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1
acute promyelocytic leukemia t 15 17 q22 q11 12 morphologic abnormality 2005:2010[pubdate] *count=100
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1.
Reshetniak TM, Shirokova IE, Lisitskaia TL:
[The role of hyperhomocysteinemia in systemic lupus erythematosus and antiphospholipid syndrome].
Ter Arkh
; 2006;78(6):24-30
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[Title]
[The role of hyperhomocysteinemia in systemic lupus erythematosus and
antiphospholipid
syndrome].
AIM: To assess the role of hyperhomocysteinemia (HHC) in development of vascular complications in systemic lupus erythematosus (SLE) and
antiphospholipid
syndrome (APS).
The patients had the
disease
for 14 +/- 11 years.
HHC (HC >
15
mcg/l) was diagnosed in 82 of 125 (66%) patients: in 59% patients of group 1, 67%--of group 2 and 76%--of group 3.
There was a relationship between HHC and digital necrosis (DN): 80% of DN patients had HHC while HHC was diagnosed in 57% patients free of DN (chi-square = 4.76, p = 0.
03
).
Elevated
levels
of HC in blood was registered in 43 of 55 (78%) APS patients with thromboses vs. 9 of 19 (47%) patients with APS free of thromboses (p = 0.
03
).
HHC occurred significantly more frequently in patients with arterial thromboses (in all 14 patients) than in patients with venous thromboses (in 16 of 23--69.6%, p = 0.
03
) and in the absence of thromboses (in 9 of 19, 47.4%, p = 0.04).
CONCLUSION: More than 50% patients with SLE and APS, irrespective of APS variants, had an elevated HC
level
in the blood.
[MeSH-major]
Antiphospholipid
Syndrome / epidemiology. Hyperhomocysteinemia / epidemiology. Hyperhomocysteinemia / physiopathology. Lupus Erythematosus, Systemic / epidemiology
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.
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consumer health - Systemic lupus erythematosus
.
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.
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(PMID = 16881359.001).
[ISSN]
0040-3660
[Journal-full-title]
Terapevticheskiĭ arkhiv
[ISO-abbreviation]
Ter. Arkh.
[Language]
rus
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / Antibodies, Anticardiolipin
2.
Persaud SP, Donermeyer DL, Weber KS, Kranz DM, Allen PM:
High-affinity T cell receptor differentiates cognate peptide-MHC and altered peptide ligands with distinct kinetics and thermodynamics.
Mol Immunol
; 2010 May;47(9):1793-801
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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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[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
3.
Shen H, Li R, Xiao H, Zhou Q, Cui Q, Chen J:
Higher serum clozapine level is associated with increased antiphospholipid antibodies in schizophrenia patients.
J Psychiatr Res
; 2009 Mar;43(6):615-9
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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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4.
Matsuura E, Kobayashi K, Lopez LR:
Atherosclerosis in autoimmune diseases.
Curr Rheumatol Rep
; 2009 Feb;11(1):61-9
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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
5.
Asou N:
[Treatment of acute promyelocytic leukemia].
Nihon Rinsho
; 2007 Jan 28;65 Suppl 1:483-7
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[Title]
[Treatment of
acute promyelocytic leukemia
].
[MeSH-major]
Leukemia
,
Promyelocytic
,
Acute
/ drug therapy
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ALL-TRANS-RETINOIC ACID
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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
6.
Motta S, Monti M:
Photodynamic therapy-a promising treatment option for autoimmune skin ulcers: a case report.
Photochem Photobiol Sci
; 2007 Nov;6(11):1150-1
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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
7.
Bonati A, Rizzoli V, Lunghi P:
Arsenic trioxide in hematological malignancies: the new discovery of an ancient drug.
Curr Pharm Biotechnol
; 2006 Dec;7(6):397-405
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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
8.
Zhang ZL, Kong YY, Wan LG:
[Apoptosis of retinoic acid resistant NB4-R1 cells induced with curcumin and its mechanism].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2010 Apr;18(2):340-3
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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
9.
Ostertag MV, Liu X, Henderson V, Pierangeli SS:
A peptide that mimics the Vth region of beta-2-glycoprotein I reverses antiphospholipid-mediated thrombosis in mice.
Lupus
; 2006;15(6):358-65
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[Title]
A peptide
that mimics the Vth region of beta-2-glycoprotein I reverses
antiphospholipid
-mediated thrombosis in mice.
Antiphospholipid
(
aPL
) antibodies bind to beta2glycoprotein I (beta2GPI) and cause endothelial cell (EC) activation and thrombosis in mice. beta2GPI binds to EC through its Vth domain and induces their activation.
TIFI is a 20 amino acid synthetic
peptide
that shares similarity with the Vth domain of beta2GPI.
Our objectives were to examine the ability of TIFI to affect
aPL
-mediated thrombosis in mice and the interactions of TIFI, beta2GPI
with phospholipid
surfaces and target cells.
CD1 mice were injected with IgG from a patient
with antiphospholipid
syndrome (IgG-APS) or with control IgG-NHS and with either TIFI or with control
peptide
(VITT).
Inhibition and competition studies were done using
aPL
antibodies, cardiolipin (
CL
) liposomes in the presence of varying amounts of TIFI and beta2GPI.
TIFI reverted the beta2GPI-dependent binding of
aPL
antibodies to
CL
liposomes in a dose-dependent fashion.
This effect was abrogated by addition of beta2GPI, suggesting that TIFI displaces the binding of beta2GPI to
phospholipids
.
The data indicate that TIFI abrogates thrombogenic properties of
aPL
in mice by competing with beta2GPI and preventing its binding to target cells.
[MeSH-major]
Antiphospholipid
Syndrome / immunology. Fibrinolytic Agents / therapeutic use. Peptides / therapeutic use. Thrombosis / prevention & control. beta 2-Glycoprotein I / chemistry
[MeSH-minor]
Amino Acid Sequence. Animals. Antibodies,
Antiphospholipid
/ blood. Antibodies,
Antiphospholipid
/ immunology. Antibodies,
Antiphospholipid
/ toxicity. Binding, Competitive. Cardiolipins / immunology. Cells, Cultured. Endothelium, Vascular / drug effects. Endothelium, Vascular / physiopathology. Enzyme-Linked Immunosorbent Assay. Humans. Immunoglobulin G / toxicity. Liposomes. Macrophages / drug effects. Macrophages / immunology. Male. Mice. Molecular Mimicry. Molecular Sequence Data. Neutralization Tests. Protein Binding / drug effects. Protein Structure, Tertiary
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(PMID = 16830882.001).
[ISSN]
0961-2033
[Journal-full-title]
Lupus
[ISO-abbreviation]
Lupus
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / G12-RR03034; United States / NIGMS NIH HHS / GM / S02GM08248
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Cardiolipins; 0 / Fibrinolytic Agents; 0 / Immunoglobulin G; 0 / Liposomes; 0 / Peptides; 0 / TIFI peptide; 0 / beta 2-Glycoprotein I
10.
Bizzaro N, Tonutti E, Villalta D, Tampoia M, Tozzoli R:
Prevalence and clinical correlation of anti-phospholipid-binding protein antibodies in anticardiolipin-negative patients with systemic lupus erythematosus and women with unexplained recurrent miscarriages.
Arch Pathol Lab Med
; 2005 Jan;129(1):61-8
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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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.
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.
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.
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.
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.
NCI CPTC Antibody Characterization Program.
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.
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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
11.
Pourrat O, Jollit C, Gombert JM, Boinot C, Pierre F:
Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients.
J Thromb Haemost
; 2006 Oct;4(10):2276-7
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[Title]
Clinical
relevance of the recent update of the classification criteria for definite
antiphospholipid
syndrome: an obstetric medicine clinic series of 107 patients.
