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1. Coutre S: Classification and risk stratification for acute promyelocytic leukemia. Clin Lymphoma Myeloma Leuk; 2010 Oct;10 Suppl 3:S127-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification and risk stratification for acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (APL) as a distinct clinical entity was first described only 50 years ago.
  • The last twenty years are notable for rapid advances in understanding the molecular basis of the disease as well as dramatic improvements in treating APL.
  • A new classification system that stratifies patients by risk has also lead to dramatic improvement in managing the disease.
  • Molecular monitoring for minimal residual disease holds great promise for continued improvement in decreasing relapse risk.
  • We are now able to tailor our therapy based on risk of relapse, and ongoing clinical trials use this risk-adapted framework in an attempt to further improve outcomes.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Prognosis. Recurrence. Risk. Survival Analysis. Treatment Outcome

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  • (PMID = 21115430.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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2. Tridapalli E, Stella M, Capretti MG, Faldella G: Neonatal arterial iliac thrombosis in type-I protein C deficiency: a case report. Ital J Pediatr; 2010;36:23
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  • [Title] Neonatal arterial iliac thrombosis in type-I protein C deficiency: a case report.
  • Normal vitamin K coagulation proteins levels.
  • FV Leiden and antiphospholipid antibodies were negative.
  • The child was followed-up yearly until 4 years of age: he was well and had a normal body and mental development.The final diagnosis is likely to be of a permanent protein C deficiency in heterozygous form.
  • Our case is interesting because the first manifestation was an important thrombosis of large vessel that occurred within a few hours of life in absence of perinatal risk factors, as if it was a homozygous disease, but the patient had a heterozygotic form.

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  • [Cites] J Clin Pathol. 2000 Jun;53(6):419-23 [10911798.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2001;:358-74 [11722993.001]
  • [Cites] Br J Haematol. 2002 Nov;119(2):295-309 [12406062.001]
  • [Cites] Pediatr Res. 1981 Jul;15(7):1015-8 [7254945.001]
  • [Cites] Thromb Res. 1988 Dec 15;52(6):517-27 [3232122.001]
  • [Cites] Haemophilia. 2008 Nov;14(6):1214-21 [19141162.001]
  • [Cites] Pediatrics. 1995 Nov;96(5 Pt 1):939-43 [7478839.001]
  • [Cites] Arch Dis Child Fetal Neonatal Ed. 1997 May;76(3):F163-7 [9175945.001]
  • [Cites] Chest. 2008 Jun;133(6 Suppl):887S-968S [18574281.001]
  • [Cites] Wien Med Wochenschr. 2008;158(13-14):385-95 [18677590.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1990 Spring;12(1):95-104 [2178462.001]
  • (PMID = 20211026.001).
  • [ISSN] 1824-7288
  • [Journal-full-title] Italian journal of pediatrics
  • [ISO-abbreviation] Ital J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Protein C; 9005-49-6 / Heparin
  • [Other-IDs] NLM/ PMC2848059
  • [General-notes] NLM/ Original DateCompleted: 20100609
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3. Asherson RA, D'Cruz D: Vascular occlusions in a patient with low positive antiphospholipid antibodies and subsequent development of breast carcinoma: a diagnostic dilemma. Clin Rheumatol; 2007 Sep;26(9):1531-3
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  • [Title] Vascular occlusions in a patient with low positive antiphospholipid antibodies and subsequent development of breast carcinoma: a diagnostic dilemma.
  • A 61-year-old female with a history of previous digital ischemia and stroke, developed bilateral brachial artery thromboses thought originally to be due to fibromuscular hyperplasia.
  • Minimal elevations of anti-B2GP1 were demonstrated with levels of other isotypes measurable at just below cut off levels for normality.
  • Three years later, all aPl determinations were negative with levels well below the cutoff levels for all isotypes.
  • The minimal anti-B2GP1 elevation may have been triggered by the vascular damage caused by the thromboses or may perhaps have been pathogenic in the causation of these thromboses.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Brachial Artery / pathology. Carcinoma, Ductal, Breast / blood. Thrombosis / immunology

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  • [Cites] J Rheumatol. 2006 Oct;33(10):2091-6 [17014025.001]
  • [Cites] Clin Rheumatol. 2006 Nov;25(6):840-4 [16435159.001]
  • [Cites] Immunobiology. 2003;207(1):13-6 [12638897.001]
  • [Cites] Lupus. 1995 Aug;4(4):309-13 [8528229.001]
  • [Cites] Clin Exp Rheumatol. 2005 Mar-Apr;23(2):199-204 [15895890.001]
  • [Cites] Semin Arthritis Rheum. 2006 Apr;35(5):322-32 [16616155.001]
  • (PMID = 17661122.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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4. Kataoka-Hamai C, Higuchi M, Iwai H, Miyahara Y: Detergent-mediated formation of polymer-supported phospholipid bilayers. Langmuir; 2010 Sep 21;26(18):14600-5
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  • [Title] Detergent-mediated formation of polymer-supported phospholipid bilayers.
  • Supported phospholipid bilayers can be formed by established methods such as vesicle fusion and the Langmuir-Blodgett (LB) technique.
  • (1) incubation of phospholipid-poly(ethylene glycol) (PEG)-grafted glass with lipid-detergent micelles;.
  • While anionic phospholipids inhibited the attachment of fluid bilayers in the absence of calcium ions, supported bilayers with almost full mobility were obtained from lipid mixtures containing 10-20 mol % anionic lipids in the presence of calcium ions.
  • The incorporation of the anionic lipids in the bulk-facing leaflet was demonstrated by the binding of dye-labeled annexin V.
  • [MeSH-major] Detergents / chemistry. Lipid Bilayers / chemistry. Phospholipids / chemistry. Polyethylene Glycols / chemistry

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  • (PMID = 20726608.001).
  • [ISSN] 1520-5827
  • [Journal-full-title] Langmuir : the ACS journal of surfaces and colloids
  • [ISO-abbreviation] Langmuir
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Detergents; 0 / Lipid Bilayers; 0 / Phospholipids; 0 / Silanes; 30IQX730WE / Polyethylene Glycols
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5. Karp DR: Complement and systemic lupus erythematosus. Curr Opin Rheumatol; 2005 Sep;17(5):538-42
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  • RECENT FINDINGS: The antiphospholipid syndrome is a major feature of systemic lupus erythematosus.
  • Secondly, a potential mechanism explaining the association of anti-C1q autoantibodies with lupus glomerulonephritis has been elucidated in a mouse model system.
  • These findings point to more precise, mechanism-based therapies for autoimmune and inflammatory disease.

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  • (PMID = 16093830.001).
  • [ISSN] 1040-8711
  • [Journal-full-title] Current opinion in rheumatology
  • [ISO-abbreviation] Curr Opin Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-36-7 / Complement System Proteins
  • [Number-of-references] 45
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6. Yang Z, Su X, Wu F, Gong Y, Kuang T: Effect of phosphatidylglycerol on molecular organization of photosystem I. Biophys Chem; 2005 May 1;115(1):19-27
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  • Phosphatidylglycerol (PG) is the only anionic phospholipid in photosynthetic membrane.
  • Simultaneously, an increase in alpha-helix and a decrease particularly in the disordered conformations of protein secondary structures are observed.

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  • (PMID = 15848280.001).
  • [ISSN] 0301-4622
  • [Journal-full-title] Biophysical chemistry
  • [ISO-abbreviation] Biophys. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Liposomes; 0 / Phosphatidylglycerols; 0 / Photosystem I Protein Complex; 0 / Plant Extracts; 8DUH1N11BX / Tryptophan
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7. Zhao XS, Song PL, Sun B, Jiang HC, Liu TF: Arsenic trioxide inhibits metastatic potential of mouse hepatoma H22 cells in vitro and in vivo. Hepatobiliary Pancreat Dis Int; 2009 Oct;8(5):510-7
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  • Low-dose ATO can effectively alleviate acute promyelocytic leukemia (APL).
  • The purpose of this study was to investigate the effect of ATO at low concentrations on the metastatic potential of mouse hepatoma H(22) cells and the anti-metastatic mechanism of ATO.
  • A total of 15 different protein peaks were identified between the lysate of H(22) cells treated with ATO and controls.
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Male. Matrix Metalloproteinase 2 / metabolism. Mice. NM23 Nucleoside Diphosphate Kinases / metabolism. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 19822495.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Oxides; EC 2.7.4.6 / Nme1 protein, mouse; EC 3.4.24.24 / Matrix Metalloproteinase 2; S7V92P67HO / arsenic trioxide
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8. Diallo M, Niang SO, Kane A, Dieng MT, Ndiaye B: [Antiphospholipid antibodies syndrome in dermatology in Dakar: 11 case report]. Dakar Med; 2007;52(1):41-5
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  • [Title] [Antiphospholipid antibodies syndrome in dermatology in Dakar: 11 case report].
  • [Transliterated title] Syndrome des anticorps antiphospholipides en dermatologie à Dakar: a propos de 11 cas.
  • INTRODUCTION: Our aim was to report the cutaneous features of antiphospholipid antibodies syndrome in Dermatology in Dakar.
  • All patients were diagnosed according to the criteria of the international consensus statement in 1999 on the antiphospholipid antibodies.
  • RESULTS: Eleven cases (all female) were collected with a median age of 28 years.
  • The mean level of anticardiolipin antibodies was 60 UGPL and a dissociation of the syphilitic serology was present in 9 patients.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Pregnancy Complications / etiology. Skin Diseases / etiology


9. Matsuura E, Lopez LR: Autoimmune-mediated atherothrombosis. Lupus; 2008 Oct;17(10):878-87
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  • Circulating oxLDL/beta2GPI complexes have been detected in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).
  • The in vitro macrophage uptake of oxLDL/beta2GPI complexes was significantly increased in the presence of antiphospholipid antibodies, either beta2GPI-dependent anticardiolipin or anti-beta2GPI antibodies, suggesting that macrophage Fcgamma receptors are involved in lipid intracellular influx and foam cell formation.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Atherosclerosis / etiology
  • [MeSH-minor] Antibodies, Antiphospholipid / physiology. Humans. Lipoproteins, LDL / physiology. Oxidative Stress / physiology. beta 2-Glycoprotein I / physiology

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  • (PMID = 18827052.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Lipoproteins, LDL; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 95
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10. Aldous S: An interesting presentation of antiphospholipid syndrome. BMJ Case Rep; 2009;2009:bcr2007121210
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An interesting presentation of antiphospholipid syndrome.

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  • (PMID = 21687285.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3106044
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11. Kim S, Moskowitz NK, DiCarlo EF, Bass AR, Erkan D, Lockshin MD: Catastrophic antiphospholipid syndrome triggered by sepsis. HSS J; 2009 Feb;5(1):67-72
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  • [Title] Catastrophic antiphospholipid syndrome triggered by sepsis.

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  • [Cites] Semin Arthritis Rheum. 2001 Oct;31(2):127-32 [11590582.001]
  • [Cites] Circ Res. 2002 Jan 11;90(1):29-37 [11786515.001]
  • [Cites] Ann Rheum Dis. 2008 Mar;67(3):395-401 [17644539.001]
  • [Cites] Lupus. 2008 Jan;17(1):50-5 [18089684.001]
  • [Cites] J Rheumatol. 2007 May;34(5):923-6 [17477476.001]
  • [Cites] Autoimmun Rev. 2006 Dec;6(2):98-103 [17138252.001]
  • [Cites] Curr Opin Hematol. 2006 Sep;13(5):366-75 [16888443.001]
  • [Cites] J Intensive Care Med. 2006 May-Jun;21(3):144-59 [16672637.001]
  • [Cites] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]
  • [Cites] Transfus Apher Sci. 2005 Aug;33(1):11-7 [15951243.001]
  • [Cites] Ann Rheum Dis. 2005 Aug;64(8):1205-9 [15708888.001]
  • [Cites] Am J Med. 1998 Apr;104(4):381-5 [9576413.001]
  • [Cites] Thromb Res. 2004;114(5-6):391-6 [15507269.001]
  • [Cites] Trends Pharmacol Sci. 2004 Jun;25(6):306-10 [15165745.001]
  • [Cites] Arthritis Rheum. 2003 Dec;48(12):3320-7 [14673983.001]
  • [Cites] Lupus. 2003;12(7):530-4 [12892393.001]
  • [Cites] J Rheumatol. 2002 Sep;29(9):2006-11 [12233899.001]
  • [Cites] Rheumatology (Oxford). 2002 Aug;41(8):924-9 [12154210.001]
  • [Cites] Rheumatology (Oxford). 2000 Apr;39(4):421-6 [10817776.001]
  • (PMID = 19096893.001).
  • [ISSN] 1556-3316
  • [Journal-full-title] HSS journal : the musculoskeletal journal of Hospital for Special Surgery
  • [ISO-abbreviation] HSS J
  • [Language] eng
  • [Publication-type] Clinical Conference; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2642545
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12. Kaiser R, Barton JL, Chang M, Catanese JJ, Li Y, Begovich AB, Criswell LA: Factor V Leiden and thrombosis in patients with systemic lupus erythematosus: a meta-analysis. Genes Immun; 2009 Jul;10(5):495-502
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  • The aim of this study was to perform a meta-analysis of the association between the factor V Leiden polymorphism (FVL) and thrombosis among patients with systemic lupus erythematosus (SLE) and/or antiphospholipid antibody (aPL) positivity.
  • Included studies recruited patients based on SLE or aPL-positive status, confirmed subjects' SLE diagnosis as defined by the American College of Rheumatology, and documented thrombotic events.
  • In the secondary analysis with our individual patient dataset (n=1447 European-derived individuals), SLE subjects with the FVL polymorphism still had more than two times the odds of thrombosis compared to subjects without this polymorphism, even when adjusting for covariates such as gender, age and aPL status.
  • SLE and/or aPL-positive patients with the FVL variant have more than two times the odds of thrombosis compared to those without this polymorphism.

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  • [Cites] Arterioscler Thromb Vasc Biol. 2008 Jan;28(1):173-9 [17975119.001]
  • [Cites] Scand J Rheumatol. 2007 May-Jun;36(3):198-205 [17657674.001]
  • [Cites] Ann Rheum Dis. 2009 Feb;68(2):238-41 [18782792.001]
  • [Cites] Clin Appl Thromb Hemost. 2000 Jan;6(1):41-5 [10726048.001]
  • [Cites] Br J Haematol. 2000 Mar;108(4):865-70 [10792297.001]
  • [Cites] Haematologica. 2001 Jul;86(7):735-41 [11454529.001]
  • [Cites] Clin Rheumatol. 2001;20(4):259-61 [11529632.001]
  • [Cites] J Rheumatol. 2001 Sep;28(9):2018-24 [11550969.001]
  • [Cites] J Rheumatol. 2002 Aug;29(8):1683-8 [12180730.001]
  • [Cites] J Rheumatol. 2003 Nov;30(11):2385-91 [14677182.001]
  • [Cites] Blood. 2004 Jul 1;104(1):143-8 [15026314.001]
  • [Cites] Arthritis Rheum. 1982 Nov;25(11):1271-7 [7138600.001]
  • [Cites] Lancet. 1995 Jan 14;345(8942):132-3 [7815875.001]
  • [Cites] J Rheumatol. 1995 Jun;22(6):1215 [7674266.001]
  • [Cites] Thromb Haemost. 1995 Oct;74(4):1029-31 [8560406.001]
  • [Cites] Lupus. 1996 Aug;5(4):303-6 [8869903.001]
  • [Cites] Thromb Haemost. 1996 Oct;76(4):514-7 [8902988.001]
  • [Cites] Thromb Res. 1996 Dec 1;84(5):361-5 [8948063.001]
  • [Cites] Lupus. 1996 Dec;5(6):598-601 [9116703.001]
  • [Cites] BMJ. 1997 Sep 13;315(7109):629-34 [9310563.001]
  • [Cites] Arthritis Rheum. 1997 Sep;40(9):1720-1 [9324029.001]
  • [Cites] Thromb Haemost. 1998 Jan;79(1):46-9 [9459321.001]
  • [Cites] J Rheumatol. 1999 Mar;26(3):588-90 [10090167.001]
  • [Cites] Medicine (Baltimore). 1999 May;78(3):167-75 [10352648.001]
  • [Cites] Thromb Haemost. 2004 Dec;92(6):1312-9 [15583739.001]
  • [Cites] Arthritis Rheum. 2004 Dec;50(12):3947-57 [15593203.001]
  • [Cites] Arthritis Rheum. 2005 Jun 15;53(3):452-9 [15934123.001]
  • [Cites] Arthritis Rheum. 2005 Sep;52(9):2774-82 [16142761.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2005 Oct;25(10):2043-53 [16100033.001]
  • [Cites] J Rheumatol. 2006 Sep;33(9):1715-7 [16960931.001]
  • [Cites] Bull NYU Hosp Jt Dis. 2006;64(1-2):57-9 [17121491.001]
  • [Cites] Arch Pathol Lab Med. 2007 Jun;131(6):866-71 [17550313.001]
  • [Cites] Arch Pathol Lab Med. 2007 Jun;131(6):872-84 [17550314.001]
  • [Cites] Genes Immun. 2007 Jun;8(4):279-87 [17344889.001]
  • [Cites] Blood. 2008 Jul 1;112(1):19-27 [18574041.001]
  • (PMID = 19421222.001).
  • [ISSN] 1476-5470
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P60 AR053308-020001; United States / NIAMS NIH HHS / AR / P60 AR053308; United States / NCRR NIH HHS / RR / M01 RR000079; United States / NIAMS NIH HHS / AR / P60 AR053308-010001; United States / NIAMS NIH HHS / AR / AR002175-05; United States / NCRR NIH HHS / RR / 5 M01 RR-00079; United States / NIAMS NIH HHS / AR / K24 AR002175-03; United States / NIAMS NIH HHS / AR / AR053308-030001; United States / NIAMS NIH HHS / AR / K24 AR002175-01A1; United States / NIAMS NIH HHS / AR / K24 AR002175-04; United States / NIAMS NIH HHS / AR / AR053308-010001; United States / NIAMS NIH HHS / AR / K24 AR002175-02; United States / NIAMS NIH HHS / AR / AR053308-020001; United States / NIAMS NIH HHS / AR / P60 AR0533008; United States / NIAMS NIH HHS / AR / AR002175-01A1; United States / NIAMS NIH HHS / AR / K24 AR02175; United States / NIAMS NIH HHS / AR / K24 AR002175-05; United States / NIAMS NIH HHS / AR / AR002175-02; United States / NIAMS NIH HHS / AR / P60 AR053308-030001; United States / NIAMS NIH HHS / AR / R01 AR22804; United States / NIAMS NIH HHS / AR / AR002175-03; United States / NIAMS NIH HHS / AR / K24 AR002175; United States / NIAMS NIH HHS / AR / AR002175-04
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V
  • [Other-IDs] NLM/ NIHMS106580; NLM/ PMC2766554
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13. Cherrier-De Wilde S, Herregods MC, Verhoef G, Arnout J: A patient with Hodgkin's lymphoma, antiphospholipid syndrome and severe mitral insufficiency. Acta Clin Belg; 2006 Jul-Aug;61(4):183-7
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  • [Title] A patient with Hodgkin's lymphoma, antiphospholipid syndrome and severe mitral insufficiency.
  • The association between Hodgkin's lymphoma, antiphospholipid syndrome and severe mitral insufficiency is a very rare event.
  • The possible link between these symptoms being antiphospholipid antibodies, is discussed briefly.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Hodgkin Disease / complications. Mitral Valve Insufficiency / complications

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  • (PMID = 17091916.001).
  • [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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14. 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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  • [Cites] J Biol Chem. 2007 Aug 31;282(35):25231-9 [17609203.001]
  • [Cites] J Invest Dermatol. 1999 Dec;113(6):954-9 [10594736.001]
  • [Cites] Clin Exp Dermatol. 2001 Jan;26(1):59-71 [11260183.001]
  • [Cites] Genes Dev. 2001 Oct 15;15(20):2687-701 [11641275.001]
  • [Cites] J Invest Dermatol. 2001 Dec;117(6):1662-5 [11886538.001]
  • [Cites] J Invest Dermatol. 2002 May;118(5):887-90 [11982770.001]
  • [Cites] J Am Acad Dermatol. 2002 Oct;47(4):519-23 [12271294.001]
  • [Cites] J Invest Dermatol. 2003 Aug;121(2):430-2 [12880440.001]
  • [Cites] Cell. 1988 Jul 29;54(3):383-91 [2840205.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7717-21 [8052649.001]
  • [Cites] J Invest Dermatol. 1997 Feb;108(2):224-8 [9008239.001]
  • [Cites] Science. 1998 Jan 30;279(5351):720-4 [9445480.001]
  • [Cites] Am J Hum Genet. 1998 Feb;62(2):386-90 [9463324.001]
  • [Cites] J Invest Dermatol. 1998 Nov;111(5):744-50 [9804332.001]
  • [Cites] Genomics. 1999 Mar 1;56(2):141-8 [10051399.001]
  • [Cites] Am J Hum Genet. 1999 May;64(5):1323-9 [10205263.001]
  • [Cites] J Invest Dermatol. 1999 Aug;113(2):281-3 [10469319.001]
  • [Cites] Dermatologica. 1954 Feb;108(2):114-21 [13150805.001]
  • [Cites] Clin Exp Dermatol. 2005 Jul;30(4):363-5 [15953070.001]
  • [Cites] Eur J Dermatol. 2005 Sep-Oct;15(5):332-8 [16172039.001]
  • [Cites] Arch Dermatol Res. 2007 Jun;299(3):157-61 [17372750.001]
  • (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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15. Subbarayan PR, Lee K, Ardalan B: Arsenic trioxide suppresses thymidylate synthase in 5-FU-resistant colorectal cancer cell line HT29 In Vitro re-sensitizing cells to 5-FU. Anticancer Res; 2010 Apr;30(4):1157-62
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  • [Title] Arsenic trioxide suppresses thymidylate synthase in 5-FU-resistant colorectal cancer cell line HT29 In Vitro re-sensitizing cells to 5-FU.
  • Arsenic trioxide (As(2)O(3)), a Food and Drug Administration (FDA) approved drug is successfully being used to treat acute promyelocytic leukemia (APL).
  • Several clinical trials also suggest its ineffectiveness on solid tumors.

