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[Title] High-affinity T cell receptor differentiates cognate peptide-MHC and altered peptide ligands with distinct kinetics and thermodynamics.

Interactions between the T cell receptor and cognate peptide-MHC are crucial initiating events in the adaptive immune response.

In this work, we used M15, a high-affinity TCR engineered from the 3.L2 TCR system, to study the binding properties, thermodynamics, and specificity of two altered peptide ligands (APLs).

Our affinity measurements of the high-affinity TCR support the view that the wild type TCR binds these APLs in the millimolar affinity range, and hence very low affinities can still elicit biological functions.

As the identical TCR was analyzed with several structurally similar ligands, the distinct thermodynamic binding profiles provide a mechanistic perspective on how exquisite antigen specificity is achieved by the T cell receptor.

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[Copyright] (c) 2010 Elsevier Ltd. All rights reserved.

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(PMID = 20334923.001).

[ISSN] 1872-9142

[Journal-full-title] Molecular immunology

[ISO-abbreviation] Mol. Immunol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / AI061173-05; United States / NIAID NIH HHS / AI / R37 AI024157-24; United States / NIAID NIH HHS / AI / AI024157-24; United States / NIAID NIH HHS / AI / P01 AI071195-040002; United States / NIAID NIH HHS / AI / R37 AI024157; United States / NIAID NIH HHS / AI / R01 AI061173-05; United States / NIAID NIH HHS / AI / P01 AI071195; United States / NIAID NIH HHS / AI / R01 AI061173; United States / NIAID NIH HHS / AI / AI071195-040002

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] England

[Chemical-registry-number] 0 / Histocompatibility Antigens Class II; 0 / Ligands; 0 / Peptides; 0 / Receptors, Antigen, T-Cell

[Other-IDs] NLM/ NIHMS191933; NLM/ PMC2860700

   

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[Title] Higher serum clozapine level is associated with increased antiphospholipid antibodies in schizophrenia patients.

OBJECTIVES: This study was to evaluate the relationship between clozapine and aPL in schizophrenia patients.

A fasting blood sample was taken for serum aPL and serum clozapine level.

Serum aPL were measured by ELISA technique and HPLC method was used for the determination of serum clozapine level.

RESULTS: The unmedicated schizophrenia patients showed higher IgG aCL level [mean+/-SD: 1.51+/-0.81 and 1.25+/-0.13 U, respectively (t=2.77, df=111, p<0.01)] and IgM aCL level [mean+/-SD: 1.53+/-0.54. and 1.33+/-0.15 U, respectively (t=-2.98, df=111, p<0.01)] compared with the healthy controls.

The comparison of the clozapine-treated schizophrenia patients and the healthy controls showed significant difference in IgG aCL level [mean+/-SD: 1.74+/-0.90 and 1.25+/-0.13 U, respectively (t=-4.77, df=124, p<0.01)] and IgM aCL level [mean+/-SD: 1.62+/-0.83 and 1.33+/-0.15 U, respectively (t=-4.35, df=124, p<0.01)].

In clozapine-treated schizophrenia patients, the results of Pearson correlation coefficients showed that there was a significant positive relationship between serum IgM aCL and serum clozapine level (r=0.461, p<0.01), and serum IgG aCL were significantly correlated with serum IgM aCL (r=0.279, p<0.05).

Stepwise multiple regression analysis was performed with various characteristics, such as duration of medication, daily dose and serum clozapine level as candidate factors for serum aCL (IgG and IgM isotypes) in clozapine-treated schizophrenia patients.

Only serum clozapine level was able to enter into the regression model of IgM aCL (Model R(2)=0.212, p<0.05).

CONCLUSIONS: A higher serum clozapine level is associated with an increased aPL in schizophrenia patients.

[MeSH-major] Antibodies, Antiphospholipid / blood. Antipsychotic Agents / blood. Clozapine / blood. Schizophrenia / blood

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(PMID = 18976782.001).

[ISSN] 0022-3956

[Journal-full-title] Journal of psychiatric research

[ISO-abbreviation] J Psychiatr Res

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antipsychotic Agents; 0 / Immunoglobulin G; 0 / Immunoglobulin M; J60AR2IKIC / Clozapine

   

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Circulating oxLDL/beta2GPI complexes and autoantibodies to these complexes have been demonstrated in patients with systemic lupus erythematosus and antiphospholipid syndrome.

The in vitro macrophage uptake of oxLDL/beta2GPI complexes increased significantly in the presence of antiphospholipid antibodies (anti-beta2GPI), suggesting that macrophage Fcgamma receptors are involved in the lipid intracellular influx that leads to foam cell formation.

These findings provide an immunologic explanation for the accelerated development of atherosclerosis seen in systemic lupus erythematosus and antiphospholipid syndrome.

[MeSH-major] Antiphospholipid Syndrome / complications. Atherosclerosis / complications. Lupus Erythematosus, Systemic / complications

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(PMID = 19171113.001).

[ISSN] 1534-6307

[Journal-full-title] Current rheumatology reports

[ISO-abbreviation] Curr Rheumatol Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antigen-Antibody Complex; 0 / Autoantibodies; 0 / Lipoproteins, LDL; 0 / beta 2-Glycoprotein I; 0 / oxidized low density lipoprotein

[Number-of-references] 64

   

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[Title] [Treatment of acute promyelocytic leukemia].

[MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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(PMID = 17474452.001).

[ISSN] 0047-1852

[Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine

[ISO-abbreviation] Nippon Rinsho

[Language] jpn

[Publication-type] Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 5688UTC01R / Tretinoin

[Number-of-references] 15

   

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We describe a 38-year-old woman with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) who developed two symmetric paramalleolar ulcers with similar diameters, depths and borders, that were successfully treated with photodynamic therapy with 5-aminolevulinic acid (ALA-PDT).

[MeSH-minor] Adult. Aminolevulinic Acid / therapeutic use. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / drug therapy. Antiphospholipid Syndrome / pathology. Female. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / drug therapy. Lupus Erythematosus, Systemic / pathology. Photosensitizing Agents / therapeutic use

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(PMID = 17973045.001).

[ISSN] 1474-905X

[Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology

[ISO-abbreviation] Photochem. Photobiol. Sci.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid

   

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Currently, Arsenic Trioxide (ATO) is considered the treatment of choice for patients with relapsed acute promyelocytic leukemia (APL).

Recently, a durable remission with minimal toxicity by single agent ATO or ATO + ATRA in newly diagnosed APL was reported by different groups.

These regimens have minimal toxicity and can be administered on an outpatient basis after remission induction, thus they could become a real, less toxic and more economic option to ATRA + anthracyclines in particular in low risk APL, or in patients that cannot undergo chemotherapy because of age or comorbid conditions and in patients that refuse chemotherapy.

Significantly, these therapies are a successful attempt to cure a tumoral disease without chemotherapy.

The results of clinical trials of ATO administration as single agent in multiple myeloma (MM) and myelodisplastic syndromes (MDS) were encouraging and showed clinical effects but they were not close to APL success.

On the contrary, results of clinical trials to treat non-APL acute myeloid leukemia (AML) were disappointing.

We suggest that a combination therapy with drugs targeting specific pro-survival molecules or capable to enhance pro-apoptotic pathways may lead to an improvement of ATO efficacy against hematological malignancies, in particular AML.

Our pre-clinical studies showed that ATO is capable to induce cell death in acute leukemia cells but the apoptotic function is limited since it can induce also a mechanism of cell defense by activating pro-survival molecules such as MEK-ERK, Bcl-xL, Bcl-2.

By combining ATO with specific MEK inhibitors, we demonstrated that the block of MEK-ERK phosphorylation, the induction of Bad de-phosphorylation, and activation of p53AIP1 apoptotic pathway interrupt the pro-survival mechanisms of ATO and kill the leukemic cells by apoptotic synergism.

Our results provide an experimental basis for combined or sequential treatment with MEK inhibitors and ATO in AML.