[MeSH-major]
Antiphospholipid
Syndrome / classification.
Antiphospholipid
Syndrome /
diagnosis
[MeSH-minor]
Antibodies,
Antiphospholipid
/ blood. Female. Humans. Lupus Coagulation Inhibitor / blood. Partial Thromboplastin Time.
Phospholipids
/ chemistry. Pregnancy. Pregnancy Complications / classification. Pregnancy Complications /
diagnosis
. Pregnancy Complications / immunology. Prognosis. Retrospective Studies
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[CommentOn]
J Thromb Haemost. 2006 Feb;4(2):295-306
[
16420554.001
]
(PMID = 16869832.001).
[ISSN]
1538-7933
[Journal-full-title]
Journal of thrombosis and haemostasis : JTH
[ISO-abbreviation]
J. Thromb. Haemost.
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids
12.
Tsukamoto H, Irie A, Chen YZ, Takeshita K, Kim JR, Nishimura Y:
TCR ligand avidity determines the mode of B-Raf/Raf-1/ERK activation leading to the activation of human CD4+ T cell clone.
Eur J Immunol
; 2006 Jul;36(7):1926-37
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[Title]
TCR
ligand
avidity determines the mode of B-Raf/Raf-1/ERK activation leading to the activation of human CD4+ T cell clone.
The interactions between
peptide
/MHC complexes and their cognate TCR are essential for various T cell responses.
However, the relationship between the avidity of TCR
ligand
and the subsequent intracellular signaling through the TCR is still unclear.
To investigate the effects of TCR
ligand
avidity on TCR-mediated signaling, we established L cells expressing HLA-DR4 molecules covalently linked with agonistic
peptide
(high-affinity
ligand
) or
altered peptide ligand
(
APL
; low-affinity
ligand
) at various densities as APC for a cognate human CD4(+) T cell clone.
Using this system, we demonstrated that the T cell clone stimulated
with APL
/HLA-DR4 complexes presented at an excessive density provoked the up-regulation of CD69, IL-2 production and proliferation, but no detectable phosphorylation of ZAP-70/LAT/SLP-76.
The strength and duration of B-Raf/ERK activations closely correlated with the density of the TCR
ligand
.
A knockdown approach confirmed that B-Raf activation was indispensable for the
APL
-induced T cell responses.
These observations suggest that the differences in TCR-
peptide
/MHC interactions reflect the strength and duration of B-Raf/Raf-1/ERK activation in the human CD4(+) T cells.
[MeSH-minor]
Amino Acid Sequence. Animals. Aotidae. Cell Transformation, Viral. Cells, Cultured. Clone Cells. Enzyme Activation / immunology. HLA-DR4 Antigen / physiology. Herpesvirus 2, Saimiriine. Humans. Jurkat Cells. L Cells (Cell Line).
Ligands
. Mice. Mice, Inbred C57BL. Molecular Sequence Data. NIH 3T3 Cells. PC12 Cells. Rats
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.
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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16791876.001).
[ISSN]
0014-2980
[Journal-full-title]
European journal of immunology
[ISO-abbreviation]
Eur. J. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / HLA-DR4 Antigen; 0 / Ligands; 0 / Receptors, Antigen, T-Cell; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
13.
El Bougrini J, Pampin M, Chelbi-Alix MK:
Arsenic enhances the apoptosis induced by interferon gamma: key role of IRF-1.
Cell Mol Biol (Noisy-le-grand)
; 2006;52(1):9-15
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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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.
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ARSENIC, ELEMENTAL
.
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.
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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
14.
Vassilakopoulos TP, Pangalis GA, Siakantaris MP, Levidou G, Yiakoumis X, Floudas C, Gribabis D, Bouros S, Metaxas I, Dimitriadou EM, Pantazi L, Tsoukala C, Korkolopoulou P, Andreopoulos A, Vaiopoulos G:
Kikuchi's lymphadenopathy: a relatively rare but important cause of lymphadenopathy in Greece, potentially associated with the antiphospholipid syndrome.
Rheumatol Int
; 2010 May;30(7):925-32
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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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[Cites]
Diagn Cytopathol. 2001 Oct;25(4):220-4
[
11599104.001
]
[Cites]
Am J Surg Pathol. 1995 Jul;19(7):798-809
[
7793478.001
]
[Cites]
Clin Rheumatol. 1991 Mar;10(1):90-3
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]
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Ann Hematol. 2002 Dec;81(12):732-5
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J Microbiol Immunol Infect. 2005 Feb;38(1):35-40
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15692625.001
]
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N Engl J Med. 2002 Mar 7;346(10):752-63
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In Vivo. 2002 Sep-Oct;16(5):311-6
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12675765.001
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3217625.001
]
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[
15272543.001
]
[Cites]
Arch Pathol Lab Med. 1985 Feb;109(2):107-8
[
3883942.001
]
[Cites]
Lupus. 2005;14(12):967-9
[
16425578.001
]
[Cites]
Medicine (Baltimore). 2000 Sep;79(5):338-47
[
11039082.001
]
[Cites]
Rheumatol Int. 2005 May;25(4):303-6
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15645234.001
]
[Cites]
Clin Rheumatol. 2005 Feb;24(1):60-3
[
15517448.001
]
[Cites]
Am J Med. 1996 Oct;101(4):401-5
[
8873511.001
]
[Cites]
Lupus. 2001;10(2):126-8
[
11237125.001
]
[Cites]
Semin Oncol. 1993 Dec;20(6):570-82
[
8296196.001
]
[Cites]
In Vivo. 2003 Jan-Feb;17(1):51-3
[
12655790.001
]
(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
15.
Kwaan HC, Huyck T:
Thromboembolic and bleeding complications in acute leukemia.
Expert Rev Hematol
; 2010 Dec;3(6):719-30
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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
16.
Bassani MA, de Oliveira AB, Oliveira Neto AF:
Noninvasive ventilation in a pregnant patient with respiratory failure from all-trans-retinoic-acid (ATRA) syndrome.
Respir Care
; 2009 Jul;54(7):969-72
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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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.
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.
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ALL-TRANS-RETINOIC ACID
.
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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
17.
Tincani A, Casu C, Cartella S, Ziglioli T, Cattaneo R:
[Antiphospholipid antibody: laboratory, pathogenesis and clinical manifestations].
Reumatismo
; 2010 Jan-Mar;62(1):65-75
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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
18.
Asai E, Okouchi M, Momiyama M, Kajikawa A, Ueda K:
Free flap failure in an anticardiolipin antibody-positive patient with neoplasm--a case report.
Microsurgery
; 2010;30(3):238-41
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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
19.
Le Hello C, Blacher J, Conard J, Piette JC, Constans J:
[Thrombophilias and peripheral arterial occlusive disease].
J Mal Vasc
; 2008 Sep;33(3):126-36
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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
20.
Etsuda H, Miyamoto A, Nakajima Y, Hakamata N, Yamauchi Y, Akita T, Fukuda M:
[Acute myocardial infarction with variable clinical manifestations: probable catastrophic primary antiphospholipid antibody syndrome: a case report].
J Cardiol
; 2005 Oct;46(4):155-60
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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
21.
Onetti L, Villafañe S, Menso E, Drenkard C, Gamron S, Barberis G, Onetti CM:
[Hyperhomocysteine like thrombocytic risk factor in patient with systemic lupus erythematous with antiphospholipid syndrome].
Rev Fac Cien Med Univ Nac Cordoba
; 2005;62(1):21-5
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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
22.
