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  1. Book: Clinical hematology and oncology

    Furie, Bruce

    presentation, diagnosis, and treatment

    2003  

    Author's details Bruce Furie
    Keywords Hematologic Diseases / diagnosis ; Hematologic Diseases / therapy ; Neoplasms / diagnosis ; Neoplasms / therapy ; Hematology / methods ; Medical Oncology / methods ; Hematology ; Hematology/Technique ; Oncology ; Oncology/Technique
    Subject code 616.15
    Language English
    Size XXII, 23, 1300 S. : Ill., graph. Darst.
    Publisher Churchill Livingstone
    Publishing place Philadelphia, Pa
    Publishing country United States
    Document type Book
    HBZ-ID HT013804679
    ISBN 0-443-06556-X ; 978-0-443-06556-9
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2003 A 3303 order for loan Magazin

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  2. Article ; Online: Do pharmacogenetics have a role in the dosing of vitamin K antagonists?

    Furie, Bruce

    The New England journal of medicine

    2013  Volume 369, Issue 24, Page(s) 2345–2346

    MeSH term(s) Acenocoumarol/administration & dosage ; Algorithms ; Anticoagulants/administration & dosage ; Aryl Hydrocarbon Hydroxylases/genetics ; Cytochrome P-450 CYP2C9 ; Female ; Genotype ; Humans ; Male ; Phenprocoumon/administration & dosage ; Vitamin K Epoxide Reductases/genetics ; Warfarin/administration & dosage
    Chemical Substances Anticoagulants ; Warfarin (5Q7ZVV76EI) ; CYP2C9 protein, human (EC 1.14.13.-) ; Cytochrome P-450 CYP2C9 (EC 1.14.13.-) ; Aryl Hydrocarbon Hydroxylases (EC 1.14.14.1) ; VKORC1 protein, human (EC 1.17.4.4) ; Vitamin K Epoxide Reductases (EC 1.17.4.4) ; Acenocoumarol (I6WP63U32H) ; Phenprocoumon (Q08SIO485D)
    Language English
    Publishing date 2013-12-12
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe1313682
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Regulatory role of thiol isomerases in thrombus formation.

    Sharda, Anish / Furie, Bruce

    Expert review of hematology

    2018  Volume 11, Issue 5, Page(s) 437–448

    Abstract: Introduction: The protein disulfide isomerase (PDI) family of thiol isomerases are intracellular enzymes known to catalyze the oxidation, reduction and isomerization of disulfide bonds during protein synthesis in the endoplasmic reticulum. PDI and ... ...

    Abstract Introduction: The protein disulfide isomerase (PDI) family of thiol isomerases are intracellular enzymes known to catalyze the oxidation, reduction and isomerization of disulfide bonds during protein synthesis in the endoplasmic reticulum. PDI and related members of the thiol isomerase family are known to localize extracellularly where they possess various functions. Among these, the role of PDI in the initiation of thrombus formation is best characterized. PDI is secreted within seconds from activated platelets and endothelial cells at the site of vascular injury and accumulates in the developing platelet-fibrin thrombus. Inhibition of PDI by antibodies or small molecule inhibitors blocks thrombus formation. Efforts are underway to identify extracellular substrates of PDI that participate in the network pathways linking thiol isomerases to thrombus formation. ERp57, ERp5 and ERp72 also play a role in initiation of thrombus formation but their specific extracellular substrates are unknown. Areas covered: The following review gives an overview of biochemistry of vascular thiol isomerases followed by a detailed description of their role in thrombosis and its clinical implications. Expert commentary: The thiol isomerase system, by controlling the initiation of thrombus formation, provides the regulatory switch by which the normal vasculature is protected under physiologic conditions from thrombi generation.
    MeSH term(s) Animals ; Blood Coagulation/physiology ; Blood Platelets/cytology ; Blood Platelets/metabolism ; Fibrin/metabolism ; Humans ; Platelet Activation/physiology ; Protein Disulfide-Isomerases/metabolism
    Chemical Substances Fibrin (9001-31-4) ; Protein Disulfide-Isomerases (EC 5.3.4.1)
    Language English
    Publishing date 2018-03-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2516804-6
    ISSN 1747-4094 ; 1747-4086
    ISSN (online) 1747-4094
    ISSN 1747-4086
    DOI 10.1080/17474086.2018.1452612
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Sustained glucocorticoid tapering in the phase 3 trials of anifrolumab: a post hoc analysis of the TULIP-1 and TULIP-2 trials.