[MeSH-major] Arsenicals / therapeutic use. Clinical Trials as Topic / trends. Hematologic Neoplasms / drug therapy. Multiple Myeloma / drug therapy. Oxides / therapeutic use

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(PMID = 17168655.001).

[ISSN] 1873-4316

[Journal-full-title] Current pharmaceutical biotechnology

[ISO-abbreviation] Curr Pharm Biotechnol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide

[Number-of-references] 62

   

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This study was purposed to explore the inhibitory effect of Curcumin on growth of retinoic acid-resistant acute promyelocytic leukemia (APL) cells and its mechanism.

The NB4-R1, an APL cell line resistant to retinoic acid, was used as a model.

The growth level of NB4-R1 was detected by MTT assay, the morphologic features of cells were observed by light microscopy, the mitochondrial transmembrane potential was determined by flow cytometry, the expressions of apoptosis-related proteins procaspase 3, caspase 3, PARP and BCL-XL were measured by Western blot.

The morphologic observation showed existence of apoptotic bodies in NB4-R1 cells treated with 20 micromol/L of Curcumin.

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(PMID = 20416164.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / bcl-X Protein; 5688UTC01R / Tretinoin; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin

   

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[Title] Prevalence and clinical correlation of anti-phospholipid-binding protein antibodies in anticardiolipin-negative patients with systemic lupus erythematosus and women with unexplained recurrent miscarriages.

CONTEXT: Anti-phospholipid antibodies (aPL) are a heterogeneous group of autoantibodies, the presence of which is associated with thrombotic events and miscarriage.

OBJECTIVE: To establish whether antibodies directed against phospholipid-binding plasma proteins such as beta(2)-glycoprotein I (beta(2)GPI), prothrombin (PT), and annexin V (Anx V) constitute a risk factor for thromboembolism in patients with systemic lupus erythematosus (SLE) and for miscarriage in women with recurrent pregnancy loss (RPL), independently of the presence of the classic anticardiolipin (aCL) antibodies, and whether their determination together with that of aCL would help to increase the diagnostic sensitivity of aPL tests.

DESIGN: The prevalence of various antibodies directed toward phospholipids (CL and other anionic phospholipids [APL]) and phospholipid-binding proteins (beta(2)GPI, PT, and Anx V) was determined by immunoenzymatic methods in 311 serum samples.

PATIENTS: Twenty-five patients with aCL-positive primary anti-phospholipid syndrome (pAPS); 89 patients with SLE, 23 of whom had thrombotic complications (SLE/APS) and 66 of whom had no thrombosis; and 77 women with unexplained recurrent pregnancy loss comprised our study group.

RESULTS: Immunoglobulin (Ig) G and/or IgM aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 25 (100%), 20 (80%), 15 (60%), and 6 (24%), respectively, of the 25 aCL-positive pAPS patients; IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 33 (37%), 42 (47%), 31 (35%), 40 (45%), and 12 (13%) of the 89 SLE patients, respectively.

Of the 56 SLE patients who proved to be aCL negative, anti-beta(2)GPI was present in 3 patients (5%), anti-PT in 13 (23%) patients, and anti-Anx V in 5 (9%) patients.

In the subset of 23 SLE/APS patients, IgG anti-PT prevalence was higher than that of the other autoantibodies (87% vs 70% aCL, 66% aAPL, 57% anti-beta(2)GPI, and 4% anti-Anx V), and in 26% of cases, IgG anti-PT was the only antibody present.

Anti-PT had a slightly lower specificity than aCL (46% vs 49%); however, the occurrence of both antibodies brought the specificity to 92.4%.

The highest risk for thrombosis in SLE patients was associated with the presence of IgG anti-PT antibody (odds ratio [OR] 15.3, P < .001, vs 6.5 aCL, 3.5 aAPL, 3.4 anti-beta(2)GPI, 0.2 anti-Anx V).

Fifty-one of the 77 women with recurrent pregnancy loss were negative for all antibodies investigated; the prevalence of IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies was 6% (5), 12% (9), 6% (5), 16% (12), and 17% (13), respectively.

Of the 67 aCL-negative women, none had anti-beta(2)GPI antibodies, 7 (11%) were anti-PT positive, and 13 (19%) were anti-Anx V positive.

In the subgroup of 26 recurrent pregnancy loss patients who had at least one antibody, anti-Anx V was present in 50% of cases (in 42% as the sole antibody) and was the only antibody significantly associated with miscarriage (P = .02).

CONCLUSIONS: The results of this study indicate that it is useful to measure anti-PT antibodies in addition to the more widely used aCL and anti-beta(2)GPI antibodies in the prognostic evaluation of SLE patients for the risk of thrombosis, and the results also confirm that anti-Anx V antibodies may play an important role in recurrent pregnancy loss.

[MeSH-major] Abortion, Spontaneous / blood. Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / blood. Lupus Erythematosus, Systemic / blood

[MeSH-minor] Adult. Annexin A5 / blood. Annexin A5 / immunology. Autoantibodies / blood. Cardiolipins / immunology. Enzyme-Linked Immunosorbent Assay / methods. Female. Glycoproteins / blood. Glycoproteins / immunology. Humans. Male. Middle Aged. Phospholipids / immunology. Pregnancy. Prevalence. Prothrombin / immunology. Thromboembolism / etiology. beta 2-Glycoprotein I

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(PMID = 15628909.001).

[ISSN] 1543-2165

[Journal-full-title] Archives of pathology & laboratory medicine

[ISO-abbreviation] Arch. Pathol. Lab. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Cardiolipins; 0 / Glycoproteins; 0 / Phospholipids; 0 / beta 2-Glycoprotein I; 9001-26-7 / Prothrombin

   

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[Title] Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients.

[MeSH-major] Antiphospholipid Syndrome / classification. Antiphospholipid Syndrome / diagnosis

[MeSH-minor] Antibodies, Antiphospholipid / blood. Female. Humans. Lupus Coagulation Inhibitor / blood. Partial Thromboplastin Time. Phospholipids / chemistry. Pregnancy. Pregnancy Complications / classification. Pregnancy Complications / diagnosis. Pregnancy Complications / immunology. Prognosis. Retrospective Studies

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[CommentOn] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]

(PMID = 16869832.001).

[ISSN] 1538-7933

[Journal-full-title] Journal of thrombosis and haemostasis : JTH

[ISO-abbreviation] J. Thromb. Haemost.

[Language] eng

[Publication-type] Comment; Letter

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids

   

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We have shown earlier that IFNgamma and As2O3 act synergistically in acute promyelocytic leukemia cells to upregulate IRF-1 expression and to induce apoptosis.

Here, we show that in the human fibrosarcoma cell line 2fTGH, As2O3 prolongs IFNgamma-induced STAT1 phosphorylation resulting in persistent binding of STAT1 to GAS motif leading to an increase in IRF-1 expression which correlated with both higher anti-proliferative effect and increased apoptosis.

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(PMID = 16914093.001).

[ISSN] 1165-158X

[Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)

[ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / GAS1 protein, human; 0 / GPI-Linked Proteins; 0 / Growth Inhibitors; 0 / Interferon Regulatory Factor-1; 0 / Membrane Proteins; 0 / STAT1 Transcription Factor; 82115-62-6 / Interferon-gamma; N712M78A8G / Arsenic

   

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[Title] Kikuchi's lymphadenopathy: a relatively rare but important cause of lymphadenopathy in Greece, potentially associated with the antiphospholipid syndrome.

Kikuchi-Fujimoto disease is a form of reactive lymphadenopathy, which was firstly described in Japan, but is uncommon in the Western world.

We retrospectively reviewed the medical records of nine cases of adult or adolescent Kikuchi's disease diagnosed in a single Haematology Unit in Athens, Greece between 1990 and 2006.

The median leukocyte count was 4.7 x 10(9)/l (2.2-4.9) with a normal differential in 7/9 patients.

One patient had clinical and laboratory evidence of primary antiphospholipid syndrome (APLS).