Filip B, Milczarek M, Wietrzyk J, Chodyński M, Kutner A:
Antitumor properties of (5E,7E) analogs of vitamin D3.
J Steroid Biochem Mol Biol
; 2010 Jul;121(1-2):399-402
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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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CHOLECALCIFEROL
.
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CALCIUM, ELEMENTAL
.
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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
23.
Zhang X, Lian Z, Padden C, Gerstein MB, Rozowsky J, Snyder M, Gingeras TR, Kapranov P, Weissman SM, Newburger PE:
A myelopoiesis-associated regulatory intergenic noncoding RNA transcript within the human HOXA cluster.
Blood
; 2009 Mar 12;113(11):2526-34
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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
24.
Jiang WQ, Zhong ZH, Henson JD, Reddel RR:
Identification of candidate alternative lengthening of telomeres genes by methionine restriction and RNA interference.
Oncogene
; 2007 Jul 12;26(32):4635-47
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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
25.
Wu L, Xiao B, Jia X, Zhang Y, Lü S, Chen J, Long M:
Impact of carrier stiffness and microtopology on two-dimensional kinetics of P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) interactions.
J Biol Chem
; 2007 Mar 30;282(13):9846-54
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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
26.
Marai I, Tincani A, Balestrieri G, Shoenfeld Y:
Anticardiolipin and anti-beta-2-glycoprotein I antibodies.
Autoimmunity
; 2005 Feb;38(1):33-8
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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
27.
Mohsen H, Faouzi A, Khaldoun BH, Fatma A, Hanéne H, Zohra D, Habib G, Fethi B, Faouzi M, Mohamed BF:
[Abnormalities of haemostasis in myocardial infarction with normal coronary artery].
Tunis Med
; 2005 Nov;83(11):675-80
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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
28.
Iero M, Squarcina P, Romero P, Guillaume P, Scarselli E, Cerino R, Carrabba M, Toutirais O, Parmiani G, Rivoltini L:
Low TCR avidity and lack of tumor cell recognition in CD8(+) T cells primed with the CEA-analogue CAP1-6D peptide.
Cancer Immunol Immunother
; 2007 Dec;56(12):1979-91
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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
29.
Ozpolat B, Mehta K, Lopez-Berestein G:
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.
Leuk Lymphoma
; 2005 Oct;46(10):1497-506
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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
30.
Tebo AE, Jaskowski TD, Hill HR, Branch DW:
Clinical relevance of multiple antibody specificity testing in anti-phospholipid syndrome and recurrent pregnancy loss.
Clin Exp Immunol
; 2008 Dec;154(3):332-8
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[Title]
Clinical
relevance of multiple antibody specificity testing in
anti
-
phospholipid
syndrome and recurrent pregnancy loss.
We wanted to evaluate whether testing for
anti
-phosholipid antibodies other than
anti
-cardiolipin (aCL) and
anti
-beta-2 glycoprotein I (abeta2GPI) immunoglobulin (Ig)G and IgM identifies patients with recurrent pregnancy loss (RPL) who may be positive for
anti
-
phospholipid
syndrome (APS).
In a cross-sectional study comprising 62 patients with APS, 66 women with RPL, 50 healthy blood donors and 24 women
with a
history of successful pregnancies, we tested IgM and IgG antibodies to phosphatidic acid, phosphatidyl choline, phosphatidyl ethanolamine, phosphatidyl glycerol, phosphatidyl inositol and phosphatidyl serine with and without beta-2 glycoprotein I (beta2GPI) from a single manufacturer as well as aCL and abeta2GPI antibodies.
Diagnostic accuracies of individual and combined
anti
-
phospholipid
(
aPL
) assays were assessed by computing sensitivities, specificities, positive predictive values and negative predictive values together with their 95% confidence intervals.
The overall combined sensitivity of the non-recommended
aPL
assays was not significantly higher than that of the aCL and aB2GPI tests.
Multiple
aPL
specificities in RPL group is not significantly different from controls and therefore of no
clinical
significance.
[MeSH-major]
Abortion, Habitual / immunology.
Antiphospholipid
Syndrome /
diagnosis
[MeSH-minor]
Adolescent. Adult. Aged. Antibodies,
Antiphospholipid
/ blood. Antibody Specificity. Autoantibodies / blood. Biomarkers / blood. Cross-Sectional Studies. Female. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. Male. Middle Aged. Pregnancy. Sensitivity and Specificity. Young Adult. beta 2-Glycoprotein I / blood
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[Cites]
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[Cites]
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Blood. 1994 Nov 1;84(9):2854-67
[
7949161.001
]
(PMID = 18826497.001).
[ISSN]
1365-2249
[Journal-full-title]
Clinical and experimental immunology
[ISO-abbreviation]
Clin. Exp. Immunol.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / beta 2-Glycoprotein I
[Other-IDs]
NLM/ PMC2633231
31.
Stern C, Chamley L:
Antiphospholipid antibodies and coagulation defects in women with implantation failure after IVF and recurrent miscarriage.
Reprod Biomed Online
; 2006 Jul;13(1):29-37
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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
32.
Fischer MJ, Rauch J, Levine JS:
The antiphospholipid syndrome.
Semin Nephrol
; 2007 Jan;27(1):35-46
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[Title]
The
antiphospholipid
syndrome.
The
antiphospholipid
syndrome (APS) is an autoimmune
disorder
characterized by the
clinical
association of
antiphospholipid
autoantibodies (
aPL
)
with a
syndrome of hypercoagulability that can affect any blood vessel, irrespective of
type
or size.
We also discuss the impact that APS may have on pre-existing renal
disease
as well as current recommendations for treatment of APS.
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.
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[Cites]
N Engl J Med. 2003 Oct 16;349(16):1526-33
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(PMID = 17336687.001).
[ISSN]
0270-9295
[Journal-full-title]
Seminars in nephrology
[ISO-abbreviation]
Semin. Nephrol.
[Language]
ENG
[Grant]
None / None / / 67101; Canada / Canadian Institutes of Health Research / / 67101
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
32
[Other-IDs]
NLM/ CAMS2313; NLM/ PMC3440307
33.
Laskin CA, Spitzer KA, Clark CA, Crowther MR, Ginsberg JS, Hawker GA, Kingdom JC, Barrett J, Gent M:
Low molecular weight heparin and aspirin for recurrent pregnancy loss: results from the randomized, controlled HepASA Trial.
J Rheumatol
; 2009 Feb;36(2):279-87
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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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.
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.
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commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
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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
34.
Pagnoux C, Korach JM, Guillevin L:
Indications for plasma exchange in systemic lupus erythematosus in 2005.
Lupus
; 2005;14(11):871-7
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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
35.
Tallman MS:
What is the role of arsenic in newly diagnosed APL?
Best Pract Res Clin Haematol
; 2008 Dec;21(4):659-66
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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
36.
Markowski TR, Martin DB, Kao GF, Lutz L, Deng A, Gaspari AA:
Leukemia cutis: a presenting sign in acute promyelocytic leukemia.
Arch Dermatol
; 2007 Sep;143(9):1220-1
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[Title]
Leukemia
cutis: a presenting sign in
acute promyelocytic leukemia
.
[MeSH-major]
Leukemia
,
Promyelocytic
,
Acute
/
diagnosis
. Skin Neoplasms /
diagnosis
[MeSH-minor]
Diagnosis
, Differential. Female. Humans. Leg Dermatoses /
diagnosis
. Middle Aged
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(PMID = 17875899.001).
[ISSN]
0003-987X
[Journal-full-title]
Archives of dermatology
[ISO-abbreviation]
Arch Dermatol
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
37.
Lu J, Chew EH, Holmgren A:
Targeting thioredoxin reductase is a basis for cancer therapy by arsenic trioxide.
