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1. Ioachimescu OC, Stoller JK: Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med; 2008 Apr;75(4):258, 260, 264-5 passim
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  • [Title] Diffuse alveolar hemorrhage: diagnosing it and finding the cause.
  • Diffuse alveolar hemorrhage is an acute, life-threatening event, and repeated episodes can lead to organizing pneumonia, collagen deposition in small airways, and, ultimately, fibrosis.
  • Among the many conditions it can accompany are Wegener granulomatosis, microscopic polyangiitis, Goodpasture syndrome, connective tissue disorders, antiphospholipid antibody syndrome, infectious or toxic exposures, and neoplastic conditions.
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / therapeutic use. Bronchoscopy. Humans. Immunosuppressive Agents / therapeutic use. Prognosis. Risk Factors. Vasculitis

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  • (PMID = 18491433.001).
  • [ISSN] 0891-1150
  • [Journal-full-title] Cleveland Clinic journal of medicine
  • [ISO-abbreviation] Cleve Clin J Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents
  • [Number-of-references] 62
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2. Obón Azuara B, Ortas Nadal MR, Gutiérrez Cía I, Bustamante Rodríguez R, Velilla Soriano C, Villanueva Anadón B: [Mortality due to heart involvement in the catastrophic antiphospholipid syndrome]. An Med Interna; 2008 May;25(5):229-30
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  • [Title] [Mortality due to heart involvement in the catastrophic antiphospholipid syndrome].
  • We reported a CAPS case, possibily afterward sting wasp triggering, with acute heart failure during evolution.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Heart Failure / etiology. Heart Failure / mortality
  • [MeSH-minor] Acute Disease. Fatal Outcome. Female. Humans. Middle Aged


3. Cervera R, CAPS Registry Project Group: Catastrophic antiphospholipid syndrome (CAPS): update from the 'CAPS Registry'. Lupus; 2010 Apr;19(4):412-8
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  • [Title] Catastrophic antiphospholipid syndrome (CAPS): update from the 'CAPS Registry'.
  • Although less than 1% of patients with the antiphospholipid syndrome (APS) develop the catastrophic variant, its potentially lethal outcome emphasizes its importance in clinical medicine today.
  • In order to put together all of the published case reports as well as the new diagnosed cases from all over the world, an international registry of patients with catastrophic APS (CAPS Registry) was created in 2000 by the European Forum on Antiphospholipid Antibodies (see http://www.med.ub.es/MIMMUN/FORUM/CAPS.HTM).
  • Currently, it documents the entire clinical, laboratory and therapeutic data of more than 300 patients whose data has been fully registered.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Registries
  • [MeSH-minor] Adolescent. Adult. Antibodies, Antiphospholipid / immunology. Catastrophic Illness. Child. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 20353979.001).
  • [ISSN] 1477-0962
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
  • [Investigator] Cervera R; Bucciarelli S; Espinosa G; Erkan D; Shoenfeld Y; Asherson RA; Amigo MC; Barile-Fabris L; Boffa JJ; Boffa MC; Chávez I; Chapman J; Davidson C; Denes AE; Derksen RH; Coto JF; Disdier P; Egan RM; Ehrenfeld M; Enriquez R; Falcini F; Fang LS; García-Carrasco M; Grandone JT; Gurjal A; Hayem G; Hughes GR; Inam S; Kant KS; Khamashta MA; Kitchens CS; Kupferminc MJ; de Larrañaga G; Levy RA; Lockshin MD; Lui SF; Maddison PJ; Mekori YA; Miyamae T; Moore J; Moutsopoulos HM; Muñoz-Rodríguez FJ; Musial J; Nakajima A; Neuwelt MC; Parke A; Piette JC; Praprotnik S; Roca B; Rojas-Rodriguez J; Roldan R; Sawitzke AD; Schaar CG; Shoenfeld Y; Sipek-Dolnicar A; Spyropoulos AC; Sinico R; Stojanovich L; Tan D; Tektonidou M; Veloso MP; Wislowska M
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4. Park JA, Yun JH, Kang HJ, Shin HY, Ahn HS: Acute intestinal pseudo-obstruction after induction treatment of relapsed acute promyelocytic leukemia with arsenic trioxide. Pediatr Blood Cancer; 2008 Apr;50(4):872-4
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  • [Title] Acute intestinal pseudo-obstruction after induction treatment of relapsed acute promyelocytic leukemia with arsenic trioxide.
  • Arsenic trioxide (As(2)O(3)) is an effective agent for the treatment of relapsed acute promyelocytic leukemia (APL).
  • We report a patient with intestinal pseudo-obstruction, which occurred while treating relapsed APL with As(2)O(3).
  • A 6-year-old female with relapsed APL developed paralytic ileus, hyperleukocytosis, and a high fever while being treated with As(2)O(3).
  • Pathologic findings revealed APL cells involving the entire intestinal layers.
  • This case history suggests that As(2)O(3) when used for reinduction therapy for APL may adversely affect the intestine and cause acute intestinal pseudo-obstruction.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Intestinal Pseudo-Obstruction / chemically induced. Intestinal Pseudo-Obstruction / pathology. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17635008.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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5. Kumar A, Malik F, Bhushan S, Sethi VK, Shahi AK, Kaur J, Taneja SC, Qazi GN, Singh J: An essential oil and its major constituent isointermedeol induce apoptosis by increased expression of mitochondrial cytochrome c and apical death receptors in human leukaemia HL-60 cells. Chem Biol Interact; 2008 Feb 15;171(3):332-47
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  • [Title] An essential oil and its major constituent isointermedeol induce apoptosis by increased expression of mitochondrial cytochrome c and apical death receptors in human leukaemia HL-60 cells.
  • An essential oil from a lemon grass variety of Cymbopogon flexuosus (CFO) and its major chemical constituent sesquiterpene isointermedeol (ISO) were investigated for their ability to induce apoptosis in human leukaemia HL-60 cells because dysregulation of apoptosis is the hallmark of cancer cells.
  • The easy and abundant availability of the oil combined with its suggested mechanism of cytotoxicity make CFO highly useful in the development of anti-cancer therapeutics.
  • [MeSH-major] Apoptosis / drug effects. Cytochromes c / biosynthesis. Leukemia, Promyelocytic, Acute / drug therapy. Mitochondria / drug effects. Oils, Volatile / pharmacology. Receptors, Tumor Necrosis Factor / biosynthesis. Receptors, Tumor Necrosis Factor, Type I / biosynthesis. Sesquiterpenes / pharmacology
  • [MeSH-minor] Caspase 8 / biosynthesis. Caspase 8 / drug effects. Caspase 8 / metabolism. Caspase 9 / drug effects. Caspase 9 / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cymbopogon / chemistry. DNA / drug effects. DNA / metabolism. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. HL-60 Cells. Humans. Molecular Conformation. NF-kappa B / biosynthesis. NF-kappa B / drug effects. Reactive Oxygen Species / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand. Signal Transduction / drug effects. Tumor Cells, Cultured. bcl-2-Associated X Protein / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18070620.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / NF-kappa B; 0 / Oils, Volatile; 0 / Reactive Oxygen Species; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Sesquiterpenes; 0 / TNFRSF10A protein, human; 0 / bcl-2-Associated X Protein; 0 / isointermedeol; 9007-43-6 / Cytochromes c; 9007-49-2 / DNA; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
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6. Cervera R, Espinosa G: Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies. Expert Opin Ther Targets; 2010 Dec;14(12):1279-82
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  • [Title] Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies.
  • The antiphospholipid syndrome is characterized by the presence of arterial or venous thrombosis or recurrent miscarriages in a patient with positive laboratory tests for antiphospholipid antibodies (anticardiolipin antibodies and/or lupus anticoagulant and/or anti-beta2-glycoprotein I).
  • Despite the strong association between antiphospholipid antibodies and thrombosis and obstetric morbidity, their pathogenic role in the development of these clinical features has not been fully elucidated.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / pharmacology. Anticoagulants / therapeutic use. Antiphospholipid Syndrome / drug therapy. Immunologic Factors / pharmacology
  • [MeSH-minor] Abortion, Habitual / immunology. Abortion, Habitual / pathology. Antibodies, Anticardiolipin / physiology. Antibodies, Antiphospholipid / immunology. Female. Humans. Lupus Coagulation Inhibitor / immunology. Lupus Coagulation Inhibitor / physiology. Pregnancy. Pregnancy Complications / drug therapy. Pregnancy Complications / immunology. Rituximab. Thrombosis / immunology. Thrombosis / pathology. Venous Thrombosis / immunology. beta 2-Glycoprotein I / immunology. beta 2-Glycoprotein I / physiology

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  • (PMID = 21058919.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Anticoagulants; 0 / Immunologic Factors; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I; 4F4X42SYQ6 / Rituximab
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7. Lee KW, Kim HJ, Lee YS, Park HJ, Choi JW, Ha J, Lee KT: Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte. Carcinogenesis; 2007 Sep;28(9):1928-36
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  • [Title] Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte.
  • We investigated the in vitro effects of acteoside on the proliferation, cell cycle regulation and differentiation of HL-60 human promyelocytic leukemia cells.
  • DNA flow cytometric analysis indicated that acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells.
  • Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by acteoside, whereas the steady-state level of CDK4 was unaffected.
  • The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after acteoside treatment in a time-dependent manner.
  • Our results further suggest that acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigen.
  • In conclusion, the onset of acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities.
  • These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of acteoside on human promyelocytic HL-60 cells.

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  • (PMID = 17634406.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Glucosides; 0 / Phenols; 0 / Stilbenes; 61276-17-3 / acteoside; 62229-50-9 / Epidermal Growth Factor; NI40JAQ945 / Tetradecanoylphorbol Acetate; Q369O8926L / resveratrol
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8. Shah AA, Higgins JP, Chakravarty EF: Thrombotic microangiopathic hemolytic anemia in a patient with SLE: diagnostic difficulties. Nat Clin Pract Rheumatol; 2007 Jun;3(6):357-62
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  • INVESTIGATIONS: At a general hospital, the investigations included brain MRI, echocardiography, laboratory tests including measurement of the amount of protein excreted daily, platelet count, levels of lactate dehydrogenase, creatinine and anticardiolipin antibodies, direct Coombs' test, peripheral blood smear, and measurement of blood pressure.
  • At a tertiary institution the investigations included physical examination, electroencephalography, brain MRI, magnetic resonance angiography, repetition of laboratory tests plus measurement of von Willebrand factor-cleaving protease activity, measurement of levels of antibodies to double-stranded DNA and platelets, and renal biopsy.
  • DIAGNOSIS: Thrombotic microangiopathic hemolytic anemia with a possible underlying diagnosis of malignant hypertension, antiphospholipid antibody syndrome, catastrophic antiphospholipid antibody syndrome, thrombotic thrombocytopenic purpura, or active SLE.
  • MANAGEMENT: At the general hospital, therapy included a single dose of intravenous cyclophosphamide 500 mg, eight daily plasma exchange treatments, three daily infusions of methylprednisolone 1 g followed by methylprednisolone 60 mg every 8 h, an infusion of rituximab 657 mg and ultrafiltration via hemodialysis.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Hypertension, Malignant / diagnosis. Lupus Erythematosus, Systemic / complications. Lupus Nephritis / diagnosis. Purpura, Thrombotic Thrombocytopenic / diagnosis. Purpura, Thrombotic Thrombocytopenic / therapy
  • [MeSH-minor] Adult. Anemia, Hemolytic / etiology. Diagnosis, Differential. Erythrocytes. Erythrocytes, Abnormal. Female. Humans. Plasma Exchange. Seizures / etiology. Thrombocytopenia / etiology. Vascular Diseases / complications. Vascular Diseases / etiology. Vascular Diseases / pathology

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  • (PMID = 17538567.001).
  • [ISSN] 1745-8382
  • [Journal-full-title] Nature clinical practice. Rheumatology
  • [ISO-abbreviation] Nat Clin Pract Rheumatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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9. Ashrafuzzaman M, Andersen OS, McElhaney RN: The antimicrobial peptide gramicidin S permeabilizes phospholipid bilayer membranes without forming discrete ion channels. Biochim Biophys Acta; 2008 Dec;1778(12):2814-22
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  • [Title] The antimicrobial peptide gramicidin S permeabilizes phospholipid bilayer membranes without forming discrete ion channels.
  • We examined the permeabilization of lipid bilayers by the beta-sheet, cyclic antimicrobial decapeptide gramicidin S (GS) in phospholipid bilayers formed either by mixtures of zwitterionic diphytanoylphosphatidylcholine and anionic diphytanoylphosphatidylglycerol or by single zwitterionic unsaturated phosphatidylcholines having various hydrocarbon chain lengths, with and without cholesterol.
  • In the zwitterionic bilayers formed by the phosphatidylcholines, without or with cholesterol, the peptide concentrations and membrane potentials required to initiate membrane permeabilization vary little as function of bilayer thickness and cholesterol content.
  • In the zwitterionic phosphatidylcholine bilayers, the effect of GS does not depend on the polarity of the transmembrane potential; however, in bilayers formed from mixtures of phosphatidylcholines and anionic phospholipids, the polarity of the transmembrane potential becomes important, with the GS-induced conductance events being much more frequent when the GS-containing solution is positive relative to the GS-free solution.
  • Overall, these results suggest that GS does not form discrete, well-defined, channel-like structures in phospholipid bilayers, but rather induces a wide variety of transient, differently sized defects which serve to compromise the bilayer barrier properties for small electrolytes.