    Bruce, Ian N / van Vollenhoven, Ronald F / Morand, Eric F / Furie, Richard A / Manzi, Susan / White, William B / Abreu, Gabriel / Tummala, Raj

    Rheumatology (Oxford, England)

    2022  Volume 62, Issue 4, Page(s) 1526–1534

    Abstract: Objectives: Glucocorticoid sparing is a key priority for SLE management. We evaluated the effects of sustained glucocorticoid tapering in patients with SLE.: Material and methods: This was a post hoc analysis of the randomized, placebo-controlled, 52- ...

    Abstract Objectives: Glucocorticoid sparing is a key priority for SLE management. We evaluated the effects of sustained glucocorticoid tapering in patients with SLE.
    Material and methods: This was a post hoc analysis of the randomized, placebo-controlled, 52-week phase 3 Treatment of Uncontrolled Lupus via the Interferon Pathway (TULIP)-1 and TULIP-2 trials of anifrolumab (300 mg i.v. once every 4 weeks for 48  weeks) plus standard therapy in patients with moderate to severe SLE. In a cohort of patients receiving glucocorticoids (prednisone or equivalent) 10 mg or more per day at baseline, we assessed changes in glucocorticoid dosage, patient-reported outcomes (PROs) and safety. Outcome measures were compared between sustained glucocorticoid taper responders (7.5 mg or less per day by week 40 sustained through week 52) and non-responders, regardless of treatment group, and between patients receiving anifrolumab or placebo.
    Results: Among the 726 patients in the TULIP trials, 375 patients received glucocorticoids 10 mg or more per day at baseline, and of these, 155 (41%) patients were sustained glucocorticoid taper responders. Compared with non-responders (n = 220), sustained glucocorticoid taper responders reduced their mean cumulative glucocorticoid dose by 32%, improved PRO scores, reduced blood pressure and experienced fewer serious adverse events. Sustained glucocorticoid tapering was achieved by 51% (96/190) of patients receiving anifrolumab vs 32% (59/185) receiving placebo. Compared with placebo, more anifrolumab-treated patients achieved both sustained glucocorticoid taper and reduced overall disease activity [38% (72/190) vs 23% (43/185)].
    Conclusions: Sustained glucocorticoid tapering is associated with clinical benefits. Anifrolumab treatment has potential to reduce disease activity and glucocorticoid exposure, a key goal of SLE management.
    Study registration: ClinicalTrials.gov identifier: NCT02446912 and NCT02446899.
    MeSH term(s) Humans ; Antibodies, Monoclonal, Humanized/therapeutic use ; Glucocorticoids ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/chemically induced ; Treatment Outcome ; Tulipa
    Chemical Substances anifrolumab (38RL9AE51Q) ; Antibodies, Monoclonal, Humanized ; Glucocorticoids
    Language English
    Publishing date 2022-08-26
    Publishing country England
    Document type Clinical Trial, Phase III ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keac491
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 497: Show issues

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  5. Article ; Online: Efficacy of anifrolumab across organ domains in patients with moderate-to-severe systemic lupus erythematosus: a post-hoc analysis of pooled data from the TULIP-1 and TULIP-2 trials.

    Morand, Eric F / Furie, Richard A / Bruce, Ian N / Vital, Edward M / Dall'Era, Maria / Maho, Emmanuelle / Pineda, Lilia / Tummala, Raj

    The Lancet. Rheumatology

    2022  Volume 4, Issue 4, Page(s) e282–e292

    Abstract: Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterised by multisystem involvement. We aimed to evaluate the efficacy of anifrolumab on organ domain-specific SLE disease activity.: Methods: In this post-hoc ... ...