Proc Natl Acad Sci U S A
; 2007 Jul 24;104(30):12288-93
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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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.
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.
The Lens.
Cited by Patents in
.
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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
38.
Campos B, Chames M, Lantry JM, Bill JP, Eis A, Brockman D, Neil J, Tischner E, Barton J, Wong C, Schwemberger S, Cornelius J, Myatt L, Baeza I, Hnat M:
Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy.
Placenta
; 2006 Feb-Mar;27(2-3):215-24
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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
39.
Ma J:
Advances in management of acute promyelocytic leukemia with arsenic trioxide.
Chin J Integr Med
; 2007 Jun;13(2):92-4
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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
Genetic Alliance.
consumer health - Acute Promyelocytic Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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ARSENIC TRIOXIDE
.
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ALL-TRANS-RETINOIC ACID
.
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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
40.
Pan M, Chu M, Sun Y, Song X, Zhu J:
[Preparation and characterization of quantum dots-peptides bioconjugations and their specificity related to recognizing tumor cells].
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi
; 2007 Jun;24(3):577-81
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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
41.
Crowder C, Dahle Ø, Davis RE, Gabrielsen OS, Rudikoff S:
PML mediates IFN-alpha-induced apoptosis in myeloma by regulating TRAIL induction.
Blood
; 2005 Feb 1;105(3):1280-7
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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
NCI CPTAC Assay Portal.
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.
NCI CPTAC Assay Portal.
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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
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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
42.
Liu BH, Wu TS, Yu FY, Su CC:
Induction of oxidative stress response by the mycotoxin patulin in mammalian cells.
Toxicol Sci
; 2007 Feb;95(2):340-7
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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.
Hazardous Substances Data Bank.
PATULIN
.
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NCI CPTAC Assay Portal
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NCI CPTAC Assay Portal.
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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
43.
Araujo FD, Stracker TH, Carson CT, Lee DV, Weitzman MD:
Adenovirus type 5 E4orf3 protein targets the Mre11 complex to cytoplasmic aggresomes.
J Virol
; 2005 Sep;79(17):11382-91
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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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[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
44.
van Os GM, Urbanus RT, Agar C, Meijers JC, de Groot PG:
Antiphospholipid syndrome. Current insights into laboratory diagnosis and pathophysiology.
Hamostaseologie
; 2010 Aug;30(3):139-43
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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
45.
Tennent-Brown BS, Wilkins PA, Lindborg S, Russell G, Boston RC:
Assessment of a point-of-care lactate monitor in emergency admissions of adult horses to a referral hospital.
J Vet Intern Med
; 2007 Sep-Oct;21(5):1090-8
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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
46.
Ortona E, Capozzi A, Colasanti T, Conti F, Alessandri C, Longo A, Garofalo T, Margutti P, Misasi R, Khamashta MA, Hughes GR, Valesini G, Sorice M:
Vimentin/cardiolipin complex as a new antigenic target of the antiphospholipid syndrome.
Blood
; 2010 Oct 21;116(16):2960-7
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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
47.
Graw-Panzer KD, Verma S, Rao S, Miller ST, Lee H:
Venous thrombosis and pulmonary embolism in a child with pneumonia due to Mycoplasma pneumoniae.
J Natl Med Assoc
; 2009 Sep;101(9):956-8
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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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.
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.
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.
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.
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HEPARIN
.
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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
48.
Miesbach W, Chapman J, Scharrer I:
Focal seizures after treatment with fluvastatin in a patient with a history of catastrophic antiphospholipid syndrome.
J Neurol Sci
; 2005 Nov 15;238(1-2):93-5
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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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.
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.
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.
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.
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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
49.
Cheunsuchon B, Rungkaew P, Chawanasuntorapoj R, Pattaragarn A, Parichatikanond P:
Prevalence and clinicopathologic findings of antiphospholipid syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies.
Nephrology (Carlton)
; 2007 Oct;12(5):474-80
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[Title]
Prevalence and clinicopathologic findings of
antiphospholipid
syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies.
AIM: To determine the prevalence of
antiphospholipid
syndrome nephropathy (APSN) in Thai systemic lupus erythematosus (SLE) patients who underwent renal biopsy and to compare the relationship of renal histopathology and other significant
clinical
parameters between SLE patients with and without APSN.
METHODS: A retrospective analysis was undertaken in systemic lupus erythematosus patients (n = 150, 44 <
15
years old, 106 0e;
15
years old) who underwent renal biopsy.
The specimens were evaluated for histological features of APSN and other significant
clinical
parameters.
The result of
antiphospholipid
antibodies,
clinical
course, and renal function from chart review were analysed.
RESULTS: The prevalence of APSN in systemic lupus erythematosus patients who underwent renal biopsies was 34% (16% in <
15
-year-old group, 41.5% in > or =
15
-year-old group).
APSN was associated with more severe hypertension (P = 0.002 for systolic and P = 0.004 for diastolic blood pressure),
acute
renal failure (P = 0.003), persistent heavy proteinuria (P < 0.001 for 4+ proteinuria), severe lupus nephritis (class III and IV, P = 0.014, high activity and chronicity indices, P < 0.001) and a tendency to progress to end-stage renal
disease
.
[MeSH-major]
Antiphospholipid
Syndrome / complications.
Antiphospholipid
Syndrome / epidemiology. Kidney / pathology. Kidney Diseases / etiology. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / physiopathology
[MeSH-minor]
Adolescent. Adult. Biopsy. Child. Child, Preschool. Chronic
Disease
.
Disease
Progression. Female. Humans. Infant. Kidney Failure, Chronic / etiology. Male. Middle Aged. Prevalence. Retrospective Studies. Severity of Illness Index. Thailand
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.
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.
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(PMID = 17803471.001).
[ISSN]
1320-5358
[Journal-full-title]
Nephrology (Carlton, Vic.)
[ISO-abbreviation]
Nephrology (Carlton)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Australia
50.
de Meis E, Monteiro RQ, Levy RA:
Lung adenocarcinoma and antiphospholipid antibodies.
Autoimmun Rev
; 2009 May;8(6):529-32
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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
51.
Miwako I, Kagechika H:
Tamibarotene.
Drugs Today (Barc)
; 2007 Aug;43(8):563-8
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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
52.
Ramkumar B, Chadha MK, Barcos M, Sait SN, Heyman MR, Baer MR:
Acute promyelocytic leukemia after mitoxantrone therapy for multiple sclerosis.
Cancer Genet Cytogenet
; 2008 Apr 15;182(2):126-9
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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
53.
Jia PM, Pan XR, Xiao S, Li D, Wang ZY, Tong JH:
[In vitro study of the effects of CDA-II combined with cAMP on apoptosis induction in retinoic acid resistant acute promyelocytic leukemia cells].
Zhonghua Xue Ye Xue Za Zhi
; 2008 Sep;29(9):603-6
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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
54.
Sayarlioglu M, Topcu N, Harman M, Guntekin U, Erkoc R:
A case of antiphospholipid syndrome presenting with pulmonary truncus and main pulmonary artery thrombosis.
Rheumatol Int
; 2005 Jan;25(1):65-8
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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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J Rheumatol. 1995 Jan;22(1):62-6
[
7699684.001
]
[Cites]
Surg Today. 1992;22(6):548-52
[
1472796.001
]
[Cites]
Arthritis Rheum. 2002 Apr;46(4):1019-27
[
11953980.001
]
[Cites]
Medicine (Baltimore). 1998 May;77(3):195-207
[
9653431.001
]
(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
55.
