - Treatment"]
[{"$nulls":4},"Mieloma múltiple"]
[{"$nulls":4},"Resistència als medicaments"]
[{"$nulls":4},"Llibres electrònics"]
[null,null,"Lingua di pubblicazione",null,"Inglese"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,null,"Nota di contenuto",null,"Intro -- Aims and Scope -- Objective -- Preface -- Contents -- Series Editor Biography -- About the Series Editor -- Contributors -- About the Editors -- Chapter 1: The Role of Targeted Therapy in Multiple Myeloma -- 1.1 Multiple Myeloma Overview -- 1.2 Historical Treatment of Multiple Myeloma Until Present -- 1.3 Immunomodulatory Imide Drugs -- 1.4 Proteasome Inhibitors -- 1.5 Monoclonal Antibodies -- 1.6 Histone Deacetylase Inhibitors -- 1.7 Bone Targeted Therapy -- 1.8 New Agents on the Horizon -- 1.9 Conclusion -- References -- Chapter 2: Lenalidomide -- 2.1 Introduction -- 2.2 Indications -- 2.3 Efficacy of Lenalidomide -- 2.3.1 Efficacy in Relapsed or Refractory Multiple Myeloma -- 2.3.1.1 Lenalidomide and Dexamethasone -- 2.3.1.2 Bortezomib, Lenalidomide, and Dexamethasone -- 2.3.1.3 Daratumumab, Lenalidomide, and Dexamethasone -- 2.3.1.4 Carfilzomib, Lenalidomide, and Dexamethasone -- 2.3.2 Efficacy in Newly Diagnosed Multiple Myeloma -- 2.3.2.1 Transplant Ineligible Patients -- Lenalidomide and Dexamethasone -- Cyclophosphamide, Lenalidomide, and Dexamethasone -- Bortezomib, Lenalidomide, and Dexamethasone -- 2.3.2.2 Transplant Eligible Patients -- Bortezomib, Lenalidomide, and Dexamethasone -- 2.4 Mechanisms of Action -- 2.4.1 Cereblon Pathway -- 2.4.2 Effect on Cytokines -- 2.4.3 T Cell Activation -- 2.4.4 Effect on Natural Killer Cells -- 2.4.5 "]
[{"$nulls":4},"Anti-Angiogenic Activity -- 2.4.6 Direct Antitumor Activity -- 2.4.7 Myeloma Microenvironment -- 2.5 Lenalidomide Resistance -- 2.5.1 Potential Mechanisms of Lenalidomide Resistance -- 2.5.1.1 Decreased Cereblon Expression and Downstream Factors -- 2.5.1.2 Increase in c-Myc -- 2.5.2 Management of Lenalidomide-Resistant Disease -- 2.5.2.1 Pomalidomide-Based Regimes -- 2.5.2.2 Proteasome Inhibitor and Daratumumab-Based Regimes -- 2.6 Conclusion -- References -- Chapter 3: Pomalidomide."]
