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46. Rainaldi G, Romano R, Indovina P, Ferrante A, Motta A, Indovina PL, Santini MT: Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used. Radiat Res; 2008 Feb;169(2):170-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used.
  • High-resolution proton nuclear magnetic resonance ((1)H-NMR) spectroscopy was used to examine and compare the metabolic variations that occur in cells of the HL60 promyelocytic leukemia cell line after induction of apoptosis by ionizing radiation and the antineoplastic drug doxorubicin as well as after induction of necrosis by heating.

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

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

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

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

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

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

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

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  • (PMID = 17606455.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; S7V92P67HO / arsenic trioxide
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5
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4. Nestvold JM, Omdal BK, Dai KZ, Martens A, Benestad HB, Vaage JT, Rolstad B: A second prophylactic MHC-mismatched bone marrow transplantation protects against rat acute myeloid leukemia (BNML) without lethal graft-versus-host disease. Transplantation; 2008 Jan 15;85(1):102-11
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  • [Title] A second prophylactic MHC-mismatched bone marrow transplantation protects against rat acute myeloid leukemia (BNML) without lethal graft-versus-host disease.
  • BACKGROUND: We have employed a rat model for human acute myeloid leukemia, a promyelocytic leukemia in the BN rat strain (BNML), to develop new protocols for immunotherapy in combination with allogeneic bone marrow transplantation (alloBMT).
  • In addition to T or natural killer (NK) cells, we introduced a second infusion of bone marrow cells as prophylactic donor lymphocyte infusions (DLI) to test whether an effective graft-versus-leukemia (GVL) response could be obtained without clinical graft-versus-host disease (GVHD).
  • METHODS: BN rats were sublethally irradiated and transplanted with T-cell depleted bone marrow cells from either fully major histocompatibility complex (MHC)-mismatched (PVG) donor rats or MHC-matched (PVG.1N) as controls.
  • Seven days after transplantation, rats were given 500 leukemic cells to mimic minimal residual disease.
  • RESULTS: Rats receiving infusions of NK cells succumbed to leukemia.
  • A second alloBMT protected against leukemia.
  • If applicable to humans, repeated alloBMT may provide a novel approach to leukemia therapy.
  • [MeSH-major] Bone Marrow Transplantation / immunology. Bone Marrow Transplantation / methods. Graft vs Host Disease / prevention & control. Leukemia, Myeloid, Acute / therapy. Major Histocompatibility Complex / immunology
  • [MeSH-minor] Animals. Chimerism. Disease Models, Animal. Graft vs Leukemia Effect. Immunotherapy / methods. Killer Cells, Natural / immunology. Killer Cells, Natural / pathology. Killer Cells, Natural / physiology. Male. Neoplasm, Residual / immunology. Rats. Rats, Inbred BN. Rats, Nude. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / physiology

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

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  • [CommentIn] Cancer. 2011 Jan 15;117(2):435; author reply 435-6 [20845483.001]
  • (PMID = 19950129.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  • [Other-IDs] NLM/ NIHMS629441; NLM/ PMC4180261
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56. Quenby S, Mountfield S, Cartwright JE, Whitley GS, Chamley L, Vince G: Antiphospholipid antibodies prevent extravillous trophoblast differentiation. Fertil Steril; 2005 Mar;83(3):691-8
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  • [Title] Antiphospholipid antibodies prevent extravillous trophoblast differentiation.
  • OBJECTIVE: We investigated the hypothesis that antiphospholipid antibodies (aPL) have a detrimental effect on human extravillous trophoblast (EVT) differentiation into giant multinucleated cells "in vitro."
  • MAIN OUTCOME MEASURE(S): This model was then used to investigate the effect of two different monoclonal aPL to beta2-glycoprotein 1 (IIC5 and ID2), and control mouse IgG antibody on EVT differentiation.
  • The aPL, IIC5, and ID2 significantly inhibited GMC formation, whereas the mouse IgG control had no effect.
  • CONCLUSION(S): Antiphospholipid antibodies can inhibit EVT differentiation and GMC formation "in vitro" suggesting that a failure of trophoblast differentiation and subsequent uteroplacental development may be an underlying pathology in antiphospholipid syndrome-associated pregnancy loss.
  • [MeSH-major] Antibodies, Antiphospholipid / pharmacology. Trophoblasts / cytology. Trophoblasts / immunology

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

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

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

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

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

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

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


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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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