Andreoli L, Malacarne F, Ceribelli A, Kutschera I, Tincani A:
Anti-cardiolipin and anti-beta2-glycoprotein I antibodies: performance of new commercial ELISA kits.
Ann N Y Acad Sci
; 2007 Aug;1109:531-7
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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
56.
Avetisov SE, Smirnova TV, Kozlovskaia NL, Kazarian EE, Budzinskaia MV:
[Multifocal electroretinography in ophtalmological symptoms in patients with antiphospholipid syndrome].
Vestn Oftalmol
; 2009 Jan-Feb;125(1):46-9
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[Title]
[Multifocal electroretinography in ophtalmological symptoms in patients
with antiphospholipid
syndrome].
The paper describes the first experience in using multifocal electroretinography (mfERG) in patients
with antiphospholipid
syndrome (APS).
In the latter, thrombogenesis is mosaic in most cases so the techniques providing a spatial imaging of the pathological process is of interest in the examination of patients with this
disease
.
[MeSH-major]
Antiphospholipid
Syndrome / physiopathology. Electroretinography / methods. Retina / physiopathology. Retinal Diseases / physiopathology
[MeSH-minor]
Adolescent. Adult.
Diagnosis
, Differential. Humans. Middle Aged. Visual Field Tests. Visual Fields / physiology. Young Adult
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(PMID = 19284102.001).
[ISSN]
0042-465X
[Journal-full-title]
Vestnik oftalmologii
[ISO-abbreviation]
Vestn Oftalmol
[Language]
rus
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
Russia (Federation)
57.
Singh A, Blank M, Shoenfeld Y, Illges H:
Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-beta2-glycoprotein-I autoantibodies.
Rheumatol Int
; 2008 May;28(7):661-5
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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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[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
58.
Kondo H, Nakayama M, Ishikawa H:
[Mitral valve replacement for mitral valve stenosis and insufficiency in a patient with antiphospholipid syndrome and systemic lupus erythematosus; report of a case].
Kyobu Geka
; 2010 Dec;63(13):1173-5
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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
59.
Bougie JK, Lim T, Farah CA, Manjunath V, Nagakura I, Ferraro GB, Sossin WS:
The atypical protein kinase C in Aplysia can form a protein kinase M by cleavage.
J Neurochem
; 2009 May;109(4):1129-43
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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
60.
Bokarev IN, Arshinov AV, Mel'nikov AL:
[Antiphospholipid syndrome: modern problems].
Klin Med (Mosk)
; 2007;85(11):4-8
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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
61.
Choi SH, Worswick S, Byun HM, Shear T, Soussa JC, Wolff EM, Douer D, Garcia-Manero G, Liang G, Yang AS:
Changes in DNA methylation of tandem DNA repeats are different from interspersed repeats in cancer.
Int J Cancer
; 2009 Aug 1;125(3):723-9
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Hypomethylation of DNA repetitive elements is a common
finding
in cancer, but very little is known about the DNA methylation changes of different types of DNA repetitive elements, such as interspersed repeats (LINE1 and Alu Yb8) and tandem repeats (Sat-
alpha
, NBL-2 and D4Z4).
In all we studied 10 different tissues from four individuals undergoing autopsy, 34 paired normal and tumor tissues from patients with bladder cancer, 58 patients with chronic myelogenous
leukemia
and 23 patients with
acute promyelocytic leukemia
.
In bladder cancer we found clear hypomethylation of LINE1, Alu Yb8, Sat-
alpha
and NBL-2.
Conversely, we found an increase in the DNA methylation
levels
of D4Z4 from normal to cancer.
In contrast
leukemia
showed no significant changes in the DNA methylation of LINE1 and Alu Yb8, but DNA methylation increases in NBL-2 and D4Z4 tandem repeats.
Our findings show that the changes in DNA methylation
levels
of individual DNA repetitive elements are unique for each repetitive element, which may reflect distinct epigenetic factors and may have important implications in the use of DNA methylation of repetitive elements as global DNA methylation biomarkers.
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Hum Mol Genet. 2000 Mar 1;9(4):597-604
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10699183.001
]
(PMID = 19437537.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA086871; United States / NIEHS NIH HHS / ES / P30 ES007048; United States / NIEHS NIH HHS / ES / 5P30ES07048; United States / NCI NIH HHS / CA / P01 CA86871
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS587075; NLM/ PMC4086885
62.
Dutta P, Sazawal S, Kumar R, Saxena R:
Does acute promyelocytic leukemia in Indian patients have biology different from the West?
Indian J Pathol Microbiol
; 2008 Jul-Sep;51(3):437-9
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[Title]
Does
acute promyelocytic leukemia
in Indian patients have biology different from the West?
Acute promyelocytic leukemia
(
APML
) is a well-characterized malignancy with typical clinico-hematological and molecular features.
This study was conducted to determine the clinico-hematological profile of
APML
in India.
Thirty-five patients
with APML
presenting to Hematology Department, AIIMS, New Delhi, between July 2003 and June 2005 were evaluated for presenting
clinical
features, hemogram, peripheral smear, bone marrow morphology and cytochemistry.
Reverse transcriptase PCR (RT-PCR) for
PML
-RARalpha was done in all cases.
Male-to-female ratio was 0.9:1 (males--
17
and females--18) with median age 25 years (range 11-57 years).
RT-PCR showed
PML
-RARalpha in 33/35 cases with the bcr3 isoform being present in 24/33 positive cases (72.7%).
The two cases negative for
PML
-RARalpha showed typical morphology and responded to ATRA.
APML
in India has certain unusual features, which may reflect a different biology.
[MeSH-major]
Leukemia
,
Promyelocytic
,
Acute
/ pathology
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(PMID = 18723985.001).
[ISSN]
0377-4929
[Journal-full-title]
Indian journal of pathology & microbiology
[ISO-abbreviation]
Indian J Pathol Microbiol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Chemical-registry-number]
0 / Azo Compounds; 0 / Naphthalenes; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.- / Esterases
63.
Riviello C, Ammannati F, Lamassa M, Mariotti F, Mennonna P, Parretti E, Tondi F, Mello G:
Atypical onset of antiphospholipid syndrome in pregnancy: a case report.
Thromb Res
; 2005;115(5):405-8
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[Title]
Atypical onset of
antiphospholipid
syndrome in pregnancy: a case report.
BACKGROUND: We present a case of an atypical onset of
antiphospholipid
syndrome (APS).
After 1 month, laboratory tests revealed high
level
of
antiphospholipid
antibodies.
After 6 weeks,
antiphospholipid
antibodies, tested again, result positive.
CONCLUSION:
Antiphospholipid
antibodies often cause pregnancy complications, but, to our knowledge, this is the first report of an association of
antiphospholipid
antibodies, with cerebral cavernoma thrombosis and early onset HELLP syndrome.
[MeSH-major]
Antiphospholipid
Syndrome / complications. Pregnancy Complications, Hematologic
[MeSH-minor]
Abortion, Spontaneous. Adult. Antibodies,
Antiphospholipid
/ blood. Cerebral Hemorrhage / complications. Cerebral Hemorrhage /
diagnosis
. Cerebral Hemorrhage / surgery. Female. HELLP Syndrome / complications. HELLP Syndrome /
diagnosis
. Humans. Pregnancy. Prognosis. Risk Factors. Thrombosis / complications. Thrombosis /
diagnosis
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(PMID = 15733974.001).
[ISSN]
0049-3848
[Journal-full-title]
Thrombosis research
[ISO-abbreviation]
Thromb. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid
64.
Savickiene J, Treigyte G, Gineitis A, Navakauskiene R:
A critical role of redox state in determining HL-60 cell granulocytic differentiation and apoptosis via involvement of PKC and NF-kappaB.