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  • (PMID = 20530422.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 0 / RNA, Messenger; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.1.1.45 / Thymidylate Synthase; S7V92P67HO / arsenic trioxide; U3P01618RT / Fluorouracil
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16. O'Neil KM: Role of complement in antiphospholipid antibody-mediated thrombosis. Curr Rheumatol Rep; 2007 Jun;9(3):205-11
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  • [Title] Role of complement in antiphospholipid antibody-mediated thrombosis.
  • The mechanisms by which an antibody that reacts with phospholipids (universal components of mammalian membranes) causes thrombosis are not immediately obvious.
  • The development of an animal model of antiphospholipid antibody syndrome has moved the field forward in dissecting the pathogenesis of antiphospholipid antibody syndrome and has implicated the complement system in the mechanism of disease.
  • Understanding complement's role in promoting thrombosis will be important in designing safer, more effective approaches to the treatment of patients with antiphospholipid antibodies, and may shed light on which patients are at greatest risk for thrombosis, perhaps permitting primary prophylaxis before irreversible tissue and organ damage occur.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Complement System Proteins / immunology. Thrombosis / immunology
  • [MeSH-minor] Animals. Antibodies, Antiphospholipid / immunology. Complement Activation / immunology. Disease Models, Animal. Female. Humans. Male. Pregnancy. Pregnancy Complications, Hematologic / immunology

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  • [Cites] Inflamm Res. 1999 Oct;48(10):524-6 [10563468.001]
  • [Cites] Thromb Haemost. 1997 Feb;77(2):394-8 [9157602.001]
  • [Cites] Thromb Res. 2004;114(5-6):467-76 [15507280.001]
  • [Cites] J Thromb Haemost. 2005 May;3(5):848-53 [15869575.001]
  • [Cites] Am J Obstet Gynecol. 1987 Jan;156(1):114-9 [3799744.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2353-8 [15226179.001]
  • [Cites] J Exp Med. 1995 Jan 1;181(1):151-9 [7528766.001]
  • [Cites] Lupus. 1996 Jun;5(3):196-205 [8803890.001]
  • [Cites] J Rheumatol. 1995 Feb;22(2):227-35 [7738943.001]
  • [Cites] Arthritis Rheum. 1988 Sep;31(9):1211-2 [3422020.001]
  • [Cites] Ann Rheum Dis. 1995 Jun;54(6):530-1 [7632103.001]
  • [Cites] Arthritis Rheum. 2006 Feb;54(2):670-4 [16447243.001]
  • [Cites] Thromb Haemost. 2000 May;83(5):728-31 [10823270.001]
  • [Cites] Ann Med Interne (Paris). 1996;147(2):115-6 [8760690.001]
  • [Cites] Lupus. 2003;12(7):535-8 [12892394.001]
  • [Cites] Ann Intern Med. 1992 Aug 15;117(4):303-8 [1637025.001]
  • [Cites] J Immunol. 2006 Oct 1;177(7):4794-802 [16982920.001]
  • [Cites] J Rheumatol. 1988 Jan;15(1):80-6 [3351843.001]
  • [Cites] Ann Rheum Dis. 2002 Nov;61 Suppl 2:ii46-50 [12379621.001]
  • [Cites] Circulation. 1999 Apr 20;99(15):1997-2002 [10209004.001]
  • [Cites] Am J Obstet Gynecol. 1998 Jul;179(1):226-34 [9704792.001]
  • [Cites] N Engl J Med. 2003 Sep 18;349(12):1133-8 [13679527.001]
  • [Cites] Lupus. 1999;8(6):423-9 [10483009.001]
  • [Cites] Arthritis Rheum. 1987 Jun;30(6):601-6 [3111489.001]
  • [Cites] Exp Clin Immunogenet. 1992;9(2):72-9 [1489552.001]
  • [Cites] Ann Rheum Dis. 1991 Apr;50(4):249-50 [2029207.001]
  • [Cites] Lupus. 2005;14(12):953-8 [16425575.001]
  • [Cites] Nat Med. 2004 Nov;10(11):1222-6 [15489858.001]
  • [Cites] Arch Intern Med. 2002 May 27;162(10):1164-9 [12020188.001]
  • [Cites] Arthritis Rheum. 2005 Jul;52(7):2120-4 [15986360.001]
  • [Cites] Arthritis Rheum. 1989 Mar;32(3):259-64 [2522783.001]
  • [Cites] Am J Obstet Gynecol. 1990 Jul;163(1 Pt 1):210-6 [2197866.001]
  • [Cites] N Engl J Med. 1995 Apr 13;332(15):993-7 [7885428.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2340-6 [15956288.001]
  • [Cites] Mol Immunol. 2005 Jan;42(1):87-97 [15488947.001]
  • [Cites] J Exp Med. 2002 Jan 21;195(2):211-20 [11805148.001]
  • [Cites] Science. 2000 Jan 21;287(5452):498-501 [10642554.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1644-54 [14660741.001]
  • [Cites] Ann N Y Acad Sci. 2005 Jun;1051:413-20 [16126983.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):485-90 [15611274.001]
  • [Cites] Clin Exp Rheumatol. 1992 Sep-Oct;10(5):455-60 [1458697.001]
  • [Cites] Scand J Immunol. 1995 May;41(5):427-32 [7725061.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1867-75 [12000738.001]
  • [Cites] J Clin Invest. 1995 Nov;96(5):2211-9 [7593607.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3069-73 [2014226.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):451-7 [9054647.001]
  • [Cites] Thromb Res. 2004;114(5-6):391-6 [15507269.001]
  • [Cites] Arthritis Rheum. 1998 Jun;41(6):1026-39 [9627012.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 1991 Oct 8;41(3):179-86 [1936501.001]
  • (PMID = 17531173.001).
  • [ISSN] 1523-3774
  • [Journal-full-title] Current rheumatology reports
  • [ISO-abbreviation] Curr Rheumatol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 9007-36-7 / Complement System Proteins
  • [Number-of-references] 50
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17. Chim CS, Chan WW, Kwong YL: Epigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias. J Clin Pathol; 2008 Jul;61(7):844-7
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  • [Title] Epigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias.
  • AIM AND METHODS: To analyse the potential inactivation of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway by aberrant promoter methylation in acute leukaemias.
  • At diagnosis, DAP kinase methylation occurred in eight (25%) APL patients and none of the other AML patients (8/32 vs 0/50, p = 0.001).
  • DAP kinase methylation was detected in four (16%) ALL patients. p14 and Apaf-1 methylation was not detected in any of the 32 cases of acute promyelocytic leukaemia (APL), 50 cases of other subtypes of acute myeloid leukaemia (AML), and 25 cases of acute lymphoblastic leukaemia.
  • CONCLUSION: Among AML subtypes, DAP kinase is preferentially hypermethylated in APL.
  • [MeSH-major] Apoptosis / genetics. Death-Associated Protein Kinases / genetics. Epigenesis, Genetic. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Adult. Apoptotic Protease-Activating Factor 1 / genetics. Apoptotic Protease-Activating Factor 1 / metabolism. Base Sequence. DNA Methylation. Humans. Molecular Sequence Data. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Polymerase Chain Reaction / methods. Proto-Oncogene Proteins c-mdm2 / genetics. Proto-Oncogene Proteins c-mdm2 / metabolism. Signal Transduction. Tumor Cells, Cultured. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18587015.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ J04238
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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18. Wyllie S, Fairlamb AH: Differential toxicity of antimonial compounds and their effects on glutathione homeostasis in a human leukaemia monocyte cell line. Biochem Pharmacol; 2006 Jan 12;71(3):257-67
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  • [Title] Differential toxicity of antimonial compounds and their effects on glutathione homeostasis in a human leukaemia monocyte cell line.
  • Trivalent antimonial compounds (Sb(III)), originally used in the treatment of leishmaniasis, are now being proposed as a novel therapy for acute promyelocytic leukaemia (APL).
  • Here, we examine the effects of Sb(III) and pentavalent antimonial drugs (Sb(V)) on glutathione homeostasis, oxidative stress and apoptosis in the human leukaemia monocyte cell line, THP-1.
  • On exposure to Sb(III), intracellular free glutathione (GSH) levels in macrophages decrease linearly by 50% over 4h, associated with efflux of both GSH and accumulation of intracellular glutathione disulphide (GSSG).
  • Sb(III)-treated THP-1 macrophages go on to exhibit elevated levels of reactive oxygen species and show the early signs of apoptosis.
  • Collectively, these findings suggest that Sb(III) seriously compromises thiol homeostasis in THP-1 macrophages and that this may be an early defining event in the mode of action of antimonials against leukaemia cells.
  • [MeSH-minor] Cell Line, Tumor. Glutathione Reductase / metabolism. Humans. Leukemia. Oxidation-Reduction. Reactive Oxygen Species / metabolism

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  • (PMID = 16318845.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; DL6OZ476V3 / Antimony Potassium Tartrate; EC 1.8.1.7 / Glutathione Reductase; GAN16C9B8O / Glutathione; V083S0159D / Antimony Sodium Gluconate
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19. Giner V, Oltra MR, Esteban MJ, García-Fuster MJ, Salvador A, Núñez J, Redón J: Catastrophic antiphospholipid syndrome related to severe ovarian hyperstimulation. Clin Rheumatol; 2007 Jun;26(6):991-3
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  • [Title] Catastrophic antiphospholipid syndrome related to severe ovarian hyperstimulation.
  • Antiphospholipid syndrome (APS) is a cause of infertility and fetal loss.
  • In spite of the life-threatening risk of this situation, the indication for preventive anti-aggregation and/or anticoagulation is not clear.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Aortic Aneurysm / etiology. Myocardial Infarction / etiology. Ovarian Hyperstimulation Syndrome / complications. Ovarian Hyperstimulation Syndrome / immunology. Sinus of Valsalva. Stroke / etiology


20. Kon Y, Atsumi T, Hagiwara H, Furusaki A, Kataoka H, Horita T, Yasuda S, Amengual O, Takao K: Thrombotic microangiopathy in patients with phosphatidylserine dependent antiprothrombin antibodies and antiphospholipid syndrome. Clin Exp Rheumatol; 2008 Jan-Feb;26(1):129-32
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  • [Title] Thrombotic microangiopathy in patients with phosphatidylserine dependent antiprothrombin antibodies and antiphospholipid syndrome.
  • Thrombotic microangiopathy (TMA) is a rare disorder characterized by microvascular thrombosis.
  • TMA has been reported in patients with antiphospholipid antibodies and/or antiphospholipid syndrome but its pathogenesis is not clarified.
  • Both patients were successfully treated with a series of plasma exchange.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Autoantibodies / blood. Phosphatidylserines / physiology. Thrombosis / complications. Vascular Diseases / complications
  • [MeSH-minor] Adult. Female. Humans. Lupus Erythematosus, Systemic / complications. Plasma Exchange. Pregnancy. Pregnancy Complications

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  • (PMID = 18328160.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Phosphatidylserines
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21. Dellaire G, Bazett-Jones DP: Beyond repair foci: subnuclear domains and the cellular response to DNA damage. Cell Cycle; 2007 Aug 1;6(15):1864-72
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  • Besides chromatin, DNA damage also affects the dynamic behaviour, morphology and biochemical composition of various subnuclear domains, including the nucleolus, promyelocytic leukemia (PML) nuclear bodies and Cajal bodies.

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  • (PMID = 17660715.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
  • [Number-of-references] 137
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22. Godlewska J, Luniewski W, Zagrodzki B, Kaczmarek L, Bielawska-Pohl A, Dus D, Wietrzyk J, Opolski A, Siwko M, Jaromin A, Jakubiak A, Kozubek A, Peczyñska-Czoch W: Biological evaluation of omega-(dialkylamino)alkyl derivatives of 6H-indolo[2,3-b]quinoline--novel cytotoxic DNA topoisomerase II inhibitors. Anticancer Res; 2005 Jul-Aug;25(4):2857-68
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  • They also showed cytotoxic activity against KB (human cervix carcinoma) cells (ID50 varied from 2.1 to 9.0 microM) and were able to overcome multidrug resistance in colorectal adenocarcinoma LoVo/DX, uterine sarcoma MES-SA/DX5 and promyelocytic leukemia HL-60/MX2 cells (the values of the resistance index RI fell between 0.54 and 2.4).
  • The compounds induced G2M-phase cell cycle arrest in Jurkat T-cell leukemia cells, revealed DNA-binding properties and inhibited topoisomerase II activity.

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  • (PMID = 16080538.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents, Phytogenic; 0 / DNA Adducts; 0 / Indoles; 0 / Quinolines; 0 / Topoisomerase II Inhibitors; 9007-49-2 / DNA; 91080-16-9 / calf thymus DNA
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23. d'Angeac AD, Stefas I, Duperray C, Rucheton M, Graafland H, Montero JL, Chicheportiche R: Oxidation and biotinylation of beta 2 glycoprotein I glycan chains induce an increase in its affinity for anionic phospholipids similar to that obtained by the addition of anti-beta 2 glycoprotein I or anti-cardiolipin antibodies. J Immunol Methods; 2005 May;300(1-2):160-78
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  • [Title] Oxidation and biotinylation of beta 2 glycoprotein I glycan chains induce an increase in its affinity for anionic phospholipids similar to that obtained by the addition of anti-beta 2 glycoprotein I or anti-cardiolipin antibodies.
  • Binding of beta 2 glycoprotein I (beta2GPI) to apoptotic cells plays a key role in the opsonization of apoptotic bodies and the formation of antiphospholipids antibodies.
  • Binding equilibrium studies, performed on solid-state anionic phospholipids (AnPL), revealed that beta2GPI-bh had a greater apparent affinity for AnPL than native beta2GPI.
  • In presence of the anti-beta2GPI mAb 8C3, the ability of native beta2GPI to bind to AnPL was increased and binding to apoptotic PI+ and PI- CEM cells was observed whereas binding of beta2GPI-bh was barely affected by the addition of 8C3.
  • It is not clear why the oxidation and biotinylation of glycan chains of beta2GPI increases its affinity for AnPL, but it seems that if such oxidative process occurs naturally, it could participate in enhancing antiphospholipid formation.
  • [MeSH-major] Antibodies, Anticardiolipin / metabolism. Glycoproteins / chemistry. Glycoproteins / metabolism. Phospholipids / metabolism

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  • (PMID = 15904931.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Phospholipids; 0 / Polysaccharides; 0 / Recombinant Proteins; 0 / beta 2-Glycoprotein I
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24. Pilarska E, Lemka M, Bakowska A: [Antiphospholipid antibodies in children with migraine]. Neurol Neurochir Pol; 2006 Jul-Aug;40(4):291-6
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  • [Title] [Antiphospholipid antibodies in children with migraine].
  • We tried to assess whether the type of migraine (with aura or without aura) had the influence on those values.
  • The type of migraine had no influence on the values of aCL.

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  • (PMID = 16967350.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Biomarkers; 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M
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25. Makhija S, Aneja S, Tripathi RP, Narayan S: Etiological profile of stroke and its relation with prothrombotic states. Indian J Pediatr; 2008 Jun;75(6):579-84
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  • METHODS: Children with acute stroke with no evidence of CNS infection or head injury were studied.
  • Presenting symptoms were motor deficit (72%), seizure (66%), altered sensorium (36%), aphasia (27%).
  • Causes identified were antiphospholipid antibody syndrome (25%), Moya Moya disease (16.6%), cardiac disease (11.1%), vasculitis (5.5%), ATIII deficiency (5.5%), Protein C deficiency (2.7%).
  • Hemorrhage was seen in 8.2% of cases and they had DIC or liver disease as the underlying cause.
  • CONCLUSIONS: Magnetic Resonance Angiography and ELISA for antiphospholipid antibody should be done in all patients with stroke without an obvious cause.
  • [MeSH-minor] Antibodies, Antiphospholipid. Antithrombin III / analysis. Case-Control Studies. Child. Child, Preschool. Enzyme-Linked Immunosorbent Assay. Female. Humans. Infant. Magnetic Resonance Angiography. Male. Moyamoya Disease / complications. Prospective Studies. Protein C / analysis. Risk Factors

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  • [CommentIn] Indian J Pediatr. 2009 Jun;76(6):661; author reply 661 [19618149.001]
  • [Cites] Acta Paediatr. 1994 Jul;83(7):762-5 [7949809.001]
  • [Cites] Pediatr Neurol. 1995 Nov;13(4):323-6 [8771168.001]
  • [Cites] Pediatrics. 1994 Oct;94(4 Pt 1):500-3 [7936859.001]
  • [Cites] J Neurol. 1985;232(3):137-43 [4031955.001]
  • [Cites] Ann Neurol. 1997 May;41(5):565-6 [9153515.001]
  • [Cites] Pediatr Neurosurg. 1999 Jul;31(1):45-8 [10545822.001]
  • [Cites] J Clin Epidemiol. 1995 Nov;48(11):1343-8 [7490597.001]
  • [Cites] Childs Brain. 1976;2(4):257-71 [991668.001]
  • [Cites] Acta Paediatr Scand. 1983 May;72(3):391-5 [6880725.001]
  • [Cites] Dev Med Child Neurol. 1968 Oct;10(5):621-5 [5708281.001]
  • [Cites] Acta Neurol Scand. 1994 Oct;90(4):251-5 [7839810.001]
  • [Cites] Acta Neurol Scand. 1997 Dec;96(6):401-6 [9449480.001]
  • [Cites] Neuropadiatrie. 1973 Jan;4(1):7-19 [4739779.001]
  • [Cites] N Engl J Med. 1988 May 5;318(18):1148-52 [3362165.001]
  • [Cites] Ann Neurol. 1991 Jun;29(6):585-9 [1892360.001]
  • [Cites] Neurology. 1978 Aug;28(8):763-8 [567292.001]
  • [Cites] Eur J Pediatr. 1989 Dec;149(3):216-8 [2612512.001]
  • [Cites] Neurology. 1973 Jul;23 (7):734-44 [4736492.001]
  • (PMID = 18759085.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Protein C; 9000-94-6 / Antithrombin III
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26. Zhao Y, Leal K, Abi-Farah C, Martin KC, Sossin WS, Klein M: Isoform specificity of PKC translocation in living Aplysia sensory neurons and a role for Ca2+-dependent PKC APL I in the induction of intermediate-term facilitation. J Neurosci; 2006 Aug 23;26(34):8847-56
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  • [Title] Isoform specificity of PKC translocation in living Aplysia sensory neurons and a role for Ca2+-dependent PKC APL I in the induction of intermediate-term facilitation.
  • In Aplysia, there are two major phorbol ester-activated PKCs, Ca2+-activated PKC Apl I and Ca2+-independent PKC Apl II.
  • Functional Apl II, but not Apl I, in sensory neurons is required for a form of short-term facilitation induced at sensorimotor synapses by the facilitatory transmitter serotonin (5-HT).
  • Because PKCs are activated by translocating from the cytoplasm to the membrane, we used fluorescently tagged PKCs to determine the isoform and cell-type specificity of translocation in living Aplysia neurons.
  • In Sf9 cells, low levels of diacylglycerol translocate Apl II, but not Apl I, which requires calcium for translocation at low concentrations of diacylglycerol.
  • Accordingly, application of 5-HT to Aplysia sensory neurons in the absence of neuronal firing translocates Apl II, but not Apl I, consistent with the role of Apl II in short-term facilitation.
  • Apl I translocates only if 5-HT is coupled to firing in the sensory neuron; firing alone is ineffective.
  • Because combined 5-HT and firing are required for the induction of one type of intermediate-term facilitation at these synapses, we asked whether this form of synaptic plasticity involves activation of Apl I.
  • We report here that dominant-negative Apl I, but not Apl II, blocks intermediate-term facilitation.
  • Thus, different isoforms of PKC translocate under different conditions to mediate distinct types of synaptic plasticity: Ca2+-independent Apl II is involved in short-term facilitation, and Ca2+-dependent Apl I contributes to intermediate-term facilitation.