In conclusion, Kikuchi's disease represents a rare but important diagnostic possibility for patients presenting with lymphadenopathy in Greece and other western countries.

[MeSH-major] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / physiopathology. Histiocytic Necrotizing Lymphadenitis / diagnosis. Histiocytic Necrotizing Lymphadenitis / physiopathology

[MeSH-minor] Adolescent. Adult. Antibodies, Antiphospholipid / analysis. Antibodies, Antiphospholipid / blood. Autoimmune Diseases / diagnosis. Autoimmune Diseases / epidemiology. Autoimmune Diseases / physiopathology. Comorbidity. Diagnosis, Differential. Diagnostic Errors / prevention & control. Female. Greece. Humans. Leukocyte Count. Lymph Nodes / pathology. Male. Prevalence. Spleen / pathology. Spleen / physiopathology. Splenomegaly / diagnosis. Splenomegaly / epidemiology. Splenomegaly / physiopathology. Young Adult

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(PMID = 19693507.001).

[ISSN] 1437-160X

[Journal-full-title] Rheumatology international

[ISO-abbreviation] Rheumatol. Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid

   

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[Title] Thromboembolic and bleeding complications in acute leukemia.

The risk of both thromboembolic and bleeding complications is high in acute leukemia.

This double hazard has a significant negative impact on the morbidity and mortality of patients with this disease.

The clinical manifestations of both complications show special features specific to the form of acute leukemia.

Recognition of these characteristics is important in the diagnosis and management of acute leukemia.

In this article, several additional issues are addressed, including the features of bleeding and thrombosis in acute promyelocytic leukemia, the current understanding of the leukostasis syndrome and the iatrogenic complications including catheter-associated thrombosis, and the adverse effects of therapeutic agents used in acute leukemia.

[MeSH-major] Hemorrhage / etiology. Leukemia / complications. Thromboembolism / etiology

[MeSH-minor] Acute Disease. Blood Vessels / pathology. Drug-Related Side Effects and Adverse Reactions. Humans. Thrombophilia. Thrombosis / complications. Thrombosis / epidemiology

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(PMID = 21091148.001).

[ISSN] 1747-4094

[Journal-full-title] Expert review of hematology

[ISO-abbreviation] Expert Rev Hematol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

   

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We saw a 34-year-old pregnant woman with acute promyelocytic leukemia, who developed acute respiratory failure from all-trans-retinoic acid (ATRA) syndrome.

She was discharged from the intensive care unit after 12 days.

[MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Respiration, Artificial. Respiratory Insufficiency / chemically induced. Tretinoin / adverse effects

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(PMID = 19558746.001).

[ISSN] 0020-1324

[Journal-full-title] Respiratory care

[ISO-abbreviation] Respir Care

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

   

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[Title] [Antiphospholipid antibody: laboratory, pathogenesis and clinical manifestations].

Antiphospholipid antibodies (aPL) represent a heterogeneous group of antibodies that recognize various antigenic targets including beta2 glycoprotein I (beta2GPI), prothrombin (PT), activated protein C, tissue plasminogen activator, plasmin and annexin A2.

The most commonly used tests to detect aPL are: lupus anticoagulant (LAC), a functional coagulation assay, anticardiolipin antibody (aCL) and anti-beta2GPI antibody (anti-beta2GPI), which are enzyme-linked immunoassay (ELISA).

Clinically aPL are associated with thrombosis and/or with pregnancy morbidity.

Apparently aPL alone are unable to induce thrombotic manifestations, but they increase the risk of vascular events that can occur in the presence of another thrombophilic condition; on the other hand obstetrical manifestations were shown to be associated not only to thrombosis but mainly to a direct antibody effect on the trophoblast.

[MeSH-major] Antibodies, Anticardiolipin. Antibodies, Antiphospholipid. Antiphospholipid Syndrome. Lupus Coagulation Inhibitor. Pregnancy Complications. Thrombosis / immunology

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(PMID = 20390120.001).

[ISSN] 0048-7449

[Journal-full-title] Reumatismo

[ISO-abbreviation] Reumatismo

[Language] ita

[Publication-type] Comparative Study; English Abstract; Journal Article; Review

[Publication-country] Italy

[Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I

[Number-of-references] 69

   

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Laboratory findings, 7 days postoperatively, showed high levels of immunoglobulin G anticardiolipin antibody.

This case does not match the criteria for antiphospholipid syndrome, but some English-language reports have shown rising antiphospholipid antibody levels, particularly anticardiolipin antibodies, in patients with neoplasm.

In those cases, levels have normalized after successful therapy.

Antiphospholipid antibody levels should be examined before surgery to identify risks of hypercoagulability.

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(PMID = 20049910.001).

[ISSN] 1098-2752

[Journal-full-title] Microsurgery

[ISO-abbreviation] Microsurgery

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Anticardiolipin

   

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[Title] [Thrombophilias and peripheral arterial occlusive disease].

Peripheral arterial occlusive disease is a frequent disease due to the classical vascular risk factors such as smoking, diabetes mellitus, dyslipidemia, and hypertension.

Despite these risk factors, many thrombophilias (physiological inhibitors defects, Factor V Leiden and 20210A prothrombin gene variant, antiphospholipid antibodies, mild hyperhomocysteinemia 15-30micromol/l) can be evoked in some clinical forms of peripheral arterial occlusive disease.

Screening for these thrombophilias is justified in patients with venous thromboembolic disease, or signs of antiphospholipid syndrome and possibly in different situations such as premature atheroma of lower limbs, chronic ischaemia, evolutive disease despite adapted treatment and revascularisation failures without evident technical explanation.

Except for the antiphospholipid syndrome, there is currently no consensus for systematic screening of thrombophilia and treatment in patients with peripheral arterial occlusive disease.

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(PMID = 18554834.001).

[ISSN] 0398-0499

[Journal-full-title] Journal des maladies vasculaires

[ISO-abbreviation] J Mal Vasc

[Language] fre

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] France

[Chemical-registry-number] 0 / Antithrombins; 0 / factor V Leiden; 9001-24-5 / Factor V; 9001-26-7 / Prothrombin

[Number-of-references] 62

   

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[Title] [Acute myocardial infarction with variable clinical manifestations: probable catastrophic primary antiphospholipid antibody syndrome: a case report].

A 62-year-old diabetic man was admitted to our hospital because of acute myocardial infarction.

Emergent coronary angiography showed multiple thromboembolic occlusions in the distal circumflex and anterior descending arteries.

These clinical manifestations and laboratory findings suggested catastrophic antiphospholipid antibody syndrome.

Acute myocardial infarction is rare as the initial manifestation of catastrophic antiphospholipid antibody syndrome.

[MeSH-major] Antiphospholipid Syndrome / complications. Myocardial Infarction / etiology

[MeSH-minor] Anticoagulants / therapeutic use. Coronary Angiography. Diabetic Retinopathy / complications. Diagnosis, Differential. Humans. Kidney Diseases / complications. Male. Middle Aged. Prognosis

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(PMID = 16252568.001).

[ISSN] 0914-5087

[Journal-full-title] Journal of cardiology

[ISO-abbreviation] J Cardiol

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Anticoagulants

   

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[Title] [Hyperhomocysteine like thrombocytic risk factor in patient with systemic lupus erythematous with antiphospholipid syndrome].

[Transliterated title] Hiperhomocisteinemia como factor de riesgo trombótico en pacientes con lupus eritematoso sistémico y síndrome antifosfolípido.

OBJECTIVES: to detect the prevalence of hyperhcy in SLE patients with and without antiphospholipid syndrom; to compare the Hcy levels between those patients and healthy controls and to determine the correlation between hyperhcy and antiphospholipid antibodies.

PATIENTS AND METHODS: we studied 44 SLE patients: 17 had antiphospholipid syndrom and 27 didn't have it, and we compared them to 24 healthy controls.

Hyperhcy was present in 27 SLE patients (61,4%), 12 of them had antiphospholipid syndrom.

15(75%) of them had hiperhcy.