In Vitro Cell Dev Biol Anim
; 2010 Jun;46(6):547-59
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Here, a causal relationship among redox state, granulocytic differentiation induced by all-trans retinoic acid (RA) or dibutyryl cAMP (dbcAMP) and apoptosis have been studied in the human
acute promyelocytic
leukaemia
HL-60 cells.
The modulation of intracellular reactive oxygen species
levels
by D: , L: -buthionine-(S, R) sulfoximide (BSO), and N: -acetyl-L: -cysteine (NAC) caused inducer- and time-dependent or stage-specific effects on HL-60 cell growth inhibition, differentiation and subsequent apoptosis.
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N-ACETYLCYSTEINE
.
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(PMID = 20224971.001).
[ISSN]
1543-706X
[Journal-full-title]
In vitro cellular & developmental biology. Animal
[ISO-abbreviation]
In Vitro Cell. Dev. Biol. Anim.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / NF-kappa B; EC 2.7.11.13 / Protein Kinase C; WYQ7N0BPYC / Acetylcysteine
65.
Karasawa M, Yamane A, Mitsui T, Irisawa H, Sakura T, Matsushima T, Tsukamoto N, Nojima Y, Miyawaki S:
Long-term persistence of host cells detected by X-chromosome gene-based assay in patients undergoing gender-mismatched hematopoietic stem cell transplantation.
Am J Hematol
; 2005 Oct;80(2):101-5
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After restriction digestion of samples, we detected a small number of female-derived cells within a large population of male-derived cells,
with a
sensitivity from 0.1% to 0.05%.
Chimerism was examined in four patients
with myeloid
malignancies: two patients with
acute
myeloid
leukemia
(
AML
) from myelodysplastic syndrome (MDS), and one patient each
with AML M3
and
AML
M4.
All patients underwent myeloablative conditioning regimens and exhibited good
clinical
results during a median follow-up period of 6.6 years (range, 3.4-7.5 years).
[MeSH-minor]
Adult. Chromosomes, Human, X. Female. Hematopoietic Stem Cell Transplantation. Humans.
Leukemia
,
Myeloid
/ therapy. Longitudinal Studies. Middle Aged. Receptors, Androgen / genetics. Sensitivity and Specificity. Sex Factors
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.
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 16184584.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / AR protein, human; 0 / Receptors, Androgen
66.
Crowther M, Crowther MA:
Intensity of warfarin coagulation in the antiphospholipid syndrome.
Curr Rheumatol Rep
; 2010 Feb;12(1):64-9
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[Title]
Intensity of warfarin coagulation in the
antiphospholipid
syndrome.
Antiphospholipid
syndrome is a condition with an increased propensity for both arterial and venous thrombosis.
[MeSH-major]
Anticoagulants / therapeutic use.
Antiphospholipid
Syndrome / drug therapy. Thromboembolism / prevention & control. Warfarin / therapeutic use
Genetic Alliance.
consumer health - Antiphospholipid Syndrome
.
Genetic Alliance.
consumer health - Warfarin syndrome
.
MedlinePlus Health Information.
consumer health - Blood Thinners
.
Hazardous Substances Data Bank.
WARFARIN
.
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(PMID = 20425536.001).
[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 / Anticoagulants; 5Q7ZVV76EI / Warfarin
[Number-of-references]
27
67.
Franchini M, Di Minno MN, Coppola A:
Disseminated intravascular coagulation in hematologic malignancies.
Semin Thromb Hemost
; 2010 Jun;36(4):388-403
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A variety of
disease
- or treatment-related factors may affect this condition, enhancing the risk of thrombosis or of bleeding and further triggering mechanisms of DIC in this setting.
An overt DIC is diagnosed in approximately
15
% of patients with
acute leukemia
, and bleeding manifestations prevail over thrombosis, with the highest and most harmful
clinical
impact in
acute promyelocytic leukemia
(
APL
).
In this review the coagulation abnormalities,
clinical
manifestations, and the presently known pathophysiologic mechanisms of DIC in patients with hematologic malignancies are discussed, focusing on the most extensively studied condition of
APL
.
The Lens.
Cited by Patents in
.
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[Copyright]
Copyright Thieme Medical Publishers.
(PMID = 20614391.001).
[ISSN]
1098-9064
[Journal-full-title]
Seminars in thrombosis and hemostasis
[ISO-abbreviation]
Semin. Thromb. Hemost.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
132
68.
Sirulnik LA, Stone RM:
Acute promyelocytic leukemia: current strategies for the treatment of newly diagnosed disease.
Clin Adv Hematol Oncol
; 2005 May;3(5):391-7, 429
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[Title]
Acute promyelocytic leukemia
: current strategies for the treatment of newly diagnosed
disease
.
Acute promyelocytic leukemia
(
APL
) is a distinct subtype of
acute
myeloid
leukemia
that comprises about 10% of cases.
It is characterized by the accumulation of granulocytic cells blocked at the
promyelocytic
stage of differentiation in the bone marrow and the peripheral blood, life-threatening coagulopathy, and a remarkable response to treatment with all-trans-retinoic acid (ATRA), arsenic trioxide, and anthracyclines.
Current treatment strategies with ATRA and anthracycline-based chemotherapy has dramatically transformed
APL
into the most curable of all
acute
leukemias
.
In this review we explore current treatment strategies in the management of newly diagnosed
APL
.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Promyelocytic
,
Acute
/ drug therapy
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.
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(PMID = 16167012.001).
[ISSN]
1543-0790
[Journal-full-title]
Clinical advances in hematology & oncology : H&O
[ISO-abbreviation]
Clin Adv Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
69
69.
Tsai WH, Shih CH, Lin CC, Ho CK, Hsu FC, Hsu HC:
Monocyte chemotactic protein-1 in the migration of differentiated leukaemic cells toward alveolar epithelial cells.
Eur Respir J
; 2008 May;31(5):957-62
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All-trans retinoic acid (ATRA) can induce
acute
respiratory distress syndrome in patients with
acute promyelocytic
leukaemia
(
APL
).
The current study investigated the role of monocyte chemotactic protein (MCP)-1 in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4)
APL
cells toward A549 alveolar epithelial cells.
Monocyte chemotactic protein-1 secreted from alveolar epithelial cells plays an important role in the cell-cell interaction involved in the chemotactic transmigration of all-trans retinoic acid-treated
acute promyelocytic
leukaemia
cells toward alveolar epithelial cells.
[MeSH-major]
Antineoplastic Agents / adverse effects. Chemotaxis / drug effects. Epithelial Cells / drug effects. Granulocyte Precursor Cells / drug effects.
Leukemia
,
Promyelocytic
,
Acute
/ drug therapy. Tretinoin / adverse effects
[MeSH-minor]
Cell Differentiation / drug effects. Cells, Cultured. Chemokine CCL2 / drug effects. Coculture Techniques. Humans.
Pulmonary
Alveoli / cytology.
Pulmonary
Alveoli / drug effects. Receptors, CCR2
Hazardous Substances Data Bank.
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.
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(PMID = 18216048.001).
[ISSN]
1399-3003
[Journal-full-title]
The European respiratory journal
[ISO-abbreviation]
Eur. Respir. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CCR2 protein, human; 0 / Chemokine CCL2; 0 / Receptors, CCR2; 5688UTC01R / Tretinoin
70.
Mimura Y, Takahashi K, Kawata K, Akazawa T, Inoue N:
Two-step colocalization of MORC3 with PML nuclear bodies.
J Cell Sci
; 2010 Jun 15;123(Pt 12):2014-24
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[Title]
Two-step colocalization of MORC3
with PML
nuclear bodies.