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  • (PMID = 18809374.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM021342-26; United States / NIGMS NIH HHS / GM / R01 GM021342; United States / NIGMS NIH HHS / GM / GM 21342; United States / NIGMS NIH HHS / GM / R01 GM021342-26
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Ion Channels; 0 / Lipid Bilayers; 0 / Phospholipids; 1405-97-6 / Gramicidin
  • [Other-IDs] NLM/ NIHMS82601; NLM/ PMC2614689
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10. Russell AI, Cunninghame Graham DS, Chadha S, Roberton C, Fernandez-Hart T, Griffiths B, D'Cruz D, Nitsch D, Whittaker JC, Vyse TJ: No association between E- and L-selectin genes and SLE: soluble L-selectin levels do correlate with genotype and a subset in SLE. Genes Immun; 2005 Aug;6(5):422-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] No association between E- and L-selectin genes and SLE: soluble L-selectin levels do correlate with genotype and a subset in SLE.
  • Altered function of selectin glycoprotein adhesion molecules may modulate severity and organ-specific manifestations of autoimmune and inflammatory disease via changes in leukocyte trafficking.
  • We identified increased levels of soluble L-selectin (sL-selectin), but not soluble E-selectin (sE-selectin) in 278 European-Caucasian lupus patients compared to 230 healthy siblings (P=0.002).
  • sL-selectin levels were markedly elevated in patients with IgG antiphospholipid autoantibodies (P=0.002), suggesting that perhaps sL-selectin defines a subgroup of lupus with vasculopathy. sL-selectin level was also influenced by two L-selectin polymorphisms: 665C>T, F206L in the epidermal growth factor-like domain (P=0.015) and rs12938 in the 3'-untranslated region (P=0.06).
  • Having shown increased sL-selectin levels in lupus patients, we used genetics to investigate whether this was a secondary phenomena or the result of an underlying genetic mechanism.
  • [MeSH-major] E-Selectin / genetics. Genetic Predisposition to Disease. L-Selectin / genetics. Lupus Erythematosus, Systemic / genetics. Polymorphism, Single Nucleotide. Quantitative Trait Loci / genetics
  • [MeSH-minor] Adult. Antibodies, Antiphospholipid / blood. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Middle Aged. Risk Factors

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  • (PMID = 15902275.001).
  • [ISSN] 1466-4879
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / E-Selectin; 126880-86-2 / L-Selectin
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11. Takahashi S, Harigae H, Kameoka J, Sasaki T, Kaku M: AML1B transcriptional repressor function is impaired by the Flt3-internal tandem duplication. Br J Haematol; 2005 Aug;130(3):428-36
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  • Fms-like tyrosine kinase 3 (Flt3) is a type III receptor tyrosine kinase.
  • The internal tandem duplication (ITD) of the juxtamembrane region of this receptor is the most prevalent mutation in acute myeloid leukaemia (AML).
  • We recently reported that Flt3-ITD interferes with the transcriptional and biological action of promyelocytic leukaemia zinc finger transcriptional repressor by dissociating it from SMRT.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Gene Duplication. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences. Transcription Factors / metabolism
  • [MeSH-minor] Acute Disease. Animals. COS Cells. Core Binding Factor Alpha 2 Subunit. Humans. Mice. Nuclear Receptor Co-Repressor 2. RNA, Messenger / analysis. Repressor Proteins / metabolism. Transcription, Genetic. Transfection. Two-Hybrid System Techniques. fms-Like Tyrosine Kinase 3

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  • (PMID = 16042694.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / NCOR2 protein, human; 0 / Ncor2 protein, mouse; 0 / Nuclear Receptor Co-Repressor 2; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Runx1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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12. Pourrat O, Jollit C, Gombert JM, Boinot C, Pierre F: Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients. J Thromb Haemost; 2006 Oct;4(10):2276-7
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  • [Title] Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients.
  • [MeSH-major] Antiphospholipid Syndrome / classification. Antiphospholipid Syndrome / diagnosis
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. Female. Humans. Lupus Coagulation Inhibitor / blood. Partial Thromboplastin Time. Phospholipids / chemistry. Pregnancy. Pregnancy Complications / classification. Pregnancy Complications / diagnosis. Pregnancy Complications / immunology. Prognosis. Retrospective Studies

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  • [CommentOn] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]
  • (PMID = 16869832.001).
  • [ISSN] 1538-7933
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids
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13. Sato J, Kawakami T, Nakabayashi K, Fukuoka K, Hirano K, Terado Y, Yokoyama K, Ohtsuka T, Ohkura Y, Fujioka Y, Kurata A: Multiple aortic aneurysms complicated by a rupture in the systemic lupus erythematosus: a case report. Pathol Res Pract; 2008;204(11):845-50
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  • At 59 years of age, she was found to be affected by antiphospholipid antibody syndrome (APS).
  • Although SLE with APS is common, a complication of the disease by CMN, multiple AAs, or ruptured AA has been described in several cases to date.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Age of Onset. Antiphospholipid Syndrome / complications. Fatal Outcome. Female. Humans. Middle Aged

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  • (PMID = 18653288.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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14. Cavazzana A, Ruffatti A, Tonello M, Bortolati M, De Moerloose P, Reber G: An analysis of experimental conditions influencing the anti-beta2-glycoprotein I ELISA assay results. Ann N Y Acad Sci; 2007 Aug;1109:484-92
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  • [Title] An analysis of experimental conditions influencing the anti-beta2-glycoprotein I ELISA assay results.
  • Five components of the anti-beta(2)-glycoprotein I (abeta(2)GPI) enzyme-linked immunosorbent assay (ELISA) (coating buffer, microplate brand, blocking buffer, dilution buffer, and conjugate) were analyzed to evaluate how they affect variability in test results.
  • Thirty-two samples from patients with antiphospholipid syndrome (APS) positive for abeta(2)GPI IgG antibodies and three calibrators (a pool of abeta(2)GPI-positive patients, the monoclonal HCAL antibody, and a home-made calibrator) were tested.

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  • (PMID = 17785337.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Buffers; 0 / beta 2-Glycoprotein I
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15. Pierangeli SS, Vega-Ostertag M, Liu X, Girardi G: Complement activation: a novel pathogenic mechanism in the antiphospholipid syndrome. Ann N Y Acad Sci; 2005 Jun;1051:413-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complement activation: a novel pathogenic mechanism in the antiphospholipid syndrome.
  • Antiphospholipid antibodies (aPLs) have been shown to induce thrombosis, activate endothelial cells, and induce fetal loss.
  • The pathogenesis of aPL-induced thrombosis is incompletely understood, but it is thought to involve platelet and endothelial cell activation as well as pro-coagulant effects of aPL antibody directly on clotting pathway components.
  • Recent studies have shown that uncontrolled complement activation leads to fetal death in aPL-antibody treated mice.
  • We hypothesized that aPL antibodies activate complement, generating split products that induce thrombosis.
  • To test this hypothesis, we used an in vivo model of thrombosis in which aPL antibodies induce a significant increase in thrombus size and a mouse model of endothelial cell activation in which aPLs induce significant adhesion of leukocytes (WBCs) to endothelial cells.
  • We found that mice deficient in complement components C3 and C5 were resistant to enhanced thrombosis and endothelial cell activation induced by aPL antibodies.
  • Furthermore, inhibition of C5 activation using anti-C5 mAb prevented thrombophilia induced by aPL antibodies.
  • Our data show that complement activation mediates two important effectors of aPL antibodies: induction of thrombosis and endothelial activation.
  • [MeSH-major] Antiphospholipid Syndrome / etiology. Complement Activation
  • [MeSH-minor] Animals. Antibodies, Antiphospholipid / blood. Complement C3 / physiology. Complement C5 / physiology. Humans. Mice. Thrombosis / prevention & control

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  • (PMID = 16126983.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR 03034; United States / NIGMS NIH HHS / GM / S02 GM M 08248
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Complement C3; 0 / Complement C5
  • [Number-of-references] 39
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16. Glienke W, Chow KU, Bauer N, Bergmann L: Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds. Leuk Lymphoma; 2006 Aug;47(8):1629-38
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  • [Title] Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds.
  • Arsenic trioxide (As2O3) induces remission in patients with acute promyelocytic leukemia (APL).
  • The Wilms' tumor gene (wt1) is up-regulated in acute myeloid leukemia (AML) and a variety of leukemia cell lines.
  • The expression of wt1 in these cells is proposed to have an anti-apoptotic effect.
  • Low concentrations of 0.1 microM arsenic induced expression of the anti-apoptotic bcl-2 gene in both cell lines HL-60 and K562.
  • After arsenic treatment of the leukemia cell lines HL-60 and K562 the up-regulation of par-4 may contribute to the induction of apoptosis rather than down-regulation of bcl-2.
  • The therapeutic effect of arsenic is the induction of apoptosis by modulating the gene expression profile of pro- and anti-apoptotic genes including the wt1 gene.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Carrier Proteins / genetics. Leukemia / drug therapy. WT1 Proteins / genetics

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  • (PMID = 16966277.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / Arsenites; 0 / Carrier Proteins; 0 / Oxides; 0 / Sodium Compounds; 0 / WT1 Proteins; 0 / WTIP protein, human; 48OVY2OC72 / sodium arsenite; S7V92P67HO / arsenic trioxide
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17. Tussié-Luna MI, Rozo L, Roy AL: Pro-proliferative function of the long isoform of PML-RARalpha involved in acute promyelocytic leukemia. Oncogene; 2006 Jun 8;25(24):3375-86
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  • [Title] Pro-proliferative function of the long isoform of PML-RARalpha involved in acute promyelocytic leukemia.
  • The promyelocytic leukemia (PML) gene codes for a tumor suppressor protein that is associated with distinct subnuclear macromolecular structures called the PML bodies.
  • The PML gene is frequently involved in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL).
  • The translocation results in a fusion gene product, PML-RARalpha, in which the PML gene fuses to the retinoic acid receptor alpha (RARalpha) gene.
  • PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA).
  • However, there are several alternatively spliced isoforms of PML-RARalpha.
  • Here, we addressed the differences between the short and the long isoforms of PML-RARalpha (L and S) since both are associated with APL.
  • We demonstrate that PML-RARalphaL, but not PML-RARalphaS, can directly promote cell growth by transcriptionally activating the pro-proliferative gene, c-fos, in response to mitogenic stimulation.
  • The activity of the PML-RARalphaL is completely sensitive to ATRA.
  • Our results suggest that in addition to antagonizing the PML-tumor suppressor or the PML-pro-apoptotic activity, PML-RARalpha proteins can also directly promote cell growth by activating c-fos.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / metabolism. Neoplasm Proteins / chemistry. Oncogene Proteins, Fusion / chemistry

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  • (PMID = 16434964.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI056240
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-fos; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Hdac1 protein, mouse; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
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18. He J, Luster TA, Thorpe PE: Radiation-enhanced vascular targeting of human lung cancers in mice with a monoclonal antibody that binds anionic phospholipids. Clin Cancer Res; 2007 Sep 1;13(17):5211-8
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  • [Title] Radiation-enhanced vascular targeting of human lung cancers in mice with a monoclonal antibody that binds anionic phospholipids.
  • We recently showed that anionic phospholipids, principally phosphatidylserine, are specifically exposed on the luminal surface of tumor blood vessels.
  • Here we tested the hypothesis that radiation therapy can increase phosphatidylserine exposure on lung tumor vasculature, thereby enhancing the antitumor properties of the anti-phosphatidylserine antibody 2aG4.
  • Bavituximab, a chimeric version of 2aG4 in clinical trials, has the potential to enhance the therapeutic efficacy of radiation therapy in lung cancer patients.

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  • (PMID = 17785577.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Phosphatidylserines; 0 / bavituximab
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19. Vasse M: Protein Z, a protein seeking a pathology. Thromb Haemost; 2008 Oct;100(4):548-56
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  • Protein Z (PZ) is a vitamin K-dependent factor identified in human plasma in 1984 characterized by an homology with other vitamin K-dependent factors (factor VII, IX, X, protein C).
  • ZPI inhibits the activated factor X (FXa) on phospholipid surface.
  • In humans, PZ is characterized by an unusual wide distribution in plasma, and a major decrease induced by warfarin.
  • Unexpectedly, a relationship between PZ deficiency and ischemic arterial diseases such as stroke, acute coronary syndromes or peripheral arterial disease was described but not confirmed by all studies.
  • PZ deficiency could be also a risk factor for early fetal losses, and increases the arterial risk in antiphospholipid syndrome.

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  • (PMID = 18841275.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / plasma protein Z; 12001-79-5 / Vitamin K
  • [Number-of-references] 98
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20. Kim TM, Kim JS, Han SW, Hong YS, Kim I, Ha J, Kim SJ, Chung JW, Park JH, Lee D, Park S, Kim BK, Kim NK, Yoon SS: Clinical predictors of recurrent venous thromboembolism: a single institute experience in Korea. Thromb Res; 2009;123(3):436-43
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  • [Title] Clinical predictors of recurrent venous thromboembolism: a single institute experience in Korea.
  • Independent predictors for recurrent VTE were presence of residual thrombosis (hazard ratio [HR]=3.1, 95% confidence interval [CI] 1.0-9.3; p=0.044), antiphospholipid syndrome (APS) (HR=4.3, 95% CI 1.0-19.0; p=0.052), and age 50 years or younger (HR=2.5, 95% CI 1.0-6.6; p=0.053) by multivariate analysis.

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  • [CommentIn] Thromb Res. 2009 Jun;124(2):236 [18849061.001]
  • (PMID = 18579181.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants
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21. Yamaguchi Y, Usui N, Dobashi N, Yano S, Yahagi Y, Takei Y, Sugiyama K, Ogasawara Y, Saito T, Minami J, Kobayashi T, Katsube A, Kamiyama Y, Machishima T, Morikawa N, Otsubo H, Kaito K, Asai O, Aiba K: Gemtuzumab ozogamicin (GO) in relapsed/refractory patients with acute myeloid leukemia. Gan To Kagaku Ryoho; 2009 Jul;36(7):1105-9
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  • [Title] Gemtuzumab ozogamicin (GO) in relapsed/refractory patients with acute myeloid leukemia.
  • OBJECTIVE: Gemtuzumab ozogamicin (GO) is a humanized anti-CD33 antibody, linked to calicheamicin, which has been approved in Japan recently.
  • We conducted to evaluate the efficacy and toxicity of GO in our patients with relapsed or refractory AML retrospectively.
  • PATIENTS AND METHODS: Data were collected between March 1, 2000, and March 1, 2006, on 10 patients with relapsed or refractory AML(excluding FAB: M3).
  • No patient developed hepatic veno-occlusive disease including 2 patients who underwent HSCT.
  • CONCLUSION: GO is a valuable new treatment option for relapsed or refractory AML patients, however, the benefit from single agent appears insufficient.
  • On going clinical trials including combination with other antileukemic agents might better define the role of GO.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19620797.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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22. Nakano D, Matsumoto H, Yamaguchi T, Iwasaki Y, Ohashi M, Nunobe S, Iwanaga T, Takahashi K, Mori T: [CT-guided radiofrequency ablation therapy for pelvic recurrence from rectal carcinoma--a case report]. Gan To Kagaku Ryoho; 2008 Nov;35(12):2156-8
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  • A 48-year-old man, who had undergone a low anterior resection for advanced lower rectal cancer on May 27, 2003, was admitted to our hospital with anastomosis recurrence in November 2004.
  • Because of presence of complication of acute promyelocytic leukemia (APL), this patient had a poor general condition.
  • He died of APL on August 27, 2007.
  • [MeSH-minor] Biomarkers, Tumor / blood. Combined Modality Therapy. Humans. Leukemia, Promyelocytic, Acute / complications. Leukemia, Promyelocytic, Acute / drug therapy. Male. Middle Aged. Recurrence. Tomography, X-Ray Computed. Treatment Failure

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  • (PMID = 19106555.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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23. Amadori S, Stasi R: Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):95-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia.
  • PURPOSE OF REVIEW: This review addresses use of monoclonal antibodies and immunoconjugates to treat acute myeloid leukemia.
  • RECENT FINDINGS: Monoclonal antibodies used in acute myeloid leukemia have been directed against the antigens CD33, CD45, and CD66.
  • Unconjugated monoclonal antibodies such as lintuzumab have modest activity against overt acute myeloid leukemia but can eliminate minimal residual disease in acute promyelocytic leukemia.
  • Most experience with immunoconjugates is with gemtuzumab ozogamicin, an anti-CD33 monoclonal antibody linked to the potent antitumor antibiotic calicheamicin.
  • Gemtuzumab ozogamicin has shown activity both singly, particularly in acute promyelocytic leukemia, and combined with conventional cytotoxic chemotherapy.
  • The most promising results were obtained with radiolabeled anti-CD45 antibodies.
  • Antibodies reactive with CD66 have been used to deliver targeted radiation to hematopoietic tissues in patients with advanced myeloid malignancies.
  • SUMMARY: Both unlabeled monoclonal antibodies and immunoconjugates appear to have a limited role if used as single agents to treat acute myeloid leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoconjugates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Antigens, Differentiation, Myelomonocytic / drug effects. Antigens, Differentiation, Myelomonocytic / immunology. Clinical Trials as Topic. Humans