[MeSH-major] Antiphospholipid Syndrome / physiopathology. Hyperhomocysteinemia / complications. Lupus Erythematosus, Systemic / physiopathology. Thrombosis / etiology

[MeSH-minor] Adult. Aged. Antibodies, Antiphospholipid / blood. Argentina. Female. Homocysteine / blood. Humans. Male. Middle Aged. Risk Factors. Venous Thrombosis / blood

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(PMID = 16281418.001).

[ISSN] 0014-6722

[Journal-full-title] Revista de la Facultad de Ciencias Médicas (Córdoba, Argentina)

[ISO-abbreviation] Rev Fac Cien Med Univ Nac Cordoba

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Argentina

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0LVT1QZ0BA / Homocysteine

   

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The analogs were examined for their antiproliferative activity in vitro against human breast cancer cells (MCF-7) and promyelocytic leukemia (HL-60) cells.

The studies of calcemic activity in vivo showed that analogs PRI-2208 and PRI-2209 did not influence the serum calcium level in doses, in which 1alpha,25(OH)2D3 or (24R)-1,24(OH)2D3 significantly increased this level.

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[Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.

(PMID = 20227499.001).

[ISSN] 1879-1220

[Journal-full-title] The Journal of steroid biochemistry and molecular biology

[ISO-abbreviation] J. Steroid Biochem. Mol. Biol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 1C6V77QF41 / Cholecalciferol; SY7Q814VUP / Calcium

   

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We have identified an intergenic transcriptional activity that is located between the human HOXA1 and HOXA2 genes, shows myeloid-specific expression, and is up-regulated during granulocytic differentiation.

The novel gene, termed HOTAIRM1 (HOX antisense intergenic RNA myeloid 1), is transcribed antisense to the HOXA genes and originates from the same CpG island that embeds the start site of HOXA1.

HOTAIRM1 is the most prominent intergenic transcript expressed and up-regulated during induced granulocytic differentiation of NB4 promyelocytic leukemia and normal human hematopoietic cells; its expression is specific to the myeloid lineage.

Its induction during retinoic acid (RA)-driven granulocytic differentiation is through RA receptor and may depend on the expression of myeloid cell development factors targeted by RA signaling.

Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes.

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(PMID = 19144990.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NHGRI NIH HHS / HG / U01 HG003147; United States / NIDDK NIH HHS / DK / R01 DK054369; United States / NIDDK NIH HHS / DK / DK54369; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400; United States / NHGRI NIH HHS / HG / U01-HG003147

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Intergenic; 0 / HOXA2 protein, human; 0 / Homeodomain Proteins; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / Regulatory Sequences, Ribonucleic Acid; 0 / Transcription Factors; 0 / homeobox A1 protein; 0 / long non-coding RNA HOTAIRM1, human; 157907-48-7 / HoxA protein; EC 2.7.7.- / RNA Polymerase II

[Other-IDs] NLM/ PMC2656274

   

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We reported previously that sequestration of MRE11/RAD50/NBS1 complexes represses ALT-mediated telomere length maintenance, and suppresses formation of ALT-associated promyelocytic leukemia (PML) bodies (APBs).

APBs are PML bodies containing telomeric DNA and telomere-binding proteins, and are observed only in a small fraction of cells within asynchronously dividing ALT-positive cell populations.

We combined methionine restriction with RNA interference to test whether the following proteins are required for APB formation: PML body-associated proteins, PML and Sp100; telomere-associated proteins, TRF1, TRF2, TIN2 and RAP1; and DNA repair proteins, MRE11, RAD50, NBS1 and 53BP1.

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(PMID = 17297460.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRE11A protein, human; 0 / NBN protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / Rad50 protein, human; 0 / TINF2 protein, human; 0 / TP53BP1 protein, human; 0 / Telomere-Binding Proteins; 0 / Telomeric Repeat Binding Protein 1; 0 / Telomeric Repeat Binding Protein 2; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 135844-47-2 / Sp100 protein, human; 143220-95-5 / PML protein, human; AE28F7PNPL / Methionine; EC 6.5.1.- / DNA Repair Enzymes

   

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[Title] Impact of carrier stiffness and microtopology on two-dimensional kinetics of P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) interactions.

Interactions of P-selectin with P-selectin glycoprotein ligand-1 (PSGL-1) were used to demonstrate such effects by presenting the molecules on three carrier systems: human red blood cells (RBCs), human promyelocytic leukemia HL-60 cells, and polystyrene beads.

These results demonstrate that the carrier stiffness and microtopology of a receptor influences its rate of encountering and binding a surface ligand but does not subsequently affect the stability of binding.

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(PMID = 17267403.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / P-Selectin; 0 / P-selectin ligand protein

   

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[Title] Anticardiolipin and anti-beta-2-glycoprotein I antibodies.

The anticardiolipin (aCL) antibody test was first established in 1983, using cardiolipin (negatively charged phospholipid) as an antigen in a solid-phase immunoassAy.

The wide use of this test was determinant in the definition of the "aCL or antiphospholipid syndrome" (APS).Later, it was demonstrated that aCL antibodies do not recognize anionic phospholipids but are directed against plasma proteins bound to anionic phospholipids, mainly beta-2-glycoprotein I, which is now considered as the autoantigen in APS.

Anti-beta-2-glycoprotein I (anti-beta2GPI) is not yet accepted as a serological criterion for APS, but most investigators would consider a patient with anti-beta2GPI antibodies and clinical features of APS to have the syndrome. aCL and anti-beta2GPI are a heterogeneous group of antibodies with different clinical significances and can be present in different autoimmune diseases as well as in infectious diseases.

[MeSH-major] Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Glycoproteins / immunology

[MeSH-minor] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / immunology. Autoimmune Diseases / immunology. Female. History, 20th Century. Humans. Pregnancy. beta 2-Glycoprotein I

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(PMID = 15804703.001).

[ISSN] 0891-6934

[Journal-full-title] Autoimmunity

[ISO-abbreviation] Autoimmunity

[Language] eng

[Publication-type] Historical Article; Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I

[Number-of-references] 60

   

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[Transliterated title] Anomalies de l'hemostase dans l'infarctus du myocarde sur coronaires angiographiquement saines: a propos de 39 cas.

Myocardial infarction with normal coronary artery is ussually inaugural, with electric and clinical characteristics similar to those with atheroma.

They were 33 males and 6 females aged between 22 and 75 years (44 + 13 years), in whom the deficiency in protein C and S. antithrombin, activated protein C resistance and antiphospholipid antibodies were assessed.

RESULTS: Concurrent abnormalities of haemostasis were found in 10 patients: Antiphospholipid antibodies, found in 5 patients constitute the most frequent abnormality.

[MeSH-major] Blood Coagulation Disorders / diagnosis. Coronary Angiography. Myocardial Infarction / blood

[MeSH-minor] Activated Protein C Resistance / diagnosis. Adult. Aged. Antibodies, Antiphospholipid / blood. Antithrombins / analysis. Antithrombins / deficiency. Coronary Vessels / pathology. Female. Humans. Immunoglobulin G / blood. Male. Middle Aged. Protein C / analysis. Protein C Deficiency / diagnosis. Protein S / analysis. Protein S Deficiency / diagnosis. Retrospective Studies

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(PMID = 16422365.001).

[ISSN] 0041-4131

[Journal-full-title] La Tunisie médicale

[ISO-abbreviation] Tunis Med

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] Tunisia

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antithrombins; 0 / Immunoglobulin G; 0 / Protein C; 0 / Protein S

   

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[Title] Low TCR avidity and lack of tumor cell recognition in CD8(+) T cells primed with the CEA-analogue CAP1-6D peptide.

The use of "altered peptide ligands" (APL), epitopes designed for exerting increased immunogenicity as compared with native determinants, represents nowadays one of the most utilized strategies for overcoming immune tolerance to self-antigens and boosting anti-tumor T cell-mediated immune responses.

However, the actual ability of APL-primed T cells to cross-recognize natural epitopes expressed by tumor cells remains a crucial concern.