    Abstract Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterised by multisystem involvement. We aimed to evaluate the efficacy of anifrolumab on organ domain-specific SLE disease activity.
    Methods: In this post-hoc analysis, data were pooled from the randomised, placebo-controlled, phase 3 TULIP-1 (NCT02446912) and TULIP-2 (NCT02446899) trials of anifrolumab (300 mg intravenously once every 4 weeks for 48 weeks) in patients aged 18-70 years with moderate-to-severe SLE. We evaluated changes from baseline to week 52 in British Isles Lupus Assessment Group 2004 (BILAG-2004) and SLE Disease Activity Index 2000 (SLEDAI-2K) organ domain scores, Cutaneous Lupus Erythematosus Disease Area and Severity Index activity score (CLASI-A), swollen and tender joint counts, haematology, and serology.
    Findings: Among the 726 patients included, the mean age was 41·8 years (SD 11·9); 674 (93%) were female, 52 (7%) were male, and 479 (66%) were White. 360 patients received anifrolumab 300 mg (180 patients in each trial), and 366 received placebo (184 patients in TULIP-1 and 182 patients in TULIP-2). The most frequently affected organ domains at baseline were musculoskeletal (645 [89%] patients based on BILAG-2004; 684 [94%] with SLEDAI-2K) and mucocutaneous (627 [86%] with BILAG-2004; 699 [96%] based on SLEDAI-2K). At week 52, anifrolumab treatment resulted in greater improvements versus placebo in the musculoskeletal system (176 [56%] of 317 patients vs 143 [44%] of 328 with BILAG-2004; 164 [49%] of 335 vs 141 [40%] of 349 with SLEDAI-2K), the mucocutaneous system (168 [54%] of 315 vs 119 [38%] of 312 with BILAG-2004; 190 [55%] of 348 vs 138 [39%] of 351 SLEDAI-2K), and immunological system (44 [19%] of 237 vs 26 [11%] of 230 with SLEDAI-2K). Less frequently affected domains had varied responses. Among patients with a CLASI-A of 10 or more at baseline, greater proportions of patients receiving anifrolumab than placebo achieved a reduction of 50% or more in CLASI-A at week 52 (49 [46%] of 107 vs 24 [25%] of 94). Among patients with at least six swollen joints, more patients in the anifrolumab group than in the placebo group had a 50% or more reduction from baseline to week 52 in swollen joint count (99 [57%] of 174 vs 92 [46%] of 200), but the difference between groups was not significant for 50% or more reduction in tender joint count.
    Interpretation: Across the two pivotal phase 3 trials, anifrolumab treatment improved SLE disease activity across multiple organ domains.
    Funding: AstraZeneca.
    Language English
    Publishing date 2022-02-03
    Publishing country England
    Document type Journal Article
    ISSN 2665-9913
    ISSN (online) 2665-9913
    DOI 10.1016/S2665-9913(21)00317-9
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  6. Article ; Online: Identification of PDI Substrates by Mechanism-Based Kinetic Trapping.

    Eriksson, Oskar / Stopa, Jack / Furie, Bruce

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 1967, Page(s) 165–182

    Abstract: Protein disulphide isomerase (PDI) is secreted by activated platelets and endothelial cells and is required for thrombus formation upon vascular injury. PDI catalyzes the reduction, oxidation, or isomerization of disulphide bonds in its substrate ... ...

    Abstract Protein disulphide isomerase (PDI) is secreted by activated platelets and endothelial cells and is required for thrombus formation upon vascular injury. PDI catalyzes the reduction, oxidation, or isomerization of disulphide bonds in its substrate proteins. The specific substrates of PDI during thrombus formation have largely remained elusive, in part due to the transient nature of the PDI-substrate interaction.To overcome this challenge we have adapted and developed a kinetic substrate trapping strategy to identify extracellular substrates of PDI. By substitution of selected amino acids in the PDI active sites, we have generated PDI variants that form stable complexes with their substrates for subsequent isolation and identification. We here describe the substrate trapping methodology in detail, including generation and characterization of PDI variants, kinetic trapping experiments, and isolation and identification of bound substrates. The protocol can be adapted for most any biological fluid or sample, and can be applied to other extracellular thiol isomerases.
    MeSH term(s) Animals ; Blood Platelets/chemistry ; Catalysis ; Catalytic Domain ; Disulfides/chemistry ; Endothelial Cells/chemistry ; Humans ; Kinetics ; Oxidation-Reduction ; Protein Disulfide-Isomerases/chemistry ; Substrate Specificity
    Chemical Substances Disulfides ; Protein Disulfide-Isomerases (EC 5.3.4.1)
    Language English
    Publishing date 2019-05-09
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9187-7_10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Pathogenesis of thrombosis.

    Furie, Bruce

    Hematology. American Society of Hematology. Education Program

    2009  , Page(s) 255–258

    Abstract: The hemostatic process is a host defense mechanism to preserve the integrity of the closed high pressure circulatory system. This process must remain inactive but poised to minimize extravasation of blood from the vasculature following tissue injury. ... ...