Many functional subdomains, including
promyelocytic leukemia
nuclear bodies (
PML
NBs), are formed in the mammalian nucleus.
Various proteins are constitutively or transiently accumulated in
PML
NBs in
a PML
-dependent manner.
MORC3 (microrchidia family CW-
type
zinc-finger 3), also known as NXP2, which consists of GHL-ATPase, a CW-
type
zinc-finger and coiled-coil domains, is localized in
PML
NBs, where it recruits and activates p53 to induce cellular senescence.
Interestingly, we found that MORC3 can form
PML
-independent nuclear domains (NDs) in mouse hematopoietic cells and even in
Pml
-deficient cells.
Here, we show that MORC3 colocalizes
with PML
by a two-step molecular mechanism: the
PML
-independent formation of MORC3 NDs by the ATPase cycle, and the association of MORC3
with PML
via the SUMO1-SUMO-interacting motif (SIM).
Furthermore, the SUMOylation of MORC3 at five sites was involved in the association of MORC3
with PML
, and SUMO1-unmodified MORC3 formed NDs independently of
PML
.
[MeSH-major]
Adenosine
Triphosphatases / metabolism. DNA-Binding Proteins / metabolism. Intranuclear Inclusion Bodies / metabolism. Nuclear Proteins / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Animals. HeLa Cells. Humans.
Leukemia
,
Promyelocytic
,
Acute
/ genetics.
Leukemia
,
Promyelocytic
,
Acute
/ metabolism. Mice. Protein Structure, Tertiary. Protein Transport. SUMO-1 Protein / genetics. SUMO-1 Protein / metabolism
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(PMID = 20501696.001).
[ISSN]
1477-9137
[Journal-full-title]
Journal of cell science
[ISO-abbreviation]
J. Cell. Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / MORC3 protein, human; EC 3.6.1.- / MORC3 protein, mouse
71.
Chu Q, Amano O, Kanda Y, Kunii S, Wang Q, Sakagami H:
Tumor-specific cytotoxicity and type of cell death induced by gefitinib in oral squamous cell carcinoma cell lines.
Anticancer Res
; 2009 Dec;29(12):5023-31
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[Title]
Tumor-specific cytotoxicity and
type
of cell death induced by gefitinib in oral squamous cell carcinoma cell lines.
Gefitinib alone and combined with docetaxel induced internucleosomal DNA fragmentation and caspase-3 activation in human
promyelocytic leukemia
HL-60 cells, but not in HSC-2 or T98G cells.
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(PMID = 20044612.001).
[ISSN]
1791-7530
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Plant Extracts; 0 / Quinazolines; 80168379AG / Doxorubicin; 8ZYQ1474W7 / Sodium Fluoride; BZ114NVM5P / Mitoxantrone; EC 3.4.22.- / Caspase 3; PQ6CK8PD0R / Ascorbic Acid; Q20Q21Q62J / Cisplatin; S65743JHBS / gefitinib; YL5FZ2Y5U1 / Methotrexate
72.
Kwaan HC:
Double hazard of thrombophilia and bleeding in leukemia.
Hematology Am Soc Hematol Educ Program
; 2007;:151-7
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[Title]
Double hazard of thrombophilia and bleeding in
leukemia
.
Thrombotic complications in
acute leukemia
are often overlooked because bleeding complications generally dominate the
clinical
picture.
While there are many thrombogenic factors shared by both solid tumors and
leukemia
, many additional prothrombotic features are present in
leukemia
.
In addition, comorbid conditions including hereditary thrombophilia, infection, endothelial cell activation by cytokines,
antiphospholipid
syndrome and acquired activated protein C resistance are major contributory factors.
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(PMID = 18024623.001).
[ISSN]
1520-4391
[Journal-full-title]
Hematology. American Society of Hematology. Education Program
[ISO-abbreviation]
Hematology Am Soc Hematol Educ Program
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
44
73.
Basova LV, Kurnikov IV, Wang L, Ritov VB, Belikova NA, Vlasova II, Pacheco AA, Winnica DE, Peterson J, Bayir H, Waldeck DH, Kagan VE:
Cardiolipin switch in mitochondria: shutting off the reduction of cytochrome c and turning on the peroxidase activity.
Biochemistry
; 2007 Mar 20;46(11):3423-34
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Upon interaction
with anionic phospholipids
, particularly mitochondria-specific cardiolipin (
CL
), cytochrome c (cyt c) loses its tertiary structure and its peroxidase activity dramatically increases.
CL
-induced peroxidase activity of cyt c has been found to be important for selective
CL
oxidation in cells undergoing programmed death.
During apoptosis, the peroxidase activity and the fraction of
CL
-bound cyt c markedly increase, suggesting that
CL
may act as a switch to regulate cyt c's mitochondrial functions.
Using cyclic voltammetry and equilibrium redox titrations, we show that the redox potential of cyt c shifts negatively by 350-400 mV upon binding to
CL
-containing membranes.
Further,
CL
/cyt c complexes are not effective in scavenging superoxide anions and are not effectively reduced by ascorbate.
Thus, both redox properties and functions of cyt c change upon interaction
with CL
in the mitochondrial membrane, diminishing cyt c's electron donor/acceptor role and stimulating its peroxidase activity.
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(PMID = 17319652.001).
[ISSN]
0006-2960
[Journal-full-title]
Biochemistry
[ISO-abbreviation]
Biochemistry
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01 HL070755; United States / NIOSH CDC HHS / OH / R01 OH008282; United States / NIAID NIH HHS / AI / U19 AI068021; United States / NIAID NIH HHS / AI / U19 AI 068021; None / None / / R01 HL070755-08; United States / NHLBI NIH HHS / HL / R01 HL061411; United States / NHLBI NIH HHS / HL / HL 61411; United States / NHLBI NIH HHS / HL / HL 70755; United States / NIOSH CDC HHS / OH / OH 008282; United States / NHLBI NIH HHS / HL / R01 HL070755-08
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / 1,1',2,2'-tetraoleoylcardiolipin; 0 / Cardiolipins; 0 / Liposomes; 9007-43-6 / Cytochromes c; EC 1.11.1.- / Peroxidases; EC 1.9.3.1 / Electron Transport Complex IV; PQ6CK8PD0R / Ascorbic Acid
[Other-IDs]
NLM/ NIHMS62066; NLM/ PMC3356783
74.
Varjo SJ, Hautala JT, Wiedmer SK, Riekkola ML:
Small diamines as modifiers for phosphatidylcholine/phosphatidylserine coatings in capillary electrochromatography.
J Chromatogr A
; 2005 Jul 15;1081(1):92-8
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The
phospholipid
coatings consisted of 1 mM of 8:2 mol% phosphatidylcholine (PC)/phosphatidylserine (PS) and 5 mM of modifier in buffer solutions (acetate, phosphate, or Tris) at pH 4.0-7.4.
The results showed that under optimal conditions, the small linear diamines increased the packing density of
anionic phospholipids
, leading to improved separations.
While buffers with amino groups take part in the
phospholipid
bilayer formation, buffers like phosphate may even have negative effect on coating formation.
The factors affecting
phospholipid
coatings with diamines as modifiers are clarified.
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(PMID = 16013604.001).
[ISSN]
0021-9673
[Journal-full-title]
Journal of chromatography. A
[ISO-abbreviation]
J Chromatogr A
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Buffers; 0 / Coated Materials, Biocompatible; 0 / Diamines; 0 / Ethylenediamines; 0 / Liposomes; 0 / Phosphatidylcholines; 0 / Phosphatidylserines; 0 / Steroids; 023C2WHX2V / Tromethamine; 60V9STC53F / ethylenediamine; 64431-96-5 / 1,3-bis(tris(hydroxymethyl)methylamino)propane; CB3ISL56KG / trimethylenediamine; RWW266YE9I / HEPES
75.