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  • [ErratumIn] J Neurosci. 2006 Sep 20;26(38):9833
  • (PMID = 16928874.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS47646
  • [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 / Diglycerides; 0 / Isoenzymes; 333DO1RDJY / Serotonin; EC 2.7.1.- / Apl II protein kinase C; EC 2.7.11.13 / Protein Kinase C; SY7Q814VUP / Calcium
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27. Iwagawa T, Hashimoto K, Okamura H, Kurawaki J, Nakatani M, Hou DX, Fujii M, Doe M, Morimoto Y, Takemura K: Biscembranes from the soft coral Sarcophyton glaucum. J Nat Prod; 2006 Aug;69(8):1130-3
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  • Four novel biscembranes have been isolated from the soft coral Sarcophyton glaucum, collected at Amami Oshima, two of which showed weak activity against proliferation of human promyelocytic leukemia cells (HL-60).

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  • (PMID = 16933862.001).
  • [ISSN] 0163-3864
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diterpenes
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28. Tossidou I, Dangers M, Koch A, Brandt DT, Schiffer M, Kardinal C: Tyrosine phosphatase SHP-2 is a regulator of p27(Kip1) tyrosine phosphorylation. Cell Cycle; 2008 Dec 15;7(24):3858-68
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  • Considering the associated dephosphorylation as a pivotal event in the regulation of cell cycle proteins, we focused on the tyrosine phosphatase SHP-2, which is regulated in promyelocytic leukemia cells on G-CSF stimulation.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism

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  • (PMID = 19066472.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / SH2 Domain-Containing Protein Tyrosine Phosphatases
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29. Abaza L, Talorete TP, Yamada P, Kurita Y, Zarrouk M, Isoda H: Induction of growth inhibition and differentiation of human leukemia HL-60 cells by a Tunisian gerboui olive leaf extract. Biosci Biotechnol Biochem; 2007 May;71(5):1306-12
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  • [Title] Induction of growth inhibition and differentiation of human leukemia HL-60 cells by a Tunisian gerboui olive leaf extract.
  • Cancer protection associated with the consumption of olive products is well established, but not for leukemia.
  • The protective effects of olive (Olea europaea L.) leaves were investigated by incubating human promyelocytic leukemia HL-60 cells with olive leaf extracts (OLEs) from seven principal Tunisian olive varieties, namely, Chemchali, Chemlali, Chétoui, Gerboui, Sayali, Zalmati and Zarrazi.
  • The results showed significant growth inhibition of HL-60 cells incubated for 48 h with a 100-fold dilution of each OLE which had been obtained by incubating 10 g of dried leaves in 100 ml of 70% ethanol for one week with subsequent ultrafiltration.
  • DNA fragmentation was observed in the cells incubated for 19 h with a 100-fold dilution of the Chemchali, Chemlali and Zalmati extracts.
  • [MeSH-major] Cell Differentiation / drug effects. Cell Proliferation / drug effects. Leukemia / drug therapy. Olea / chemistry. Plant Extracts / pharmacology. Plant Leaves / chemistry

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  • (PMID = 17485840.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Plant Extracts; 298-83-9 / Nitroblue Tetrazolium; 3K9958V90M / Ethanol
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30. Zhang HL, Yang YM, Meng WT, Deng CQ: [Effects of Tanshinone IIA on procoagulant activity of human ECV304 cell line induced by NB4 cells]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2006 Jan;37(1):55-9
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  • OBJECTIVE: To investigate the effects of Tanshinone IIA (Tan IIA) on procoagulant activity (PCA) of human ECV304 cells induced by acute promyelocytic leukemia cell line NB4 cells.
  • CONCLUSION: Tan IIA-NB4-CM can increase the levels of PCA and TF: Act of ECV304 cells through some unidentified factor; however, Tan IIA can obviously decrease the PCA and TF: Act levels of ECV304 cells induced by Tan IIA-NB4-CM.
  • [MeSH-minor] Anticoagulants / pharmacology. Cell Differentiation / drug effects. Cell Line. Cell Line, Tumor. Diterpenes, Abietane. Drugs, Chinese Herbal / pharmacology. Humans. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Tretinoin / pharmacology. Umbilical Veins / cytology

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  • (PMID = 16468642.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Culture Media, Conditioned; 0 / Diterpenes, Abietane; 0 / Drugs, Chinese Herbal; 0 / Phenanthrenes; 0 / endothelial cell procoagulant activity; 03UUH3J385 / tanshinone; 5688UTC01R / Tretinoin; 9035-58-9 / Thromboplastin
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31. Sobieszczuk DF, Poliakov A, Xu Q, Wilkinson DG: A feedback loop mediated by degradation of an inhibitor is required to initiate neuronal differentiation. Genes Dev; 2010 Jan 15;24(2):206-18
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  • Btbd6a is an adaptor for the Cul3 ubiquitin ligase complex, and we find that it binds to the transcriptional repressor Plzf (promyelocytic leukemia zinc finger).

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  • [Cites] Development. 2002 Jun;129(11):2639-48 [12015292.001]
  • [Cites] Nat Rev Neurosci. 2002 Jul;3(7):517-30 [12094208.001]
  • [Cites] EMBO Rep. 2002 Jul;3(7):688-94 [12101103.001]
  • [Cites] Mol Cell Biol. 2002 Oct;22(19):6854-65 [12215542.001]
  • [Cites] Curr Opin Neurobiol. 2003 Feb;13(1):16-25 [12593978.001]
  • [Cites] Int J Dev Biol. 2003;47(7-8):643-51 [14756340.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):647-52 [15156142.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):653-9 [15156143.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):551-3 [15167928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8378-83 [15148389.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7130-9 [15282312.001]
  • [Cites] Trends Genet. 2004 Oct;20(10):481-90 [15363902.001]
  • [Cites] Mol Cell Biol. 2004 Oct;24(19):8477-86 [15367669.001]
  • [Cites] Neuron. 1991 Dec;7(6):947-63 [1764246.001]
  • [Cites] Development. 1991 Dec;113(4):1193-206 [1811936.001]
  • [Cites] Trends Genet. 1992 Jun;8(6):202-8 [1496555.001]
  • [Cites] EMBO J. 1993 Mar;12(3):1161-7 [8384553.001]
  • [Cites] Nucleic Acids Res. 1993 Mar 11;21(5):1087-95 [8464695.001]
  • [Cites] Genes Dev. 1993 Jun;7(6):1085-96 [8504931.001]
  • [Cites] Development. 1993 Jun;118(2):417-25 [8223269.001]
  • [Cites] Nucleic Acids Res. 1994 Nov 11;22(22):4673-80 [7984417.001]
  • [Cites] Cell. 1995 Feb 10;80(3):453-62 [7859287.001]
  • [Cites] Cell. 1995 Feb 10;80(3):463-72 [7888014.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 14;92(6):2249-53 [7892256.001]
  • [Cites] Neuron. 1995 May;14(5):913-25 [7748559.001]
  • [Cites] Development. 1994 Apr;120(4):935-45 [7600969.001]
  • [Cites] Development. 2003 Apr;130(8):1591-604 [12620984.001]
  • [Cites] J Biol Chem. 2003 Jun 13;278(24):21592-600 [12682069.001]
  • [Cites] Neuron. 2003 Jul 3;39(1):13-25 [12848929.001]
  • [Cites] Nature. 2003 Sep 18;425(6955):311-6 [13679921.001]
  • [Cites] Nature. 2003 Sep 18;425(6955):316-21 [13679922.001]
  • [Cites] Neuron. 2000 May;26(2):313-29 [10839352.001]
  • [Cites] Neuron. 2000 May;26(2):331-43 [10839353.001]
  • [Cites] Development. 2000 Jul;127(13):2933-43 [10851137.001]
  • [Cites] Development. 2000 Oct;127(19):4203-16 [10976052.001]
  • [Cites] J Cell Sci. 2000 Nov;113 ( Pt 22):3897-905 [11058077.001]
  • [Cites] Mol Cell. 2003 Sep;12(3):783-90 [14527422.001]
  • [Cites] Nat Cell Biol. 2003 Nov;5(11):1001-7 [14528312.001]
  • [Cites] Nat Cell Biol. 2003 Nov;5(11):950-1 [14593416.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(24):9375-88 [14645547.001]
  • [Cites] J Neurosci. 1995 Jul;15(7 Pt 1):4927-42 [7623123.001]
  • [Cites] Dev Dyn. 1995 Jul;203(3):253-310 [8589427.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Cell. 1997 Aug 8;90(3):459-67 [9267026.001]
  • [Cites] Cell. 1997 Aug 8;90(3):469-78 [9267027.001]
  • [Cites] Development. 1997 Nov;124(22):4557-69 [9409673.001]
  • [Cites] Development. 1998 Feb;125(3):359-70 [9425132.001]
  • [Cites] Genes Dev. 1998 Jul 1;12(13):2036-47 [9649507.001]
  • [Cites] Mol Cell Biol. 1998 Sep;18(9):5533-45 [9710637.001]
  • [Cites] Oncogene. 1999 Jan 28;18(4):925-34 [10023668.001]
  • [Cites] Nature. 1999 May 20;399(6733):267-71 [10353250.001]
  • [Cites] Trends Biochem Sci. 2004 Dec;29(12):634-7 [15544948.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jan;6(1):9-20 [15688063.001]
  • [Cites] Development. 2005 Mar;132(6):1375-85 [15716337.001]
  • [Cites] Exp Cell Res. 2005 Jun 10;306(2):343-8 [15925590.001]
  • [Cites] Genome Biol. 2005;6(10):R82 [16207353.001]
  • [Cites] Nat Rev Neurosci. 2006 Feb;7(2):93-102 [16429119.001]
  • [Cites] Trends Cell Biol. 2006 Nov;16(11):578-87 [16996269.001]
  • [Cites] Bioessays. 2006 Dec;28(12):1194-202 [17120193.001]
  • [Cites] Curr Top Microbiol Immunol. 2007;313:31-48 [17217037.001]
  • [Cites] PLoS Genet. 2007 May 25;3(5):e78 [17530925.001]
  • [Cites] Dev Cell. 2007 Aug;13(2):283-97 [17681138.001]
  • [Cites] Mol Cell Biol. 2007 Sep;27(18):6334-49 [17636022.001]
  • [Cites] Biochem Biophys Res Commun. 2008 May 16;369(4):1209-14 [18348865.001]
  • [Cites] Dev Dyn. 2008 Nov;237(11):3352-60 [18855900.001]
  • [Cites] J Cell Biol. 2008 Dec 1;183(5):933-47 [19047466.001]
  • [Cites] Mech Dev. 2001 Apr;102(1-2):119-33 [11287186.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7186-203 [11704847.001]
  • [Cites] Mol Cell. 2000 Nov;6(5):1131-41 [11106752.001]
  • (PMID = 20080956.001).
  • [ISSN] 1549-5477
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U117532048; United Kingdom / Medical Research Council / / MC/ U117560481; United Kingdom / Medical Research Council / / U117532048
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Btbd6a protein, zebrafish; 0 / Carrier Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Nerve Tissue Proteins; 0 / Zebrafish Proteins
  • [Other-IDs] NLM/ PMC2807355
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32. Dalen JE: Should patients with venous thromboembolism be screened for thrombophilia? Am J Med; 2008 Jun;121(6):458-63
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  • The most common acquired cause is antiphospholipid syndrome.
  • Therefore, thrombophilia screening to prevent initial episodes of VTE is not indicated, except possibly in women with a family history of idiopathic VTE who are considering oral contraceptive therapy.
  • However, several studies have demonstrated that, with the exception of antiphospholipid syndrome, thrombophilia does not significantly increase the risk of recurrent VTE.
  • [MeSH-major] Thromboembolism / etiology. Thrombophilia / diagnosis

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  • (PMID = 18501222.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / factor V Leiden; 12001-79-5 / Vitamin K; 5Q7ZVV76EI / Warfarin; 9001-24-5 / Factor V
  • [Number-of-references] 34
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33. Santin M, Rhys-Williams W, O'Reilly J, Davies MC, Shakesheff K, Love WG, Lloyd AW, Denyer SP: Calcium-binding phospholipids as a coating material for implant osteointegration. J R Soc Interface; 2006 Apr 22;3(7):277-81
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  • [Title] Calcium-binding phospholipids as a coating material for implant osteointegration.
  • Among the many biomolecules involved in the bone mineralization processes, anionic phospholipids play an important role because of their ability to bind calcium.
  • In the present work, we demonstrate that calcium-binding phospholipids can be used as biomimetic coating materials for improving the osteointegration of metal implants.
  • Upon dehydration in a simulated body fluid phospholipids were quickly crosslinked by calcium and re-arranged into a three-dimensional matrix able to induce rapid formation of a calcium phosphate mineral phase.
  • In the attempt to closely mimic the cell membrane composition, heterogeneous formulations based on the mixing of anionic phospholipids (either phosphatidylserine or phosphatidylinositol) with phosphatidylcholine and cholesterol were synthesized.

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  • [Cites] Biomed Mater Eng. 2000;10(3-4):157-88 [11202145.001]
  • [Cites] J Mater Sci Mater Med. 2006 Sep;17(9):789-94 [16932859.001]
  • [Cites] Calcif Tissue Int. 1985 Jul;37(4):390-4 [3930037.001]
  • [Cites] J Bone Miner Res. 1986 Oct;1(5):409-15 [3503556.001]
  • [Cites] Calcif Tissue Int. 1992 Feb;50(2):149-56 [1315188.001]
  • [Cites] Calcif Tissue Int. 1992 May;50(5):439-44 [1596779.001]
  • [Cites] Bone Miner. 1992 May;17(2):269-72 [1611319.001]
  • [Cites] FEBS Lett. 1992 Sep 28;310(2):143-7 [1397263.001]
  • [Cites] Glycobiology. 1992 Dec;2(6):571-8 [1472764.001]
  • [Cites] J Biomed Mater Res. 1993 Jan;27(1):35-45 [8380597.001]
  • [Cites] J Biomed Mater Res. 1995 Jul;29(7):875-81 [7593027.001]
  • [Cites] J Biomed Mater Res. 1996 Mar;30(3):273-9 [8698689.001]
  • [Cites] J Biomed Mater Res. 1997 Mar 5;34(3):305-15 [9086400.001]
  • [Cites] J Biomed Mater Res. 1998 Mar 15;39(4):611-20 [9492223.001]
  • [Cites] Science. 1981 May 22;212(4497):921-3 [7233185.001]
  • (PMID = 16849237.001).
  • [ISSN] 1742-5689
  • [Journal-full-title] Journal of the Royal Society, Interface
  • [ISO-abbreviation] J R Soc Interface
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium Phosphates; 0 / Coated Materials, Biocompatible; 0 / Phospholipids
  • [Other-IDs] NLM/ PMC1578739
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34. Moreno R, Sobotzik JM, Schultz C, Schmitz ML: Specification of the NF-kappaB transcriptional response by p65 phosphorylation and TNF-induced nuclear translocation of IKK epsilon. Nucleic Acids Res; 2010 Oct;38(18):6029-44
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  • Here we investigated the regulation of NF-κB activity by post-translational modifications upon reconstitution of NF-κB p65-deficient cells with the wild-type protein or phosphorylation-defect mutants.
  • Analysis of NF-κB target gene expression showed that p65 phosphorylations alone or in combination function to direct transcription in a highly target gene-specific fashion, a finding discussed here as the NF-κB barcode hypothesis.
  • TNF stimulation resulted in the translocation of the cytosolic p65 kinase IKKε to the nucleus and also to promyelocytic leukemia (PML) nuclear bodies.
  • This inducible IKKε translocation was dependent on p65 phosphorylation and was prevented by the oncogenic PML-RARα fusion protein.
  • [MeSH-major] Cell Nucleus / enzymology. Gene Expression Regulation. I-kappa B Kinase / metabolism. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / pharmacology


35. Kleger A, Busch T, Liebau S, Prelle K, Paschke S, Beil M, Rolletschek A, Wobus A, Wolf E, Adler G, Seufferlein T: The bioactive lipid sphingosylphosphorylcholine induces differentiation of mouse embryonic stem cells and human promyelocytic leukaemia cells. Cell Signal; 2007 Feb;19(2):367-77
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  • [Title] The bioactive lipid sphingosylphosphorylcholine induces differentiation of mouse embryonic stem cells and human promyelocytic leukaemia cells.
  • Sphingosylphosphorylcholine (SPC) is the major component of high-density lipoproteins (HDL) in blood plasma.
  • Similar to ligands of other GPCRs, SPC has multiple biological roles including the regulation of proliferation, migration, angiogenesis, wound healing and heart rate.
  • Here we examined the effect of SPC on the differentiation of mouse embryonic stem (ES) cells and of human NB4 promyelocytic leukemia cells, a well established tumour differentiation model.
  • We demonstrate both at the level of morphology and of gene expression that SPC induces neuronal and cardiac differentiation of mouse ES cells.
  • [MeSH-major] Embryonic Stem Cells / physiology. Leukemia, Promyelocytic, Acute / metabolism. Phosphorylcholine / analogs & derivatives. Receptors, G-Protein-Coupled / metabolism. Sphingosine / analogs & derivatives

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  • (PMID = 16978842.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Receptors, G-Protein-Coupled; 10216-23-6 / sphingosine phosphorylcholine; 107-73-3 / Phosphorylcholine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; NGZ37HRE42 / Sphingosine
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36. Lin TL, Vala MS, Barber JP, Karp JE, Smith BD, Matsui W, Jones RJ: Induction of acute lymphocytic leukemia differentiation by maintenance therapy. Leukemia; 2007 Sep;21(9):1915-20
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  • [Title] Induction of acute lymphocytic leukemia differentiation by maintenance therapy.
  • Despite extensive study in many malignancies, maintenance therapy has clinically benefited only two diseases: acute lymphocytic leukemia (ALL) and acute promyelocytic leukemia (APL).
  • ALL maintenance therapy utilizes low-dose 6-mercaptopurine (6MP) and methotrexate (MTX), while maintenance in APL primarily consists of all-trans-retinoic acid (ATRA).
  • 6MP and MTX as used in ALL are also now usually added to maintenance ATRA for APL, based on data suggesting an improved disease-free survival.
  • Thus, we studied whether maintenance therapy in ALL, like ATRA in APL, may be inducing terminal differentiation of ALL progenitors.
  • The APL cell line NB4, the ALL cell lines REH and RS4;11, and patients' ALL blasts were incubated with ATRA, 6MP, and MTX in vitro.
  • All three drugs inhibited the clonogenic growth of the APL and ALL cell lines without inducing immediate apoptosis, but associated with induction of phenotypic differentiation.
  • These data suggest that induction of leukemia progenitor differentiation plays an important role in the mechanism of action of maintenance therapy in ALL.