[{"$nulls":4},"3.1 Introduction -- 3.2 Clinical Indication of Pomalidomide -- 3.3 Efficacy -- 3.3.1 Efficacy in Relapsed and Refractory Multiple Myeloma -- 3.3.1.1 Pomalidomide and Dexamethasone -- 3.3.1.2 Pomalidomide + Dexamethasone + Cyclophosphamide -- 3.3.1.3 Pomalidomide, Bortezomib, and Dexamethasone -- 3.3.1.4 Pomalidomide, Daratumumab, and Dexamethasone -- 3.3.1.5 Pembrolizumab, Pomalidomide, and Dexamethasone -- 3.4 Mechanisms of Pomalidomide Action -- 3.5 Potential Mechanism of Pomalidomide Resistance and Overcoming Resistance -- 3.6 Conclusion -- References -- Chapter 4: Mechanisms Driving Resistance to Proteasome Inhibitors Bortezomib, Carfilzomib, and Ixazomib in Multiple Myeloma -- 4.1 Introduction -- 4.2 The Proteasome -- 4.3 Endoplasmic Reticulum Stress -- 4.4 Proteasome Inhibitors in Multiple Myeloma -- 4.5 Bortezomib Resistance Mechanisms -- 4.5.1 Proteasome Mutation and Overexpression -- 4.5.2 Drug Efflux -- 4.5.3 Plasma Cell Differentiation -- 4.5.4 Upregulation of Heat Shock Proteins -- 4.5.5 Autophagy -- 4.5.6 The Bone Marrow Microenvironment -- 4.6 Resistance Mechanisms to Second Generation Proteasome Inhibitors -- 4.6.1 Carfilzomib Resistance Mechanisms -- 4.6.1.1 Proteasome Mutations -- 4.6.1.2 Drug Efflux -- 4.6.1.3 Autophagy -- 4.6.1.4 Bone Marrow Microenvironment -- 4.6.2 Ixazomib Resistance Mechanisms -- 4.7 Conclusion -- References -- Chapter 5: Daratumumab -- 5.1 Introduction -- 5.2 Mechanism of Action -- 5.3 Mechanisms Behind Daratumumab-Resistance -- 5.3.1 Reduced Cell Surface Expression of Target Antigen CD38 -- 5.3.2 Antibody-Dependent Cell Cytotoxicity Resistance -- 5.3.3 Antibody-Dependent Cellular Phagocytosis Resistance -- 5.3.4 Complement-Dependent Cytotoxicity Resistance -- 5.3.5 Immune Modulated Resistance -- 5.4 Clinical Efficacy of Daratumumab -- 5.4.1 Daratumumab in the Relapsed and Refractory Setting."]
[{"$nulls":4},"5.4.2 Daratumumab in Newly Diagnosed, Transplant Ineligible Patients -- 5.4.3 Daratumumab in Newly Diagnosed, Transplant Eligible Patients -- 5.5 Toxicity Profile -- 5.6 Conclusion -- References -- Chapter 6: Elotuzumab -- 6.1 Introduction -- 6.2 Mechanisms of Action -- 6.2.1 Preclinical Studies -- 6.3 Pharmacological Characteristics of Elotuzumab -- 6.4 Mechanisms of Resistance to Elotuzumab -- 6.4.1 Expression of the Antigen Target of the Monoclonal Antibody -- 6.4.2 CD16a Expression on NK Cells and Associated Polymorphisms -- 6.4.3 Interactions with the Microenvironment -- 6.4.4 Development of Neutralizing Antibodies -- 6.5 Clinical Trials -- 6.5.1 Relapsed and/or Refractory Myeloma -- 6.6 Toxicities of Elotuzumab -- 6.7 Conclusion -- References -- Chapter 7: Histone Deacetylase Inhibitors -- 7.1 Introduction -- 7.2 Histone Deacetylases -- 7.2.1 Class I Histone Deacetylases -- 7.2.2 Class II Histone Deacetylases -- 7.2.3 Class III Histone Deacetylases (Sirtuins) -- 7.2.4 Class IV Histone Deacetylases -- 7.3 Histone Deacetylases in Multiple Myeloma -- 7.3.1 Histone Deacetylases and Protein Clearance -- 7.3.2 Histone Deacetylase Overexpression and Increased Activity in Multiple Myeloma -- 7.4 Histone Deacetylase Inhibitors -- 7.4.1 Types of Histone Deacetylase Inhibitors -- 7.4.2 Mechanisms of Action -- 7.4.2.1 "]
[{"$nulls":4},"Altered Gene Expression -- 7.4.2.2 Induction of Apoptosis -- 7.4.2.3 Cell Cycle Arrest -- 7.4.2.4 Inhibition of Angiogenesis -- 7.4.2.5 Regulation of Cytokines -- 7.4.2.6 Suppressed DNA Damage Repair -- 7.4.2.7 Ubiquitin Proteasome System -- 7.4.2.8 Aggresome Pathway -- 7.5 Approved Histone Deacetylase Inhibitors -- 7.5.1 Panobinostat -- 7.5.2 Vorinostat -- 7.5.3 Ricolinostat -- 7.6 Immunomodulatory Imide Drugs and Histone Deacetylase Inhibitors -- 7.7 Potential Mechanisms of Resistance to Histone Deacetylase Inhibitors."]