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  • (PMID = 18300754.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Immunoconjugates
  • [Number-of-references] 49
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24. Asherson RA, Gómez-Puerta JA, Marinopoulos G: Recurrent pulmonary thromboembolism in a patient with systemic lupus erythematosus and HIV-1 infection associated with the presence of antibodies to prothrombin: a case report. Clin Infect Dis; 2005 Nov 15;41(10):e89-92
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  • [Title] Recurrent pulmonary thromboembolism in a patient with systemic lupus erythematosus and HIV-1 infection associated with the presence of antibodies to prothrombin: a case report.
  • Antiphospholipid antibodies are demonstrable in patients with both conditions, but clinical manifestations of the antiphospholipid syndrome (APS) in HIV-infected patients, although reported, are uncommon.
  • METHODS: We describe a patient with HIV infection and SLE who manifested 4 episodes of deep vein thrombosis (DVT) complicated by pulmonary embolism.
  • Enzyme-linked immunosorbant assay was used to test for the presence of antiphospholipid antibodies, including anticardiolipin antibodies, anti- beta 2-glycoprotein 1 antibodies, and antiprothrombin antibodies (anti-PT).
  • RESULTS: We document the case of 35-year-old African woman with HIV infection and SLE who developed recurrent episodes of DVT and pulmonary embolism in the presence of anti-PT and discuss in depth the pathogenic role of these antibodies and the clinical challenges posed to clinicians by the coexistence of HIV and SLE in the same patient.
  • [MeSH-major] Antibodies / immunology. HIV Infections / complications. Lupus Erythematosus, Systemic / complications. Prothrombin / immunology. Pulmonary Embolism / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Anti-HIV Agents / therapeutic use. Anticoagulants / therapeutic use. Female. Humans. Venous Thrombosis / etiology. Warfarin / therapeutic use


25. Lindhoff-Last E, Luxembourg B: Evidence-based indications for thrombophilia screening. Vasa; 2008 Feb;37(1):19-30
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  • The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review.
  • In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation.
  • The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population.
  • Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history.
  • While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.
  • [MeSH-major] Anticoagulants / therapeutic use. Blood Coagulation / drug effects. Mass Screening. Patient Selection. Thrombophilia / diagnosis
  • [MeSH-minor] Abortion, Spontaneous / blood. Abortion, Spontaneous / etiology. Arterial Occlusive Diseases / blood. Arterial Occlusive Diseases / etiology. Contraceptives, Oral, Hormonal / adverse effects. Estrogen Replacement Therapy / adverse effects. Evidence-Based Medicine. Female. Genetic Predisposition to Disease. Humans. Male. Pedigree. Pre-Eclampsia / blood. Pre-Eclampsia / etiology. Pregnancy. Pregnancy Complications, Cardiovascular / blood. Pregnancy Complications, Cardiovascular / etiology. Risk Factors. Thromboembolism / blood. Thromboembolism / etiology. Venous Thrombosis / blood. Venous Thrombosis / etiology

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  • [CommentIn] Vasa. 2008 May;37(2):189; author reply 190-2 [18622971.001]
  • (PMID = 18512539.001).
  • [ISSN] 0301-1526
  • [Journal-full-title] VASA. Zeitschrift für Gefässkrankheiten
  • [ISO-abbreviation] VASA
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Contraceptives, Oral, Hormonal
  • [Number-of-references] 74
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26. Bérubé NG, Healy J, Medina CF, Wu S, Hodgson T, Jagla M, Picketts DJ: Patient mutations alter ATRX targeting to PML nuclear bodies. Eur J Hum Genet; 2008 Feb;16(2):192-201
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  • [Title] Patient mutations alter ATRX targeting to PML nuclear bodies.
  • ATRX associates with the nuclear matrix, pericentromeric heterochromatin, and promyelocytic leukemia nuclear bodies (PML-NBs) in a speckled nuclear staining pattern.
  • One of the latter domains is responsible for targeting ATRX to PML-NBs.
  • More importantly, four different patient mutations within this domain resulted in an approximately 80% reduction in the number of transfected cells with ATRX nuclear speckles and PML colocalization.
  • These results demonstrate that patient mutations have a dramatic effect on subnuclear targeting to PML-NBs.
  • Moreover, these findings support the hypothesis that ATRX patient mutations represent functional hypomorphs and suggest that loss of proper targeting to PML-NBs is an important contributor to the pathogenesis of the ATR-X syndrome.

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  • (PMID = 17957225.001).
  • [ISSN] 1018-4813
  • [Journal-full-title] European journal of human genetics : EJHG
  • [ISO-abbreviation] Eur. J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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27. Liu Y, Shevchenko A, Shevchenko A, Berk AJ: Adenovirus exploits the cellular aggresome response to accelerate inactivation of the MRN complex. J Virol; 2005 Nov;79(22):14004-16
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  • During adenovirus infection, the viral protein E4orf3 associates with MRN in promyelocytic leukemia protein nuclear bodies before MRN is bound by E1B-55K.

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  • (PMID = 16254336.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA064799; United States / NCI NIH HHS / CA / CA64799
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MRE11A protein, human; 0 / Multiprotein Complexes; 0 / NBN protein, human; 0 / Nuclear Proteins; 0 / Rad50 protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC1280221
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28. Melnick A: Predicting the effect of transcription therapy in hematologic malignancies. Leukemia; 2005 Jul;19(7):1109-17
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  • As a consequence, the three-dimensional structure of the target gene is altered and its potential to support transcription is increased or decreased.
  • The success of all-trans retinoic acid in the treatment of acute promyelocytic leukemia indicates that transcription therapy can be highly effective and safe.
  • A classification scheme of these therapeutic strategies is proposed herein, which allows predictions to be made regarding specificity, efficacy, disease spectrum and side effects.
  • This framework could help facilitate discussion of the mechanisms of action of transcription therapy drugs as well as the design of preclinical and clinical trials in the future.

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  • (PMID = 15858614.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA104348
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors
  • [Number-of-references] 114
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29. Parks J, Gyeltshen T, Prachyawarakorn V, Mahidol C, Ruchirawat S, Kittakoop P: Glutarimide alkaloids and a terpenoid benzoquinone from Cordia globifera. J Nat Prod; 2010 May 28;73(5):992-4
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  • Cordiarimide B (4) exhibited radical scavenging activity, as it inhibited superoxide anion radical formation in the xanthine/xanthine oxidase (XXO) assay, and also suppressed superoxide anion generation in differentiated HL-60 human promyelocytic leukemia cells when induced by 12-O-tetradecanoylphorbol-13-acetate (TPA).

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  • (PMID = 20384317.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Benzoquinones; 0 / Free Radical Scavengers; 0 / Piperidones; 0 / Terpenes; 0 / cordiarimide A; 0 / cordiarimide B; 0 / globiferane; 11062-77-4 / Superoxides; 3T006GV98U / benzoquinone; EC 1.17.3.2 / Xanthine Oxidase; NI40JAQ945 / Tetradecanoylphorbol Acetate
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30. Ishimaru C, Yonezawa Y, Kuriyama I, Nishida M, Yoshida H, Mizushina Y: Inhibitory effects of cholesterol derivatives on DNA polymerase and topoisomerase activities, and human cancer cell growth. Lipids; 2008 Apr;43(4):373-82
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  • Compounds 2, 3 and 6 inhibited the activity of human topo II, with IC50 values of 5.0, 12.5 and 120 microM, respectively.
  • Compounds 2, 3 and 6 also suppressed human cancer cell (promyelocytic leukemia cell line, HL-60) growth, and LD50 values were 8.8, 20.2 and 72.3 microM, respectively, suggesting that cell growth inhibition had the same tendency as the inhibition of topos rather than pols.
  • From these findings, the action mode of cholesterol derivatives as anti-cancer compounds is discussed.

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  • (PMID = 18214566.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Topoisomerase Inhibitors; 97C5T2UQ7J / Cholesterol; EC 2.7.7.7 / DNA-Directed DNA Polymerase; EC 5.99.1.- / DNA Topoisomerases
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31. Ma Z, Saluta G, Kucera GL, Bierbach U: Effect of linkage geometry on biological activity in thiourea- and guanidine-substituted acridines and platinum-acridines. Bioorg Med Chem Lett; 2008 Jul 1;18(13):3799-801
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  • Novel thiourea- and guanidine-modified acridine-4-carboxamides (4, 7) and a corresponding platinum-intercalator conjugate (4') have been synthesized and evaluated as cytotoxic agents in human promyelocytic leukemia, HL-60, and a non-small cell lung cancer, NCI-H460.
  • Modification of thiourea sulfur in derivative 4 with a DNA platinating moiety, giving 4', resulted in a pronounced cytotoxic enhancement, and the conjugate proved to be the most active of the newly synthesized compounds in NCI-H460 cells.

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  • (PMID = 18515101.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101880-04; United States / NCI NIH HHS / CA / R01 CA101880; United States / NCI NIH HHS / CA / CA101880; United States / NCI NIH HHS / CA / R01 CA101880-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acridines; 0 / Antineoplastic Agents; 141-83-3 / guanidine carboxamide; 49DFR088MY / Platinum; 8W8T17847W / Urea; GYV9AM2QAG / Thiourea; JU58VJ6Y3B / Guanidine
  • [Other-IDs] NLM/ NIHMS57183; NLM/ PMC2474763
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32. Krejcí J, Harnicarová A, Kůrová J, Uhlírová R, Kozubek S, Legartová S, Hájek R, Bártová E: Nuclear organization of PML bodies in leukaemic and multiple myeloma cells. Leuk Res; 2008 Dec;32(12):1866-77
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  • [Title] Nuclear organization of PML bodies in leukaemic and multiple myeloma cells.
  • The nuclear arrangement of promyelocytic leukaemia nuclear bodies (PML NBs) was studied in vitro after the cell treatment by clinically used agents such as all-trans retinoic acid (RA) in human leukaemia and cytostatics or gamma radiation in multiple myeloma cells.
  • In addition, the influence of phorbol ester (PMA) on PML NBs formation was analyzed.
  • A reduced number of PML bodies, which led to relocation of PML NBs closer to the nuclear interior, mostly accompanied RA- and PMA-induced differentiation.
  • Centrally located PML NBs were associated with transcriptional protein RNAP II and SC35 regions, which support importance of PML NBs in RNA processing that mostly proceeds within the nuclear interior.
  • Conversely, the quantity of PML NBs was increased after cytostatic treatment, which caused re-distribution of PML NBs closer to the nuclear envelope.
  • Here we showed correlations between the number of PML NBs and average Centre-to-PML distances.
  • Moreover, a number of cells in S phase, especially during differentiation, influenced number of PML NBs.
  • Studying the proteins involved in PML compartment, such as c-MYC, cell-type specific association of c-MYC and the PML NBs was observed in selected leukaemic cells undergoing differentiation, which was accompanied by c-MYC down-regulation.
  • [MeSH-major] Cell Cycle / physiology. Cell Nucleus / pathology. Intranuclear Inclusion Bodies / pathology. Leukemia, Promyelocytic, Acute / pathology. Multiple Myeloma / pathology


33. Estey E: Therapeutic research in untreated acute promyelocytic leukemia. Leukemia; 2005 Jun;19(6):913-5
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  • [Title] Therapeutic research in untreated acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • [CommentOn] Leukemia. 2005 Jun;19(6):978-83 [15843821.001]
  • (PMID = 15843820.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 16
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34. Luo RQ, Lei YX, Zhang X, Liang F: [Clinical analysis of patients with systemic lupus erythematosus and concomitant pulmonary hypertension]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Oct;28(10):1860-3
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  • [Title] [Clinical analysis of patients with systemic lupus erythematosus and concomitant pulmonary hypertension].
  • OBJECTIVE: To investigate the clinical manifestations, diagnosis and interventions of pulmonary hypertension (PAH) in patients with systemic lupus erythematosus (SLE).
  • METHODS: From January 2001 to December 2007, 798 SLE patients without prior diagnosis were admitted in our hospital, among whom 39 were identified to have concomitant PAH defined by echocardiography.
  • The clinical data of the 39 cases were analyzed retrospectively.
  • The 39 SLE patients with concomitant PAH included 5 men and 34 women with a mean age of 34-/+12 years.
  • Positive correlations were found between the occurrence of PAH and the Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia (P < 0.05).
  • Patients with higher scores for SLE Disease Activity Index were liable to PAH.
  • The presence of Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia is correlated to greater severity PAH with poor prognosis.
  • CONCLUSION: PAH is not a rare concomitant disease in SLE patients.
  • The presence of Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia all suggest the likeliness of PAH in SLE patients, and echocardiographic examination may help derive an early diagnosis.
  • [MeSH-major] Hypertension, Pulmonary / complications. Hypertension, Pulmonary / diagnosis. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. China / epidemiology. Early Diagnosis. Echocardiography. Female. Humans. Male. Middle Aged. Raynaud Disease / complications. Retrospective Studies


35. Berman JN, Look AT: Targeting transcription factors in acute leukemia in children. Curr Drug Targets; 2007 Jun;8(6):727-37
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  • [Title] Targeting transcription factors in acute leukemia in children.
  • In many childhood acute leukemias, transcription factors are altered through chromosomal translocations that change their functional properties resulting in repressed activity or inappropriate activation.
  • The development of therapies that specifically target these molecular abnormalities holds promise for improving the outcome in diseases that remain challenging to treat, such as childhood T-cell acute lymphoblastic leukemia and acute myeloid leukemia, with improved toxicity profiles.
  • All trans-retinoic acid and arsenic trioxide have already demonstrated efficacy in acute promyelocytic leukemia in both adults and children.
  • Newer agents, such as histone deacetylase inhibitors, drugs targeting the NOTCH pathway, and short interfering RNAs have shown encouraging results in pre-clinical studies and are likely to enter the clinical arena in the near future.
  • Through an improved understanding of the pathways and mechanisms underlying the malignant transformation induced by altered transcription factors, new targeted therapies will be designed that should greatly enhance current available treatments.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia / drug therapy. Transcription Factors / drug effects
  • [MeSH-minor] Acute Disease. Arsenicals / pharmacology. Arsenicals / therapeutic use. Child. DNA Methylation / drug effects. Histone Deacetylase Inhibitors. Humans. Oxides / pharmacology. Oxides / therapeutic use. Tretinoin / pharmacology. Tretinoin / therapeutic use

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  • (PMID = 17584028.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Histone Deacetylase Inhibitors; 0 / Oxides; 0 / Transcription Factors; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 113
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36. Narita T, Suga A, Kobayashi M, Hashimoto K, Sakagami H, Motohashi N, Kurihara T, Wakabayashi H: Tumor-specific cytotoxicity and type of cell death induced by benzo[b]cyclohept[e][1,4]oxazine and 2-aminotropone derivatives. Anticancer Res; 2009 Apr;29(4):1123-30
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  • [Title] Tumor-specific cytotoxicity and type of cell death induced by benzo[b]cyclohept[e][1,4]oxazine and 2-aminotropone derivatives.
  • The highly active derivatives, 7-bromo-2-(4-hydroxyanilino)tropone [16] and 4-isopropyl-2-(2-hydroxyanilino)tropone [20], induced internucleosomal DNA fragmentation and caspase-3, -8 and -9 activation in human promyelocytic leukemia HL-60 cells, but only at concentrations twice or four times higher than CC(50) values.

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  • (PMID = 19414354.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-aminotropone; 0 / 4-isopropyl-2-(2-hydroxyanilino)tropone; 0 / 7-bromo-2-(4-hydroxyanilino)tropone; 7L6DL16P1T / Tropolone; EC 3.4.22.- / Caspases
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37. Hwang J, Kalejta RF: Human cytomegalovirus protein pp71 induces Daxx SUMOylation. J Virol; 2009 Jul;83(13):6591-8
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  • A component of promyelocytic leukemia nuclear bodies, Daxx is a transcriptional corepressor that silences the expression of viral immediate-early (IE) genes at the start of both lytic and quiescent HCMV infections. pp71 is a tegument component delivered directly to cells by infecting HCMV virions.
  • Here we report that pp71 also substantially increases the basal level of SUMOylated Daxx observed in cells.
  • Thus, while pp71 enhances the basal level of SUMOylated Daxx, the role that this modification plays in regulating Daxx activity in uninfected or HCMV-infected cells remains an enigma.