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  • [Cites] J Clin Oncol. 2003 Mar 1;21(5):774-80 [12610173.001]
  • [Cites] Br J Haematol. 2003 Apr;121(2):251-8 [12694246.001]
  • [Cites] N Engl J Med. 2003 Jun 12;348(24):2375-6 [12802021.001]
  • [Cites] Nouv Rev Fr Hematol. 1984;26(6):371-8 [6597407.001]
  • [Cites] Cancer. 1987 Apr 1;59(7):1258-63 [3469011.001]
  • [Cites] Blood. 1987 Jun;69(6):1551-62 [3555647.001]
  • [Cites] J Clin Oncol. 1989 Dec;7(12):1816-23 [2585022.001]
  • [Cites] N Engl J Med. 1990 Jul 5;323(1):17-21 [2355954.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Leukemia. 1991 May;5(5):425-31 [2033963.001]
  • [Cites] Br J Cancer. 1991 Jul;64(1):169-73 [1854617.001]
  • [Cites] Leukemia. 1992;6 Suppl 2:178-81 [1578927.001]
  • [Cites] Leukemia. 1994 Oct;8(10):1744-9 [7934171.001]
  • [Cites] J Pharmacol Exp Ther. 1994 Oct;271(1):193-9 [7965714.001]
  • [Cites] Blood. 1995 Mar 1;85(5):1151-68 [7858247.001]
  • [Cites] Blood. 1995 May 15;85(10):2742-6 [7742535.001]
  • [Cites] Lancet. 1996 Jun 29;347(9018):1783-8 [8667921.001]
  • [Cites] J Immunol. 1996 Dec 1;157(11):4908-17 [8943395.001]
  • [Cites] N Engl J Med. 1997 Oct 9;337(15):1021-8 [9321529.001]
  • [Cites] J Immunol. 1997 Oct 1;159(7):3278-87 [9317126.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3569-77 [9808549.001]
  • [Cites] Leukemia. 1999 Feb;13(2):275-81 [10025902.001]
  • [Cites] Haematologica. 1999 Jan;84(1):36-58 [10091392.001]
  • [Cites] Exp Hematol. 2002 Nov;30(11):1273-82 [12423680.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3893-903 [12124315.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2225-33 [10090931.001]
  • [Cites] Blood. 1985 Jan;65(1):21-31 [3917311.001]
  • [Cites] Exp Cell Res. 1999 Apr 10;248(1):58-73 [10094813.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1192-200 [10438706.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1442-9 [15735032.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):853-62 [15755292.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3760-7 [16105981.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • [Cites] Eur J Immunol. 2001 Apr;31(4):1261-7 [11298353.001]
  • [Cites] Immunol Res. 2000;22(2-3):281-98 [11339363.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3925-30 [11389036.001]
  • [Cites] Blood. 2002 Feb 1;99(3):863-71 [11806988.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3496-506 [12032784.001]
  • [Cites] Blood. 2002 Jul 15;100(2):640-6 [12091359.001]
  • [Cites] Cell Growth Differ. 2002 Jun;13(6):275-83 [12114217.001]
  • [Cites] Pharmacol Ther. 2003 Dec;100(3):257-90 [14652113.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8955-61 [14695213.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2919-25 [15242869.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 Feb;68(2):378-82 [5277089.001]
  • [Cites] Lancet. 1973 Jun 16;1(7816):1339-43 [4122739.001]
  • [Cites] Eur J Cancer. 1977 Apr-May;13(4-5):377-9 [194778.001]
  • [Cites] Proc Natl Acad Sci U S A. 1978 May;75(5):2458-62 [276884.001]
  • [Cites] Cancer Res. 1984 Jun;44(6):2421-9 [6586286.001]
  • [Cites] Blood. 1984 Oct;64(4):922-9 [6206904.001]
  • (PMID = 17611566.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / K23 CA107040-04; United States / NCI NIH HHS / CA / K23 CA107040; United States / NCI NIH HHS / CA / P01 CA70970; United States / NCI NIH HHS / CA / P01 CA15396; United States / NCI NIH HHS / CA / CA107040-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Cytotoxins; 5688UTC01R / Tretinoin; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS81581; NLM/ PMC2643128
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37. Barón MA, Khamashta MA, Hughes GR, D'Cruz DP: Prevalence of an abnormal ankle-brachial index in patients with primary antiphospholipid syndrome: preliminary data. Ann Rheum Dis; 2005 Jan;64(1):144-6
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  • [Title] Prevalence of an abnormal ankle-brachial index in patients with primary antiphospholipid syndrome: preliminary data.
  • OBJECTIVES: To evaluate the prevalence of abnormal ankle-brachial indexes (ABIs), their relationship with other cardiovascular risk factors and/or the presence of antiphospholipid antibodies (aPL), and the clinical use of the ABI in patients with primary antiphospholipid syndrome (primary APS).
  • No correlation between abnormal ABI and traditional cardiovascular risk factors nor with the presence of aPL was found.
  • [MeSH-major] Ankle / blood supply. Antiphospholipid Syndrome / physiopathology. Brachial Artery / physiopathology
  • [MeSH-minor] Adult. Arteriosclerosis / diagnosis. Arteriosclerosis / etiology. Blood Pressure. Cardiovascular Diseases / etiology. Case-Control Studies. Female. Humans. Male. Middle Aged. Risk Factors. Ultrasonography, Doppler

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  • (PMID = 15608314.001).
  • [ISSN] 0003-4967
  • [Journal-full-title] Annals of the rheumatic diseases
  • [ISO-abbreviation] Ann. Rheum. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1755181
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38. Diz-Kucukkaya R, Hancer VS, Artim-Esen B, Pekcelen Y, Inanc M: The prevalence and clinical significance of inherited thrombophilic risk factors in patients with antiphospholipid syndrome. J Thromb Thrombolysis; 2010 Apr;29(3):303-9
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  • [Title] The prevalence and clinical significance of inherited thrombophilic risk factors in patients with antiphospholipid syndrome.
  • In this study, we evaluated common inherited thrombophilic risk factors in patients with antiphospholipid syndrome (APS), and reviewed relevant literature.
  • Ninety-four APS patients with documented thrombosis, 40 patients with persistent antiphospholipid antibody (aPLA) positivity but without thrombosis, and healthy controls were screened.
  • [MeSH-major] Antiphospholipid Syndrome / epidemiology. Antiphospholipid Syndrome / genetics. Thrombophilia / epidemiology. Thrombophilia / genetics

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  • [Cites] Arthritis Rheum. 1997 Sep;40(9):1725 [9324032.001]
  • [Cites] Lancet. 1999 Apr 3;353(9159):1167-73 [10209995.001]
  • [Cites] N Engl J Med. 2003 Sep 18;349(12):1177-9 [13679533.001]
  • [Cites] Thromb Haemost. 1997 Dec;78(6):1527-8 [9423807.001]
  • [Cites] N Engl J Med. 2002 Mar 7;346(10):752-63 [11882732.001]
  • [Cites] Thromb Haemost. 1995 Oct;74(4):1029-31 [8560406.001]
  • [Cites] Nature. 1994 May 5;369(6475):64-7 [8164741.001]
  • [Cites] Thromb Haemost. 1996 Oct;76(4):514-7 [8902988.001]
  • [Cites] J Rheumatol. 1999 Mar;26(3):588-90 [10090167.001]
  • [Cites] J Rheumatol. 2001 Sep;28(9):2018-24 [11550969.001]
  • [Cites] Blood Coagul Fibrinolysis. 2000 Oct;11(7):679-82 [11085290.001]
  • [Cites] Blood Coagul Fibrinolysis. 2001 Dec;12(8):699-704 [11734671.001]
  • [Cites] Blood. 1996 Nov 15;88(10):3698-703 [8916933.001]
  • [Cites] J Rheumatol. 2002 Aug;29(8):1683-8 [12180730.001]
  • [Cites] Haematologica. 2001 Jul;86(7):735-41 [11454529.001]
  • [Cites] Thromb Haemost. 1995 Oct;74(4):1185-90 [8560433.001]
  • [Cites] Thromb Haemost. 1998 Jan;79(1):46-9 [9459321.001]
  • [Cites] Am J Hematol. 1998 Jul;58(3):249 [9662283.001]
  • [Cites] Br J Haematol. 2000 Mar;108(4):865-70 [10792297.001]
  • [Cites] Br J Haematol. 1990 Jan;74(1):1-9 [2178669.001]
  • [Cites] Haematologia (Budap). 2002;32(1):73-7 [12243558.001]
  • [Cites] Lupus. 1996 Aug;5(4):303-6 [8869903.001]
  • [Cites] Haematologica. 2006 May;91(5):695-8 [16670075.001]
  • [Cites] Arthritis Rheum. 1999 Jul;42(7):1309-11 [10403256.001]
  • (PMID = 19504051.001).
  • [ISSN] 1573-742X
  • [Journal-full-title] Journal of thrombosis and thrombolysis
  • [ISO-abbreviation] J. Thromb. Thrombolysis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V; OF5P57N2ZX / Alanine; TE7660XO1C / Glycine
  • [Number-of-references] 25
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39. Subramaniyam S, Nandula SV, Nichols G, Weiner M, Satwani P, Alobeid B, Bhagat G, Murty VV: Do RARA/PML fusion gene deletions confer resistance to ATRA-based therapy in patients with acute promyelocytic leukemia? Leukemia; 2006 Dec;20(12):2193-5
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  • [Title] Do RARA/PML fusion gene deletions confer resistance to ATRA-based therapy in patients with acute promyelocytic leukemia?
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gene Deletion. Leukemia, Promyelocytic, Acute / drug therapy. Oncogene Proteins, Fusion / genetics. Tretinoin / therapeutic use

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  • (PMID = 17008891.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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40. Kumar S, Savitz S, Schlaug G, Caplan L, Selim M: Antiplatelets, ACE inhibitors, and statins combination reduces stroke severity and tissue at risk. Neurology; 2006 Apr 25;66(8):1153-8; discussion 1135
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  • BACKGROUND: Antiplatelets (APL), angiotensin-converting enzyme (ACE) inhibitors (ACEI), and statins (STAT) are commonly used for stroke prevention.
  • Baseline NIH Stroke Scale (NIHSS) score and diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), and PWI-DWI mismatch lesion volumes as clinical and radiologic measures of stroke severity were measured among patients who were not taking APL, ACEI, or STAT before stroke onset vs those who were taking APL alone or in combination with either ACEI, STAT, or both.
  • RESULTS: Sixty-nine patients were not on APL, ACEI, or STAT at stroke onset; 47 were on APL alone, 43 on dual (14 APL + STAT, 29 APL + ACEI), and 20 on triple combination therapy.
  • Patients on triple therapy had lower NIHSS score (p = 0.001) and smaller mean PWI-DWI mismatch lesion volumes (p = 0.03) than those on two agents, APL alone, or no prestroke therapy.
  • Age, risk factor profile, blood pressure, glucose levels, onset to evaluation time, stroke subtypes, and DWI lesion volumes were comparable among all groups.

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  • (PMID = 16636230.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1R01NS045049-01A1
  • [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 / Angiotensin-Converting Enzyme Inhibitors; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Platelet Aggregation Inhibitors
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41. Montiel-Manzano G, Romay-Penabad Z, Papalardo de Martínez E, Meillon-García LA, García-Latorre E, Reyes-Maldonado E, Pierangeli SS: In vivo effects of an inhibitor of nuclear factor-kappa B on thrombogenic properties of antiphospholipid antibodies. Ann N Y Acad Sci; 2007 Jun;1108:540-53
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  • [Title] In vivo effects of an inhibitor of nuclear factor-kappa B on thrombogenic properties of antiphospholipid antibodies.
  • It has been shown that endothelial cell (EC) activation and tissue factor (TF) upregulation in EC and monocytes by antiphospholipid antibodies (aPL Abs) leads to a prothrombotic state and involves translocation of nuclear factor-kappa B (NF-kappaB).
  • Here we examined the effects of an NF-kappaB inhibitor on aPL-induced thrombosis, TF activity, and EC in vivo.
  • We treated CD1 mice with IgG from a patient with antiphospholipid syndrome (IgG-APS) or with control IgG (IgG-NHS).
  • [MeSH-major] Antibodies, Antiphospholipid / metabolism. Cell Adhesion / drug effects. Leupeptins / pharmacology. NF-kappa B / antagonists & inhibitors. Thrombosis / metabolism
  • [MeSH-minor] Animals. Antiphospholipid Syndrome / blood. Antiphospholipid Syndrome / immunology. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Humans. Male. Mice. Middle Aged. Thromboplastin / drug effects

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  • (PMID = 17894019.001).
  • [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-RR03034
  • [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 / Antibodies, Antiphospholipid; 0 / Leupeptins; 0 / NF-kappa B; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 9035-58-9 / Thromboplastin
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42. Leavenworth JW, Ma X, Mo YY, Pauza ME: SUMO conjugation contributes to immune deviation in nonobese diabetic mice by suppressing c-Maf transactivation of IL-4. J Immunol; 2009 Jul 15;183(2):1110-9
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  • It is not clear why the development of protective Th2 cells is poor in type 1 diabetes (T1D).
  • In transfected cells, sumoylation decreases c-Maf transactivation of IL-4p-driven luciferase reporter activity, reduces c-Maf binding to the IL-4p in chromatin immunoprecipitation assays, and enhances c-Maf localization into promyelocytic leukemia nuclear bodies.

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  • [Cites] J Immunol. 2006 Apr 15;176(8):4843-51 [16585579.001]
  • [Cites] Genes Immun. 2006 Jul;7(5):352-8 [16691184.001]
  • [Cites] Science. 2006 Sep 22;313(5794):1751 [16990542.001]
  • [Cites] J Biol Chem. 2006 Oct 20;281(42):31188-201 [16895915.001]
  • [Cites] Mol Cell Proteomics. 2006 Dec;5(12):2298-310 [17000644.001]
  • [Cites] Protein Expr Purif. 2007 Aug;54(2):289-94 [17459725.001]
  • [Cites] Eur J Immunol. 2007 Oct;37(10):2868-80 [17823980.001]
  • [Cites] Biochem Soc Trans. 2007 Dec;35(Pt 6):1393-6 [18031229.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Dec;8(12):1006-16 [17928811.001]
  • [Cites] J Immunol. 2007 Dec 15;179(12):8297-304 [18056374.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 26;104(52):20793-8 [18087039.001]
  • [Cites] J Immunol. 2008 May 1;180(9):5983-90 [18424718.001]
  • [Cites] Oncogene. 2004 Mar 15;23(11):1998-2008 [15021887.001]
  • [Cites] Biochem Biophys Res Commun. 2008 May 30;370(2):359-65 [18384750.001]
  • [Cites] J Biol Chem. 2008 Jun 27;283(26):18124-34 [18408014.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1784-96 [10669754.001]
  • [Cites] Eur J Immunol. 2000 Sep;30(9):2576-85 [11009091.001]
  • [Cites] Diabetes. 2001 Jan;50(1):39-46 [11147792.001]
  • [Cites] Nat Med. 2001 Feb;7(2):206-14 [11175852.001]
  • [Cites] J Cell Sci. 2001 May;114(Pt 10):1867-73 [11329373.001]
  • [Cites] Exp Cell Res. 2001 Nov 15;271(1):57-65 [11697882.001]
  • [Cites] J Cell Physiol. 2002 Jun;191(3):257-68 [12012321.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Jun;3(6):411-21 [12042763.001]
  • [Cites] Nat Immunol. 2002 Jul;3(7):643-51 [12055628.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] J Biol Chem. 2003 Feb 28;278(9):6862-72 [12482876.001]
  • [Cites] EMBO Rep. 2003 Feb;4(2):137-42 [12612601.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(8):2953-68 [12665592.001]
  • [Cites] J Immunol. 2004 Jan 1;172(1):688-98 [14688382.001]
  • [Cites] Science. 2004 Apr 2;304(5667):100-4 [15064418.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2793-8 [15087395.001]
  • [Cites] Annu Rev Biochem. 2004;73:355-82 [15189146.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):8870-5 [15173587.001]
  • [Cites] J Biol Chem. 2004 Jun 25;279(26):27233-8 [15123604.001]
  • [Cites] Nat Genet. 2004 Aug;36(8):837-41 [15247916.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11410-5 [15272080.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14373-8 [15388847.001]
  • [Cites] Science. 1995 May 26;268(5214):1185-8 [7761837.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11623-7 [8524816.001]
  • [Cites] Cell. 1996 Jun 28;85(7):973-83 [8674125.001]
  • [Cites] J Cell Biol. 1996 Dec;135(6 Pt 1):1457-70 [8978815.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2414-24 [9036992.001]
  • [Cites] Immunity. 1997 Sep;7(3):411-8 [9324361.001]
  • [Cites] J Immunol. 1997 Nov 15;159(10):4686-92 [9366391.001]
  • [Cites] Nucleic Acids Res. 1998 Jan 1;26(1):362-7 [9399875.001]
  • [Cites] J Cell Biol. 1998 Feb 9;140(3):499-509 [9456312.001]
  • [Cites] J Immunol. 1998 Jun 1;160(11):5280-7 [9605125.001]
  • [Cites] Diabetes Metab Rev. 1998 Jun;14(2):129-51 [9679667.001]
  • [Cites] J Autoimmun. 1998 Dec;11(6):635-42 [9878085.001]
  • [Cites] J Biol Chem. 1999 Apr 9;274(15):10618-24 [10187858.001]
  • [Cites] Mol Cell. 2004 Nov 19;16(4):549-61 [15546615.001]
  • [Cites] Nat Genet. 2005 Feb;37(2):110-1; author reply 112-3 [15678134.001]
  • [Cites] Nat Genet. 2005 Feb;37(2):111-2; author reply 112-3 [15678135.001]
  • [Cites] Nat Genet. 2005 Feb;37(2):112; author reply 112-3 [15678137.001]
  • [Cites] J Immunol. 2005 Mar 1;174(5):2720-9 [15728480.001]
  • [Cites] J Immunol. 2005 Mar 15;174(6):3484-92 [15749884.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):9937-45 [15637059.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10164-73 [15637079.001]
  • [Cites] Mol Cell. 2005 Apr 1;18(1):1-12 [15808504.001]
  • [Cites] Curr Biol. 2005 Apr 12;15(7):616-23 [15823533.001]
  • [Cites] Eur J Immunol. 2005 May;35(5):1408-17 [15832295.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(12):5095-105 [15923626.001]
  • [Cites] Cytokine. 2005 Jun 7;30(5):219-27 [15927845.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 22;102(47):16973-8 [16287980.001]
  • [Cites] Mol Cell Biol. 2006 Feb;26(3):955-64 [16428449.001]
  • [Cites] Annu Rev Immunol. 2006;24:607-56 [16551261.001]
  • (PMID = 19553542.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100223-01A1; United States / NCI NIH HHS / CA / R01 CA100223; United States / NCI NIH HHS / CA / R01 CA102630; United States / NCI NIH HHS / CA / R01 CA100223-01A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Maf protein, mouse; 0 / Proto-Oncogene Proteins c-maf; 0 / SUMO-1 Protein; 207137-56-2 / Interleukin-4; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ NIHMS243334; NLM/ PMC2965337
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43. Huang HH, Zhu JY, Zhong JH, Wang HR, Zhong H, Han JY, Chen FY: [Correlation between expression of apoptosis-related gene pnas-2 and leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):738-42
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  • [Title] [Correlation between expression of apoptosis-related gene pnas-2 and leukemia].
  • The study was purposed to explore the correlation between apoptosis-related gene pnas-2 and leukemia.
  • The RT-PCR was performed to detect the expression levels of pnas-2 gene in NB4, K562, U937 cells before and after treatment with AS(4)S(4), and to analysis the expression change of pnas-2 gene in bone marrow cells from patients with acute leukemia before and after chemotherapy.
  • The positive expression rate of pnas-2 in cells from untreated patients with acute leukemia was 100%, and was significantly higher than that in normal control group.
  • It is concluded that the pnas-2 gene may be closely related with apotosis of arsenic sulfide treated APL cells, and may consider as a molecular biological remission marker in acute leukemia.

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  • (PMID = 17708794.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / PNAS-2 protein, human; 0 / Sulfides; 44SIJ800OX / arsenic trisulfide
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44. Sano M, Tokudome S, Shimizu N, Yoshikawa N, Ogawa C, Shirakawa K, Endo J, Katayama T, Yuasa S, Ieda M, Makino S, Hattori F, Tanaka H, Fukuda K: Intramolecular control of protein stability, subnuclear compartmentalization, and coactivator function of peroxisome proliferator-activated receptor gamma coactivator 1alpha. J Biol Chem; 2007 Aug 31;282(35):25970-80
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  • Interestingly, ectopically expressed C-terminal fragment of PGC-1alpha was autonomously ubiquitinated and aggregated with promyelocytic leukemia protein.

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  • (PMID = 17620342.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Ppargc1a protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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45. Yu FY, Liao YC, Chang CH, Liu BH: Citrinin induces apoptosis in HL-60 cells via activation of the mitochondrial pathway. Toxicol Lett; 2006 Feb 20;161(2):143-51
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  • To investigate the death mode of cells exposed to CTN, human promyelocytic leukemia (HL-60) cells were chosen to identify the apoptotic process induced by CTN.