[{"$nulls":4},"7.7.1 Drug Transporters -- 7.7.2 Cell Signaling -- 7.7.3 Antioxidant Pathway -- 7.7.4 Cell Cycle Proteins -- 7.7.5 Nuclear Factor-Kappa B -- 7.7.6 Anti-Apoptotic Proteins -- 7.7.7 Altered Histone Deacetylases -- 7.7.8 Autophagy -- 7.8 Conclusion -- References -- Chapter 8: Bone Targeted Therapies -- 8.1 Myeloma Bone Disease -- 8.1.1 Diagnosis -- 8.1.2 Pathogenesis -- 8.1.3 Osteoclastic Activation -- 8.1.3.1 The RANK/RANKL Pathway -- 8.1.3.2 Interleukins -- 8.1.3.3 Hepatocyte Growth Factor -- 8.1.3.4 Notch Pathway -- 8.1.3.5 Chemokines -- 8.1.3.6 Activin A -- 8.1.3.7 The TNF Superfamily -- 8.1.3.8 BTK and SDF-1α -- 8.1.4 Osteoblastic Suppression -- 8.1.4.1 The WNT Pathway -- 8.1.4.2 Sclerostin -- 8.1.4.3 DKK1 -- 8.1.4.4 Periostin -- 8.1.4.5 RUNX2/CBFA1 and IL-7 -- 8.2 Indications for Bone Targeted Therapies -- 8.3 Utility of Bone Resorption Markers to Guide Therapy -- 8.4 Current Treatments for Myeloma Bone Disease -- 8.4.1 Bisphosphonates -- 8.4.1.1 Mechanism of Action -- 8.4.1.2 Evidence in MBD -- 8.4.1.3 Comparison Between Bisphosphonates -- 8.4.1.4 Adverse Events -- 8.4.1.5 Renal Impairment -- 8.4.1.6 Osteonecrosis of the Jaw -- 8.4.1.7 Subtrochanteric and Other Atypical Femoral Fractures -- 8.4.1.8 Duration, Frequency, and Monitoring of Therapy -- 8.4.1.9 Future of Bisphosphonate Therapy -- 8.4.2 Denosumab -- 8.4.2.1 Mechanism of Action -- 8.4.2.2 Evidence in MBD -- 8.4.2.3 Adverse Events -- 8.4.2.4 Duration and Frequency of Therapy -- 8.4.3 Novel Therapies -- 8.4.3.1 Anti-Sclerostin Antibodies -- 8.4.3.2 Anti-DKK1 Neutralizing Antibodies -- 8.4.3.3 Activin Receptor Ligand Traps -- 8.4.3.4 Bruton's Tyrosine Kinase (BTK) Inhibitors -- 8.4.3.5 B Cell Activating Factor (BAFF) Neutralizing Antibodies -- 8.4.3.6 Transforming Growth Factor-β (TGF-β) Inhibitors -- 8.4.3.7 Parathyroid Hormone -- 8.4.3.8 Proteasome Inhibitors."]
[{"$nulls":4},"8.4.3.9 Immunomodulatory Imide Drugs -- 8.5 Conclusion -- References -- Chapter 9: New Targeted Therapies for Multiple Myeloma Under Clinical Investigation -- 9.1 Introduction -- 9.2 Antibodies -- 9.2.1 Monoclonal Antibodies Directed at Plasma Cells -- 9.2.2 Bispecific Antibodies -- 9.2.3 Checkpoint Inhibitor -- 9.2.4 Cellular Therapies -- 9.2.4.1 Chimeric Antigen Receptor T Cells -- 9.2.4.2 DC Vaccination -- 9.2.5 Small-Molecule Inhibitors -- 9.2.5.1 Targeting Specific Subsets of Patients -- Venetoclax for Patients with Chromosomal Translocation t(11 -- 14) -- Patients with BRAF V600E Mutation -- Potential MEK Inhibition -- 9.2.5.2 Patients with Overexpressed FGFR3 -- 9.2.5.3 Targeting Inherent Weaknesses in MM -- SINE Compounds -- Bromodomain Inhibitors -- Kinesin Spindle Protein Inhibitors -- 9.3 Conclusion and Perspectives -- References -- Index."]