In the present study, we show that CAP1-6D, a superagonist analogue of a carcinoembriyonic antigen (CEA)-derived HLA-A*0201-restricted epitope widely used in clinical setting, reproducibly promotes the generation of low-affinity CD8(+) T cells lacking the ability to recognized CEA-expressing colorectal carcinoma (CRC) cells.

Short-term T cell cultures, obtained by priming peripheral blood mononuclear cells from HLA-A*0201(+) healthy donors or CRC patients with CAP1-6D, were indeed found to heterogeneously cross-react with saturating concentrations of the native peptide CAP1, but to fail constantly lysing or recognizing through IFN- gamma release CEA(+)CRC cells.

Characterization of anti-CAP1-6D T cell avidity, gained through peptide titration, CD8-dependency assay, and staining with mutated tetramers (D227K/T228A), revealed that anti-CAP1-6D T cells exerted a differential interaction with the two CEA epitopes, i.e., displaying high affinity/CD8-independency toward the APL and low affinity/CD8-dependency toward the native CAP1 peptide.

Our data demonstrate that the efficient detection of self-antigen expressed by tumors could be a feature of high avidity CD8-independent T cells, and underline the need for extensive analysis of tumor cross-recognition prior to any clinical usage of APL as anti-cancer vaccines.

[MeSH-minor] Antibody Affinity. Antigens, Neoplasm / chemistry. Cancer Vaccines. Colorectal Neoplasms / metabolism. Epitopes / chemistry. HLA-A Antigens / chemistry. HLA-A2 Antigen. Immunotherapy / methods. Leukocytes, Mononuclear / metabolism. Ligands. Peptides / chemistry. Risk. T-Lymphocytes / metabolism

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(PMID = 17564703.001).

[ISSN] 0340-7004

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CAP1-6D; 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Ligands; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, Antigen, T-Cell

   

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[Title] Regulation of a highly specific retinoic acid-4-hydroxylase (CYP26A1) enzyme and all-trans-retinoic acid metabolism in human intestinal, liver, endothelial, and acute promyelocytic leukemia cells.

The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels.

We studied induction and regulation of CYP26A1 expression and ATRA metabolism in human intestinal (Caco-2), liver (HepG2), endothelial (HUVEC), and APL (NB4) cell lines.

A specific RA receptor-alpha antagonist totally inhibited ATRA-induced expression of CYP26A1, indicating that RA receptor-alpha plays a major role in CYP26A1 expression in HepG2 cells.

Our data suggest that upregulation of CYP26A1 expression in intestinal, endothelial, liver, and APL cells and metabolism of ATRA may play a role in rapid clearance of ATRA after continuous oral administration.

Therapeutic strategies such as liposomal encapsulation and intermittent administration of ATRA may circumvent accelerated ATRA metabolism and improve the treatment of APL.

[MeSH-major] Colonic Neoplasms / metabolism. Cytochrome P-450 Enzyme System / metabolism. Endothelial Cells / metabolism. Gene Expression Regulation, Enzymologic. Leukemia, Promyelocytic, Acute / metabolism. Liver Neoplasms / metabolism. Tretinoin / metabolism

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(PMID = 16194896.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Grant] United States / FDA HHS / FD / FDA-FD-R000923-04-01; United States / NCI NIH HHS / CA / U54 RFA CA096300

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 5688UTC01R / Tretinoin; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / retinoic acid 4-hydroxylase

   

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[Title] Antiphospholipid antibodies and coagulation defects in women with implantation failure after IVF and recurrent miscarriage.

Testing for antiphospholipid antibodies or thrombophilia is commonly carried out, and interpretation of results in the light of the current evidence is extremely difficult.

This paper reviews the purported pathogenetic mechanisms and clinical associations between both antiphospholipid antibodies and inherited thrombophilias, and reproductive failure.

The current management strategies are also critically evaluated and recommendations are made for optimal, evidence-based clinical practice.

[MeSH-major] Abortion, Habitual / blood. Abortion, Habitual / immunology. Antibodies, Antiphospholipid / blood. Embryo Implantation / immunology. Thrombophilia / blood

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(PMID = 16820106.001).

[ISSN] 1472-6483

[Journal-full-title] Reproductive biomedicine online

[ISO-abbreviation] Reprod. Biomed. Online

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Immunoglobulins, Intravenous

[Number-of-references] 96

   

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OBJECTIVE: To compare live birth rates in women with recurrent pregnancy loss (RPL) and either autoantibodies or a coagulation abnormality, treated with low molecular weight heparin plus aspirin (LMWH/ASA) or ASA alone, and to place our results in context with other randomized clinical trials (RCT) with similar cohorts.

METHODS: The HepASA Trial was an RCT including patients with a history of RPL and at least 1 of the following: antiphospholipid antibody (aPL), an inherited thrombophilia, or antinuclear antibody.

Treatment groups were stratified by aPL status and history of early versus late pregnancy losses.

RESULTS: Over 4 years, 859 women with RPL were screened: 88 (10.2%) fulfilled inclusion criteria, became pregnant and were randomized to receive either LMWH/ASA or ASA alone. aPL were present in 42 (47.7%) patients in each group.

Neither number of prior losses nor aPL status was correlated with pregnancy outcome.

Mean change in BMD did not differ by treatment group at either the lumbar spine (p = 0.57) or femoral neck (p = 0.15).

RCT since 2000 for aPL positive women with RPL and similar inclusion criteria report a mean live birth rate of 75% with either LMWH or ASA.

Regardless of treatment regimen, number of prior losses, or aPL positivity, almost 80% of women in our RPL cohort had a successful pregnancy outcome.

[MeSH-minor] Adult. Antibodies, Antinuclear / immunology. Anticoagulants / administration & dosage. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / drug therapy. Antiphospholipid Syndrome / physiopathology. Bone Density / drug effects. Cohort Studies. Female. Humans. Platelet Aggregation Inhibitors / administration & dosage. Pregnancy. Thrombophilia / complications. Thrombophilia / drug therapy. Thrombophilia / physiopathology. Treatment Outcome

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[CommentIn] J Rheumatol. 2010 Jan;37(1):202; author reply 203 [20040643.001]

[CommentIn] Curr Rheumatol Rep. 2010 Feb;12(1):1-3 [20425526.001]

(PMID = 19208560.001).

[ISSN] 0315-162X

[Journal-full-title] The Journal of rheumatology

[ISO-abbreviation] J. Rheumatol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] Canada

[Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Anticoagulants; 0 / Heparin, Low-Molecular-Weight; 0 / Platelet Aggregation Inhibitors; R16CO5Y76E / Aspirin

   

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[Title] Indications for plasma exchange in systemic lupus erythematosus in 2005.

Plasma exchange can remove putative pathogenic autoantibodies and circulating immune complexes from the blood of patients with systemic lupus erythematosus (SLE).

We review herein the principal historical steps of the use of plasma exchange to treat SLE, based upon the main trials and case reports that have highlighted its most pertinent indications.

Acute life-threatening manifestations and severe therapy-resistant manifestations, like refractory SLE renal disease, diffuse alveolar hemorrhage, neuropsychiatric SLE, thrombotic thrombocytopenic purpura, catastrophic antiphospholipid syndrome, hyperviscosity syndrome and cryoglobulinemia, are the indications for which plasma exchange might have a beneficial therapeutic role.

Although few SLE patients undergo plasma exchange each year nowadays (10-20 per year in France), adverse events are very rare and recent advances in plasma exchange technologies, like immunoadsorption, might, in the future, counterbalance their cost and broaden their place in the therapeutic armamentarium for SLE.

[MeSH-major] Lupus Erythematosus, Systemic / therapy. Plasma Exchange / methods. Plasma Exchange / trends

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(PMID = 16335578.001).

[ISSN] 0961-2033

[Journal-full-title] Lupus

[ISO-abbreviation] Lupus

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 100

   

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[Title] What is the role of arsenic in newly diagnosed APL?