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  • (PMID = 16183218.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 3S697X6SNZ / Citrinin; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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46. Kitagawa Y, Ohkuma H, Tokuoka K: [Ischemic stroke with antiphospholipid antibody]. Brain Nerve; 2008 Oct;60(10):1144-58
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  • [Title] [Ischemic stroke with antiphospholipid antibody].
  • Antiphospholipid syndrome is considered to be associated with a hypercoagulable state that leads to stroke and other ischemic events, and is currently diagnosed based on the modified Sapporo criteria that was proposed in 2006.
  • Antiphospholipid antibodies (aPL) comprise a heterogeneous group of autoantibodies.
  • Among them, the level of beta2-glycoprotein I-dependent anticardiolipin antibody, lupus anticoagulant (LA), and IgG anticardiolipin antibody are commonly measured.
  • Recently, phosphatidylserine dependent anti-prothrombin antibody has been suggested to be closely related to LA. aPL is an independent risk factor for a first-ever ischemic stroke, especially in young female patients.
  • It is still debatable whether aPL is a marker for recurrent stroke risk.
  • The precipitating factors for the occurrence of stroke are beta2-GPI-dependent aCL, aGPL, and aCL levels of greater than 40, and the simultaneous presence of LA.
  • Several mechanisms are considered to be involved in the thrombotic process in patients with antiphospholipid antibodies.
  • Activation of protein C is impaired in patients with aPL.
  • In addition, the presence of aPL is associated with the development of atherosclerosis.
  • Several therapeutic options are available for the prevention of ischemic stroke in patients with aPL.
  • For cases of cryptogenic ischemic stroke and positive aPL antibodies, antiplatelet therapy is reasonable.
  • Oral anticoagulation with a target international normalized ratio (INR) of 2 to 3 is reasonable for patients with ischemic stroke who meet the criteria for antiphospholipid syndrome with venous and arterial occlusive disease in multiple organs.
  • [MeSH-major] Antibodies, Antiphospholipid. Antiphospholipid Syndrome / complications. Stroke / etiology
  • [MeSH-minor] Age of Onset. Anticoagulants / administration & dosage. Aspirin / administration & dosage. Biomarkers / blood. Clinical Trials as Topic. Female. Heparin / administration & dosage. Humans. Middle Aged. Platelet Aggregation Inhibitors / administration & dosage. Prognosis. Risk Factors. Warfarin / administration & dosage

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  • (PMID = 18975602.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Biomarkers; 0 / Platelet Aggregation Inhibitors; 5Q7ZVV76EI / Warfarin; 9005-49-6 / Heparin; R16CO5Y76E / Aspirin
  • [Number-of-references] 76
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47. Favaloro EJ, Wong RC: The antiphospholipid syndrome: a large elephant with many parts or an elusive chameleon disguised by many colours? Auto Immun Highlights; 2010 May;1(1):5-14
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  • [Title] The antiphospholipid syndrome: a large elephant with many parts or an elusive chameleon disguised by many colours?
  • The antiphospholipid syndrome (APS) is characterized by a range of clinical features (primarily thrombosis and/or obstetric-related), together with the presence of antiphospholipid antibody (aPL) as detected by a diverse range of laboratory tests.
  • APS remains a significant diagnostic and management challenge for clinicians across a wide range of specialties, some 30 years after APS was first described as a discrete clinical entity.
  • This is due to ongoing issues regarding nomenclature, the diagnosis of APS in individual patients, the expanding range of recognized clinical manifestations and of APS-related laboratory tests, and management issues in particular APS patient subgroups (including obstetric and catastrophic APS).
  • In addition to the presence of appropriate clinical features, the diagnosis of APS fundamentally requires the finding of positive aPL test result(s), which is hampered by ongoing problems with assay reproducibility and standardization.
  • This review focuses on ongoing dilemmas and issues related to clinical and laboratory aspects of APS including:.
  • (1) diagnostic challenges posed by the protean clinical manifestations of APS;.
  • (3) an overview of some key issues related to aPL testing;.
  • (4) potential pitfalls of applying the APS classification criteria as diagnostic criteria; and (5) the controversial subgroups of seronegative APS and non-APS aPL positivity.

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  • (PMID = 26000102.001).
  • [ISSN] 2038-0305
  • [Journal-full-title] Auto- immunity highlights
  • [ISO-abbreviation] Auto Immun Highlights
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC4389063
  • [Keywords] NOTNLM ; APS / Anti-beta-2-glycoprotein-I antibodies / Anticardiolipin antibodies / Antiphospholipid antibodies / Antiphospholipid syndrome / Clinical features / Criteria / Diagnosis / aPL
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48. Buliková A, Zavrelová J, Penka M: [Antiphospholipid syndrome in the year 2009]. Vnitr Lek; 2009 Mar;55(3):253-62
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  • [Title] [Antiphospholipid syndrome in the year 2009].
  • Antiphospholipid syndrome is a prothrombotic disorder characterized by vascular occlusions and/or pregnancy morbidity in the presence of antiphospholipid antibodies.
  • A number of criteria for diagnosis of antiphospholipid syndrome have been proposed.
  • [MeSH-major] Antiphospholipid Syndrome
  • [MeSH-minor] Animals. Biomedical Research. Female. Humans. Pregnancy. Pregnancy Complications, Hematologic / classification. Pregnancy Complications, Hematologic / diagnosis

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  • (PMID = 19378856.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 57
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49. Walewska E, Rupińiski R, Filipowicz-Sosnowska A, Wojciechowska B: [Follow-up studies of rheumatoid arthritis patients with the presence of antiphospholipid antibodies]. Pol Arch Med Wewn; 2006 May;115(5):438-42
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  • [Title] [Follow-up studies of rheumatoid arthritis patients with the presence of antiphospholipid antibodies].
  • The aim of the study was 2 years follow-up observation of clinical course in RA patients with the presence of anticardiolipin antibodies (aCL).
  • Patients positive for antiphospholipid antibodies were invited to the Clinic on the beginning of 2006 (after 2 years from previous hospitalization) to analyze clinical course of disease and to perform laboratory examination.
  • RESULTS: In the group of patients with RA positive for antiphospholipid antibodies, 3 had active RA with vascular changes.
  • Aggressive therapy with disease modifying antirheumatic drugs (DMARDs) and corticosteroids caused conversion of anticardiolipin antibodies.
  • CONCLUSION: Presence of anticardiolipin antibodies can be the indicator of serious prognosis, it can predict vasculitis, persistent infections, cardiovascular complications or neoplasmatic disease.
  • We suggest that antiphospholipid antibodies should be measure in patient with aggressive course of rheumatoid arthritis.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Arthritis, Rheumatoid / diagnosis. Arthritis, Rheumatoid / therapy

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  • (PMID = 17195357.001).
  • [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, Antiphospholipid; 0 / Antirheumatic Agents; 0 / Biomarkers
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50. Alijotas-Reig J, Casellas-Caro M, Ferrer-Oliveras R, Llurba-Olive E, Hermosilla E, Vilardell-Tarres M, Cabero-Roura L: Are anti-beta-glycoprotein-I antibodies markers for recurrent pregnancy loss in lupus anticoagulant/anticardiolipin seronegative women? Am J Reprod Immunol; 2008 Sep;60(3):229-37
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  • [Title] Are anti-beta-glycoprotein-I antibodies markers for recurrent pregnancy loss in lupus anticoagulant/anticardiolipin seronegative women?
  • PROBLEM: Anti-beta(2)-Glicoprotein-1 antibodies (anti-beta(2)GPI-ab) have been related to recurrent miscarriage (RM) with conflicting results.
  • The aim was to evaluate the role of anti-beta(2)-GPI-ab as unique biological marker in RM related to antiphospholipid (aPL).
  • METHOD OF STUDY: A cohort study that included 59 cases, divided in two groups, was designed: group 1 comprised 43 pregnant women with 'obstetric' antiphospholipid syndrome (APS) and group 2 included 16 cases with similar complaints but only having repeatedly anti-beta(2)-GPI-ab.
  • Lupus anticoagulant, anticardiolipin antibodies (aCA), anti-beta(2)-GPI-ab, and other autoantibodies were analyzed.
  • CONCLUSION: These results suggest that anti-beta(2)-GPI-ab may be considered a biological marker for obstetric APS.
  • [MeSH-major] Abortion, Habitual / immunology. Antiphospholipid Syndrome / immunology. Autoantibodies / blood. beta 2-Glycoprotein I / immunology
  • [MeSH-minor] Adult. Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Anticoagulants / administration & dosage. Anticoagulants / therapeutic use. Aspirin / administration & dosage. Aspirin / therapeutic use. Biomarkers. Cohort Studies. Enoxaparin / administration & dosage. Enoxaparin / therapeutic use. Female. Humans. Lupus Coagulation Inhibitor / blood. Platelet Aggregation Inhibitors / administration & dosage. Platelet Aggregation Inhibitors / therapeutic use. Pregnancy. Pregnancy Complications / immunology

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  • (PMID = 18782284.001).
  • [ISSN] 1046-7408
  • [Journal-full-title] American journal of reproductive immunology (New York, N.Y. : 1989)
  • [ISO-abbreviation] Am. J. Reprod. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Autoantibodies; 0 / Biomarkers; 0 / Enoxaparin; 0 / Lupus Coagulation Inhibitor; 0 / Platelet Aggregation Inhibitors; 0 / beta 2-Glycoprotein I; R16CO5Y76E / Aspirin
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51. Kang LC, Smith SV, Kaiser-Rogers K, Rao K, Dunphy CH: Two cases of acute myeloid leukemia with t(11;17) associated with varying morphology and immunophenotype: rearrangement of the MLL gene and a region proximal to the RARalpha gene. Cancer Genet Cytogenet; 2005 Jun;159(2):168-73
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  • [Title] Two cases of acute myeloid leukemia with t(11;17) associated with varying morphology and immunophenotype: rearrangement of the MLL gene and a region proximal to the RARalpha gene.
  • This report describes 2 cases of acute myeloid leukemia (AML), which based on the WHO classification would be classified as AML with an 11q23 (MLL) abnormality, but with contrasting morphologic and immunophenotypic profiles.
  • One case had monocytic features (morphologically and immunophenotypically) with a t(11;17)(q23;q21), a previously identified variant translocation in acute promyelocytic leukemia (APL).
  • The second case had morphologic and immunophenotypic features of APL associated with a t(11;17)(q23;q25).
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Receptors, Retinoic Acid / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15899392.001).
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / retinoic acid receptor alpha; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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52. Douer D, Tallman MS: Arsenic trioxide: new clinical experience with an old medication in hematologic malignancies. J Clin Oncol; 2005 Apr 1;23(10):2396-410
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  • [Title] Arsenic trioxide: new clinical experience with an old medication in hematologic malignancies.
  • Arsenic trioxide has shown great promise in the treatment of patients with relapsed or refractory acute promyelocytic leukemia (APL).
  • In clinical trials, arsenic trioxide induces complete remission in 87% of patients and molecular remission in 83% of patients.
  • Treatment with arsenic trioxide may be associated with the APL differentiation syndrome, leukocytosis, and electrocardiographic abnormalities.
  • The expanded use of arsenic trioxide in APL for postremission therapy, in conjunction with transplantation, and in patients with newly diagnosed APL is under investigation.
  • The multiple mechanisms of action of arsenic trioxide suggest that it may have antitumor activity in malignancies other than APL and that it may be used in combination with other agents to expand its potential use.
  • This article reviews the clinical use of arsenic trioxide to date and discusses new therapeutic strategies evolving from its diverse biologic activities.
  • [MeSH-minor] Clinical Trials as Topic. Humans

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  • (PMID = 15800332.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 95
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53. Gore SD, Gojo I, Sekeres MA, Morris L, Devetten M, Jamieson K, Redner RL, Arceci R, Owoeye I, Dauses T, Schachter-Tokarz E, Gallagher RE: Single cycle of arsenic trioxide-based consolidation chemotherapy spares anthracycline exposure in the primary management of acute promyelocytic leukemia. J Clin Oncol; 2010 Feb 20;28(6):1047-53
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  • [Title] Single cycle of arsenic trioxide-based consolidation chemotherapy spares anthracycline exposure in the primary management of acute promyelocytic leukemia.
  • PURPOSE Event-free survival following all-trans-retinoic acid (ATRA) -based therapy for acute promyelocytic leukemia (APL) averages 70% at 5 years.
  • While arsenic trioxide (ATO) can induce remissions in 95% of relapsed patients, few studies have addressed the integration of ATO into the primary management of APL.
  • PATIENTS AND METHODS After induction with ATRA and daunorubicin (DRN), untreated patients with APL received 3 days of cytarabine and DRN followed by 30 doses of ATO beginning on day 8.
  • With a median follow-up of 2.7 years, estimated disease-free survival was 90%; overall survival for all patients was 88%.
  • CONCLUSION These data, combined with other recent studies using ATO in the primary management of APL, demonstrate the important role that ATO can play in the primary management of this curable disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasm Recurrence, Local / drug therapy


54. Kogure T, Noguchi J, Yanagisawa N, Haizuka H, Sato M: [Case of primary antiphospholipid antibody syndrome with repeated renal biopsies]. Nihon Jinzo Gakkai Shi; 2005;47(4):445-50
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  • [Title] [Case of primary antiphospholipid antibody syndrome with repeated renal biopsies].
  • Antiphospholipid antibody syndrome (APS) is characterized by the presence of repeated arterial and venous thrombosis, recurrent fetal loss and thrombocytopenia.
  • [MeSH-major] Antiphospholipid Syndrome / pathology. Kidney / pathology

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  • (PMID = 15971887.001).
  • [ISSN] 0385-2385
  • [Journal-full-title] Nihon Jinzo Gakkai shi
  • [ISO-abbreviation] Nihon Jinzo Gakkai Shi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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55. Vujović S, Zidverc J, Stojanović M, Penezić Z, Ivović M, Dukić V, Drezgić M: Drospirenone in the treatment of severe premenstrual cerebral edema in a woman with antiphospholipid syndrome, lateral sinus thrombosis, situs inversus and epileptic seizures. Gynecol Endocrinol; 2005 Nov;21(5):243-7
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  • [Title] Drospirenone in the treatment of severe premenstrual cerebral edema in a woman with antiphospholipid syndrome, lateral sinus thrombosis, situs inversus and epileptic seizures.
  • We report herein the case of 32-year-old woman with situs inversus, thrombophilia, antiphospholipid syndrome and severe premenstrual syndrome (PMS) with cerebral edema and epileptic seizures prior to menstruation.
  • Daily hormone analyses prior to and during menstruation confirmed an ovulatory cycle with extremely high progesterone, prolactin and insulin levels in the late luteal phase.
  • [MeSH-major] Androstenes / therapeutic use. Antiphospholipid Syndrome / complications. Brain Edema / drug therapy. Lateral Sinus Thrombosis / complications. Mineralocorticoid Receptor Antagonists / therapeutic use. Premenstrual Syndrome / drug therapy
  • [MeSH-minor] Abortion, Habitual / etiology. Adult. Anticoagulants / therapeutic use. Diuretics / therapeutic use. Epilepsy / complications. Female. Humans. Intracranial Pressure. Menstrual Cycle. Mutation. Pregnancy. Progesterone / blood. Prolactin / blood. Prothrombin / genetics. Situs Inversus / complications. Situs Inversus / diagnosis


56. Moosavi MA, Yazdanparast R, Lotfi A: 3-Hydrogenkwadaphnin induces monocytic differentiation and enhances retinoic acid-mediated granulocytic differentiation in NB4 cell line. J Biochem Mol Biol; 2006 Nov 30;39(6):722-9
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  • Recently, we have reported that 3-hydrogenkwadaphnin (3-HK), a diterpene ester isolated from Dendrostellera lessertii (Thymealeaceae), is very effective against leukemia cell lines without any detectable effects on normal cells (Moosavi et al., 2005b).
  • In this study, we report that 3-HK induces G1 cell-cycle arrest, differentiation and apoptosis in APL NB4 cell line.
  • According to flow cytomtry results, 3-HK (15 nM) induced a significant G1-arrest up to 24 h which was consequently followed with appearance of sub-G(1) peak at 72 to 96 h.
  • Based on these results, 3-HK might become an ideal candidate for treatment of APL patients pending full exploration of its biological functions.
  • [MeSH-minor] Cell Cycle / drug effects. Cell Proliferation / drug effects. Cell Survival. Drug Interactions. G1 Phase / drug effects. Guanosine / pharmacology. Humans. Leukemia, Promyelocytic, Acute. Macrophages / cytology. Macrophages / drug effects. Thymelaeaceae / chemistry. Thymelaeaceae / drug effects. Tretinoin. Tumor Cells, Cultured

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  • (PMID = 17129408.001).
  • [ISSN] 1225-8687
  • [Journal-full-title] Journal of biochemistry and molecular biology
  • [ISO-abbreviation] J. Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / 3-hydrogenkwadaphnin; 0 / Diterpenes; 12133JR80S / Guanosine; 5688UTC01R / Tretinoin
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57. Teh CL, Wong JS, Ngeh NK, Loh WL: Systemic lupus erythematosus pregnancies: a case series from a tertiary, East Malaysian hospital. Lupus; 2009 Mar;18(3):278-82
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  • We performed a retrospective study of all systemic lupus erythematosus (SLE) pregnancies during a two-year period (2006-2007) to describe the clinical features, maternal and foetal outcomes in our centre.
  • There were 17 pregnancies in 16 women with SLE.
  • Our patients have a mean age of 28.31 years (SD 5.24) and a mean disease duration of 38.62 months (SD 38.03).
  • There were 15.8% foetal losses and 12.5% preterm deliveries in our patients.
  • The low incidence of antiphospholipid syndrome, the high usage of hydroxychloroquine and the high SLE remission rate in our patients before conceptions are the possible factors contributing to the good outcome.


58. Ahn T, Kim M, Yun CH, Chae HJ: Functional regulation of hepatic cytochrome p450 enzymes by physicochemical properties of phospholipids in biological membranes. Curr Protein Pept Sci; 2007 Oct;8(5):496-505
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  • [Title] Functional regulation of hepatic cytochrome p450 enzymes by physicochemical properties of phospholipids in biological membranes.
  • P450 is a membrane-anchored protein that shows a variety of interaction with membrane phospholipids, which affect the membrane topology and catalytic activities of the protein.
  • In particular, anionic phospholipids, nonbilayer forming lipids, and the degree of saturation of the lipid fatty acyl chain play important roles in the functional regulation of P450, as well as in the bilayer structure of the membrane.
  • However, despite the importance of phospholipids in the regulation of P450s, the interaction of the protein with membrane phospholipids, and the membrane properties induced by phospholipids which regulate P450, are unclear.
  • In this review, we describe the effect of the physicochemical properties of the phospholipid constituents of biological membranes on hepatic P450 catalytic activity, membrane insertion (and/or penetration), and structural changes.
  • [MeSH-major] Cytochrome P-450 Enzyme System / metabolism. Intracellular Membranes / enzymology. Liver / enzymology. Phospholipids / physiology

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  • (PMID = 17979764.001).
  • [ISSN] 1389-2037
  • [Journal-full-title] Current protein & peptide science
  • [ISO-abbreviation] Curr. Protein Pept. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Phospholipids; 9035-51-2 / Cytochrome P-450 Enzyme System
  • [Number-of-references] 116
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59. Beck Z, Karasavvas N, Tong J, Matyas GR, Rao M, Alving CR: Calcium modulation of monoclonal antibody binding to phosphatidylinositol phosphate. Biochem Biophys Res Commun; 2007 Mar 16;354(3):747-51
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  • The binding characteristics of two monoclonal antibodies (mAb) to phosphatidylinositol-4-phosphate (PIP) were examined: a murine IgM mAb to PIP; and a human IgG mAb (4E10) that binds both to HIV-1 envelope protein and also to neutral and anionic phospholipids, including PIP.
  • When studied by surface plasmon resonance, liposomes containing PIP could be stripped (i.e., removed) by either Ca(2+) or phosphorylated haptens after binding of the liposomes to the murine anti-PIP antibody attached to a BIAcore chip.
  • [MeSH-minor] Animals. Binding Sites. Cations, Divalent. Dose-Response Relationship, Drug. Edetic Acid / metabolism. Enzyme-Linked Immunosorbent Assay. HIV-1 / immunology. HIV-1 / metabolism. Humans. Hydrophobic and Hydrophilic Interactions. Liposomes / immunology. Liposomes / metabolism. Mice. Phospholipids / immunology. Phospholipids / metabolism. Viral Envelope Proteins / immunology. Viral Envelope Proteins / metabolism

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  • (PMID = 17257584.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cations, Divalent; 0 / Immunoglobulin M; 0 / Liposomes; 0 / Phosphatidylinositol Phosphates; 0 / Phospholipids; 0 / Viral Envelope Proteins; 0 / phosphatidylinositol 4-phosphate; 9G34HU7RV0 / Edetic Acid; SY7Q814VUP / Calcium
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60. Nayak SR, Hussein M, Krishnamurthy A, Mansur DI, Prabhu LV, D'Souza P, Potu BK, Chettiar GK: Variation and clinical significance of extensor pollicis brevis: a study in South Indian cadavers. Chang Gung Med J; 2009 Nov-Dec;32(6):600-4
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  • [Title] Variation and clinical significance of extensor pollicis brevis: a study in South Indian cadavers.
  • BACKGROUND: de Quervain's disease is a condition in which there is pain in the radial styloid process caused by stenosing tenosynovitis of the abductor pollicis longus (APL) or/and extensor pollicis brevis (EPB) tendons in the first extensor compartment of the wrist.
  • RESULTS: The EPB had a single tendon in 133 limbs, double tendons in 17 limbs and triple tendons in only 6 limbs.
  • In 34.6% of cases, the tendons of the EPB were separated from the tendons of APL by an osseo-fibrous septum in the first extensor compartment.
  • CONCLUSION: Variation in the number of EPB tendons and site of insertion should be taken into consideration by clinicians and surgeons when performing surgical decompression of the first extensor compartment of the wrist in de Quervain's syndrome.
  • [MeSH-minor] Adult. Aged. Cadaver. De Quervain Disease / surgery. Humans. Male. Middle Aged