    Abstract The hemostatic process is a host defense mechanism to preserve the integrity of the closed high pressure circulatory system. This process must remain inactive but poised to minimize extravasation of blood from the vasculature following tissue injury. Given the complexity of the hemostatic mechanism, paradigms developed from biochemical and cell biological approaches have been revisited by studying thrombus formation in a live animal by intravital microscopy. Many of these paradigms have proven accurate, but others need to be reconsidered given the results of whole animal experiments.
    MeSH term(s) Animals ; Blood Coagulation Factors/physiology ; Cell-Derived Microparticles/physiology ; Chlorides ; Collagen/physiology ; Disease Models, Animal ; Ferric Compounds/toxicity ; Fibrin/biosynthesis ; Integrin beta3/physiology ; Lasers/adverse effects ; Mesentery/blood supply ; Mice ; Mice, Knockout ; Microscopy, Fluorescence/methods ; Muscle, Skeletal/blood supply ; Platelet Aggregation ; Protein Disulfide-Isomerases/physiology ; Thromboplastin/physiology ; Thrombosis/etiology ; Thrombosis/pathology ; Thrombosis/physiopathology
    Chemical Substances Blood Coagulation Factors ; Chlorides ; Ferric Compounds ; Integrin beta3 ; Fibrin (9001-31-4) ; Collagen (9007-34-5) ; Thromboplastin (9035-58-9) ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; ferric chloride (U38V3ZVV3V)
    Language English
    Publishing date 2009-11-04
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1520-4383
    ISSN (online) 1520-4383
    DOI 10.1182/asheducation-2009.1.255
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  8. Article ; Online: Vascular thiol isomerases.

    Flaumenhaft, Robert / Furie, Bruce

    Blood

    2016  Volume 128, Issue 7, Page(s) 893–901

    Abstract: Thiol isomerases are multifunctional enzymes that influence protein structure via their oxidoreductase, isomerase, and chaperone activities. These enzymes localize at high concentrations in the endoplasmic reticulum of all eukaryotic cells where they ... ...

    Abstract Thiol isomerases are multifunctional enzymes that influence protein structure via their oxidoreductase, isomerase, and chaperone activities. These enzymes localize at high concentrations in the endoplasmic reticulum of all eukaryotic cells where they serve an essential function in folding nascent proteins. However, thiol isomerases can escape endoplasmic retention and be secreted and localized on plasma membranes. Several thiol isomerases including protein disulfide isomerase, ERp57, and ERp5 are secreted by and localize to the membranes of platelets and endothelial cells. These vascular thiol isomerases are released following vessel injury and participate in thrombus formation. Although most of the activities of vascular thiol isomerases that contribute to thrombus formation are yet to be defined at the molecular level, allosteric disulfide bonds that are modified by thiol isomerases have been described in substrates such as αIIbβ3, αvβ3, GPIbα, tissue factor, and thrombospondin. Vascular thiol isomerases also act as redox sensors. They respond to the local redox environment and influence S-nitrosylation of surface proteins on platelets and endothelial cells. Despite our rudimentary understanding of the mechanisms by which thiol isomerases control vascular function, the clinical utility of targeting them in thrombotic disorders is already being explored in clinical trials.
    MeSH term(s) Animals ; Blood Vessels/enzymology ; Blood Vessels/pathology ; Hemostasis ; Humans ; Models, Biological ; Oxidation-Reduction ; Protein Disulfide-Isomerases/metabolism ; Thrombosis/enzymology ; Thrombosis/pathology
    Chemical Substances Protein Disulfide-Isomerases (EC 5.3.4.1)
    Language English
    Publishing date 2016-06-29
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2016-04-636456
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  9. Article ; Online: Formation of the clot.

    Furie, Bruce / Furie, Barbara C

    Thrombosis research

    2012  Volume 130 Suppl 1, Page(s) S44–6

    Abstract: An electron transport system regulates the initiation of thrombus formation through the activation of critical receptors involved in hemostasis and thrombosis. Protein disulfide isomerase along with other thiol isomerases, important for intracellular ... ...