Acute promyelocytic leukemia (APL), a highly curable subtype of acute myeloid leukemia (AML) is characterized by the chromosomal translocation t(15;17) and, consequently, the presence of the PML-RARalpha fusion transcript.

Most patients are treated with all-trans retinoic acid (ATRA), which targets the RAR-alpha moiety of the PML/RAR-alpha fusion transcript, and anthracycline-based chemotherapy.

Arsenic trioxide (ATO) targets the PML moiety and has different mechanisms of action at different concentrations, and induces differentiation and apoptosis.

Several clinical trials have tested the combination of ATRA and ATO with outstanding results.

ATRA plus ATO has emerged as a promising strategy, even for those with high-risk disease.

[MeSH-major] Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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(PMID = 19041605.001).

[ISSN] 1532-1924

[Journal-full-title] Best practice & research. Clinical haematology

[ISO-abbreviation] Best Pract Res Clin Haematol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Anthracyclines; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

[Number-of-references] 31

   

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Arsenic trioxide (ATO) is an effective cancer therapeutic drug for acute promyelocytic leukemia and has potential anticancer activity against a wide range of solid tumors.

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(PMID = 17640917.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Arsenicals; 0 / Enzyme Inhibitors; 0 / Oxides; EC 1.8.1.9 / Thioredoxin-Disulfide Reductase; GAN16C9B8O / Glutathione; S7V92P67HO / arsenic trioxide

[Other-IDs] NLM/ PMC1940330

   

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[Title] Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy.

Antiphospholipid antibodies (APA) in circulation are also associated with vascular diseases.

In fact, the pathology of placentae from PE and Antiphospholipid syndrome patients is similar; atherosis, thrombosis and infarction, and endothelium activation represent the pathological mechanisms.

We identified a new antibody which recognizes non-bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, and which triggered an autoimmune-like disease in mice.

Results showed increased levels of NPA in the syncytiotrophoblast, extravillous cytotrophoblast, syncytial knots and the amnion epithelial cell membranes of the placenta, as well as increases in NPA and NPA antibodies in sera from HDP patients, when compared with controls.

[MeSH-major] Antibodies, Antiphospholipid / analysis. Membrane Lipids / analysis. Phospholipids / analysis. Placenta / chemistry. Pre-Eclampsia / etiology

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(PMID = 16338467.001).

[ISSN] 0143-4004

[Journal-full-title] Placenta

[ISO-abbreviation] Placenta

[Language] eng

[Grant] United States / NICHD NIH HHS / HD / HD40363

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Membrane Lipids; 0 / Phospholipids

   

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[Title] Advances in management of acute promyelocytic leukemia with arsenic trioxide.

[MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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(PMID = 17609904.001).

[ISSN] 1672-0415

[Journal-full-title] Chinese journal of integrative medicine

[ISO-abbreviation] Chin J Integr Med

[Language] eng

[Publication-type] Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

   

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Water-soluble CdTe quantum dots synthesized in aqueous solution have been conjugated with peptide LyP-1 using N-Succinimidyl 3-[2-pyridyldithio]-propionate (SPDP) as a cross-linking reagent.

Capillary electrophoresis (CE), UV-Vis absorption and photoluminescent (PL) spectra suggested that the peptide had been successfully linked to the QDs.

The QDs-peptides conjugates could specifically recognize the lung adenoma cancer cells (SPCA-1), but did not recognize promyelocytic leukemia cells (HL-60).

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(PMID = 17713265.001).

[ISSN] 1001-5515

[Journal-full-title] Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi

[ISO-abbreviation] Sheng Wu Yi Xue Gong Cheng Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / LyP-1 protein, mouse; 0 / Oligopeptides; 0 / Peptides; 0 / Peptides, Cyclic; 99896-85-2 / arginyl-glycyl-aspartic acid

   

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[Title] PML mediates IFN-alpha-induced apoptosis in myeloma by regulating TRAIL induction.

Interferon (IFN) induces expression of proapoptotic genes and has been used in the clinical treatment of multiple myeloma.

The promyelocytic leukemia (PML) gene is an IFN-induced target that encodes a tumor suppressor protein.

PML protein is typically localized within discrete speckled nuclear structures termed PML nuclear bodies (NBs).

Herein, we show that growth inhibition effects of IFN-alpha in myeloma cells correlate with PML NBs and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induction, whereas known IFN targets including signal transducer and activator of transcription-1 (STAT1), STAT3, p38, and Daxx cannot account for these differential responses.

RNAi silencing of PML blocks IFN-alpha-induced apoptosis in myeloma cells and correspondingly down-regulates TRAIL expression.

These results demonstrate that PML and TRAIL play important roles in IFN-induced apoptosis and identify TRAIL as a novel downstream transcriptional target of PML.

Identification of PML and PML NBs as effectors of IFN responses provides insights into mechanisms by which tumor cells exhibit resistance to this class of agents and may prove useful in assessing treatment regimens.

[MeSH-major] Apoptosis / drug effects. Interferon-alpha / pharmacology. Membrane Glycoproteins / physiology. Neoplasm Proteins / physiology. Nuclear Proteins / physiology. Transcription Factors / physiology. Tumor Necrosis Factor-alpha / physiology

[MeSH-minor] Apoptosis Regulatory Proteins. Cell Division / drug effects. Cell Line, Tumor. Humans. Leukemia, Promyelocytic, Acute. Multiple Myeloma. RNA, Small Interfering / genetics. TNF-Related Apoptosis-Inducing Ligand. Transfection. Tumor Suppressor Proteins

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(PMID = 15459016.001).

[ISSN] 0006-4971

[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 / Apoptosis Regulatory Proteins; 0 / Interferon-alpha; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human

   

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When cell-permeating fluorescent dyes were used as indicators of the generation of reactive oxygen species (ROS), we found that PAT treatment directly increased intracellular oxidative stress in human embryonic kidney (HEK293) and human promyelocytic leukemia (HL-60) cells.

Lipid peroxidation levels were also significantly increased in HL-60 cells and mouse kidney homogenates treated with PAT.

Pretreatment of HEK293 cells with Tiron, a free radical scavenger, reduced the phosphorylation levels of extracellular signal-regulated kinase (ERK) 1/2 elicited by PAT.

The ERK1/2 signaling pathway inhibitor, U0126, also significantly decreased the levels of ROS associated with PAT treatment.

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(PMID = 17090621.001).

[ISSN] 1096-6080

[Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology

[ISO-abbreviation] Toxicol. Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Free Radical Scavengers; 0 / Reactive Oxygen Species; 95X2BV4W8R / Patulin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases

   

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[Title] Adenovirus type 5 E4orf3 protein targets the Mre11 complex to cytoplasmic aggresomes.

Rearrangement of Mre11 and Rad50 by Ad5 E4orf3 is not dependent on interactions with Nbs1 or promyelocytic leukemia protein nuclear bodies.

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(PMID = 16103189.001).

[ISSN] 0022-538X

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA097093; United States / NIAID NIH HHS / AI / AI43341; United States / NCI NIH HHS / CA / CA97093

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Adenovirus E4 Proteins; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MRE11A protein, human; 0 / Multiprotein Complexes; 0 / NBN protein, human; 0 / Nuclear Proteins; 0 / Rad50 protein, human; 0 / Tubulin; EC 6.5.1.- / DNA Repair Enzymes

[Other-IDs] NLM/ PMC1193610

   

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[Title] Antiphospholipid syndrome. Current insights into laboratory diagnosis and pathophysiology.

The antiphospholipid syndrome (APS) is a non-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL) in the plasma of patients with vascular thrombosis, recurrent complications of pregnancy, or both (1, 2).

The presence of aPL in plasma of patients can be detected with either a prolongation of phospholipid dependent coagulation tests (lupus anticoagulant, LAC), or with solid phase immune assays against the protein beta2-glycoprotein I (beta2-GPI) or the phospholipid cardiolipin (anti-beta2-GPI antibody ELISA and anti-cardiolipin antibody ELISA, respectively) (3).