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  • (PMID = 20035638.001).
  • [ISSN] 2309-835X
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
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61. Erzin Y, Yalin AS, Erdamar AS, Celik AF: Necrosis of small intestine. Antiphospholipid syndrome. Neth J Med; 2008 Oct;66(9):400-1
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  • [Title] Necrosis of small intestine. Antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Intestine, Small / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged. Necrosis / diagnosis. Necrosis / etiology

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  • (PMID = 18931405.001).
  • [ISSN] 0300-2977
  • [Journal-full-title] The Netherlands journal of medicine
  • [ISO-abbreviation] Neth J Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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62. Basso C, Bottio T, Rubino M, Ruffatti A, Pittarello D, Thiene G, Gerosa G: Antiphospholipid syndrome and right atrial mass. J Thorac Cardiovasc Surg; 2005 Nov;130(5):1462-3
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  • [Title] Antiphospholipid syndrome and right atrial mass.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Heart Diseases / etiology. Thrombosis / etiology


63. Zhang H, Huang J: Henoch-Schönlein purpura associated with antiphospholipid syndrome. Pediatr Nephrol; 2010 Feb;25(2):377-8
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  • [Title] Henoch-Schönlein purpura associated with antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Purpura, Schoenlein-Henoch / complications
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. Child. Female. Humans

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  • [Cites] J Rheumatol. 1993 Nov;20(11):1964-6 [8308787.001]
  • [Cites] Pediatr Neurol. 2007 May;36(5):345-7 [17509470.001]
  • [Cites] Neurology. 2000 Nov 14;55(9):1379-81 [11087785.001]
  • [Cites] Arch Dermatol Res. 1989;281(4):296-8 [2789020.001]
  • [Cites] Arch Dis Child. 2002 Feb;86(2):132-3 [11827910.001]
  • [Cites] Pediatr Nephrol. 2001 May;16(5):458-9; discussion 460-2 [11405122.001]
  • (PMID = 19705156.001).
  • [ISSN] 1432-198X
  • [Journal-full-title] Pediatric nephrology (Berlin, Germany)
  • [ISO-abbreviation] Pediatr. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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64. Matsuura E, Shen L, Matsunami Y, Quan N, Makarova M, Geske FJ, Boisen M, Yasuda S, Kobayashi K, Lopez LR: Pathophysiology of beta2-glycoprotein I in antiphospholipid syndrome. Lupus; 2010 Apr;19(4):379-84
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  • [Title] Pathophysiology of beta2-glycoprotein I in antiphospholipid syndrome.
  • Since beta(2)-glycoprotein I (beta(2)GPI) was described as the major antigenic target for antiphospholipid antibodies, many studies have focused their attention to the physiological role of beta(2)GPI and anti-beta(2)GPI antibodies on autoimmune-mediated thrombosis.
  • Studies reporting the physiological role of beta(2)GPI have been numerous, but the exact mechanism of action(s) has yet to be completely determined. beta(2)GPI's epitopes for anti-beta(2)GPI autoantibodies have been characterized, however, not all of the heterogeneous anti-beta(2)GPI antibodies are pathogenic.
  • Our understanding of the impact of beta(2)GPI, its metabolites and autoantibodies to beta(2)GPI on these physiological functions may contribute to the development of better therapeutic strategies to treat and prevent autoimmune-mediated atherothrombotic vascular disease.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Autoantibodies / immunology. beta 2-Glycoprotein I / immunology

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  • (PMID = 20353973.001).
  • [ISSN] 1477-0962
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Epitopes; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 50
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65. Boehm I: Drug treatment-induced downregulation of antiphospholipid antibodies in PAPS. Clin Rheumatol; 2009 Nov;28(11):1347-8
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  • [Title] Drug treatment-induced downregulation of antiphospholipid antibodies in PAPS.
  • Although low-dose methotrexate (MTX) has been used to treat several autoimmune diseases like lupus erythematosus, rheumatoid arthritis, etc., it has not yet been used to treat patients with primary antiphospholipid syndrome (PAPS).
  • Parallel to clinical follow-up of female patient with a severe form of PAPS, antiphospholipid antibodies (aPL), blood coagulation, and hematological parameters in the peripheral blood have been monitored.
  • MTX improved ulcers, livedo reticularis, decreased aPL titers, increased platelet counts, and improved blood coagulation parameters (e.g., factor VIII) and was well tolerated.
  • The clinical benefit may be due to the downregulation of increased aPL titers and amelioration of disturbed coagulation parameters.
  • [MeSH-major] Antibodies, Antiphospholipid / drug effects. Antiphospholipid Syndrome / drug therapy. Immunosuppressive Agents / therapeutic use. Methotrexate / therapeutic use

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  • [Cites] JAMA. 2006 Mar 1;295(9):1050-7 [16507806.001]
  • [Cites] Ther Apher. 1998 May;2(2):157-9 [10225719.001]
  • [Cites] Immunobiology. 2005;210(10):749-54 [16325493.001]
  • [Cites] Lupus. 2005;14(7):499-504 [16130503.001]
  • [Cites] Ann Hematol. 2006 Feb;85(2):134-5 [16292550.001]
  • [Cites] Arthritis Rheum. 2008 Sep;58(9):2824-34 [18759321.001]
  • [Cites] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]
  • [Cites] Rheumatol Int. 1998;18(2):59-62 [9782534.001]
  • [Cites] Front Biosci. 2007 May 01;12:3093-103 [17485284.001]
  • [Cites] Biomed Pharmacother. 2003 Sep;57(7):278-81 [14499173.001]
  • [Cites] J Rheumatol. 2008 Sep;35(9):1768-75 [18634157.001]
  • (PMID = 19693642.001).
  • [ISSN] 1434-9949
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Immunosuppressive Agents; YL5FZ2Y5U1 / Methotrexate
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66. Yang L, Gong YP, Yang YM, Luo S: [A successful case of tanshinone II A treatment for relapsed acute promyelocytic leukemia after maintainance therapy of all-trans retinoic acid and arsenic trioxide]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2010 Nov;41(6):1065-7
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  • [Title] [A successful case of tanshinone II A treatment for relapsed acute promyelocytic leukemia after maintainance therapy of all-trans retinoic acid and arsenic trioxide].
  • OBJECTIVE: To observe the effects of Tanshinone II A (Tan II A) on acute promyelocytic leukemia (APL) characterized by resistance to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO).
  • METHODS: A 21-year-old male patient with relapsed APL, who previously received the maintenance therapy with ATRA,ATO, 6-Mercaptopurine (6-MP) and Methotrexate (MTX) for 1 year, was given Tan II A 80 mg intravenously once a day, and the changes of hematological parameters and side effects of Tan II A were observed.
  • CONCLUSION: Tan II A treatment may be effective in relapsed APL cases with ATRA and ATO resistance.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diterpenes, Abietane / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 21265116.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Arsenicals; 0 / Diterpenes, Abietane; 0 / Oxides; 03UUH3J385 / tanshinone; 5688UTC01R / Tretinoin; E7WED276I5 / 6-Mercaptopurine; S7V92P67HO / arsenic trioxide; YL5FZ2Y5U1 / Methotrexate
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67. Gao Y, Camacho LH, Mehta K: Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome. Leuk Res; 2007 Apr;31(4):455-63
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  • [Title] Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome.
  • All-trans retinoic acid (RA) treatment of patients with acute promyelocytic leukemia (APL) induces complete remission in more than 90% of the cases.
  • Although RA therapy is well tolerated, about 25% of APL patients develop a potentially fatal condition called retinoic acid syndrome (RAS).
  • In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients.
  • Importantly, RA-induced CD38 expression promoted strong attachment of leukemia cells to endothelial cells, and incubation of endothelial cells with either high concentration (100 ng/ml) of IFN-gamma alone or low concentration of IL-1beta and IFN-gamma (10 ng/ml, each) induced strong apoptotic responses as revealed by caspase-8 activation and DNA fragmentation.
  • Our results suggest that these RA-induced events could contribute to the development of RAS pathogenesis in patients with APL.
  • [MeSH-major] Antigens, CD38 / metabolism. Apoptosis / drug effects. Endothelium, Vascular / pathology. Interferon-gamma / pharmacology. Interleukin-1beta / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Tretinoin / pharmacology

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  • (PMID = 16920192.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA092115; United States / PHS HHS / / P01 PA 55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-1beta; 0 / Receptors, Retinoic Acid; 31C4KY9ESH / Nitric Oxide; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; EC 3.2.2.5 / Antigens, CD38
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68. Pengo V, Ruffatti A, Legnani C, Gresele P, Barcellona D, Erba N, Testa S, Marongiu F, Bison E, Denas G, Banzato A, Padayattil Jose S, Iliceto S: Clinical course of high-risk patients diagnosed with antiphospholipid syndrome. J Thromb Haemost; 2010 Feb;8(2):237-42
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  • [Title] Clinical course of high-risk patients diagnosed with antiphospholipid syndrome.
  • BACKGROUND: The characteristics and the clinical course of antiphospholipid syndrome (APS) in high-risk patients that are positive for all three recommended tests that detect the presence of antiphospholipid (aPL) antibodies have not been described.
  • METHODS: This retrospective analysis of prospectively collected data examined patients referred to Italian Thrombosis Centers that were diagnosed with definite APS and tested positive for aPL [lupus anticoagulant (LA), anti-cardiolipin (aCL), and anti-beta2-glycoprotein I (beta2GPI) antibodies].
  • The qualifying events at diagnosis were venous thromboembolism (76 cases; 47.5%), arterial thromboembolism (69 cases; 43.1%) and pregnancy morbidity (11 cases; 9.7%).
  • The cumulative incidence of thromboembolic events in the follow-up period was 12.2% (95% CI, 9.6-14.8) after 1 year, 26.1% (95% CI, 22.3-29.9) after 5 years and 44.2% (95% CI, 38.6-49.8) after 10 years.
  • CONCLUSIONS: Patients with APS and triple positivity for aPL are at high risk of developing future thromboembolic events.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / diagnosis. Pregnancy Complications, Cardiovascular / etiology. Venous Thromboembolism / etiology
  • [MeSH-minor] Administration, Oral. Adult. Aged. Antibodies, Anticardiolipin / blood. Anticoagulants / administration & dosage. Anticoagulants / adverse effects. Biomarkers / blood. Catastrophic Illness. Disease Progression. Female. Hemorrhage / chemically induced. Humans. Incidence. Italy. Kaplan-Meier Estimate. Lupus Coagulation Inhibitor / blood. Male. Middle Aged. Predictive Value of Tests. Pregnancy. Proportional Hazards Models. Recurrence. Retrospective Studies. Risk Assessment. Risk Factors. Time Factors. Treatment Outcome. beta 2-Glycoprotein I / immunology

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  • [CommentIn] J Thromb Haemost. 2010 Feb;8(2):234-6 [19912514.001]
  • (PMID = 19874470.001).
  • [ISSN] 1538-7836
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Biomarkers; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I
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69. Zhu B, Zhang LH, Zhao YM, Cui JR, Strada SJ: 8-chloroadenosine induced HL-60 cell growth inhibition, differentiation, and G(0)/G(1) arrest involves attenuated cyclin D1 and telomerase and up-regulated p21(WAF1/CIP1). J Cell Biochem; 2006 Jan 1;97(1):166-77
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  • 8-Chloroadenosine, an active dephosphorylated metabolite of the antineoplastic agent 8-chloroadenosine 3',5'-monophosphate (8-Cl-cAMP), induces growth inhibition in multiple carcinomas.
  • Here we report that 8-chloroadenosine inhibits growth in human promyelocytic leukemia HL-60 cells by a G(0)/G(1) phase arrest and terminates cell differentiation along the granulocytic lineage.
  • Therefore, anti-proliferation of HL-60 cells by 8-chloroadenosine involves coordination of cyclin D1 suppression, reduction of telomerase activity, and up-regulation of p21(WAF1/CIP1) that arrest cell-cycle progression at G(0)/G(1) phase and terminate cell differentiation.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16173047.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 136601-57-5 / Cyclin D1; 146-77-0 / 2-Chloroadenosine; 34408-14-5 / 8-chloroadenosine; EC 2.7.7.49 / Telomerase
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70. Tirado CA, Chen W, Valdez F, Karandikar N, Arbini A, Acevedo I, Garcia R, Davila O, Smart RL, Matthews E, Kirk A, Collins RH: Unusual presentation of myeloid sarcoma in a case of acute promyelocytic leukemia with a cryptic PML-RARA rearrangement involving multiple sites including the atrium. Cancer Genet Cytogenet; 2010 Jul 1;200(1):47-53
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  • [Title] Unusual presentation of myeloid sarcoma in a case of acute promyelocytic leukemia with a cryptic PML-RARA rearrangement involving multiple sites including the atrium.
  • Myeloid sarcoma is an extramedullary tumor mass composed of immature myeloid cells.
  • Myeloid sarcoma may develop de novo, concurrently with acute myeloid leukemia (AML), or at relapse.
  • Although myeloid sarcoma can occur at any site, myeloid sarcoma involving the heart is extremely rare.
  • Reported here is the case of a 30-year-old man, initially diagnosed with acute promyelocytic leukemia (APL) in bone marrow, who presented later with myeloid sarcoma at multiple anatomical sites (left scapula, thoracic vertebra, right atrium, and supraclavicular mass) in multiple relapses.
  • Fluorescence in situ hybridization studies confirmed a cryptic PML-RARA fusion on the short arm of chromosome 7, as well as a second fusion on one copy of chromosome 15.
  • With the fourth and latest relapse, molecular cytogenetic studies performed on interphase nuclei of the myeloid sarcoma specimen (a supraclavicular mass) showed evidence of six related abnormal clones with a PML-RARA fusion, suggesting clonal evolution.
  • This represents a rare case of APL with a cryptic PML-RARA rearrangement presenting as myeloid sarcoma at multiple relapses and involving multiple anatomical sites, including cardiac atrium.
  • [MeSH-major] Gene Rearrangement. Heart Neoplasms / genetics. Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. Sarcoma, Myeloid / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20513534.001).
  • [ISSN] 1873-4456
  • [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 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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71. Tan LA, Yu B, Sim FC, Kishore U, Sim RB: Complement activation by phospholipids: the interplay of factor H and C1q. Protein Cell; 2010 Nov;1(11):1033-49
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  • [Title] Complement activation by phospholipids: the interplay of factor H and C1q.
  • The anionic phospholipid (aPL) cardiolipin binds both complement proteins C1q and factor H.
  • To examine opposing effects of C1q and factor H on complement activation by aPL, we surveyed C1q and factor H binding, and complement activation by aPL, either coated on microtitre plates or in liposomes.
  • Both C1q and factor H bound to all aPL tested, and competed directly with each other for binding.
  • All the aPL activated the complement classical pathway, but negligibly the alternative pathway, consistent with accepted roles of C1q and factor H.
  • However, in this system, factor H, by competing directly with C1q for binding to aPL, acts as a direct regulator of the complement classical pathway.
  • Regulation of classical pathway activation by factor H was confirmed by measuring C4 activation by aPL in human sera in which the C1q:factor H molar ratio was adjusted over a wide range.
  • Thus factor H, which is regarded as a down-regulator only of the alternative pathway, has a distinct role in downregulating activation of the classical complement pathway by aPL.
  • Recombinant globular domains of C1q A, B and C chains bound aPL similarly to native C1q, confirming that C1q binds aPL via its globular heads.

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  • (PMID = 21153520.001).
  • [ISSN] 1674-8018
  • [Journal-full-title] Protein & cell
  • [ISO-abbreviation] Protein Cell
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Phospholipids; 80295-33-6 / Complement C1q; 80295-65-4 / Complement Factor H
  • [Other-IDs] NLM/ PMC4875149
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72. Dixon KS, Hassoun A: Pseudotumor cerebri due to the potentiation of all-trans retinoic acid by voriconazole. J Am Pharm Assoc (2003); 2010 Nov-Dec;50(6):742-4
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  • CASE SUMMARY: The patient had been diagnosed with acute promyelocytic leukemia 5 months before admission and continued on ATRA throughout induction and two consolidation therapies.
  • On day 15 of voriconazole therapy, the patient complained of blurred vision, farsightedness, and dry skin with pruritus and was subsequently diagnosed with pseudotumor cerebri secondary to ATRA toxicity.

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  • (PMID = 21071321.001).
  • [ISSN] 1544-3450
  • [Journal-full-title] Journal of the American Pharmacists Association : JAPhA
  • [ISO-abbreviation] J Am Pharm Assoc (2003)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Triazoles; 5688UTC01R / Tretinoin; JFU09I87TR / Voriconazole
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73. Wang Y, An R, Dong X, Pan S, Duan G, Sun X: Protein kinase C is involved in arsenic trioxide-induced apoptosis and inhibition of proliferation in human bladder cancer cells. Urol Int; 2009;82(2):214-21
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  • OBJECTIVE: Arsenic trioxide (ATO) is a potent antitumor agent used to treat acute promyelocytic leukemia, and recently solid tumors including bladder cancers.

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19322013.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Enzyme Activators; 0 / Oxides; 0 / Protein Kinase Inhibitors; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; EC 2.7.11.13 / Protein Kinase C; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; NI40JAQ945 / Tetradecanoylphorbol Acetate; S7V92P67HO / arsenic trioxide
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74. Wierema TK, Stehouwer CD: [Premature cardiovascular disease: no indication for the determination of antiphospholipid antibodies or lupus anticoagulant as a possible risk factor]. Ned Tijdschr Geneeskd; 2007 Mar 31;151(13):735-8
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  • [Title] [Premature cardiovascular disease: no indication for the determination of antiphospholipid antibodies or lupus anticoagulant as a possible risk factor].
  • In patients with premature atherothrombotic disease, the antiphospholipid syndrome (APS, defined as any thrombosis plus the repeated presence ofantiphospholipid antibodies) is sometimes looked for, as observational studies have suggested a link between APS and premature atherothrombosis.
  • However, recent reviews that evaluated the prognostic value of antiphospholipid antibodies have concluded that the prognostic significance ofAPS for recurrent thrombotic disease is, at best, unclear and that its presence has no therapeutic consequences.
  • A study in patients with a recent ischaemic stroke found no additional benefit from warfarin (standard dosage) versus aspirin in patients with or without antiphospholipid antibodies.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Cardiovascular Diseases / diagnosis. Lupus Coagulation Inhibitor / blood. Thrombosis / diagnosis

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  • (PMID = 17471773.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Biomarkers; 0 / Lupus Coagulation Inhibitor; 5Q7ZVV76EI / Warfarin
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75. Szczepańiska M, Muszewska E, Szprynger K, Niwińska-Faryna B: [Systemic lupus erythematosus and pregnancy]. Wiad Lek; 2008;61(4-6):161-5
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  • Systemic lupus erythematosus (SLE) is an autoimmune chronic disease, which involves multiple organs, particularly joints, skin, heart, lungs, nervous system and kidneys.
  • In the study authors report the risk factors for spontaneous abortions and premature births in women with SLE particularly in the group with the presence of antiphospholipid syndrome.
  • [MeSH-major] Lupus Erythematosus, Systemic / diagnosis. Lupus Erythematosus, Systemic / drug therapy. Pregnancy Complications / diagnosis. Pregnancy Complications / drug therapy


76. Profumo E, Buttari B, Alessandri C, Conti F, Capoano R, Valesini G, Salvati B, Riganò R: Beta2-glycoprotein I is a target of T cell reactivity in patients with advanced carotid atherosclerotic plaques. Int J Immunopathol Pharmacol; 2010 Jan-Mar;23(1):73-80
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  • Evidence in animal models that beta2-glycoprotein I (beta2GPI), the principal target of autoimmune antiphospholipid antibodies, is involved in the initiation and progression of atherosclerosis, prompted us to investigate the possible role of this self protein as a target autoantigen of immune reactions in patients with carotid atherosclerosis.
  • ELISA was used to detect cytokine production in culture supernatants and anti-beta2GPI/anti-cardiolipin antibodies in serum samples.
  • Patients PBMC samples that proliferated in response to beta2GPI produced significantly higher IFN-gamma and TNF-alpha than non-proliferating PBMC. beta2GPI-specific plaque-derived T lymphocytes expressed IFN-gamma, TNF-alpha and IL-4, suggesting concomitant Th1 and Th2 activation.
  • Only one patients serum was positive for anti-beta2GPI and anti-cardiolipin IgM antibodies.
  • These new findings indicate that beta2GPI induces a cellular immune response in a subpopulation of patients with carotid atherosclerosis thus contributing to the inflammatory responses involved in carotid atherosclerotic disease.