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  • (PMID = 19369322.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI074984; United States / NIAID NIH HHS / AI / R56 AI064703; United States / NIAID NIH HHS / AI / R01-AI074984; United States / NIAID NIH HHS / AI / R56-AI064703
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DAXX protein, human; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Viral Proteins; 107852-97-1 / cytomegalovirus phosphoprotein 71kDa
  • [Other-IDs] NLM/ PMC2698545
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38. Johnson JE, Varkonyi RJ, Schwalm J, Cragle R, Klein-Szanto A, Patchefsky A, Cukierman E, von Mehren M, Broccoli D: Multiple mechanisms of telomere maintenance exist in liposarcomas. Clin Cancer Res; 2005 Aug 1;11(15):5347-55
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  • EXPERIMENTAL DESIGN: Tumor samples were analyzed with respect to telomerase activity, telomere length, and the presence of ALT-specific subcellular structures, ALT-associated promyelocytic leukemia nuclear bodies.
  • In addition, telomere length was always shorter in recurrent disease, regardless of the telomere maintenance mechanism.

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  • (PMID = 16061847.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA006927; United States / NCI NIH HHS / CA / CA098087-03; United States / NCI NIH HHS / CA / CA109442-01; United States / NCI NIH HHS / CA / T32 CA09035-29
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nucleoproteins; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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39. Dikmen M, Canturk Z, Ozturk Y, Tunali Y: Investigation of the apoptotic effect of curcumin in human leukemia HL-60 cells by using flow cytometry. Cancer Biother Radiopharm; 2010 Dec;25(6):749-55
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  • [Title] Investigation of the apoptotic effect of curcumin in human leukemia HL-60 cells by using flow cytometry.
  • Curcumin exhibits a variety of pharmacological effects including antitumor, anti-inflammatory, and anti-infectious activities.
  • In the present study, the effects of curcumin on apoptosis in the acute promyelocytic human leukemia (HL-60) cells was evaluated.
  • Concentrations of 15, 20, and 40 μM curcumin significantly reduced cell proliferations.
  • When HL-60 cells were treated with 10, 15, 20, and 40 μM concentration of curcumin, apoptotic rates were determined as 1.2, 81.1, 84.5, and 88.6%, respectively.
  • It was suggested that curcumin may have a potential therapeutic role for human leukemia.
  • [MeSH-minor] Caspase 3 / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Leukemia / drug therapy

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  • (PMID = 21204771.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
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40. Donadini MP, Crowther M: Antiphospholipid syndrome: a challenging hypercoagulable state with systemic manifestations. Hematol Oncol Clin North Am; 2010 Aug;24(4):669-76, vii
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  • [Title] Antiphospholipid syndrome: a challenging hypercoagulable state with systemic manifestations.
  • Antiphospholipid syndrome (APS) is a systemic disease that causes venous and arterial thrombosis in virtually any organ and is responsible for fetal losses and pregnancy disorders.
  • The spectrum of clinical manifestations is wide, because the thrombotic process may involve arterial and venous vessels of any size in any organ.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Thrombophilia / diagnosis

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20659651.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Makhoul BF, Guralnik L, Azzam ZS: Catastrophic antiphospholipid syndrome presented with abdominal, pulmonary, and bone marrow complications. Rheumatol Int; 2010 Jan;30(3):401-4
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  • [Title] Catastrophic antiphospholipid syndrome presented with abdominal, pulmonary, and bone marrow complications.
  • We are presenting a case of catastrophic antiphospholipid syndrome in an adult female manifesting with abdominal thrombosis, pancytopenia, and alveolar hemorrhage.
  • The diagnosis should be made promptly based on clinical symptoms coupled with radiological features.
  • Once this diagnosis is suspected, treatment with corticosteroids and anticoagulation must be initiated as soon as possible in order to reduce severe morbidity and high mortality.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Hemorrhage / etiology. Lung Diseases / etiology. Pancytopenia / etiology. Thrombosis / etiology
  • [MeSH-minor] Abdominal Pain / etiology. Acute Disease / therapy. Anticoagulants / therapeutic use. Dyspnea / etiology. Dyspnea / physiopathology. Female. Humans. Lung / diagnostic imaging. Lung / pathology. Lung / physiopathology. Middle Aged. Pleural Effusion / diagnostic imaging. Pleural Effusion / etiology. Pleural Effusion / pathology. Portal Vein / pathology. Portal Vein / physiopathology. Pulmonary Alveoli / pathology. Pulmonary Alveoli / physiopathology. Steroids / therapeutic use. Tomography, X-Ray Computed. Treatment Outcome


42. Saito T, Ikezoe T, Daibata M, Takeuchi T, Ohtsuki Y, Taguchi H, Miyoshi I: Disseminated mucormycosis (zygomycosis) in acute myeloid leukemia. Intern Med; 2006;45(18):1073-4
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  • [Title] Disseminated mucormycosis (zygomycosis) in acute myeloid leukemia.
  • [MeSH-major] Dexamethasone / adverse effects. Glucocorticoids / adverse effects. Immunocompromised Host. Leukemia, Promyelocytic, Acute / immunology. Mucormycosis / etiology

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  • (PMID = 17043382.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone
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43. Ieko M, Naito S, Yoshida M: [Laboratory examinations in antiphospholipid syndrome]. Rinsho Byori; 2010 Apr;58(4):343-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Laboratory examinations in antiphospholipid syndrome].
  • Antiphospholipid syndrome (APS), formerly detected by the association between clinical events (venous/arterial thrombosis or pregnancy morbidity) and positivity in at least one of the laboratory tests used to detect antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), IgG- or IgM-class anticardiolipin antibodies (aCL), and IgG or IgM-class anti-beta2GPI antibodies (abeta2GPI), is now diagnosed using revised APS classification criteria.
  • However, there are a number of problems with the methods used to detect aPL.
  • According to the guidelines for detection of LA recently published by ISTH-SSC, APTT reagents with silica as an activator and double centrifugation-treated samples (including control plasma) are recommended to detect LA, while 50% patient plasma mixed with control plasma is recommended for a cross-mixing test.
  • In the present study, we obtained favorable results for LA detection with cross-mixing tests by measuring APTT in mixtures of control plasma with 0%, 10%, 20%, 50%, and 100% concentrations of patient plasma treated with a 0.2 microm filter.
  • In the future, laboratory examinations for APS will change with diagnostic criteria, as APS has not yet been established as a distinct disease concept.
  • [MeSH-major] Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / diagnosis

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  • (PMID = 20496762.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Biomarkers; 0 / Lupus Coagulation Inhibitor; 0 / Reagent Kits, Diagnostic; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 27
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44. Carmona F, Lázaro I, Reverter JC, Tàssies D, Font J, Cervera R, Balasch J: Impaired factor XIIa-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications. Am J Obstet Gynecol; 2006 Feb;194(2):457-65
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  • [Title] Impaired factor XIIa-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
  • OBJECTIVE: The objective of the study was to investigate the potential role of impaired factor XII-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
  • STUDY DESIGN: This was a prospective study in a third-level teaching hospital, including 75 patients: 25 pregnant patients having the antiphospholipid syndrome and carrying their pregnancies until 26 weeks' gestation or later (group 1); 25 pregnant patients having normal term pregnancies and delivery and no previous miscarriage (group 2); and 25 pregnant patients being diagnosed as having severe pre-eclampsia and/or intrauterine growth restriction but testing negative for antiphospholipid antibodies (group 3).
  • RESULTS: Patients in group 1 were characterized by increased factor VIIa levels, increased prothrombin fragment 1+2 levels, reduced factor XIIa levels, diminished functional urokinase-type plasminogen activator levels, and decreased levels of plasmin/alpha-2-plasmin inhibitor complexes.
  • CONCLUSIONS: Impaired factor XIIa-dependent activation of fibrinolysis seems to be a key mechanism related to late-pregnancy complications in patients with the antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Factor XIIa / physiology. Fibrinolysis / physiology. Pregnancy Complications / physiopathology

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  • (PMID = 16458646.001).
  • [ISSN] 1097-6868
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Coagulation Factors; EC 3.4.21.38 / Factor XIIa
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45. Pu YS, Jan KY, Wang TC, Wang AS, Gurr JR: 8-Oxoguanine DNA glycosylase and MutY homolog are involved in the incision of arsenite-induced DNA adducts. Toxicol Sci; 2007 Feb;95(2):376-82
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  • Treatment of human promyelocytic leukemia NB4 cells with 0.5muM As(2)O(3) for 30 min induced no DNA breaks, as analyzed by a standard comet assay.

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  • (PMID = 17101720.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / DNA Adducts; 0 / Environmental Pollutants; 0 / Ferrous Compounds; 0 / Oxides; 39R4TAN1VT / ferrous sulfate; BBX060AN9V / Hydrogen Peroxide; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human; S7V92P67HO / arsenic trioxide
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46. Rainaldi G, Romano R, Indovina P, Ferrante A, Motta A, Indovina PL, Santini MT: Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used. Radiat Res; 2008 Feb;169(2):170-80
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  • [Title] Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used.
  • High-resolution proton nuclear magnetic resonance ((1)H-NMR) spectroscopy was used to examine and compare the metabolic variations that occur in cells of the HL60 promyelocytic leukemia cell line after induction of apoptosis by ionizing radiation and the antineoplastic drug doxorubicin as well as after induction of necrosis by heating.

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  • (PMID = 18220461.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cytotoxins; 0 / Proteome; 0 / Protons; 80168379AG / Doxorubicin
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47. Lindhoff-Last E, Luxembourg B, Pabinger I: [Update thrombophilia]. Hamostaseologie; 2008 Dec;28(5):365-75
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  • A survey on definitions, epidemiology, clinical manifestations of congenital and acquired thrombophilias is given with focus on evidence-based data.
  • The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population.
  • Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis to be able to decide whether anticoagulation is necessary when these patients become pregnant.

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  • (PMID = 19132167.001).
  • [ISSN] 0720-9355
  • [Journal-full-title] Hämostaseologie
  • [ISO-abbreviation] Hamostaseologie
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V; 9001-26-7 / Prothrombin; 9001-27-8 / Factor VIII; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 3.4.21.5 / Thrombin
  • [Number-of-references] 136
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48. Lopes AA: Pathophysiological basis for anticoagulant and antithrombotic therapy in pulmonary hypertension. Cardiovasc Hematol Agents Med Chem; 2006 Jan;4(1):53-9
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  • [Title] Pathophysiological basis for anticoagulant and antithrombotic therapy in pulmonary hypertension.
  • In pulmonary hypertension (PH), thrombosis and thromboembolism may occur as primary events associated with inherited or acquired thrombophilia.
  • Alternatively, in situ thrombosis may develop as a complication of pre-existing vasculopathy as in the case of idiopathic PH and related disorders (so called pulmonary arterial hypertension).
  • These abnormalities are suggestive of a shift of pulmonary vascular microenvironment toward a procoagulant, prothrombotic and antifibrinolytic pattern.
  • The abnormalities described so far include circulating antiphospholipid antibodies, increased plasma levels of platelet aggregating agents (serotonin, thromboxane), adhesion molecules (P-selectin, von Willebrand factor), antifibrinolytic enzymes (plasminogen activator inhibitor 1) and cytokines.
  • The present review is focused on the procoagulant, prothrombotic and antifibrinolytic mechanisms so far identified in PH, in both clinical setting and animal models.
  • [MeSH-major] Anticoagulants / therapeutic use. Fibrinolytic Agents / therapeutic use. Hypertension, Pulmonary / drug therapy. Hypertension, Pulmonary / physiopathology

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  • (PMID = 16529549.001).
  • [ISSN] 1871-5257
  • [Journal-full-title] Cardiovascular & hematological agents in medicinal chemistry
  • [ISO-abbreviation] Cardiovasc Hematol Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Fibrinolytic Agents
  • [Number-of-references] 88
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49. Rosen BP, Tamás MJ: Arsenic transport in prokaryotes and eukaryotic microbes. Adv Exp Med Biol; 2010;679:47-55
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  • As- and Sb-containing compounds are toxic to cells, yet both metalloids are used as chemotherapeutic agents for treating acute promyelocytic leukemia and diseases caused by protozoan parasites.

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  • (PMID = 20666223.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R37 GM055425; United States / NIAID NIH HHS / AI / AI043428; United States / NIGMS NIH HHS / GM / GM55425
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporins; 0 / Arsenicals; 0 / Metals; 9IT35J3UV3 / Antimony; N712M78A8G / Arsenic
  • [Number-of-references] 61
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50. Harder J, Thürmel K, Maier M, Lanzl I: [Bilateral recurrent retinal thrombosis in a young man]. Ophthalmologe; 2009 Oct;106(10):924-7
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  • An antiphospholipid antibody syndrome was diagnosed which was treated with anticoagulants.
  • [MeSH-major] Anticoagulants / therapeutic use. Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / drug therapy. Retinal Diseases / diagnosis. Retinal Diseases / therapy. Thrombosis / diagnosis. Thrombosis / drug therapy
  • [MeSH-minor] Adult. Humans. Macular Edema / diagnosis. Macular Edema / drug therapy. Male. Secondary Prevention. Treatment Outcome

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  • [Cites] Semin Thromb Hemost. 1999;25(3):333-50 [10443963.001]
  • [Cites] Ophthalmology. 2002 Jan;109(1):126-31 [11772591.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1827-32 [12393574.001]
  • [Cites] JAMA. 2006 Mar 1;295(9):1050-7 [16507806.001]
  • (PMID = 19495773.001).
  • [ISSN] 1433-0423
  • [Journal-full-title] Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft
  • [ISO-abbreviation] Ophthalmologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticoagulants
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51. Lou YJ, Pan XR, Jia PM, Li D, Xiao S, Zhang ZL, Chen SJ, Chen Z, Tong JH: IRF-9/STAT2 [corrected] functional interaction drives retinoic acid-induced gene G expression independently of STAT1. Cancer Res; 2009 Apr 15;69(8):3673-80
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  • Retinoic acid-induced gene G (RIG-G), a gene originally identified in all-trans retinoic acid-treated NB4 acute promyelocytic leukemia cells, is also induced by IFNalpha in various hematopoietic and solid tumor cells.
  • Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid.
  • [MeSH-major] Gene Expression Regulation, Leukemic / physiology. Interferon-Stimulated Gene Factor 3, gamma Subunit / metabolism. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Promyelocytic, Acute / genetics. STAT1 Transcription Factor / metabolism. STAT2 Transcription Factor / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Interferon Regulatory Factor-1 / genetics. Interferon Regulatory Factor-1 / metabolism. Interferon-alpha / metabolism. Phosphorylation. Promoter Regions, Genetic. RNA, Small Interfering. Signal Transduction. Tretinoin / pharmacology