To solve this dispute, an international consensus meeting was organized in Sapporo in 1999 to formulate classification criteria for patients with the antiphospholipid syndrome (4).

This is very unfortunate because the specificity of the different aPL assays to detect the clinical manifestations that characterize APS are disputable.

One of the aims of defining the criteria was to initiate studies to determine the value of the different anti-phospholipid antibody assays to serve as biomarker for the risk of thrombosis and pregnancy morbidity.

[MeSH-major] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / physiopathology

[MeSH-minor] Antibodies, Antiphospholipid / blood. Antibodies, Antiphospholipid / physiology. Clinical Laboratory Techniques. Female. Humans. Pregnancy. Pregnancy Complications / blood

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(PMID = 20680233.001).

[ISSN] 0720-9355

[Journal-full-title] Hämostaseologie

[ISO-abbreviation] Hamostaseologie

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid

   

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BACKGROUND: Blood lactate concentration [LAC] is considered a useful indicator of disease severity in horses.

HYPOTHESIS: It was hypothesized that results from a POC lactate monitor would be in agreement with a laboratory-based measurement of [LAC].

[LAC] was measured with whole blood (AWB) and plasma (APL) by means of a POC monitor (Accutrend) and compared with results from whole blood measured by a laboratory blood gas analyzer (NOVA).

Agreement (p +/- SE) was closest between APL and NOVA (0.97 +/- 0.01); an average observed difference of 0.15 +/- 0.89 (mean +/- SD) and 95% limits of agreement (LOA) -1.89, 1.59 also were found.

CONCLUSIONS AND CLINICAL IMPORTANCE: Results indicate close agreement between NOVA and the POC monitor when [LAC] was measured with plasma.

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(PMID = 17939569.001).

[ISSN] 0891-6640

[Journal-full-title] Journal of veterinary internal medicine

[ISO-abbreviation] J. Vet. Intern. Med.

[Language] ENG

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 33X04XA5AT / Lactic Acid

   

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[Title] Vimentin/cardiolipin complex as a new antigenic target of the antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by arterial and venous thrombosis, recurrent abortions, and antiphospholipid antibodies (aPL).

However, it is possible to find patients with clinical signs of APS who persistently test negative for aPL (seronegative APS, or SN-APS).

We tested sera from patients with SN-APS with a proteomic approach by analyzing endothelial cell-surface membrane proteins.

Our results prompt to identify vimentin as a "new" cofactor for aPL, which may represent a useful tool mainly in SN-APS patients.

[MeSH-major] Antiphospholipid Syndrome / diagnosis. Autoantibodies / immunology. Cardiolipins / immunology. Vimentin / immunology

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[CommentIn] Blood. 2010 Oct 21;116(16):2867-9 [20966174.001]

(PMID = 20634382.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Autoantibodies; 0 / Cardiolipins; 0 / NF-kappa B; 0 / Vimentin; EC 2.7.11.1 / IRAK1 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases

   

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[Title] Venous thrombosis and pulmonary embolism in a child with pneumonia due to Mycoplasma pneumoniae.

A 13-year-old boy with Mycoplasma pneumoniae pulmonary infection developed deep vein thrombosis and pulmonary embolism.

He was found to have protein S deficiency and transient antiphospholipid antibodies.

Though uncommon, it is important to consider venous thromboembolic disease in children whose clinical course is atypically severe.

[MeSH-major] Lupus Erythematosus, Systemic / complications. Pneumonia, Mycoplasma / complications. Pulmonary Embolism / etiology. Venous Thrombosis / etiology

[MeSH-minor] Adolescent. Anticoagulants / therapeutic use. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / immunology. Heparin / therapeutic use. Humans. Male. Protein S Deficiency / complications. Protein S Deficiency / immunology. Warfarin / therapeutic use

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(PMID = 19806855.001).

[ISSN] 1943-4693

[Journal-full-title] Journal of the National Medical Association

[ISO-abbreviation] J Natl Med Assoc

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Anticoagulants; 5Q7ZVV76EI / Warfarin; 9005-49-6 / Heparin

   

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[Title] Focal seizures after treatment with fluvastatin in a patient with a history of catastrophic antiphospholipid syndrome.

The symptoms appeared one day after start of the treatment with fluvastatin (40 mg) administered in order to diminish the endothelial activation induced by antiphospholipid antibodies (aPL).

The patient suffered from severe manifestations of the antiphospholipid syndrome (APS) including Catastrophic Antiphospholipid Syndrome (CAPS, Asherson's syndrome).

[MeSH-major] Antiphospholipid Syndrome / complications. Epilepsies, Partial / chemically induced. Fatty Acids, Monounsaturated / adverse effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects. Indoles / adverse effects. Seizures / chemically induced

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(PMID = 16111706.001).

[ISSN] 0022-510X

[Journal-full-title] Journal of the neurological sciences

[ISO-abbreviation] J. Neurol. Sci.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Fatty Acids, Monounsaturated; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Indoles; 4L066368AS / fluvastatin

   

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[Title] Lung adenocarcinoma and antiphospholipid antibodies.

Thrombosis is a frequent finding in cancer patients, being referred to as a poor prognostic factor.

A number of studies have demonstrated the presence of antiphospholipid antibodies (aPL) in cancer patients, suggesting a potential role in tumor-associated thrombosis.

A prospective analysis has been performed in a group of lung adenocarcinoma patients in respect to the presence of aPL and thrombotic manifestations.

On the other hand, patients that displayed IgM anti-beta2-glycoprotein I (abeta2GPI) (22/80) showed an unexpected decrease in thrombosis risk (2/22, with IgM abeta2GPI vs 18/58, without IgM abeta2GPI RR=0.29; p=0.04).

Considerations on the mechanisms that link cancer, thrombosis and aPL are discussed in this article.

[MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / immunology. Antibodies, Antiphospholipid / blood. Lung Neoplasms / diagnosis. Lung Neoplasms / immunology

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(PMID = 19185619.001).

[ISSN] 1873-0183

[Journal-full-title] Autoimmunity reviews

[ISO-abbreviation] Autoimmun Rev

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I

   

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Tamibarotene is a new synthetic retinoid drug recently approved for relapsed or refractory acute promyelocytic leukemia (APL) in Japan.

It is a specific agonist for retinoic acid receptor alpha/beta.

Compared to all-trans retinoic acid (ATRA), a natural retinoid indicated for a first-line treatment of APL, tamibarotene is chemically more stable and several times more potent as an inducer of differentiation in promyelocytic leukemia cells.

In contrast to ATRA, whose plasma concentration declines considerably during daily administration, tamibarotene sustains plasma level probably due to a lower affinity for cellular retinoic acid binding protein.

Furthermore, adverse side effects were milder than those of ATRA in clinical trials.

Clinical trials held in Japan showed that tamibarotene had efficacy in APL patients who had relapsed from ATRA-induced complete remission.

Tamibarotene is being investigated for treatment of multiple myeloma and Crohn's disease in clinical trials.

This review focuses on tamibarotene's mechanisms of action, chemical properties, pharmacokinetics and its use in APL as well as its potential use in various disorders.

[MeSH-major] Antineoplastic Agents / therapeutic use. Benzoates / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tetrahydronaphthalenes / therapeutic use

[MeSH-minor] Animals. Controlled Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans

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[Copyright] (c) 2007 Prous Science.

(PMID = 17925887.001).

[ISSN] 1699-3993

[Journal-full-title] Drugs of today (Barcelona, Spain : 1998)

[ISO-abbreviation] Drugs Today

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Spain

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Tetrahydronaphthalenes; 08V52GZ3H9 / tamibarotene

[Number-of-references] 38

   

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[Title] Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis.

We present here two patients treated with mitoxantrone for MS who subsequently developed acute promyelocytic leukemia (APL).

These constitute, to our knowledge, the eighth and ninth reports of APL in patients treated with mitoxantrone for MS.