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  • (PMID = 20377996.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Autoantibodies; 0 / Cytokines; 0 / beta 2-Glycoprotein I
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77. Ramos-Casals M, Brito-Zerón P, Soto MJ, Cuadrado MJ, Khamashta MA: Autoimmune diseases induced by TNF-targeted therapies. Best Pract Res Clin Rheumatol; 2008 Oct;22(5):847-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Anti-TNF agents are increasingly being used for a rapidly expanding number of rheumatic and systemic autoimmune diseases.
  • As a result of this use, and of the longer follow-up periods of treatment, there are a growing number of reports of the development of autoimmune processes related to anti-TNF agents.
  • The clinical characteristics, outcomes, and patterns of association with the different anti-TNF agents used in all reports of autoimmune diseases developing after TNF-targeted therapy, were analyzed through a baseline Medline search of articles published between January 1990 and May 2008 (www.biogeas.org).
  • The anti-TNF agents were administered for rheumatoid arthritis in more than 80% of cases.
  • The use of anti-TNF agents has been associated with an increasing number of cases of autoimmune diseases, principally cutaneous vasculitis, lupus-like syndrome, systemic lupus erythematosus and interstitial lung disease.
  • Other autoimmune diseases associated with TNF-targeted therapies have been recently described, e.g. sarcoidosis, antiphospholipid syndrome-related features, and autoimmune hepatitis or uveitis.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antirheumatic Agents / adverse effects. Arthritis, Rheumatoid / drug therapy. Autoimmune Diseases / chemically induced. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 19028367.001).
  • [ISSN] 1532-1770
  • [Journal-full-title] Best practice & research. Clinical rheumatology
  • [ISO-abbreviation] Best Pract Res Clin Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antirheumatic Agents; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 30
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78. Shoenfeld Y, Katz U: IVIg therapy in autoimmunity and related disorders: our experience with a large cohort of patients. Autoimmunity; 2005 Mar;38(2):123-37
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  • [Title] IVIg therapy in autoimmunity and related disorders: our experience with a large cohort of patients.
  • It has been shown that IVIg contains anti-idiotypic antibodies, which explains its immunomodulatory action.
  • In murine models, recent investigations have demonstrated that IVIg can prevent and reduce the affliction by systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS) and scleroderma.
  • Relevant disease-specific fractions of IVIg were able to reproduce and even enhance the therapeutic effect in a murine model.IVIg treatment before tumor resection in rodents inoculated with melanoma and sarcoma cells dramatically improved the cure rate (50%) in comparison to the control group (0%).
  • In patients affected by SLE, several clinical manifestations responded to IVIg treatment including serositis, hematological manifestations, treatment-resistant nephritis and central nervous system involvement.
  • We suggest that in the presence of a steroid and immunosuppressive-resistant autoimmune disease, IVIg is a rational and safe choice.

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  • (PMID = 16040333.001).
  • [ISSN] 0891-6934
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulins, Intravenous
  • [Number-of-references] 127
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79. Coe E, Schimmer AD: Catalase activity and arsenic sensitivity in acute leukemia. Leuk Lymphoma; 2008 Oct;49(10):1976-81
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  • [Title] Catalase activity and arsenic sensitivity in acute leukemia.
  • Arsenic trioxide (As2O3) is currently employed as a treatment for relapsed acute promyelocytic leukemia (APL), where it can induce remission in greater than 90% of patients, but is ineffective in patients with non-APL acute myeloid leukemia (AML).
  • As2O3 induces apoptosis in APL cells through mechanisms dependent and independent of the PML-RARalpha fusion protein.
  • Through PML-RARalpha fusion-independent mechanisms, As2O3 increases H2O2 production via its effects on glutathione and glutathione peroxidase.
  • In AML and APL cell lines, but not primary patient samples, basal catalase levels matched sensitivity to As2O3.
  • Failure of catalase inhibition to sensitise cells to As2O3 was due to a failure of catalase inhibition to increased levels of reactive oxygen species.
  • Therefore, other strategies should be explored to enhance the cytotoxicity of As2O3 in AML.
  • [MeSH-major] Arsenicals / pharmacology. Catalase / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / pharmacology

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  • (PMID = 18949620.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Enzyme Inhibitors; 0 / Oxides; EC 1.11.1.6 / Catalase; S7V92P67HO / arsenic trioxide
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80. Nie XR, Zhang Y, Pan KF, Li WQ, You WC, Zhang L: [Quantification of cyclooxygenase-2 methylation in gastric mucosa by denaturing high performance liquid chromatography assay]. Zhonghua Yu Fang Yi Xue Za Zhi; 2010 Jan;44(1):54-7
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  • RESULTS: The complete methylated human promyelocytic leukemia cells (HL-60) and unmethylated gastric cancer cell line (MGC803) were used as positive and negative control.

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  • (PMID = 20388365.001).
  • [ISSN] 0253-9624
  • [Journal-full-title] Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
  • [ISO-abbreviation] Zhonghua Yu Fang Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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81. Aburai N, Yoshida M, Ohnishi M, Kimura K: Pisiferdiol and pisiferic acid isolated from Chamaecyparis pisifera activate protein phosphatase 2C in vitro and induce caspase-3/7-dependent apoptosis via dephosphorylation of Bad in HL60 cells. Phytomedicine; 2010 Aug;17(10):782-8
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  • In the course of screening for PP2C activators from natural sources, we isolated abietane-type diterpenes, pisiferdiol and pisiferic acid from Chamaecyparis pisifera.
  • Pisiferdiol and pisiferic acid showed mixed-type activation with respect to alpha-casein, and this differed from the non-competitive activation of oleic acid in vitro.
  • In vivo, the cytotoxicity of pisiferdiol toward human promyelocytic leukemia cell line HL60 with an IC(50) value of 18.3 microM was 2-fold and 7-fold stronger than those of pisiferic acid and oleic acid, and pisiferdiol induced apoptosis through a caspase 3/7-dependent mechanism involving the dephosphorylation of Bad(1), which is a PP2C substrate.

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  • [Copyright] 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20153620.001).
  • [ISSN] 1618-095X
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Diterpenes; 0 / bcl-Associated Death Protein; 67494-15-9 / pisiferic acid; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / protein phosphatase 2C; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
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82. Crosetto N, Bienko M, Hibbert RG, Perica T, Ambrogio C, Kensche T, Hofmann K, Sixma TK, Dikic I: Human Wrnip1 is localized in replication factories in a ubiquitin-binding zinc finger-dependent manner. J Biol Chem; 2008 Dec 12;283(50):35173-85
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  • Interestingly, the nuclear pattern of Wrnip1 appears to extend to a broader landscape, as it can be detected in promyelocytic leukemia nuclear bodies.

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  • [Cites] EMBO J. 2000 Jul 3;19(13):3388-97 [10880451.001]
  • [Cites] EMBO J. 2004 Oct 1;23(19):3886-96 [15359278.001]
  • [Cites] Oncogene. 2001 May 3;20(20):2551-8 [11420665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8283-9 [11459965.001]
  • [Cites] Biotechniques. 2001 Jul;31(1):88-90, 92 [11464525.001]
  • [Cites] EMBO J. 2002 Apr 15;21(8):2019-29 [11953321.001]
  • [Cites] J Cell Sci. 2002 Oct 15;115(Pt 20):3901-7 [12244128.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):169-78 [12612652.001]
  • [Cites] Mol Biol Cell. 2003 Dec;14(12):5060-8 [14565979.001]
  • [Cites] Exp Cell Res. 1998 Aug 1;242(2):487-94 [9683536.001]
  • [Cites] Science. 2004 Dec 10;306(5703):1951-3 [15591207.001]
  • [Cites] J Biol Chem. 2005 Jan 7;280(1):515-24 [15509568.001]
  • [Cites] Genes Cells. 2005 Jan;10(1):13-22 [15670210.001]
  • [Cites] Mol Cell. 2005 Jun 10;18(6):687-98 [15949443.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):610-21 [16064137.001]
  • [Cites] Nat Struct Mol Biol. 2005 Aug;12(8):708-14 [16007098.001]
  • [Cites] EMBO J. 2005 Sep 21;24(18):3178-89 [16138082.001]
  • [Cites] Annu Rev Cell Dev Biol. 2005;21:105-31 [16212489.001]
  • [Cites] Nucleic Acids Res. 2005;33(19):6137-50 [16251400.001]
  • [Cites] Science. 2005 Dec 16;310(5755):1821-4 [16357261.001]
  • [Cites] Curr Opin Cell Biol. 2006 Jun;18(3):307-16 [16687245.001]
  • [Cites] J Biol Chem. 2006 Jun 9;281(23):16117-27 [16524884.001]
  • [Cites] Curr Opin Struct Biol. 2007 Dec;17(6):641-52 [18023171.001]
  • [Cites] Cell. 2008 Mar 7;132(5):832-45 [18329369.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Apr;9(4):297-308 [18285803.001]
  • [Cites] Genes Genet Syst. 2008 Feb;83(1):95-100 [18379138.001]
  • [Cites] EMBO Rep. 2008 Jun;9(6):536-42 [18516089.001]
  • [Cites] Mol Cell Biol. 2006 Jul;26(14):5509-17 [16809783.001]
  • [Cites] Genes Cells. 2006 Jul;11(7):731-44 [16824193.001]
  • [Cites] DNA Repair (Amst). 2006 Jul 13;5(7):816-28 [16769258.001]
  • [Cites] Biochem J. 2006 Nov 1;399(3):361-72 [17034365.001]
  • [Cites] Biol Pharm Bull. 2006 Nov;29(11):2192-6 [17077513.001]
  • [Cites] J Biol Chem. 2006 Nov 10;281(45):34687-95 [16980296.001]
  • [Cites] Mol Cell Biol. 2006 Dec;26(23):8892-900 [16982685.001]
  • [Cites] J Cell Biol. 2006 Dec 4;175(5):693-701 [17145961.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 13;104(7):2205-10 [17284601.001]
  • [Cites] EMBO Rep. 2007 Mar;8(3):247-51 [17304240.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 May;8(5):394-404 [17450177.001]
  • [Cites] Cell. 2007 May 18;129(4):665-79 [17512402.001]
  • [Cites] Science. 2007 May 25;316(5828):1198-202 [17525341.001]
  • [Cites] Science. 2007 May 25;316(5828):1202-5 [17525342.001]
  • [Cites] J Biol Chem. 2007 Aug 10;282(32):23184-93 [17550899.001]
  • [Cites] Nat Struct Mol Biol. 2007 Aug;14(8):716-20 [17643121.001]
  • [Cites] Nat Struct Mol Biol. 2007 Aug;14(8):710-5 [17643122.001]
  • [Cites] Nucleic Acids Res. 2007;35(17):5819-30 [17720710.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Dec;8(12):1006-16 [17928811.001]
  • [Cites] J Biol Chem. 2004 Feb 20;279(8):7055-63 [14645257.001]
  • [Cites] J Struct Biol. 2004 Apr-May;146(1-2):44-57 [15037236.001]
  • [Cites] J Biol Chem. 2001 Jun 8;276(23):20364-9 [11301316.001]
  • (PMID = 18842586.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Ubiquitin; 0 / WRNIP1 protein, human; 9007-49-2 / DNA; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC3259897
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83. Groysman N, Orynbayeva Z, Katz M, Kolusheva S, Khanin M, Danilenko M, Jelinek R: Membrane processes and biophysical characterization of living cells decorated with chromatic polydiacetylene vesicles. Biochim Biophys Acta; 2008 May;1778(5):1335-43
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  • This work examines the biological and chemical consequences of plasma membrane labeling of promyelocytic leukemia cells with polydiacetylene.
  • We show that the extent of fusion between incubated lipid/diacetylene vesicles and the plasma membrane is closely dependent upon the lipid composition of both vesicles and cell membrane.
  • In particular, we find that cholesterol presence increased bilayer fusion between the chromatic vesicles and the plasma membrane, suggesting that membrane organization plays a significant role in the fusion process.

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  • (PMID = 18331821.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Polymers; 25067-58-7 / Polyacetylenes; 27987-87-7 / polydiacetylene
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84. Praprotnik S, Agmon-Levin N, Porat-Katz BS, Blank M, Meroni PL, Cervera R, Miesbach W, Stojanovich L, Szyper-Kravitz M, Rozman B, Tomsic M, Shoenfeld Y: Prolactin's role in the pathogenesis of the antiphospholipid syndrome. Lupus; 2010 Nov;19(13):1515-9
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  • [Title] Prolactin's role in the pathogenesis of the antiphospholipid syndrome.
  • Increased levels of serum prolactin have been reported in patients with various autoimmune diseases and have been associated with lupus disease activity.
  • Currently, there is a lack of data regarding hyperprolactinaemia in patients with the antiphospholipid syndrome.
  • Hence, this study was carried out in order to evaluate the prevalence and clinical significance of hyperprolactinaemia in antiphospholipid syndrome.
  • A total of 172 European patients with antiphospholipid syndrome and 100 geographically and sex-matched healthy controls were included in the study; none had obvious causes of hyperprolactinaemia.
  • All patients underwent clinical assessment for disease manifestations, in addition to laboratory assessment for serum prolactin, antiphospholipid antibodies and some other biomarkers of autoimmune diseases.
  • Hyperprolactinaemia was detected in 21/172 patients with antiphospholipid syndrome and 0/100 controls (p < 0.001).
  • This significant difference was present in both genders and was obvious even after subgrouping the patients into primary and secondary antiphospholipid syndrome.
  • When clinical features were compared, hyperprolactinaemia was associated with reproductive failure, including early and late pregnancy loss (p < 0.05), as well as intrauterine growth retardation (p < 0.05).
  • Hyperprolactinaemia was negatively related to arthralgias, venous thrombosis, pulmonary microthrombosis, pulmonary hypertension in both primary antiphospholipid syndrome and antiphospholipid syndrome secondary to other diseases, and to neurological manifestations in primary antiphospholipid syndrome (p<0.05).
  • The data indirectly imply that prolactin may play a role in the pathogenesis of antiphospholipid syndrome, especially antiphospholipid syndrome-related reproductive failure.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / physiopathology. Hyperprolactinemia / physiopathology. Prolactin / blood

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  • (PMID = 20647249.001).
  • [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; 9002-62-4 / Prolactin
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85. Xia J, Yuan M, Xu HW, Zhang L, Du XP, Liu YH, Yang QD: Association between Val/Leu(247) polymorphism of apolipoprotein H and cerebral infarction in a Chinese population. J Thromb Thrombolysis; 2009 Aug;28(2):187-91
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  • BACKGROUND: Antiphospholipid antibodies (aPL) are considered to be a cause of an acquired hypercoagulable state leading to cerebral infarction (CI).
  • Apolipoprtein H (apoH) is an important target antigen for aPL and thus apoH polymorphisms may influence aPL production and the development of CI.
  • The presence of aPL was detected by ELISA utilizing irradiated ELISA plates.
  • RESULTS: Our results demonstrated an association between the Val/Leu(247) polymorphism of apoH gene and aPL in CI patients.
  • The frequency of V allele was significantly higher in aPL-positive CI patients compared with control group (chi(2) = 6.864, P < 0.05).
  • VL genotype frequency was also significantly higher in aPL-positive CI group compared with control group (chi(2) = 13.879, P < 0.05) and aPL-negative CI group (chi(2) = 5.567, P < 0.05).
  • CONCLUSIONS: The Val(247) allele of apoH gene is significantly associated with the presence of aPL in Chinese patients with CI.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Cerebral Infarction / genetics. beta 2-Glycoprotein I / genetics
  • [MeSH-minor] Adult. Aged. Asian Continental Ancestry Group. Case-Control Studies. China / epidemiology. Female. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Polymorphism, Genetic. Risk Factors

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  • [Cites] Hum Genet. 1997 Jul;100(1):57-62 [9225969.001]
  • [Cites] Ann Hum Genet. 2004 Jul;68(Pt 4):285-99 [15225155.001]
  • [Cites] Hokkaido Igaku Zasshi. 2001 Sep;76(5):289-98 [11593753.001]
  • [Cites] Arthritis Rheum. 2003 Feb;48(2):471-4 [12571857.001]
  • [Cites] Eur J Biochem. 2003 Jan;270(2):230-8 [12605674.001]
  • [Cites] Neurology. 2001;57(5 Suppl 2):S24-30 [11552051.001]
  • [Cites] Lupus. 2005;14(6):440-4 [16038107.001]
  • [Cites] J Exp Med. 1994 Feb 1;179(2):457-62 [7507506.001]
  • [Cites] Cerebrovasc Dis. 2005;20 Suppl 2:53-67 [16327254.001]
  • [Cites] Neurology. 2001 Apr 24;56(8):997-1008 [11339244.001]
  • [Cites] Neurology. 1993 Oct;43(10):2069-73 [8413969.001]
  • [Cites] Eur J Biochem. 1999 Jan;259(1-2):435-40 [9914524.001]
  • [Cites] Arthritis Rheum. 1999 Aug;42(8):1655-61 [10446865.001]
  • [Cites] Autoimmun Rev. 2007 Sep;6(8):547-52 [17854747.001]
  • [Cites] Cerebrovasc Dis. 2005;20 Suppl 2:75-83 [16327256.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):1066-72 [12648080.001]
  • [Cites] Prostaglandins Other Lipid Mediat. 1999 Jul;57(5-6):351-9 [10480489.001]
  • [Cites] Lupus. 2006;15(4):218-22 [16686261.001]
  • [Cites] Clin Rheumatol. 2007 Mar;26(3):302-7 [16724168.001]
  • [Cites] Rom J Intern Med. 2007;45(2):201-4 [18333375.001]
  • [Cites] Thromb Haemost. 1998 Nov;80(5):791-7 [9843173.001]
  • [Cites] Rheumatology (Oxford). 1999 Aug;38(8):721-3 [10501418.001]
  • [Cites] Thromb Haemost. 1995 Oct;74(4):1185-90 [8560433.001]
  • [Cites] Arthritis Rheum. 2005 Jan;52(1):212-8 [15641049.001]
  • [Cites] Thromb Res. 2004;114(5-6):489-99 [15507283.001]
  • [Cites] Cerebrovasc Dis. 2002;13 Suppl 1:7-11 [11803181.001]
  • [Cites] Intern Med. 2006;45(17):1017-8 [17016003.001]
  • (PMID = 18777117.001).
  • [ISSN] 1573-742X
  • [Journal-full-title] Journal of thrombosis and thrombolysis
  • [ISO-abbreviation] J. Thromb. Thrombolysis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / beta 2-Glycoprotein I
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86. Derksen RH, de Groot PG: Towards evidence-based treatment of thrombotic antiphospholipid syndrome. Lupus; 2010 Apr;19(4):470-4
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  • [Title] Towards evidence-based treatment of thrombotic antiphospholipid syndrome.
  • Thrombosis in the presence of persistently positive tests for antiphospholipid antibodies is termed thrombotic antiphospholipid syndrome (APS).
  • [MeSH-major] Anticoagulants / therapeutic use. Antiphospholipid Syndrome / drug therapy. Thrombosis / drug therapy
  • [MeSH-minor] Antibodies, Antiphospholipid / immunology. Brain Ischemia / drug therapy. Brain Ischemia / etiology. Brain Ischemia / immunology. Dose-Response Relationship, Drug. Evidence-Based Medicine. Humans. Platelet Aggregation Inhibitors / therapeutic use. Risk Factors. Secondary Prevention / methods. Stroke / drug therapy. Stroke / etiology. Stroke / immunology

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  • (PMID = 20353990.001).
  • [ISSN] 1477-0962
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Platelet Aggregation Inhibitors
  • [Number-of-references] 24
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87. Miyajima S, Taguchi Y, Tanaka E, Inoue T, Sakuramoto M, Minakuchi M, Maeda Y, Maniwa K, Tanizawa K, Okamoto M, Takeda T: [A case of pulmonary adenocarcinoma accompanied by minimal change nephrotic syndrome, antiphospholipid syndrome and warm-type autoimmune hemolytic anemia]. Nihon Kokyuki Gakkai Zasshi; 2006 Sep;44(9):631-5
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  • [Title] [A case of pulmonary adenocarcinoma accompanied by minimal change nephrotic syndrome, antiphospholipid syndrome and warm-type autoimmune hemolytic anemia].
  • Detailed investigations including bronchoscopy and renal biopsy led to a simultaneous diagnosis of clinical stage IIIB pulmonary adenocarcinoma, minimal change nephrotic syndrome, antiphospholipid syndrome, and warm-type autoimmune hemolytic anemia.
  • Prednisolone was administered for nephrotic syndrome, antiphospholipid syndrome and warm-type autoimmune hemolytic anemia, and 6 courses of chemotherapy with 70Gy radio-therapy were performed.
  • The pulmonary nodule significantly decreased in size and the other three autoimmune diseases appeared to be well-controlled.
  • Thirteen months after admission, multiple brain metastases developed along with worsening antiphospholipid syndrome symptoms including lupus anticoagulant.
  • Following whole-brain irradiation, the brain metastases decreased in size and antiphospholipid syndrome symptoms improved.
  • [MeSH-major] Adenocarcinoma / complications. Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiphospholipid Syndrome / etiology. Lung Neoplasms / complications. Nephrosis, Lipoid / etiology