[null,"4.","Record Nr.",null,"UNINA9911035055503321"]
[null,null,"Autore",null,"Guttzeit Gero"]
[null,null,"Titolo",null,"In/Visible Subjects : Literary Character and Narratives of Invisibility Since the Eighteenth Century / / by Gero Guttzeit"]
[null,null,"Pubbl/distr/stampa",null,"Cham : , : Springer Nature Switzerland : , : Imprint : Palgrave Macmillan, , 2025"]
[null,null,"ISBN",null,"9783032026392"]
[null,null,"Edizione",null,"[1st ed. 2025.]"]
[null,null,"Descrizione fisica",null,"1 online resource (0 pages)"]
[null,null,"Collana",null,"Literature, Cultural and Media Studies"]
[null,null,"Disciplina",null,"809.03"]
[null,null,"Soggetti",null,"Fiction"]
[{"$nulls":4},"Literature, Modern - 18th century"]
[{"$nulls":4},"Literature, Modern - 19th century"]
[{"$nulls":4},"Literature, Modern - 20th century"]
[{"$nulls":4},"Literature, Modern - 21st century"]
[{"$nulls":4},"Prose literature"]
[{"$nulls":4},"Fiction Literature"]
[{"$nulls":4},"Eighteenth-Century Literature"]
[{"$nulls":4},"Nineteenth-Century Literature"]
[{"$nulls":4},"Twentieth-Century Literature"]
[{"$nulls":4},"Contemporary Literature"]
[{"$nulls":4},"Narrative Text and Prose"]
[null,null,"Lingua di pubblicazione",null,"Inglese"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,null,"Nota di contenuto",null,"Chapter 1 Introduc+on: Projec+ng Literary Invisibility Studies -- Chapter 2 “Compound Invisible Objects”: The Inscrutability of Character and Rhetorical Ethos in Eighteenth-Century Novelis+c Narra+ves -- Chapter 3 Invisible Lovers: Triadic Character Constella+ons and Perspec+ves of Social Recogni+on in Roman+c Poetry and Prose -- Chapter 4 Invisible Monsters: Uncanny Whiteness and Inhuman -- Characters in Nineteenth-Century Transatlan+c Gothic -- 5 Invisible Author: Weak Character, Un-Visible People, and the Modernist Text -- 6 The In/Visible You: Unseeing Characters, Images of the Self, and Contemporary Surveillance Narra+ves -- 7 Conclusion: The Third Sphere of Invisibility."]
[null,null,null,"Sommario/riassunto","In/Visible Subjects explores the cultural fascination with invisible characters in literature. While the concept of social invisibility is "]
[{"$nulls":4},"common in contemporary political discourse, there exists no comprehensive analysis of the history of the cultural metaphor of invisibility. This book addresses this gap by tracing the literary evolution of invisibility in narratives from the eighteenth century to the present. The monograph examines literal and metaphorical invisibility in terms of both content and form, offering exemplary readings of literary texts by: eighteenth-century women novelists Eliza Haywood and Susanna Rowson; Romantic poets Anna Letitia Barbauld and John Keats; nineteenth-century writers of fantasy and science fiction, including James Forbes Dalton, Fitz-James O’Brien, and H.G. Wells; early and mid-twentieth-century authors such as G.K. Chesterton, Virginia Woolf, and Ralph Ellison; and contemporary writers China Miéville and Jennifer Egan. In/Visible Subjects aims to establish a new foundation in literary studies for the emerging field of invisibility studies. It is of interest to students and scholars in literary and cultural studies working on narrative, literary character, subjectivity, and identity. Gero Guttzeit teaches English Literature at Ludwig-Maximilians-Universität München in Munich, Germany. He has held visiting professorships at Milwaukee, Freiburg, and Tübingen. His work is guided by theoretical interests in authorship, character, and rhetoric. He has published widely on nineteenth-century and contemporary literature and is the author of The Figures of Edgar Allan Poe: Authorship, Antebellum Literature, and Transatlantic Rhetoric (2017)."]