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  • [ErratumIn] Cancer Res. 2009 May 15;69(10):4553
  • (PMID = 19351818.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IFIT3 protein, human; 0 / IRF9 protein, human; 0 / Interferon Regulatory Factor-1; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Interferon-alpha; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / STAT2 Transcription Factor; 0 / STAT2 protein, human; 5688UTC01R / Tretinoin
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52. Rego EM, Ruggero D, Tribioli C, Cattoretti G, Kogan S, Redner RL, Pandolfi PP: Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR alpha, PLZF/RAR alpha or NPM/RAR alpha. Oncogene; 2006 Mar 23;25(13):1974-9
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  • [Title] Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR alpha, PLZF/RAR alpha or NPM/RAR alpha.
  • Recurrent chromosomal translocations involving the RAR alpha locus on chromosome 17 are the hallmark of acute promyelocytic leukemia (APL).
  • The RAR alpha gene fuses to variable partners (PML, PLZF, NPM, NuMA and STAT5B: X genes) leading to the expression of APL-specific fusion proteins with identical RAR alpha moieties.
  • To analyse whether the variable X moiety could affect the activity of the fusion protein in vivo, we generated and characterized, on a comparative basis, NPM/RAR alpha transgenic mice (TM) in which the fusion gene is expressed under the control of a human Cathepsin G (hCG) minigene.
  • We compared the features of the leukemia observed in these TM with those in hCG-PML/RAR alpha and hCG-PLZF/RAR alpha TM.
  • In all three transgenic models, leukemia developed after a variably long latency, with variable penetrance.
  • However, the three leukemias displayed distinct cytomorphological features. hCG-NPM/RAR alpha leukemic cells resembled monoblasts.
  • This phenotype contrasts with what was observed in the hCG-PML/RAR alpha TM model in which the leukemic phase was characterized by the proliferation of promyelocytic blasts.
  • Similarly, hCG-PLZF/RAR alpha TM displayed a different phenotype where terminally differentiated myeloid cells predominated.
  • Importantly, the NPM/RAR alpha oncoprotein was found to localize in the nucleolus, unlike PML/RAR alpha and PLZF/RAR alpha, thus possibly interfering with the normal function of NPM.
  • Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments.
  • Taken together, our results underscore the critical relevance of the X moiety in dictating the biology of the disease and the activity of the APL fusion oncoprotein.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Fusion. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Receptors, Retinoic Acid / genetics. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16331271.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-74031
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Zbtb16 protein, mouse; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human; 147855-37-6 / ZBTB16 protein, human; 5688UTC01R / Tretinoin; EC 3.4.- / Cathepsins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.20 / CTSG protein, human; EC 3.4.21.20 / Cathepsin G; EC 3.4.21.20 / Ctsg protein, mouse
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53. Mathews V, Thomas M, Srivastava VM, George B, Srivastava A, Chandy M: Impact of FLT3 mutations and secondary cytogenetic changes on the outcome of patients with newly diagnosed acute promyelocytic leukemia treated with a single agent arsenic trioxide regimen. Haematologica; 2007 Jul;92(7):994-5
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  • [Title] Impact of FLT3 mutations and secondary cytogenetic changes on the outcome of patients with newly diagnosed acute promyelocytic leukemia treated with a single agent arsenic trioxide regimen.
  • Ninety-eight newly diagnosed cases of PML-RARalpha positive APL were treated with a regimen of single agent ATO.
  • FLT3 activating mutations were seen in 33% and an additional cytogenetic finding was noted in 23.2%.
  • FLT3 activating mutations were significantly associated with a bcr3 PML-RARalpha isoform (p=0.012) and a delay in achieving a molecular remission (p=0.022).
  • Neither FLT3 activating mutations nor secondary cytogenetic changes had an impact on clinical outcome.
  • [MeSH-major] Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / diagnosis. Mutation. Oxides / therapeutic use. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17606455.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; S7V92P67HO / arsenic trioxide
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54. Nestvold JM, Omdal BK, Dai KZ, Martens A, Benestad HB, Vaage JT, Rolstad B: A second prophylactic MHC-mismatched bone marrow transplantation protects against rat acute myeloid leukemia (BNML) without lethal graft-versus-host disease. Transplantation; 2008 Jan 15;85(1):102-11
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  • [Title] A second prophylactic MHC-mismatched bone marrow transplantation protects against rat acute myeloid leukemia (BNML) without lethal graft-versus-host disease.
  • BACKGROUND: We have employed a rat model for human acute myeloid leukemia, a promyelocytic leukemia in the BN rat strain (BNML), to develop new protocols for immunotherapy in combination with allogeneic bone marrow transplantation (alloBMT).
  • In addition to T or natural killer (NK) cells, we introduced a second infusion of bone marrow cells as prophylactic donor lymphocyte infusions (DLI) to test whether an effective graft-versus-leukemia (GVL) response could be obtained without clinical graft-versus-host disease (GVHD).
  • METHODS: BN rats were sublethally irradiated and transplanted with T-cell depleted bone marrow cells from either fully major histocompatibility complex (MHC)-mismatched (PVG) donor rats or MHC-matched (PVG.1N) as controls.
  • Seven days after transplantation, rats were given 500 leukemic cells to mimic minimal residual disease.
  • RESULTS: Rats receiving infusions of NK cells succumbed to leukemia.
  • A second alloBMT protected against leukemia.
  • If applicable to humans, repeated alloBMT may provide a novel approach to leukemia therapy.
  • [MeSH-major] Bone Marrow Transplantation / immunology. Bone Marrow Transplantation / methods. Graft vs Host Disease / prevention & control. Leukemia, Myeloid, Acute / therapy. Major Histocompatibility Complex / immunology
  • [MeSH-minor] Animals. Chimerism. Disease Models, Animal. Graft vs Leukemia Effect. Immunotherapy / methods. Killer Cells, Natural / immunology. Killer Cells, Natural / pathology. Killer Cells, Natural / physiology. Male. Neoplasm, Residual / immunology. Rats. Rats, Inbred BN. Rats, Nude. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / physiology

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  • [CommentIn] Transplantation. 2008 Jan 15;85(1):7-8 [18192904.001]
  • (PMID = 18192919.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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55. Dimov ND, Medeiros LJ, Kantarjian HM, Cortes JE, Chang KS, Bueso-Ramos CE, Ravandi F: Rapid and reliable confirmation of acute promyelocytic leukemia by immunofluorescence staining with an antipromyelocytic leukemia antibody: the M. D. Anderson Cancer Center experience of 349 patients. Cancer; 2010 Jan 15;116(2):369-76
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  • [Title] Rapid and reliable confirmation of acute promyelocytic leukemia by immunofluorescence staining with an antipromyelocytic leukemia antibody: the M. D. Anderson Cancer Center experience of 349 patients.
  • BACKGROUND: The authors evaluated the utility of immunofluorescence staining with an antipromyelocytic leukemia (anti-PML) antibody for patients with a suspected diagnosis of new or relapsed acute promyelocytic leukemia (APL) and correlated the findings with the results of other established diagnostic modalities.
  • METHODS: Bone marrow (BM) and/or peripheral blood (PB) smears from 349 patients in whom the diagnosis of APL was considered were assessed with the anti-PML antibody using immunofluorescence.
  • The study group included 199 patients with confirmed APL and 150 with other conditions.
  • The results of conventional cytogenetics, reverse transcription polymerase chain reaction (RT-PCR), and fluorescence in situ hybridization (FISH) performed on these patients were correlated with the PML results.
  • RESULTS: Among patients with confirmed APL, anti-PML antibody was positive in 182 of 184 BM and 32 of 33 PB smears.
  • Conventional cytogenetics demonstrated t(15;17)(q22;q12) in 166 of 182 (91%) patients; 10 had a normal karyotype, 4 had insufficient mitoses to grow in culture, 1 was inconclusive, and 1 was 48, XX, +8, +8.
  • Anti-PML staining was positive in 9 of 10 with a normal karyotype and in all 4 cases with insufficient mitoses.
  • RT-PCR and FISH were positive for PML-retinoic acid receptor-alpha in 169 of 172 (98%) and 90 of 94 (96%) cases, respectively.
  • Among the patients without APL, 148 of 150 (98.6%) were negative with anti-PML antibody.
  • CONCLUSIONS: PML immunofluorescence staining is a rapid (<4 hours turnaround time) and reliable frontline diagnostic approach that can facilitate initiation of targeted therapy, particularly in clinical settings where cytogenetic and molecular testing are not readily available.
  • [MeSH-major] Antibodies, Neoplasm. Fluorescent Antibody Technique / methods. Leukemia, Promyelocytic, Acute / diagnosis. Nuclear Proteins. Transcription Factors. Tumor Suppressor Proteins
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity

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  • (PMID = 19950129.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  • [Other-IDs] NLM/ NIHMS629441; NLM/ PMC4180261
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56. Quenby S, Mountfield S, Cartwright JE, Whitley GS, Chamley L, Vince G: Antiphospholipid antibodies prevent extravillous trophoblast differentiation. Fertil Steril; 2005 Mar;83(3):691-8
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  • [Title] Antiphospholipid antibodies prevent extravillous trophoblast differentiation.
  • OBJECTIVE: We investigated the hypothesis that antiphospholipid antibodies (aPL) have a detrimental effect on human extravillous trophoblast (EVT) differentiation into giant multinucleated cells "in vitro."
  • MAIN OUTCOME MEASURE(S): This model was then used to investigate the effect of two different monoclonal aPL to beta2-glycoprotein 1 (IIC5 and ID2), and control mouse IgG antibody on EVT differentiation.
  • The aPL, IIC5, and ID2 significantly inhibited GMC formation, whereas the mouse IgG control had no effect.
  • CONCLUSION(S): Antiphospholipid antibodies can inhibit EVT differentiation and GMC formation "in vitro" suggesting that a failure of trophoblast differentiation and subsequent uteroplacental development may be an underlying pathology in antiphospholipid syndrome-associated pregnancy loss.
  • [MeSH-major] Antibodies, Antiphospholipid / pharmacology. Trophoblasts / cytology. Trophoblasts / immunology

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  • (PMID = 15749499.001).
  • [ISSN] 0015-0282
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal
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57. Suvajac G, Stojanovich L, Milenkovich S: Ocular manifestations in antiphospholipid syndrome. Autoimmun Rev; 2007 Jun;6(6):409-14
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  • [Title] Ocular manifestations in antiphospholipid syndrome.
  • Antiphospholipid syndrome (APS) is characterized by increased hypercoagulability and divergent symptoms including ocular manifestations.
  • In APS patients arterial and/or venous thromboses and repeated fetal loss are diagnosed in presence of antiphospholipid (aPL) antibodies.
  • Antiphospholipid antibodies are heterogeneous group of immunoglobulins with different antigenic structure.
  • Primary APS is defined in the absence of underlying disease, while secondary APS is seen within another pathological condition.
  • In secondary APS occlusion of central retinal artery and vein (OACR, OVCR) is the most common finding, thus when found in younger patients it should be considered indicative of APS.
  • [MeSH-major] Antibodies, Antiphospholipid / immunology. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / immunology. Eye Diseases / etiology
  • [MeSH-minor] Anterior Eye Segment. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / immunology. Thrombosis

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  • (PMID = 17537387.001).
  • [ISSN] 1568-9972
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
  • [Number-of-references] 26
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58. Martinuc Porobic J, Avcin T, Bozic B, Kuhar M, Cucnik S, Zupancic M, Prosenc K, Kveder T, Rozman B: Anti-phospholipid antibodies following vaccination with recombinant hepatitis B vaccine. Clin Exp Immunol; 2005 Nov;142(2):377-80
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  • [Title] Anti-phospholipid antibodies following vaccination with recombinant hepatitis B vaccine.
  • This study was undertaken to evaluate the possible role of hepatitis B recombinant vaccine inducing the synthesis of IgG and IgM anti-cardiolipin antibodies (aCL), antibodies against beta(2)GPI (anti-beta(2)GPI), lupus anti-coagulant (LA), anti-nuclear antibodies and antibodies against extractable nuclear antigens (anti-ENA).
  • One month after vaccination with the first dose of hepatitis B vaccine a minority of vaccinated individuals showed changes in IgG or IgM aCL or anti-beta(2)GPI or LA activity (P < 0.001).
  • Among subjects in whom changes of IgG anti-beta(2)GPI were observed, a significantly higher number of increased (8/85) than decreased (2/85) values were found (P < 0.01).
  • Analyses of paired data showed that differences in aCL or anti-beta(2)GPI levels before vaccination or 1 month later did not reach statistical significance.
  • In two people aCL transitorily reached medium positivity after the first dose of hepatitis B vaccine with a drop 5 months later.
  • Similar evident anti-beta(2)GPI fluctuation was also observed in one person.
  • Another participant was initially low positive for IgG anti-beta2GPI and the levels were increasing after vaccination.
  • Two participants became positive for anti-nuclear antibodies during 6 months' follow-up.
  • There were no sex-dependent differences in tested antibodies observed and no associations between levels of aPL and levels of anti-HBV antibodies.
  • We conclude that HBV can induce aPL, although rarely.
  • [MeSH-major] Antibodies, Antiphospholipid / biosynthesis. Hepatitis B Vaccines / immunology. Vaccines, Synthetic / immunology

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  • (PMID = 16232227.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Engerix-B; 0 / Glycoproteins; 0 / Hepatitis B Vaccines; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / Vaccines, Synthetic; 0 / beta 2-Glycoprotein I
  • [Other-IDs] NLM/ PMC1809502
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59. Gopal M, Cohn CD, McEntire MR, Alperin JB: Thrombotic thrombocytopenic purpura and adult onset Still's disease. Am J Med Sci; 2009 May;337(5):373-6
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  • [Title] Thrombotic thrombocytopenic purpura and adult onset Still's disease.
  • Although recent literature supports the role of ADAMTS13 (a disintegrin-like metalloproteinase with thrombospondin type 1 repeats), the von Willebrand factor cleaving protease, in the pathogenesis of the disease, many aspects of the disease remain a mystery.
  • Various drugs and autoimmune conditions, such as systemic lupus erythematosus and the antiphospholipid syndrome, have been observed in association with TTP.
  • Adult onset Still's disease (AOSD) has been reported less frequently in association with TTP.
  • He responded initially to plasma exchange, but never achieved complete remission.
  • DISCUSSION: Literature review shows that the autoimmune diseases usually associated with TTP include systemic lupus erythematosus and the antiphospholipid syndrome.
  • Interestingly, the patient's AOSD-associated arthritis responded to plasma exchange, but did not resolve after splenectomy.
  • [MeSH-major] Purpura, Thrombotic Thrombocytopenic / complications. Purpura, Thrombotic Thrombocytopenic / diagnosis. Still's Disease, Adult-Onset / complications. Still's Disease, Adult-Onset / diagnosis
  • [MeSH-minor] ADAM Proteins / blood. ADAM Proteins / immunology. Adult. Antigens, CD36 / blood. Antigens, CD36 / immunology. Hematology / methods. Humans. Male. Plasma Exchange. Remission Induction. Splenectomy. Treatment Outcome

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  • (PMID = 19322066.001).
  • [ISSN] 0002-9629
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAMTS13 protein, human
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60. Liu Y, Hock JM, Sullivan C, Fang G, Cox AJ, Davis KT, Davis BH, Li X: Activation of the p38 MAPK/Akt/ERK1/2 signal pathways is required for the protein stabilization of CDC6 and cyclin D1 in low-dose arsenite-induced cell proliferation. J Cell Biochem; 2010 Dec 15;111(6):1546-55
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  • Arsenic trioxide (ATO) is a first-line anti-cancer agent for acute promyelocytic leukemia, and induces apoptosis in other solid cancer cell lines including breast cancer cells.
  • Low-dose ATO steadily increased gene transcript and protein levels of both CDC6 and cyclin D1 in a dose- and time-dependent manner.