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  • (PMID = 17037407.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9PHQ9Y1OLM / Prednisolone; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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88. Kuchenbauer F, Schoch C, Kern W, Hiddemann W, Haferlach T, Schnittger S: Impact of FLT3 mutations and promyelocytic leukaemia-breakpoint on clinical characteristics and prognosis in acute promyelocytic leukaemia. Br J Haematol; 2005 Jul;130(2):196-202
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  • [Title] Impact of FLT3 mutations and promyelocytic leukaemia-breakpoint on clinical characteristics and prognosis in acute promyelocytic leukaemia.
  • In the present study 170 newly diagnosed acute promyelocytic leukaemia patients (M3: n = 121; M3v: n = 49) were molecularly characterised with respect to PML breakpoint and additional molecular mutations.
  • Bcr3 was more frequent in M3v (65.3%) compared with M3 (41.3%) (P = 0.005).
  • Cases with bcr3 showed a significantly higher white blood cell count (median: 3.65 x 10(9)/l vs. 1.59 x 10(9)/l, P = 0.003), as well as a higher PML-RARAABL expression ratio (14.8% vs. 72.7%, P < 0.005) compared with bcr1.
  • FLT3-length-mutations were detected more frequently together with bcr3 compared with bcr1 (56.5% vs. 19.4%, P < 0.001) and in M3v compared with M3 (64.5% vs. 24.1%, P < 0.005).
  • FLT3-mutations were detected in 62 of 139 cases (44.6%) and associated with a significant lower overall survival (P = 0.0339).
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Mutation. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Disease-Free Survival. Female. Humans. Leukocyte Count. Male. Middle Aged. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Polymerase Chain Reaction / methods. Prognosis. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-bcr. Survival Rate. fms-Like Tyrosine Kinase 3

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  • (PMID = 16029447.001).
  • [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 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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89. Doudican NA, Bowling B, Orlow SJ: Enhancement of arsenic trioxide cytotoxicity by dietary isothiocyanates in human leukemic cells via a reactive oxygen species-dependent mechanism. Leuk Res; 2010 Feb;34(2):229-34
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  • Although clearly effective in acute promyelocytic leukemia (APL), arsenic trioxide (ATO) demonstrates little clinical benefit as a single agent in the treatment of non-APL hematological malignancies.
  • Cellular exposure to sulforaphane in combination with ATO resulted in a dramatic increase in levels of reactive oxygen species (ROS) compared to treatment with either agent alone.
  • Combinatorial treatment with isothiocyanates and ATO might provide a promising therapeutic approach for a variety of myeloid malignancies.

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • [Cites] Biomed Pharmacother. 2008 Nov;62(9):637-44 [18313257.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Dec;63(1):37-43 [18297286.001]
  • [Cites] Br J Cancer. 1999 Nov;81(5):796-9 [10555748.001]
  • [Cites] Oncogene. 1999 Dec 16;18(54):7794-802 [10618720.001]
  • [Cites] J Natl Cancer Inst. 2000 Jan 5;92(1):61-8 [10620635.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1426-33 [10728709.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):3065-71 [10850458.001]
  • [Cites] Oncologist. 2001;6 Suppl 2:1-2 [11331433.001]
  • [Cites] Oncologist. 2001;6 Suppl 2:11-6 [11331435.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Sep;10(9):949-54 [11535546.001]
  • [Cites] Clin Chim Acta. 2002 Feb;316(1-2):43-53 [11750273.001]
  • [Cites] Carcinogenesis. 2002 Apr;23(4):581-6 [11960909.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3893-903 [12124315.001]
  • [Cites] Mol Pharmacol. 2002 Sep;62(3):529-38 [12181429.001]
  • [Cites] Leukemia. 2003 May;17(5):931-40 [12750708.001]
  • [Cites] Mol Cancer Ther. 2003 Oct;2(10):1045-52 [14578469.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Jul;310(1):263-71 [14988420.001]
  • [Cites] J Biol Chem. 1977 Sep 25;252(18):6438-42 [893418.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7 Suppl):1976s-1981s [8137323.001]
  • [Cites] J Cell Physiol. 1998 Nov;177(2):324-33 [9766529.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1198-203 [15231573.001]
  • [Cites] Leukemia. 2005 Feb;19(2):234-44 [15538402.001]
  • [Cites] Cancer Causes Control. 2004 Dec;15(10):977-85 [15801482.001]
  • [Cites] Biochem Pharmacol. 2005 Jun 1;69(11):1543-52 [15896333.001]
  • [Cites] J Biol Chem. 2005 May 20;280(20):19911-24 [15764812.001]
  • [Cites] Anticancer Res. 2005 Sep-Oct;25(5):3375-86 [16101152.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1740-50 [16452234.001]
  • [Cites] Hematol Oncol. 2006 Dec;24(4):181-8 [16783836.001]
  • [Cites] Cell Mol Life Sci. 2007 May;64(9):1105-27 [17396224.001]
  • [Cites] Blood. 2008 Jan 15;111(2):566-73 [17959855.001]
  • [Cites] J Cell Physiol. 2008 Nov;217(2):486-93 [18636556.001]
  • [Cites] Cancer Lett. 2008 Oct 8;269(2):291-304 [18504070.001]
  • [Cites] Hematol Oncol. 2009 Mar;27(1):11-6 [18668698.001]
  • (PMID = 19540589.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR041880; United States / NIAMS NIH HHS / AR / R01 AR041880-12; United States / NIAMS NIH HHS / AR / R21 AR050645-02; United States / NIAMS NIH HHS / AR / AR041880-12; United States / NIAMS NIH HHS / AR / AR041880-11; United States / NIAMS NIH HHS / AR / AR041880-14; United States / NIAMS NIH HHS / AR / R01 AR041880-13; United States / NIAMS NIH HHS / AR / AR41880; United States / NIAMS NIH HHS / AR / R21 AR050645; United States / NIAMS NIH HHS / AR / R01 AR041880-14; United States / NIAMS NIH HHS / AR / AR050645-02; United States / NIAMS NIH HHS / AR / AR041880-13; United States / NIAMS NIH HHS / AR / R01 AR041880-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Isothiocyanates; 0 / Oxides; 0 / Reactive Oxygen Species; 0 / Sulfides; 0 / Sulfones; 0 / Thiocyanates; 4478-93-7 / sulforafan; 504-84-7 / erysolin; CTE370DL3U / erucin; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ NIHMS131574; NLM/ PMC2815001
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90. Scholz C, Richter A, Lehmann M, Schulze-Osthoff K, Dörken B, Daniel PT: Arsenic trioxide induces regulated, death receptor-independent cell death through a Bcl-2-controlled pathway. Oncogene; 2005 Oct 27;24(47):7031-42
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  • Arsenic trioxide (As2O3, arsenite) efficiently kills cells from various hematologic malignancies and has successfully been employed especially for the treatment of acute promyelocytic leukemia.
  • In detail, we demonstrate that As2O3 induces cell death independently of caspase-8 or FADD and cannot be blocked by disruption of CD95/Fas receptor ligand interaction.
  • [MeSH-minor] Caspase 8. Caspase 9. Caspase Inhibitors. Caspases / genetics. Caspases / metabolism. Enzyme Inhibitors / pharmacology. Fas-Associated Death Domain Protein. Humans. Jurkat Cells. Ligands. Mitochondria / drug effects

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  • (PMID = 16007134.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / FADD protein, human; 0 / Fas-Associated Death Domain Protein; 0 / Ligands; 0 / Oxides; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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91. Austin SK, Starke RD, Lawrie AS, Cohen H, Machin SJ, Mackie IJ: The VWF/ADAMTS13 axis in the antiphospholipid syndrome: ADAMTS13 antibodies and ADAMTS13 dysfunction. Br J Haematol; 2008 May;141(4):536-44
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  • [Title] The VWF/ADAMTS13 axis in the antiphospholipid syndrome: ADAMTS13 antibodies and ADAMTS13 dysfunction.
  • Autoantibodies to ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type I motif, member 13) play an important role in the development of microthrombosis in thrombotic thrombocytopenic purpura (TTP).
  • In severe cases of antiphospholipid syndrome (APS), microthrombosis can occur similar to that seen in TTP, suggesting possible mutual pathogenic factors.
  • We hypothesised that aberrations in ADAMTS13 may occur in APS and evaluated ADAMTS13 and von Willebrand factor (VWF) in 68 patients with antiphospholipid antibodies (aPA) including 52 with APS.
  • Thirty-three (49%) had IgG anti-ADAMTS13 with 12 of these patients having reduced ADAMTS13 activity, suggesting neutralising antibodies.
  • Low ADAMTS13 activity (median 34%) was demonstrated in 22/68 (33%), all with normal ADAMTS13 antigen levels consistent with dysfunctional ADAMTS13.
  • Analysis found no associations between the ADAMTS13 abnormalities and any aPA profile or thrombotic/obstetric complications, although this study was not adequately powered to address clinical associations.
  • Nevertheless, these findings highlight that ADAMTS13 autoantibodies and ADAMTS13 dysfunction can occur in APS, and although the clinical significance remains undetermined, ADAMTS13 dysfunction may be contributory to thrombogenesis in autoimmune conditions other than TTP.
  • [MeSH-major] ADAM Proteins / immunology. Antiphospholipid Syndrome / immunology. Autoantibodies / blood. von Willebrand Factor / metabolism

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  • (PMID = 18341632.001).
  • [ISSN] 1365-2141
  • [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 / Autoantibodies; 0 / Immunoglobulin G; 0 / von Willebrand Factor; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAMTS13 protein, human
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92. Carmier D, Marchand-Adam S, Diot P, Diot E: Respiratory involvement in systemic lupus erythematosus. Rev Mal Respir; 2010 Oct;27(8):e66-78
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  • It occurs frequently but the diagnosis may be difficult because of the heterogeneity of the anatomical and clinical presentations.
  • A precise diagnosis is crucial as new immunosuppressive drugs have considerably improved the prognosis.
  • The pathology involves genetic, endocrine, environmental, pharmacological and immunological factors with a cytotoxic reaction of auto-antibodies against complement, a circulating immune complex reaction and a hyperactivity of B lymphocytes.
  • Respiratory involvement in SLE can be classified in five groups based on the anatomy: pleural involvement, infiltrating pneumonia (lymphoid interstitial pneumonia, bronchiolitis obliterans with organizing pneumonia and acute lupus pneumonitis), airways involvement (upper airways, bronchi), vascular involvement (pulmonary hypertension, acute reversible hypoxaemia, alveolar haemorrhage, and antiphospholipid syndrome), muscular and diaphragmatic involvement (shrinking lung syndrome).Treatment is based, depending upon the type of involvement and its severity, on steroids which may be combined with immunosuppressants and plasmapherisis.
  • [MeSH-minor] Antiphospholipid Syndrome / etiology. Atrophy. Bronchial Diseases / etiology. Bronchial Diseases / physiopathology. Hemorrhage / etiology. Hemorrhage / physiopathology. Humans. Hypertension, Pulmonary / etiology. Hypertension, Pulmonary / physiopathology. Lung / blood supply. Lung / pathology. Lung Diseases / etiology. Lung Diseases / physiopathology. Organ Size. Pleural Diseases / etiology. Pleural Diseases / physiopathology. Pulmonary Alveoli / pathology. Thrombophilia / etiology

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  • [Copyright] Copyright © 2010. Published by Elsevier Masson SAS.
  • (PMID = 20965395.001).
  • [ISSN] 1776-2588
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
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93. Iqbal RK, Russell R: Anaesthesia for caesarean delivery in a parturient following a recent cerebrovascular event. Int J Obstet Anesth; 2009 Jan;18(1):55-9
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  • We report the case of a woman with known systemic lupus erythematosis and antiphospholipid syndrome who developed idiopathic thrombocytopenic purpura in pregnancy and suffered a thrombotic cerebral vascular accident at 32 weeks of gestation.
  • [MeSH-minor] Adult. Antiphospholipid Syndrome / complications. Female. Humans. Lupus Erythematosus, Systemic / complications. Pregnancy. Pregnancy Complications, Cardiovascular. Pregnancy Complications, Hematologic. Thrombelastography. Treatment Outcome

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  • (PMID = 18993055.001).
  • [ISSN] 1532-3374
  • [Journal-full-title] International journal of obstetric anesthesia
  • [ISO-abbreviation] Int J Obstet Anesth
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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94. Mansfeld J, Ulbrich-Hofmann R: Secretory phospholipase A2-alpha from Arabidopsis thaliana: functional parameters and substrate preference. Chem Phys Lipids; 2007 Dec;150(2):156-66
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  • [Title] Secretory phospholipase A2-alpha from Arabidopsis thaliana: functional parameters and substrate preference.
  • The secretory phospholipase A2-alpha from Arabidopsis thaliana (AtsPLA2-alpha), being one of the first plant sPLA2s obtained in purified state, has been characterised with respect to substrate preference and optimum conditions of catalysis.
  • In contrast to pancreatic PLA2s, AtsPLA2-alpha preferred zwitterionic phospholipids, and showed lower activity toward anionic phospholipids.
  • In substrates with two identical fatty acid chains, AtsPLA2-alpha showed optimum activity toward phospholipids with decanoyl groups.
  • Km values for short chain phospholipids were comparable to sPLA2s from animals, whereas k cat values were much smaller and interfacial activation was less important.
  • [MeSH-minor] Acetophenones / chemistry. Arachidonic Acid / chemistry. Biochemistry / methods. Calcium Chloride / pharmacology. Fatty Acids / metabolism. Hydrogen-Ion Concentration. Kinetics. Phosphatidylcholines / chemistry. Phospholipids / chemistry. Recombinant Proteins / chemistry. Substrate Specificity. Temperature. Time Factors

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  • (PMID = 17692835.001).
  • [ISSN] 0009-3084
  • [Journal-full-title] Chemistry and physics of lipids
  • [ISO-abbreviation] Chem. Phys. Lipids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Fatty Acids; 0 / Phosphatidylcholines; 0 / Phospholipids; 0 / Recombinant Proteins; 27YG812J1I / Arachidonic Acid; EC 3.1.1.4 / Phospholipases A2, Secretory; M4I0D6VV5M / Calcium Chloride; PN0FRW1G4Z / 4-bromophenacyl bromide
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95. Sherer Y, Shoenfeld Y: Mechanisms of disease: atherosclerosis in autoimmune diseases. Nat Clin Pract Rheumatol; 2006 Feb;2(2):99-106
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  • [Title] Mechanisms of disease: atherosclerosis in autoimmune diseases.
  • Atherosclerosis is a pathologic process affecting blood vessels, which leads to the development of cardiovascular disease.
  • Several autoimmune rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus and antiphospholipid syndrome, are characterized by enhanced atherosclerosis and consequently higher cardiovascular morbidity and mortality rates.
  • [MeSH-minor] Animals. Antibodies, Antiphospholipid / immunology. Antibody Formation / physiology. Arthritis, Rheumatoid / immunology. Cholesterol, LDL / metabolism. Comorbidity. Disease Progression. Endothelium, Vascular / physiopathology. Heat-Shock Proteins / analysis. Humans. Immune Tolerance. Immunity, Cellular / physiology. Immunoglobulins, Intravenous / therapeutic use. Lupus Erythematosus, Systemic / immunology. Risk Factors

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  • (PMID = 16932663.001).
  • [ISSN] 1745-8382
  • [Journal-full-title] Nature clinical practice. Rheumatology
  • [ISO-abbreviation] Nat Clin Pract Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Cholesterol, LDL; 0 / Heat-Shock Proteins; 0 / Immunoglobulins, Intravenous
  • [Number-of-references] 52
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96. Digiovanni JJ, Nair P: Spontaneous recovery of sudden sensorineural hearing loss: possible association with autoimmune disorders. J Am Acad Audiol; 2006 Jul-Aug;17(7):498-505
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  • A 46-year-old white male diagnosed with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) was seen for audiological testing 15 minutes following a sudden onset hearing loss in the right ear.
  • Specifically, symptoms were consistent with a transient ischemic attack (TIA) affecting his right cochlea in the stria vascularis region, resulting in a temporary, sensorineural hearing loss.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Auditory Threshold. Hearing Loss, Sudden / etiology. Hearing Loss, Sudden / physiopathology. Lupus Erythematosus, Systemic / complications

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  • (PMID = 16927514.001).
  • [ISSN] 1050-0545
  • [Journal-full-title] Journal of the American Academy of Audiology
  • [ISO-abbreviation] J Am Acad Audiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
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97. Gyamfi C, Cohen R, Desancho MT, Gaddipati S: Prophylactic dosing adjustment in pregnancy based upon measurements of anti-factor Xa levels. J Matern Fetal Neonatal Med; 2005 Nov;18(5):329-31
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  • [Title] Prophylactic dosing adjustment in pregnancy based upon measurements of anti-factor Xa levels.
  • OBJECTIVE: To determine the necessity for monitoring of anti-factor Xa levels in pregnant women taking low molecular weight heparin (LMWH).
  • Levels were drawn monthly.
  • They were considered suboptimal if prophylactic and therapeutic doses of LMWH had an anti-Xa value <0.2 U/mL and 0.6 U/mL, respectively.
  • Variables of interest included age, parity, thrombophilias, and antiphospholipid antibody syndrome.

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  • (PMID = 16390793.001).
  • [ISSN] 1476-7058
  • [Journal-full-title] The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians
  • [ISO-abbreviation] J. Matern. Fetal. Neonatal. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Factor Xa Inhibitors; 0 / Heparin, Low-Molecular-Weight; EC 3.4.21.6 / Factor Xa
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98. Grimwade D, Mistry AR, Solomon E, Guidez F: Acute promyelocytic leukemia: a paradigm for differentiation therapy. Cancer Treat Res; 2010;145:219-35
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  • [Title] Acute promyelocytic leukemia: a paradigm for differentiation therapy.
  • Acute promyelocytic leukemia(APL) is characterized by the t(15;17) chromosomal translocation leading to the formation of the PML-RARalpha oncoprotein.
  • This leukemia has attracted considerable interest in recent years, being the first in which therapies that specifically target the underlying molecular lesion, i.e., all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), leading to induction of differentiation and apoptosis have been successfully used in clinical practice.
  • The advent of ATRA therapy has transformed APL from being a disease with a poor outlook to one of the most prognostically favorable subsets of acute myeloid leukemia.
  • Moreover, recent studies have suggested that ATO and ATRA, or even ATO alone, used as front-line treatment of PML-RARA- associated APL can induce long-term remissions.
  • It is clear that the success of such an approach is critically dependent upon molecular diagnostics and monitoring for minimal residual disease (MRD) to distinguish those patients who can potentially be cured with differentiation therapy from those requiring additional myelosuppressive agents.
  • This represents an exciting new phase in the treatment of acute leukemia, highlighting the potential of molecularly targeted and MRD-directed therapies to achieve an individualized approach to patient management.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

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  • (PMID = 20306254.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 77
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99. Tsironi E, Gatselis N, Kotoula MG, Chatzoulis DZ, Dalekos GN: Unexplained choroidal embolisation: remember the antiphospholipid syndrome. Lancet; 2006 Nov 25;368(9550):1936
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  • [Title] Unexplained choroidal embolisation: remember the antiphospholipid syndrome.
  • [MeSH-major] Acenocoumarol / therapeutic use. Anticoagulants / therapeutic use. Antiphospholipid Syndrome / immunology. Choroid Diseases / drug therapy

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  • (PMID = 17126726.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Anticoagulants; I6WP63U32H / Acenocoumarol
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100. Carrero JL, Sanjurjo FJ: Bilateral cilioretinal artery occlusion in antiphospholipid syndrome. Retina; 2006 Jan;26(1):104-6
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  • [Title] Bilateral cilioretinal artery occlusion in antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Ciliary Arteries / pathology. Retinal Artery Occlusion / etiology
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. Anticoagulants / therapeutic use. Fluorescein Angiography. Functional Laterality. Humans. Male. Middle Aged. Visual Acuity. Warfarin / therapeutic use

  • Genetic Alliance. consumer health - Antiphospholipid Syndrome.
  • Hazardous Substances Data Bank. WARFARIN .
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  • (PMID = 16395148.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 5Q7ZVV76EI / Warfarin
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