Topoisomerase 2 inhibitors are associated with therapy-related acute myeloid leukemia (t-AML) with 11q23 abnormalities, but therapy-related APL (t-APL) is less common, and documentation of nine cases of t-APL after mitoxantrone therapy for MS suggests a specific association.

[MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / chemically induced. Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy

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[ErratumIn] Cancer Genet Cytogenet. 2008 Oct 15;186(2):130

(PMID = 18406875.001).

[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 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone

   

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[Title] [In vitro study of the effects of CDA-II combined with cAMP on apoptosis induction in retinoic acid resistant acute promyelocytic leukemia cells].

OBJECTIVE: To investigate the effects of CDA-II alone or combined with cAMP on the retinoic acid (RA)-resistant acute promyelocytic leukemia (APL) cells.

The level of Bcl-2 was detected by flow cytometry, DNA "ladder" was detected by agarose-electrophoresis.

RESULTS: CDA-II could induce NB4-R2 cell apoptosis through decreasing the level of cellular anti-apoptotic protein Bcl-2. cAMP could significantly enhance the role of CDA-II.

Bcl-2 positive cell rates decreased to (15.1 +/- 4.8)% and (7.3 +/- 2.9)% in NB4-R2 cells treated with 1 mg/ml CDA-II plus 100 micromol/L cAMP for 48 h and 72 h, respectively.

CONCLUSIONS: CDA-II combined with cAMP could exert potent apoptotic effect on RA-resistant APL cells.

[MeSH-major] Cyclic AMP / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Peptides / pharmacology. Phenylacetates / pharmacology. Tretinoin / pharmacology

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(PMID = 19175987.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD11c; 0 / Peptides; 0 / Phenylacetates; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / cell differentiation agent II; 5688UTC01R / Tretinoin; E0399OZS9N / Cyclic AMP

   

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[Title] A case of antiphospholipid syndrome presenting with pulmonary truncus and main pulmonary artery thrombosis.

In patients with antiphospholipid syndrome (APS), thromboembolism and pulmonary hypertension are the most common pulmonary manifestations.

Thrombotic obstruction at the level of the main and/or proximal pulmonary arteries is rare.

We report a 40-year-old woman without any history of previous arterial and/or venous thrombosis who presented with severe dyspnea and was found to have pulmonary hypertension and positivity for anticardiolipin antibodies.

Computed tomography revealed pulmonary truncus thrombosis extending to both right and left pulmonary arteries.

This is the first reported case with thrombosis of pulmonary truncus and main pulmonary arteries concurrent with APS.

[MeSH-major] Antiphospholipid Syndrome / pathology. Pulmonary Artery / pathology. Pulmonary Embolism / pathology

[MeSH-minor] Adult. Antibodies, Anticardiolipin / blood. Diagnosis, Differential. Echocardiography. Fatal Outcome. Female. Humans. Hypertension, Pulmonary / etiology. Hypertension, Pulmonary / pathology. Radiography, Thoracic. Tomography, X-Ray Computed

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[Cites] Ann Thorac Surg. 1998 Dec;66(6):1919-24 [9930469.001]

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(PMID = 15378261.001).

[ISSN] 0172-8172

[Journal-full-title] Rheumatology international

[ISO-abbreviation] Rheumatol. Int.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies, Anticardiolipin

   

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[Title] Anti-cardiolipin and anti-beta2-glycoprotein I antibodies: performance of new commercial ELISA kits.

Antiphospholipid antibodies (aPL) are known to be pathogenic in experimental models and are predictive of thrombosis and miscarriages in patients, so it is important to correctly evaluate their presence for identifying patients at risk.

Despite many years of work, the standardization of aPL ELISA remains an open problem, so evaluation of newly introduced commercial preparations is mandatory.

A total of 80 sera were collected (10 primary antiphospholipid syndromes (APSs), 10 APSs associated with systemic lupus erythematosus, 20 infectious diseases, 20 rheumatoid arthritis and 20 normal blood donors) and tested for IgG/IgM anti-cardiolipin and anti-beta2GPI antibodies on commercial ELISA kits (ETI) by DiaSorin and on home-made ELISA.

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(PMID = 17785342.001).

[ISSN] 0077-8923

[Journal-full-title] Annals of the New York Academy of Sciences

[ISO-abbreviation] Ann. N. Y. Acad. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies; 0 / Cardiolipins; 0 / beta 2-Glycoprotein I

   

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[Title] Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-beta2-glycoprotein-I autoantibodies.

The sCD21 is able to bind all known ligands such as CD23, sCD23, Epstein-Barr virus and C3d in immune complexes.

Here, we show the serum levels of sCD21 in sera the of antiphospholipid syndrome (APS) patients.

Antiphospholipid syndrome is an autoimmune disorder in which autoantibodies cause heart attack, stroke and miscarriage.

Antiphospholipid syndrome may appear as primary or in association with systemic lupus erythromatosus (SLE) and other autoimmune diseases.

Here, we ask whether APS patients have different sCD21 titers compared to healthy persons and whether sCD21 levels correlate with the presence of anti-beta2-GPI autoantibodies.

We show that autoimmune APS patients have significantly reduced amounts of sCD21 in their sera, irrespective of the presence of anti-beta2-GPI autoantibodies.

In our APS patients cohort additional SLE, vasculities, DVT (deep vein thrombosis), fetal loss or thrombosis did not correlate to the reduced level of sCD21.

[MeSH-major] Antiphospholipid Syndrome / blood. Autoantibodies / blood. Receptors, Complement 3d / blood. beta 2-Glycoprotein I / immunology

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(PMID = 18172655.001).

[ISSN] 0172-8172

[Journal-full-title] Rheumatology international

[ISO-abbreviation] Rheumatol. Int.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Autoantibodies; 0 / Receptors, Complement 3d; 0 / beta 2-Glycoprotein I

   

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[Title] [Mitral valve replacement for mitral valve stenosis and insufficiency in a patient with antiphospholipid syndrome and systemic lupus erythematosus; report of a case].

She was previously diagnosed as antiphospholipid syndrome (APS) because of previous pregnancy morbidity and cerebral infarction.

[MeSH-major] Antiphospholipid Syndrome / complications. Heart Valve Prosthesis Implantation. Lupus Erythematosus, Systemic / complications. Mitral Valve Insufficiency / surgery. Mitral Valve Stenosis / surgery

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(PMID = 21174670.001).

[ISSN] 0021-5252

[Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery

[ISO-abbreviation] Kyobu Geka

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

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We have cloned the atypical PKC from Aplysia, PKC Apl III.

Instead, over-expression of PKC Apl III in Aplysia sensory neurons leads to production of a PKM fragment of PKC Apl III.

Moreover, nervous system enriched spliced forms of PKC Apl III show enhanced cleavage.

PKC Apl III could also be activated through phosphorylation downstream of phosphoinositide 3-kinase.

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(PMID = 19302474.001).

[ISSN] 1471-4159

[Journal-full-title] Journal of neurochemistry

[ISO-abbreviation] J. Neurochem.

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / / 12046

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 333DO1RDJY / Serotonin; 9007-49-2 / DNA; EC 2.7.11.13 / Protein Kinase C; EC 3.4.22.- / Calpain

   

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[Title] [Antiphospholipid syndrome: modern problems].

The article describes the historical aspects of the formation of the notion antiphospholipid syndrome (AFS) as well as the development of the conception of its clinical symptoms and laboratory tests confirming the diagnosis.

Special attention is paid to the modern interpretation of the notion of AFS, which excludes a number of clinical symptoms and laboratory tests and defines more clearly the use of the rest of clinical and laboratory signs.

Theoretical concepts of the pathogenetic mechanisms of the development of this disease and its association with congenital thrombofilias are adduced.

[MeSH-major] Antiphospholipid Syndrome / physiopathology

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(PMID = 18219947.001).

[ISSN] 0023-2149

[Journal-full-title] Klinicheskaia meditsina

[ISO-abbreviation] Klin Med (Mosk)

[Language] rus

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Russia (Federation)

[Number-of-references] 29