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  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 20862710.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / CDC6 protein, human; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / Oxides; 0 / Reactive Oxygen Species; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; S7V92P67HO / arsenic trioxide
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61. Atienza MR, Respaldiza N, De La Santa E, Martín-Garrido I, Medrano FJ, Varela JM, Calderón E: Antiphospholipid antibodies investigation in Pneumocystis jirovecii carriers. Scand J Infect Dis; 2008;40(10):840-2
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  • [Title] Antiphospholipid antibodies investigation in Pneumocystis jirovecii carriers.
  • It is well documented that antiphospholipid antibodies are increased in patients with HIV-1 infection and these are most commonly seen in those with Pneumocystis jirovecii pneumonia.
  • We report here our experience concerning the possible relationship between P. jirovecii infection in non-immunocompromized adults and the production of antiphospholipid antibodies.
  • IgG anticardiolipin antibodies were positive in 2 out of 5 (40%) P. jirovecii carriers and 2 out of 10 (20%) subjects with no evidence of pulmonary infection by this microorganism (p=0.4).

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  • (PMID = 18609205.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor
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62. Jerga A, Miller DJ, White SW, Rock CO: Molecular determinants for interfacial binding and conformational change in a soluble diacylglycerol kinase. J Biol Chem; 2009 Mar 13;284(11):7246-54
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  • Anionic phospholipids, like phosphatidylglycerol (PtdGro), were required for DgkB to recognize diacylglycerol embedded in a phospholipid bilayer.
  • DgkB interaction with phospholipid vesicles was not influenced by the presence of ATP, but anionic vesicles decreased the Km of the enzyme for ATP.
  • The key residues responsible for the structural Mg2+ binding site, the conformational changes that increase ATP affinity, and interfacial recognition of anionic phospholipids were identical in DgkB and the mammalian diacylglycerol kinase catalytic cores.
  • This sequence conservation suggests that the mammalian enzymes also require a structural divalent cation and surface positively charged residues to bind phospholipid bilayers and trigger conformational changes that accelerate catalysis.

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  • (PMID = 19112175.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NIGMS NIH HHS / GM / GM34496
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Lipid Bilayers; 0 / Phosphatidylglycerols; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.1.107 / Diacylglycerol Kinase; I38ZP9992A / Magnesium
  • [Other-IDs] NLM/ PMC2652325
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63. Szewczyk M, Wielkoszyński T, Zakliczyński M, Zembala M, Szumska-Kostrzewska M: Anti-ox-LDL and anticardiolipin autoantibodies in patients after cardiac transplantation. Transplant Proc; 2007 Nov;39(9):2870-2
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  • [Title] Anti-ox-LDL and anticardiolipin autoantibodies in patients after cardiac transplantation.
  • INTRODUCTION: Among cardiac transplantation (OHT) of coronary arterial disease, the pathogenesis can be associated with autoimmunologic effects due to oxidative lipoprotein modification and their change in antigenicity.
  • These factors may lead to lipoprotein vascular changes observed in antiphospholipid syndrome or systemic lupus erythematosus.
  • The aim of the presented study was to evaluate anticardiolipin autoantibodies (ACA) and anti-ox-LDL (antibodies against oxidized LDL) levels in the plasma immunoglobulin IgG class.
  • RESULTS: OHT patients showed significantly higher ACA concentrations compared with the control group (3.53 vs 1.10 GPL U/mL), whereas anti-ox-LDL levels did not differ considerably (494 vs 385 mU/mL).
  • Significant differences between the 2 OHT patient groups regarding anti-ox-LDL concentration were demonstrated among samples taken in 2002.
  • It is necessary to focus further research on the possibilities of developing secondary antiphospholipid syndrome.


64. Zhou J, Ye J, Zhao X, Li A, Zhou J: JWA is required for arsenic trioxide induced apoptosis in HeLa and MCF-7 cells via reactive oxygen species and mitochondria linked signal pathway. Toxicol Appl Pharmacol; 2008 Jul 1;230(1):33-40
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  • Arsenic trioxide, emerging as a standard therapy for refractory acute promyelocytic leukemia, induces apoptosis in a variety of malignant cell lines.
  • JWA, a novel retinoic acid-inducible gene, is known to be involved in apoptosis induced by various agents, for example, 12-O-tetradecanoylphorbol 13-acetate, N-4-hydroxy-phenyl-retinamide and arsenic trioxide.


65. Khalifa M, Ghannouchi N, Kaabia N, BenJazia E, Hachfi W, Krifa A, Letaief A, Bahri F: Primary antiphospholipid syndrome and Evan's syndrome: 2 case reports. Acta Clin Belg; 2009 Jan-Feb;64(1):65-7
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  • [Title] Primary antiphospholipid syndrome and Evan's syndrome: 2 case reports.
  • The main clinical features of primary antiphospholipid syndrome are recurrent foetal loss, arterial or venous thrombosis and thrombocytopaenia.
  • Evan's syndrome is characterized by simultaneous or sequential association of autoimmune anaemia and thombocytopaenia, rarely reported in primary antiphospholipid syndrome.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / complications. Antiphospholipid Syndrome / complications. Thrombocytopenia / complications

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  • (PMID = 19317244.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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66. Cuong NM, Tai BH, Hoan DH, Huong TT, Kim YH, Hyun JH, Kang HK: Inhibitory effects of indirubin derivatives on the growth of HL-60 leukemia cells. Nat Prod Commun; 2010 Jan;5(1):103-6
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  • [Title] Inhibitory effects of indirubin derivatives on the growth of HL-60 leukemia cells.
  • Six indirubin derivatives have been synthesized and their inhibitory effects on the growth of HL-60 human promyelocytic leukemia cells investigated.
  • Indirubin-3'-oxime (I-1) inhibited the growth of HL-60 cells with a GI50 value of 36.6 microM, whereas I-0, I-2, I-3, I-4 and I-6 showed only weak cytotoxic activities against HL-60 cancer cells with GI50 values in the range of 97.3 to over 100 microM.

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  • (PMID = 20184032.001).
  • [ISSN] 1934-578X
  • [Journal-full-title] Natural product communications
  • [ISO-abbreviation] Nat Prod Commun
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Indoles; V86L8P74GI / indirubin
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67. Hertig A, Ridel C, Rondeau E: [Hemolytic uremic syndrome in adults]. Nephrol Ther; 2010 Jul;6(4):258-71
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  • [Transliterated title] Syndromes hémolytiques et urémiques de l'adulte.
  • Hemolytic uremic syndrome (HUS) is related to a renal thrombotic microangiopathy, inducing hypertension and acute renal failure (ARF).
  • HUS may also occur after various treatments such as mitomycin C, gemcitabine, ciclosporin A, or tacrolimus, and as reported more recently bevacizumab, an anti VEGF antibody.
  • In adults, several HUS are encountered in the course of chronic nephropathies: nephroangiosclerosis, chronic glomerulonephritis, post irradiation nephropathy, scleroderma, disseminated lupus erythematosus, antiphospholipid syndrome.
  • Overall the prognosis of HUS has improved, with a patient survival greater than 85% at 1 year.
  • Plasma infusions and plasma exchanges are effective in most of the cases to treat hemolysis and thrombocytopenia.
  • A new monoclonal anti-C5 antibody is tested, and seems to be effective in atypical HUS with abnormal complement alternate pathway activation.
  • [MeSH-minor] Acute Kidney Injury / etiology. Adult. Escherichia coli Infections / complications. Humans. Hypertension / etiology. Kidney Failure, Chronic / complications. Risk Factors. Thrombotic Microangiopathies / complications

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  • [Copyright] Copyright 2010 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.
  • (PMID = 20399168.001).
  • [ISSN] 1872-9177
  • [Journal-full-title] Néphrologie & thérapeutique
  • [ISO-abbreviation] Nephrol. Ther.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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68. Qin J, Ye N, Yu L, Liu D, Fung Y, Wang W, Ma X, Lin B: Simultaneous and ultrarapid determination of reactive oxygen species and reduced glutathione in apoptotic leukemia cells by microchip electrophoresis. Electrophoresis; 2005 Mar;26(6):1155-62
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  • [Title] Simultaneous and ultrarapid determination of reactive oxygen species and reduced glutathione in apoptotic leukemia cells by microchip electrophoresis.
  • The established method was tested to measure the intracellular ROS and GSH levels in acute promyelocytic leukemia (APL)-derived NB4 cells.
  • [MeSH-major] Apoptosis / physiology. Electrophoresis, Microchip / methods. Glutathione / analysis. Leukemia, Promyelocytic, Acute / metabolism. Reactive Oxygen Species / analysis

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  • (PMID = 15706575.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Fluorescent Dyes; 0 / Oxides; 0 / Reactive Oxygen Species; 0 / Rhodamines; 109244-58-8 / dihydrorhodamine 123; 5072-26-4 / Buthionine Sulfoximine; GAN16C9B8O / Glutathione; S7V92P67HO / arsenic trioxide
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69. Furugaki K, Pokorna K, Le Pogam C, Aoki M, Reboul M, Bajzik V, Krief P, Janin A, Noguera ME, West R, Charron D, Chomienne C, Pla M, Moins-Teisserenc H, Padua RA: DNA vaccination with all-trans retinoic acid treatment induces long-term survival and elicits specific immune responses requiring CD4+ and CD8+ T-cell activation in an acute promyelocytic leukemia mouse model. Blood; 2010 Jan 21;115(3):653-6
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  • [Title] DNA vaccination with all-trans retinoic acid treatment induces long-term survival and elicits specific immune responses requiring CD4+ and CD8+ T-cell activation in an acute promyelocytic leukemia mouse model.
  • DNA vaccination and all-trans retinoic acid (ATRA) result in a survival advantage in a mouse model of acute promyelocytic leukemia (APL).
  • Degranulation and cytotoxic carboxyfluorescein diacetate succinimidyl ester-based assays showed major histocompatibility complex-restricted APL-specific T cell-mediated immune responses.
  • Sorted APL-specific CD8(+)CD107a(+) T cells showed an increase of antileukemic activity.
  • Effectors from ATRA + DNA-treated mice were shown to secrete interferon-gamma when stimulated with either APL cells or peptides from the promyelocytic leukemia-RARalpha vaccine-derived sequences as detected by ELISpot assays.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Immunity, Cellular. Leukemia, Promyelocytic, Acute / therapy. Tretinoin / administration & dosage. Vaccines, DNA / administration & dosage
  • [MeSH-minor] Animals. Combined Modality Therapy. Disease Models, Animal. Humans. Lymphocyte Activation / drug effects. Lymphocyte Activation / genetics. Mice. Oncogene Proteins, Fusion / administration & dosage. Oncogene Proteins, Fusion / genetics. Survival Analysis. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 19965687.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Vaccines, DNA; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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70. Robinson PJ, Pinheiro TJ: Phospholipid composition of membranes directs prions down alternative aggregation pathways. Biophys J; 2010 Apr 21;98(8):1520-8
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  • [Title] Phospholipid composition of membranes directs prions down alternative aggregation pathways.
  • Atomic force microscopy is used to image the aggregation of prions on supported lipid bilayers composed of mixtures of the zwitterionic lipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) and the anionic lipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoserine (POPS).
  • Prion aggregation is observed on both zwitterionic and anionic membranes, and the morphology of the aggregates formed is dependent on the anionic phospholipid content of the membrane.
  • The presence of POPS results in larger aggregates with a distinctive sponge-like morphology that are disruptive to membranes.

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  • [Copyright] Copyright 2010 Biophysical Society. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20409471.001).
  • [ISSN] 1542-0086
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / 88/DTA19176; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D524516/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipid Bilayers; 0 / Phosphatidylcholines; 0 / Phosphatidylserines; 0 / Phospholipids; 0 / Prions; 0 / Solutions; 40290-44-6 / 1-palmitoyl-2-oleoylglycero-3-phosphoserine; TE895536Y5 / 1-palmitoyl-2-oleoylphosphatidylcholine
  • [Other-IDs] NLM/ PMC2856143
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71. Lormeau C, Falgarone G, Roulot D, Boissier MC: Rheumatologic manifestations of chronic hepatitis C infection. Joint Bone Spine; 2006 Dec;73(6):633-8
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  • Tests are usually negative for antibodies to cyclic citrullinated peptides (anti-CCP), which may help to differentiate the two conditions.
  • HCV-associated vasculitis is usually related to cryoglobulinemia, although a few cases of polyarteritis nodosa-like disease affecting the medium-sized vessels have been reported.
  • Other conditions reported in patients with chronic HCV infection include fibromyalgia, systemic lupus erythematosus (SLE), antiphospholipid syndrome, and osteosclerosis.

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  • (PMID = 17056293.001).
  • [ISSN] 1778-7254
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 59
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72. Zabek J, Noworyta J, Brasse-Rumin M, Rell-Bakalarska M: [Inhibition of cardiolipin binding antibodies from synovial fluids of patients with arthritis by endotoxin]. Pol Arch Med Wewn; 2006 May;115(5):447-51
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  • In the presented study was prooven that aCl antibodies cross-reacting with LPS (endotoxin) from arthritic synovial fluids are part of the aPL antibodies pool and correlated with presence in joints bacterial cell wall components like LPS-showing endotoxin presence in synovial fluids and they may be usefull in differential diagnosis of the different kind of arthritis and also in explanation of their aetiology at all--especially in cases of early, undifferentiated arthritis.
  • [MeSH-major] Antibodies, Anticardiolipin / immunology. Arthritis / diagnosis. Arthritis / immunology. Lipopolysaccharides / metabolism. Synovial Fluid / immunology
  • [MeSH-minor] Antibodies, Bacterial / analysis. Antigens, Bacterial / analysis. Arthritis, Rheumatoid / diagnosis. Biomarkers / metabolism. Cross Reactions. Diagnosis, Differential. Humans. Immunologic Tests. Osteoarthritis / diagnosis. Osteoarthritis / immunology

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  • (PMID = 17195359.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Bacterial; 0 / Antigens, Bacterial; 0 / Biomarkers; 0 / Lipopolysaccharides
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73. Kraemer L, Wajid M, Shimomura Y, Christiano AM: Mutations in the hairless gene underlie APL in three families of Pakistani origin. J Dermatol Sci; 2008 Apr;50(1):25-30
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  • [Title] Mutations in the hairless gene underlie APL in three families of Pakistani origin.
  • BACKGROUND: Atrichia with papular lesions (APL) (OMIM#209500) is a rare autosomal recessively inherited form of irreversible alopecia characterized by papular lesions of keratin-filled cysts on various regions of the body.
  • Males and females are equally affected and present with a distinct pattern of total hair loss on scalp, axilla and body.
  • Mutations in the hairless (HR) gene have been previously shown to be responsible for APL.
  • OBJECTIVE: In this study, we studied the molecular basis of APL in three unrelated families of Pakistani origin.
  • In family B, we identified a novel homozygous deletion of a G nucleotide at the exon 15-intron 15 boundary, termed 3097delG.