    Abstract An electron transport system regulates the initiation of thrombus formation through the activation of critical receptors involved in hemostasis and thrombosis. Protein disulfide isomerase along with other thiol isomerases, important for intracellular protein synthesis, are responsible for this extracellular activity during thrombus formation. Inhibition of these thiol isomerases blocks platelet aggregation and fibrin generation. Pharmaceuticals directed against these thiol isomerases offers a novel approach to antithrombotic therapy.
    MeSH term(s) Animals ; Blood Platelets/drug effects ; Blood Platelets/enzymology ; Drug Design ; Enzyme Inhibitors/pharmacology ; Fibrin/metabolism ; Fibrinolytic Agents/pharmacology ; Humans ; Kinetics ; Microscopy, Confocal ; Microscopy, Video ; Platelet Aggregation ; Platelet Aggregation Inhibitors/pharmacology ; Protein Disulfide-Isomerases/antagonists & inhibitors ; Protein Disulfide-Isomerases/blood ; Thrombin/metabolism ; Thrombosis/blood ; Thrombosis/drug therapy ; Thrombosis/enzymology
    Chemical Substances Enzyme Inhibitors ; Fibrinolytic Agents ; Platelet Aggregation Inhibitors ; Fibrin (9001-31-4) ; Thrombin (EC 3.4.21.5) ; Protein Disulfide-Isomerases (EC 5.3.4.1)
    Language English
    Publishing date 2012-09-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 121852-9
    ISSN 1879-2472 ; 0049-3848
    ISSN (online) 1879-2472
    ISSN 0049-3848
    DOI 10.1016/j.thromres.2012.08.272
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  10. Article ; Online: What Does It Mean to Be a British Isles Lupus Assessment Group-Based Composite Lupus Assessment Responder? Post Hoc Analysis of Two Phase III Trials.

    Furie, Richard / Morand, Eric F / Bruce, Ian N / Isenberg, David / van Vollenhoven, Ronald / Abreu, Gabriel / Pineda, Lilia / Tummala, Raj

    Arthritis & rheumatology (Hoboken, N.J.)

    2021  Volume 73, Issue 11, Page(s) 2059–2068

    Abstract: Objective: The British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) is a validated global measure of treatment response in systemic lupus erythematosus (SLE) clinical trials. To understand the relevance of BICLA in clinical ... ...

    Abstract Objective: The British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) is a validated global measure of treatment response in systemic lupus erythematosus (SLE) clinical trials. To understand the relevance of BICLA in clinical practice, we investigated relationships between BICLA response and routine SLE assessments, patient-reported outcomes (PROs), and medical resource utilization.
    Methods: This was a post hoc analysis of pooled data from the phase III, randomized, placebo-controlled, 52-week TULIP-1 (ClinicalTrials.gov identifier: NCT02446912; n = 457) and TULIP-2 (ClinicalTrials.gov identifier: NCT02446899; n = 362) trials of intravenous anifrolumab (150/300 mg once every 4 weeks) in patients with moderate-to-severe SLE. Changes from baseline to week 52 in clinical assessments, PROs, and medical resource use were compared in BICLA responders versus nonresponders, regardless of treatment assignment.
    Results: BICLA responders (n = 318) achieved significantly improved outcomes compared with nonresponders (n = 501), including lower flare rates, higher rates of attainment of sustained oral glucocorticoid taper to ≤7.5 mg/day, greater improvements in PROs (Functional Assessment of Chronic Illness Therapy-Fatigue, Short Form 36 Health Survey), and fewer SLE-related hospitalizations/emergency department visits (all nominal P < 0.001). Compared with nonresponders, BICLA responders had greater improvements in global and organ-specific disease activity (Physician's Global Assessment, SLE Disease Activity Index 2000, Cutaneous Lupus Erythematosus Disease Area and Severity Index Activity, and joint counts; all nominal P < 0.001). BICLA responders had fewer lupus-related serious adverse events than nonresponders.
    Conclusion: BICLA response is associated with clinical benefit in SLE assessments, PROs, and medical resource utilization, confirming its value as a clinical trial end point that is associated with measures important to patient care.
    MeSH term(s) Adult ; Antibodies, Monoclonal, Humanized/therapeutic use ; Female ; Glucocorticoids/therapeutic use ; Humans ; Lupus Erythematosus, Systemic/diagnosis ; Lupus Erythematosus, Systemic/drug therapy ; Male ; Middle Aged ; Outcome Assessment, Health Care/methods ; Severity of Illness Index ; Treatment Outcome
    Chemical Substances Antibodies, Monoclonal, Humanized ; Glucocorticoids ; anifrolumab (38RL9AE51Q)
    Language English
    Publishing date 2021-09-22
    Publishing country United States
    Document type Clinical Trial, Phase III ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.41778
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