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  • (PMID = 18164595.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR047338; United States / NIAMS NIH HHS / AR / R01 AR047338-06A2S1; United States / NIAMS NIH HHS / AR / R01 AR47338
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HR protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS125830; NLM/ PMC2914536
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74. Lou Y, Mai W, Jin J: Simultaneous presentation of acute myocardial infarction and acute promyelocytic leukemia. Ann Hematol; 2006 Jun;85(6):409-10
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  • [Title] Simultaneous presentation of acute myocardial infarction and acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology. Myocardial Infarction / pathology

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  • (PMID = 16557379.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
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75. Prasad AS: Zinc in human health: effect of zinc on immune cells. Mol Med; 2008 May-Jun;14(5-6):353-7
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  • In our studies in an experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, hyperammonemia, neurosensory disorders, and decreased lean body mass.
  • In HUT-78 (T helper 0 [Th(0)] cell line), we showed that a decrease in gene expression of interleukin-2 (IL-2) and IL-2 receptor alpha(IL-2Ralpha) were due to decreased activation of nuclear factor-kappaB (NF-kappaB) in zinc deficient cells.
  • Decreased NF-kappaB activation in HUT-78 due to zinc deficiency was due to decreased binding of NF-kappaB to DNA, decreased level of NF-kappaB p105 (the precursor of NF-kappaB p50) mRNA, decreased kappaB inhibitory protein (IkappaB) phosphorylation, and decreased Ikappa kappa.
  • Zinc also is an antioxidant and has anti-inflammatory actions.
  • The therapeutic roles of zinc in acute infantile diarrhea, acrodermatitis enteropathica, prevention of blindness in patients with age-related macular degeneration, and treatment of common cold with zinc have been reported.
  • In HL-60 cells (promyelocytic leukemia cell line), zinc enhances the up-regulation of A20 mRNA, which, via TRAF pathway, decreases NF-kappaB activation, leading to decreased gene expression and generation of tumor necrosis factor-alpha (TNF-alpha), IL-1beta, and IL-8.

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  • (PMID = 18385818.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 5 R01 A150698-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; J41CSQ7QDS / Zinc
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2277319
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76. Vora S, Shetty S, Salvi V, Satoskar P, Ghosh K: A comprehensive screening analysis of antiphospholipid antibodies in Indian women with fetal loss. Eur J Obstet Gynecol Reprod Biol; 2008 Apr;137(2):136-40
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  • [Title] A comprehensive screening analysis of antiphospholipid antibodies in Indian women with fetal loss.
  • STUDY DESIGN: Four hundred and thirty women (median age 26 years, range 18-39 years) with unexplained fetal loss (median number of abortions 3, range 1-13) were screened for the presence of antiphospholipid antibodies (APA), i.e. lupus anticoagulant (LA), IgG/M antibodies for cardiolipin (ACA), beta 2 glycoprotein 1 (beta2 GP1) and annexin V.
  • The overall prevalence of IgG and/or IgM antibodies for cardiolipin, beta 2 GP1 and annexin V were as follows-ACA 27.9% (OR 18.9; 95% CI, 5-70; P<0.05), beta 2 GP1 12.2% (OR 6.8; 95% CI, 1.8-25; P<0.05) and annexin V 14.6% (OR 17; 95% CI, 2.9-98; P<0.05).
  • [MeSH-major] Abortion, Spontaneous / immunology. Antibodies, Antiphospholipid / blood. Mass Screening / methods

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  • (PMID = 17644242.001).
  • [ISSN] 0301-2115
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies; 0 / Antibodies, Antiphospholipid; 0 / Cardiolipins; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I
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77. Gallien S, Milea D, Thiebaut MM, Bricaire F, Le Hoang P: Brain and optic nerve ischemia in malaria with immune disorders. J Infect; 2007 Jan;54(1):e1-3
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  • We report an unusual case of Plasmodium falciparum malaria in a European returning from tropical regions associating an anterior ischemic optic neuropathy and an asymptomatic centropontine myelinolysis.
  • The transient antiphospholipid antibodies detected in the patient may have played a role in the ischemic process at the origin of this unusual clinical association.
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. France. Humans. Male. Middle Aged. Travel

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  • (PMID = 16647756.001).
  • [ISSN] 1532-2742
  • [Journal-full-title] The Journal of infection
  • [ISO-abbreviation] J. Infect.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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78. von Scheven E, Elder ME: Association between beta2-glycoprotein I gene polymorphisms and pediatric SLE and antiphospholipid antibodies. Lupus; 2005;14(6):440-4
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  • [Title] Association between beta2-glycoprotein I gene polymorphisms and pediatric SLE and antiphospholipid antibodies.
  • Antibodies against phospholipids (PL) and PL-binding proteins have been causally implicated in antiphospholipid syndrome (APS).
  • The purpose of this study was to identify associations between beta2GPI mutations and both antiphospholipid antibodies (aPL) and their associated clinical manifestations in a pediatric and adolescent cohort and to search for novel mutations.
  • Genetic analysis of beta2GPI was performed in 58 youths with systemic lupus erythematosus (SLE) and/or aPL, to identify known polymorphisms at amino acids 247 and 306 as well as novel mutations in exon 7 of the beta2GPI gene, and their association with aPL-associated clinical manifestations.
  • Our results demonstrate an association between substitution of Val for Leu at AA247 (L247V) of beta2GPI and both the development of aPL (P = 0.05) and aPL-associated clinical manifestations (P = 0.03) among pediatric patients.
  • The odds ratio associated with risk of aPL-associated clinical manifestations for the homozygous VV polymorphism was 5.5 (CI 1.3-23, P = 0.03) for the overall cohort, and 4.75 (CI 0.66-55.49, P = 0.06) after adjusting for ethnicity.
  • Association between the VV genotype at amino acid 247 of beta2GPI and clinical disease supports a genetic cause for APS among children and adolescents.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Glycoproteins / genetics. Lupus Erythematosus, Systemic / genetics. Lupus Erythematosus, Systemic / immunology
  • [MeSH-minor] Adolescent. Adult. Alleles. Amino Acid Substitution. Antiphospholipid Syndrome / genetics. Antiphospholipid Syndrome / immunology. Base Sequence. Child. Child, Preschool. Cohort Studies. DNA, Complementary / genetics. Female. Humans. Male. Polymorphism, Genetic. beta 2-Glycoprotein I

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  • (PMID = 16038107.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR 20684; United States / NCRR NIH HHS / RR / M01 RR01271
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / DNA, Complementary; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I
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79. Gregory J, Feusner J: Acute promyelocytic leukemia in childhood. Curr Oncol Rep; 2009 Nov;11(6):439-45
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  • [Title] Acute promyelocytic leukemia in childhood.
  • Acute promyelocytic leukemia (APL) is a relatively rare form of acute myelogenous leukemia (AML).
  • In the United States, APL in children constitutes only 5% to 10% of AML.
  • Molecularly, the disease is characterized by a fusion protein, promyelocytic leukemia (PML)-retinoic acid receptor (RAR)-alpha that results from a balanced reciprocal translocation between the PML gene on chromosome 15 and the RAR-alpha (RARA) gene on chromosome 17.
  • A major advance in the field of APL treatment has been the use of all-trans-retinoic acid (ATRA).
  • Advances in the treatment of APL have taken this form of AML from a disease with significant morbidity and mortality to one with an excellent outcome.
  • Recent trials have shown a role for arsenic trioxide in both newly diagnosed and relapsed APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Anthracyclines / therapeutic use. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Humans. Prognosis. Translocation, Genetic

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  • (PMID = 19840521.001).
  • [ISSN] 1534-6269
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 47
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80. Kim DY, Choi SJ, Kim SH, Chung HY, Yi S, Kim DW, Kim CC, Han TH: Upregulated hoxC4 induces CD14 expression during the differentiation of acute promyelocytic leukemia cells. Leuk Lymphoma; 2005 Jul;46(7):1061-6
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  • [Title] Upregulated hoxC4 induces CD14 expression during the differentiation of acute promyelocytic leukemia cells.
  • Acute promyelocytic leukemia (APL) cells carrying the PML-RARa fusion protein, respond well by differentiating in their response to an all-trans-retinoic acid (ATRA) treatment.
  • Besides the constitutive expression of hoxA9 and no expression of hoxB7, the expression of hoxC4 increased significantly during differentiation of NB4 cells (PML-RAR(alpha)+).
  • We also examined the expression of hoxC4 in bone marrow cells from APL patients and found that the hoxC4 expression was reproducibly induced during an ATRA treatment.
  • To further examine this finding, HoxC4 was stably expressed in NB4 cells by retroviral transduction.
  • Upregulation of CD14 is at the transcription level and mediated by the homeodomain of the HoxC4.
  • [MeSH-major] Antigens, CD14 / genetics. Cell Differentiation. Gene Expression Regulation, Leukemic. Homeodomain Proteins / metabolism. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 16019559.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antineoplastic Agents; 0 / HOXC4 protein, human; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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81. Bao SH, Wang XP, Lin QD, Di W, Xu L, Ding CW: The investigation on the value of repeat and combination test of ACA and anti-beta2-GPI antibody in women with recurrent spontaneous abortion. Am J Reprod Immunol; 2008 Oct;60(4):372-8
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  • [Title] The investigation on the value of repeat and combination test of ACA and anti-beta2-GPI antibody in women with recurrent spontaneous abortion.
  • PROBLEM: In order to investigate the value of anticardiolipin antibodies (ACA) and anti-beta2-GPI antibodies detection in screening autoimmune type recurrent spontaneous abortion and its clinic application in antiphospholipid syndrome diagnosis, we adopt repeat combined ACA and anti-beta2-GPI antibodies detection in this study.
  • METHOD OF STUDY: Sera were collected from patients and work-up was done for detection of ACA and anti-beta2-GPI antibodies by enzyme-linked immunosorbent assay (ELISA).
  • RESULTS: The repeated and combined detection of ACA and anti-beta2-GPI antibodies detection could raise the positivity rate up to 21.8% (P < 0.05) in comparison with positive for ACA alone (14.1%), positive for anti-beta2-GPI alone (3.1%), and concurrently positive for both ACA and anti-beta2-GPI antibodies (4.6%).
  • In 91 confirmed positive antiphospholipid antibodies (APA) patients, with more frequent screening for ACA and anti-beta2-GPI antibodies, more patients with APA were found.
  • CONCLUSION: Our data implied that it would be appropriate to take over five or more screenings of combined ACA and anti-beta2-GPI antibodies detection in suspect patients to facilitate the positive diagnostic rate for autoimmune type RSA.
  • [MeSH-major] Abortion, Habitual / diagnosis. Abortion, Spontaneous / diagnosis. Antibodies, Anticardiolipin / blood. Autoimmune Diseases / diagnosis. beta 2-Glycoprotein I / blood


82. Moran DM, Shen H, Maki CG: Puromycin-based vectors promote a ROS-dependent recruitment of PML to nuclear inclusions enriched with HSP70 and Proteasomes. BMC Cell Biol; 2009 May 01;10:32
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  • [Title] Puromycin-based vectors promote a ROS-dependent recruitment of PML to nuclear inclusions enriched with HSP70 and Proteasomes.
  • BACKGROUND: Promyelocytic Leukemia (PML) protein can interact with a multitude of cellular factors and has been implicated in the regulation of various processes, including protein sequestration, cell cycle regulation and DNA damage responses.
  • Previous studies reported that misfolded proteins or proteins containing polyglutamine tracts form aggregates with PML, chaperones, and components of the proteasome, supporting a role for PML in misfolded protein degradation.
  • RESULTS: In the current study, we have identified a reactive oxygen species (ROS) dependent aggregation of PML, small ubiquitin-like modifier 1 (SUMO-1), heat shock protein 70 (HSP70) and 20S proteasomes in human cell lines that have been transiently transfected with vectors expressing the puromycin resistance gene, puromycin n-acetyl transferase (pac).
  • Immunofluorescent studies demonstrated that PML, SUMO-1, HSP70 and 20S proteasomes aggregated to form nuclear inclusions in multiple cell lines transfected with vectors expressing puromycin (puro) resistance in regions distinct from nucleoli.

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  • (PMID = 19409099.001).
  • [ISSN] 1471-2121
  • [Journal-full-title] BMC cell biology
  • [ISO-abbreviation] BMC Cell Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108843; United States / NCI NIH HHS / CA / R01 CA 108843
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Nuclear Proteins; 0 / Reactive Oxygen Species; 0 / SUMO-1 Protein; 0 / SUMO1 protein, human; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; 4A6ZS6Q2CL / Puromycin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2685373
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83. Asherson RA, Davidge-Pitts MC, Wypkema E: "Primary" antiphospholipid syndrome evolving into Waldenstrom's macroglobulinaemia: a case report. Clin Rheumatol; 2007 Feb;26(2):278-80
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  • [Title] "Primary" antiphospholipid syndrome evolving into Waldenstrom's macroglobulinaemia: a case report.
  • A 57-year-old woman with a history of transient ischaemic attacks and six recurrent foetal losses accompanied by elevations of antiphospholipid antibodies was diagnosed as having a "primary" antiphospholipid syndrome.
  • A false positive serological test for syphilis was demonstrated and apparently had been noted in her second pregnancy more than 20 years prior to her presentation with an antiphospholipid syndrome.
  • This case illustrates the importance of this investigation in any middle-aged patient presenting with an antiphospholipid syndrome and a monoclonal gammopathy This finding might presage the development of a more serious condition, even years later (as in our patient).
  • [MeSH-major] Antiphospholipid Syndrome / complications. Waldenstrom Macroglobulinemia / complications

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  • (PMID = 16547696.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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84. Naoe T, Suzuki T, Kiyoi H, Urano T: Nucleophosmin: a versatile molecule associated with hematological malignancies. Cancer Sci; 2006 Oct;97(10):963-9
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  • The NPM1 gene on 5q35 is translocated with the anaplastic lymphoma kinase (ALK) gene in anaplastic large cell lymphoma with t(2;5).
  • The MLF1 and RARA genes are fused with NPM1 in myelodysplastic syndrome and acute myeloid leukemia (AML) with t(3;5) and acute promyelocytic leukemia with t(5;17), respectively.
  • In each fused protein, the N-terminal NPM portion is associated with oligomerization of a partner protein leading to altered signal transduction or transcription.
  • Recently, mutations of exon 12 have been found in a significant proportion of de novo AML, especially in those with a normal karyotype.
  • Mutant NPM is localized aberrantly in the cytoplasm, but the molecular mechanisms for leukemia remain to be studied.
  • This review focuses on the clinical significance of the NPM1 gene in hematological malignancies and newly discovered roles of NPM associated with oncogenesis.

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  • (PMID = 16984370.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NPM-RARalpha protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 73
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85. Glasnović M, Bosnjak I, Vcev A, Kosuta M, Lenz B, Glasnović-Horvatić E: [Diagnostic and therapeutic approach to pregnant women suspect on antiphospholipid syndrome]. Reumatizam; 2008;55(1):10-5
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  • [Title] [Diagnostic and therapeutic approach to pregnant women suspect on antiphospholipid syndrome].
  • Antiphospholipid syndrome includes the presence of antiphospholipid antibodies, vascular thrombosis and reproductive function disturbances.
  • 62 women were included in study, 32 with primary antiphospholipd syndrome (PAPS), and 30 with secondary antiphospholipid syndrome (SAPS).
  • In SAPS group anticardiolipin antibodies (aCL) was positive in 8 patients (26.6%) compared to PAPS group with 3 aCL positive patients (9.4%).
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Pregnancy Complications / diagnosis


86. Kanegane H, Nomura K, Abe A, Makino T, Ishizawa S, Shimizu T, Naoe T, Miyawaki T: Spontaneous regression of aleukemic leukemia cutis harboring a NPM/RARA fusion gene in an infant with cutaneous mastocytosis. Int J Hematol; 2009 Jan;89(1):86-90
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  • [Title] Spontaneous regression of aleukemic leukemia cutis harboring a NPM/RARA fusion gene in an infant with cutaneous mastocytosis.
  • Aleukemic leukemia cutis has been rarely reported in infant leukemia.
  • This report describes a 6-month-old boy with aleukemic leukemia cutis, which regressed without any treatments within 6 months.
  • Interestingly, a cytogenetic analysis disclosed a leukemia clone with the karyotype of 46, XY, t(5;17)(q35;q12), which generated nucleophosmin (NPM)-retinoic acid receptor alpha fusion (RARA) fusion transcripts.
  • The patient simultaneously had cutaneous mastocytosis, which also disappeared with the leukemia cutis.
  • He shows no physical or laboratory abnormalities without any treatments after 12 months, although the NPM/RARA transcripts remain faintly in the bone marrow.
  • The present case is partially compatible with systemic mastocytosis with an associated clonal hematologic non-mast cell lineage disorder, proposed by the WHO classification, and it is also suggestive of the initiation or early stage of acute promyelocytic leukemia.
  • [MeSH-major] Leukemia / complications. Mastocytosis, Cutaneous / complications. Oncogene Proteins, Fusion / genetics. Remission, Spontaneous
  • [MeSH-minor] Humans. Infant. Leukemia, Promyelocytic, Acute. Male

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  • (PMID = 19052694.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / NPM-RARalpha protein, human; 0 / Oncogene Proteins, Fusion
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87. Chung RH, Hauser ER, Martin ER: Interpretation of simultaneous linkage and family-based association tests in genome screens. Genet Epidemiol; 2007 Feb;31(2):134-42
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  • Linkage tests and family-based tests of association are often applied in the same data to help fine-map disease loci or validate results.
  • We used computer simulations and theoretical statements to estimate the correlation between linkage statistics (affected sib pair maximum LOD scores) and family-based association statistics (pedigree disequilibrium test (PDT) and association in the pressure of linkage (APL)) under various hypotheses.
  • We concluded that when linkage and association tests are applied in the same data, the type I error rate of neither test will be affected and that power can be increased by applying tests conditionally.

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  • (PMID = 17123303.001).
  • [ISSN] 0741-0395
  • [Journal-full-title] Genetic epidemiology
  • [ISO-abbreviation] Genet. Epidemiol.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH59528; United States / NINDS NIH HHS / NS / NS51355
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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88. Nilsson A, Liljensten E, Bergström C, Sollerman C: Results from a degradable TMC joint Spacer (Artelon) compared with tendon arthroplasty. J Hand Surg Am; 2005 Mar;30(2):380-9
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  • Fibers of the polymer were woven into a T-shaped device in which the vertical portion separates the bone edges of the TMC joint and the horizontal portion stabilizes the joint.
  • Ten patients received the spacer device and the remaining 5 (control group) were treated with a trapezium resection arthroplasty with abductor pollicis longus (APL) stabilization.
  • The median values for both key pinch and tripod pinch increased compared with before surgery in the spacer group but not in the APL group.
  • CONCLUSIONS: This study showed significantly better pinch strength after Artelon TMC Spacer implantation into the TMC joint compared with APL arthroplasty.

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  • (PMID = 15781363.001).
  • [ISSN] 0363-5023
  • [Journal-full-title] The Journal of hand surgery
  • [ISO-abbreviation] J Hand Surg Am
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Polymers; 0 / Polyurethanes; 97343-15-2 / polyetherurethane urea
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89. Chan MY, Becker RC: Identification and treatment of arterial thrombophilia. Curr Treat Options Cardiovasc Med; 2008 Feb;10(1):3-11
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  • Once the diagnosis of a thrombophilic state has been established, management must include one or more strategies designed to attenuate thrombotic risk and the likelihood of clinical events.
  • Other specific therapies should be directed at the underlying thrombophilic disorder.
  • These treatments include direct thrombin inhibitors such as argatroban for heparin-induced thrombocytopenia (HIT), myelosuppressive drugs such as hydroxyurea for essential thrombocytosis, plasma exchange for thrombotic thrombocytopenic purpura, and phlebotomy for polycythemia vera.
  • Additionally, the treating physician must seek input early from a hematologist or rheumatologist when managing patients with known or suspected HIT, TTP, and myeloproliferative disorders, or the antiphospholipid syndrome, respectively.

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  • (PMID = 18325302.001).
  • [ISSN] 1092-8464
  • [Journal-full-title] Current treatment options in cardiovascular medicine
  • [ISO-abbreviation] Curr Treat Options Cardiovasc Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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90. Cole SM, Patterson MB, Cupp CL: Tonsillectomy in the anticoagulated patient. Ann Otol Rhinol Laryngol; 2007 Aug;116(8):589-93
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  • A case report is detailed of a 28-year-old woman with antiphospholipid syndrome on warfarin for high risk of venous thrombosis who underwent tonsillectomy.
  • [MeSH-major] Anticoagulants / adverse effects. Antiphospholipid Syndrome / drug therapy. Blood Loss, Surgical / prevention & control. Peritonsillar Abscess / surgery. Postoperative Hemorrhage / chemically induced. Tonsillectomy / methods. Venous Thrombosis / prevention & control. Warfarin / adverse effects

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  • (PMID = 17847726.001).
  • [ISSN] 0003-4894
  • [Journal-full-title] The Annals of otology, rhinology, and laryngology
  • [ISO-abbreviation] Ann. Otol. Rhinol. Laryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Enoxaparin; 0 / Heparin, Low-Molecular-Weight; 5Q7ZVV76EI / Warfarin; 9005-49-6 / Heparin
  • [Number-of-references] 21
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91. Chang YC, Huang HP, Hsu JD, Yang SF, Wang CJ: Hibiscus anthocyanins rich extract-induced apoptotic cell death in human promyelocytic leukemia cells. Toxicol Appl Pharmacol; 2005 Jun 15;205(3):201-12
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  • [Title] Hibiscus anthocyanins rich extract-induced apoptotic cell death in human promyelocytic leukemia cells.
  • [MeSH-minor] Androstadienes / pharmacology. Anthracenes / pharmacology. BH3 Interacting Domain Death Agonist Protein. Carrier Proteins / genetics. Carrier Proteins / metabolism. Caspases / genetics. Caspases / metabolism. Cell Survival / drug effects. Cytochromes c / drug effects. Cytochromes c / metabolism. DNA, Mitochondrial / drug effects. DNA, Mitochondrial / metabolism. Dose-Response Relationship, Drug. Fas Ligand Protein. Flavonoids / pharmacology. Flowers / chemistry. Humans. Imidazoles / pharmacology. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. Pyridines / pharmacology. RNA, Messenger. Time Factors. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors. p38 Mitogen-Activated Protein Kinases / drug effects. p38 Mitogen-Activated Protein Kinases / pharmacology

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  • (PMID = 15922006.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Androstadienes; 0 / Anthocyanins; 0 / Anthracenes; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Carrier Proteins; 0 / DNA, Mitochondrial; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Flavonoids; 0 / Imidazoles; 0 / Membrane Glycoproteins; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-jun; 0 / Pyridines; 0 / RNA, Messenger; 0 / SB 203580; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; 9007-43-6 / Cytochromes c; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; XVA4O219QW / wortmannin
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92. Au WY, Hon C, Yau K, Lai WW, Fong BM, Tam S, Kwong YL: Two cases of monocular visual loss during oral arsenic trioxide therapy of acute promyelocytic leukemia. Am J Hematol; 2009 Oct;84(10):699
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  • [Title] Two cases of monocular visual loss during oral arsenic trioxide therapy of acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Blindness / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects

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  • (PMID = 19705432.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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93. Di Simone N, Luigi MP, Marco D, Fiorella DN, Silvia D, Clara DM, Alessandro C: Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature. Ann N Y Acad Sci; 2007 Jun;1108:505-14
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  • [Title] Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature.
  • There are several possible mechanisms by which antiphospholipid antibodies (aPL) may have adverse effects on placental functions.
  • Examination of placentas and first-trimester decidua from antiphospholipid syndrome-complicated pregnancies has found little evidence of specific thrombotic placental pathology.
  • It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids.
  • The most important epitope for antiphospholipid syndrome-related aPL resides on beta2-glycoprotein-I (beta2GPI).
  • aPL detected by anti-beta2GPI assays are associated with fetal loss.
  • During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2GPI.
  • It might reduce the binding of aPL, inflammation by inhibiting complement activation, and might facilitate implantation.
  • Further investigations are needed to better understand how aPL induce obstetric complications and to better clarify the functional role of heparin in the human placenta, leading to more successful therapeutic options.
  • [MeSH-major] Antibodies, Antiphospholipid / immunology. Antiphospholipid Syndrome / immunology. Pregnancy Complications / etiology. Trophoblasts / immunology

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  • (PMID = 17894016.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantigens; 0 / beta 2-Glycoprotein I; 9005-49-6 / Heparin
  • [Number-of-references] 55
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94. Shanmugam VK, Price P, Attinger CE, Steen VD: Lower extremity ulcers in systemic sclerosis: features and response to therapy. Int J Rheumatol; 2010;2010
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  • Patients with diffuse scleroderma had shorter disease duration at the time of ulcer development (mean 4.05 years ± 0.05) compared to those with limited disease (mean 22.83 years ± 5.612, P value .0078).
  • In the 10 patients with ulcers, antiphospholipid antibodies were positive in 50%, and genetic prothrombotic screen was positive in 70% which is higher than expected based on prevalence reports from the general scleroderma population.
  • Of patients with biopsy specimens available (n = 5), fibrin occlusive vasculopathy was seen in 100%, and all of these patients had either positive antiphospholipid antibody screen, or positive genetic prothrombotic profile.
  • We recommend screening scleroderma patients with lower extremity ulcers for the presence of anti-phospholipid antibodies and genetic prothrombotic states.

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  • (PMID = 20827313.001).
  • [ISSN] 1687-9279
  • [Journal-full-title] International journal of rheumatology
  • [ISO-abbreviation] Int J Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2933896
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95. Patterson AM, Ford I, Graham A, Booth NA, Greaves M: The influence of anti-endothelial/antiphospholipid antibodies on fibrin formation and lysis on endothelial cells. Br J Haematol; 2006 May;133(3):323-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The influence of anti-endothelial/antiphospholipid antibodies on fibrin formation and lysis on endothelial cells.
  • The prothrombotic mechanisms associated with antiphospholipid antibodies remain incompletely defined.
  • Antibody binding to endothelial cells in vitro is a feature of antiphospholipid antibody-positive sera.
  • We hypothesised that impairment of endothelium-dependent fibrinolysis by antiphospholipid/anti-endothelial antibodies is a contributory factor in the pathogenesis of thrombosis.
  • Binding of immunoglobulin (Ig) from antiphospholipid antibody-positive sera to endothelial cells was examined using a cell-based enzyme-linked immunosorbent assay.
  • With four of 14 antiphospholipid antibody-positive sera there was some prolongation of fibrin clot lysis time, consistent with impairment of endothelial fibrinolytic activity.
  • Secretion of PAI-1 was significantly correlated with clot lysis time on endothelial cell monolayers incubated with antiphospholipid/anti-endothelial antibody-positive sera, but not with control sera.
  • IgG from antiphospholipid antibody-positive sera had little effect on endothelial cell surface annexin-V expression.
  • We conclude that impaired endothelial fibrinolysis is a potential prothrombotic mechanism in subjects with antiphospholipid antibodies.
  • We were unable to confirm enhanced displacement of annexin-V from endothelium by antiphospholipid antibodies.
  • [MeSH-minor] Annexin A5 / metabolism. Antibodies, Antiphospholipid / immunology. Blood Coagulation / immunology. Cells, Cultured. Endothelial Cells / immunology. Humans. Immunoenzyme Techniques. Plasminogen Activator Inhibitor 1 / metabolism

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  • (PMID = 16643435.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Plasminogen Activator Inhibitor 1; 9001-31-4 / Fibrin
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96. Farhat M, Venugopal P: Long-term remission of extramedullary relapse from acute promyelocytic leukemia after treatment with arsenic trioxide, intrathecal chemotherapy, and brain irradiation. Clin Adv Hematol Oncol; 2007 Apr;5(4):320-3; discussion 323-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term remission of extramedullary relapse from acute promyelocytic leukemia after treatment with arsenic trioxide, intrathecal chemotherapy, and brain irradiation.
  • [MeSH-major] Arsenicals / administration & dosage. Cranial Irradiation. Ear Neoplasms / therapy. Leukemia, Myelomonocytic, Acute. Oxides / administration & dosage. Sarcoma, Myeloid / therapy

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  • (PMID = 17607291.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 48
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97. Tempescul A, Guillerm G, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jan 1;172(1):74-6
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  • [Title] Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia.
  • We report here two cases of patients with acute myeloblastic leukemia, type M1 (FAB classification), associated with a t(10;17)(p15;q21).
  • Fluorescence in situ hybridization with the LSI PML/RARA dual-color probe showed the breakpoint to be distal to the RARA locus.
  • Four other patients with this translocation have been reported, three of them having acute undifferentiated or poorly differentiated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17175384.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human
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98. O'Neil KM: High-intensity warfarin versus conventional antithrombotic therapy to prevent thrombosis in antiphospholipid syndrome. Curr Rheumatol Rep; 2007 Jun;9(3):188-9
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  • [Title] High-intensity warfarin versus conventional antithrombotic therapy to prevent thrombosis in antiphospholipid syndrome.

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  • [CommentOn] Lupus. 2005;14(2):120-8 [15751816.001]
  • (PMID = 17531170.001).
  • [ISSN] 1523-3774
  • [Journal-full-title] Current rheumatology reports
  • [ISO-abbreviation] Curr Rheumatol Rep
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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99. Bhowmik D, Dadhwal V, Dinda AK, Handa R, Dash SC: Steroid-responsive focal segmental glomerulosclerosis in primary antiphospholipid syndrome with successful pregnancy outcome. Nephrol Dial Transplant; 2005 Aug;20(8):1726-8
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  • [Title] Steroid-responsive focal segmental glomerulosclerosis in primary antiphospholipid syndrome with successful pregnancy outcome.
  • [MeSH-major] Antiphospholipid Syndrome / drug therapy. Glomerulosclerosis, Focal Segmental / drug therapy. Glucocorticoids / therapeutic use. Nephrotic Syndrome / drug therapy. Pregnancy Complications


100. Der H, Kerekes G, Veres K, Szodoray P, Toth J, Lakos G, Szegedi G, Soltesz P: Impaired endothelial function and increased carotid intima-media thickness in association with elevated von Willebrand antigen level in primary antiphospholipid syndrome. Lupus; 2007;16(7):497-503
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  • [Title] Impaired endothelial function and increased carotid intima-media thickness in association with elevated von Willebrand antigen level in primary antiphospholipid syndrome.
  • Primary antiphospholipid syndrome (APS) is characterized by venous or arterial thrombotic events and/or recurrent abortions, fetal death, preeclasmpsia, eclampsia in the presence of anticardiolipin antibodies or lupus anticoagulant, in the absence of accompanying diseases.
  • Antiphospholipid antibodies can activate endothelial cells, and were recently implicated in atherosclerosis.
  • To assess potential endothelial impairment and early signs of atherosclerosis, flow-mediated (endothelium-dependent) and nitrate-mediated (endothelium independent) vasodilation, as well as von Willebrand factor antigen level and carotid artery intima-media thickness (IMT) were measured in patients with primary antiphospholipid syndrome and in healthy controls.
  • We also found significantly higher von Willebrand antigen levels in patients with primary APS than in the control group (157.91 +/- 52.45% versus 125.87 +/- 32.8%; P = 0.012).
  • [MeSH-major] Antigens / blood. Antiphospholipid Syndrome / physiopathology. Carotid Arteries / ultrasonography. Endothelium, Vascular / physiopathology. Vasodilation / physiology

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  • (PMID = 17670848.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Biomarkers; 0 / Vasodilator Agents; 0 / Von Willebrand antigen; 0 / von Willebrand Factor; G59M7S0WS3 / Nitroglycerin
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