Zhong Q, Gvozdenovic-Jeremic J, Webster P, Zhou J, Greenberg ML:
Loss of function of KRE5 suppresses temperature sensitivity of mutants lacking mitochondrial anionic lipids.
Mol Biol Cell
; 2005 Feb;16(2):665-75
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[Title]
Loss of function of KRE5 suppresses temperature sensitivity of mutants lacking mitochondrial
anionic
lipids.
Disruption of PGS1, which encodes the enzyme that catalyzes the committed step of cardiolipin (
CL
) synthesis, results in loss of the mitochondrial
anionic phospholipids
phosphatidylglycerol (PG) and
CL
.
To understand the essential functions of mitochondrial
anionic
lipids at elevated temperatures, we isolated suppressors of pgs1Delta that grew at 37 degrees C.
Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1Delta and suppressed the temperature sensitivity of all
CL
-deficient mutants.
These findings demonstrated that mitochondrial
anionic
lipids are required for cellular functions that are essential in cell wall biogenesis, the maintenance of cell integrity, and survival at elevated temperature.
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[ISSN]
1059-1524
[Journal-full-title]
Molecular biology of the cell
[ISO-abbreviation]
Mol. Biol. Cell
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01 HL062263; United States / NHLBI NIH HHS / HL / HL-62263
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Anions; 0 / Antigens, Bacterial; 0 / Cardiolipins; 0 / Codon, Nonsense; 0 / Enzyme Inhibitors; 0 / Fluorescent Dyes; 0 / Glycoproteins; 0 / Indoles; 0 / KRE5 protein, S cerevisiae; 0 / Phosphatidylglycerols; 0 / Polysaccharides, Bacterial; 0 / Saccharomyces cerevisiae Proteins; 0 / beta-Glucans; 0 / capsular polysaccharide K1; 1398-61-4 / Chitin; 47165-04-8 / DAPI; 9051-97-2 / beta-1,3-glucan; 9Z22C3QQCJ / nikkomycin
[Other-IDs]
NLM/ PMC545902
76.
Rantalainen KI, Christensen PA, Hafrén A, Otzen DE, Kalkkinen N, Mäkinen K:
Interaction of a potyviral VPg with anionic phospholipid vesicles.
Virology
; 2009 Dec 5;395(1):114-20
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[Title]
Interaction of a potyviral VPg
with anionic phospholipid
vesicles.
Typically, this
type
of protein gains a more stable structure upon interactions or posttranslational modifications.
It is possible that this stabilization favored the formation of
alpha
-helical structures.
Limited tryptic digestion showed that the interaction
with anionic
vesicles protected certain, otherwise accessible, trypsin cleavage sites.
[MeSH-major]
Phospholipids
/ metabolism. Potyviridae / metabolism. Ribonucleoproteins / metabolism. Viral Nonstructural Proteins / metabolism
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(PMID = 19800647.001).
[ISSN]
1096-0341
[Journal-full-title]
Virology
[ISO-abbreviation]
Virology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Phospholipids; 0 / Ribonucleoproteins; 0 / Viral Nonstructural Proteins
77.
Mora JR, Knoll JH, Rogan PK, Getts RC, Wilson GS:
Dendrimer FISH detection of single-copy intervals in acute promyelocytic leukemia.
Mol Cell Probes
; 2006 Apr;20(2):114-20
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[Title]
Dendrimer FISH detection of single-copy intervals in
acute promyelocytic leukemia
.
Acute promyelocytic leukemia
(
AML
-
M3
) is characterized by a translocation between chromosomes
15
and
17
[t(
15
;
17
)].
The detection of t(
15
;
17
) at the single cell
level
, is commonly done by fluorescence in situ hybridization (FISH) using recombinant locus specific genomic probes greater than 14 kilobases kb in length.
To allow a more thorough study of t(
15
;
17
), we designed small (0.9-3.6 kb), target-specific, single-copy probes from the human genome sequence.
(1) dendrimers modified
with anti
-biotin antibodies for detection of biotinylated bound probes, and (2) dendrimers modified with 45-base long oligonucleotides designed from the single-copy probes, for direct detection of the target region.
Furthermore, the scFISH probes were successfully detected on metaphase cells
with anti
-biotin dendrimer conjugates and on interphase cells with 45-base modified dendrimers.
[MeSH-major]
Genome, Human.
Leukemia
,
Promyelocytic
,
Acute
/ genetics. Translocation, Genetic
[MeSH-minor]
Cell Line, Tumor. Chromosomes, Human, Pair
15
/ genetics. Chromosomes, Human, Pair
17
/ genetics. DNA Probes / chemistry. Dendrimers / chemistry. Humans. In Situ Hybridization, Fluorescence. Interphase. Metaphase
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(PMID = 16460913.001).
[ISSN]
0890-8508
[Journal-full-title]
Molecular and cellular probes
[ISO-abbreviation]
Mol. Cell. Probes
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / GM08359
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Probes; 0 / Dendrimers
78.
Shishido-Hara Y, Higuchi K, Ohara S, Duyckaerts C, Hauw JJ, Uchihara T:
Promyelocytic leukemia nuclear bodies provide a scaffold for human polyomavirus JC replication and are disrupted after development of viral inclusions in progressive multifocal leukoencephalopathy.
J Neuropathol Exp Neurol
; 2008 Apr;67(4):299-308
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[Title]
Promyelocytic leukemia
nuclear bodies provide a scaffold for human polyomavirus JC replication and are disrupted after development of viral inclusions in progressive multifocal leukoencephalopathy.
Progressive multifocal leukoencephalopathy is a fatal demyelinating
disorder
due to human polyomavirus JC infection in which there are viral inclusions in enlarged nuclei of infected oligodendrocytes.
We report that the pathogenesis of this
disease
is associated with distinct subnuclear structures known as
promyelocytic leukemia
nuclear bodies (
PML
-NBs).
Postmortem brain tissues from 5 patients with the
disease
were examined.
Affected cells with enlarged nuclei contained distinct dot-like subnuclear
PML
-NBs that were immunopositive for
PML
protein and nuclear body protein Sp100.
Major and minor viral capsid proteins and proliferating cell nuclear antigen, an essential component for DNA replication, colocalized
with PML
-NBs.
By in situ hybridization, viral genomic DNA showed dot-like nuclear accumulation, and by electron microscopy, virus-like structures clustered in subnuclear domains, indicating that
PML
-NBs are the site of viral DNA replication and capsid assembly.
When viral progeny production was advanced,
PML
-NBs were disrupted.
1)
PML
-NBs allow for efficient viral propagation by providing scaffolds, 2) disruption of
PML
-NBs is independent of the ubiquitin-proteasome pathway, and 3) this disruption probably heralds oligodendrocyte degeneration and the resulting demyelination.
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(PMID = 18379438.001).
[ISSN]
0022-3069
[Journal-full-title]
Journal of neuropathology and experimental neurology
[ISO-abbreviation]
J. Neuropathol. Exp. Neurol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Capsid Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Ubiquitin; 143220-95-5 / PML protein, human
79.
Terashi H, Hashimoto S, Uchiyama S:
[Beta2-glycoprotein I polymorphism].
Brain Nerve
; 2008 Nov;60(11):1333-8
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In our study, stroke patients
with antiphospholipid
antibodies (
APL
) were significantly younger and were more likely to be women than stroke patients without
APL
.
Valvular heart
disease
, neurological complications, and hematological disorders were more frequent in the
APL
-positive group.
The mean value of thrombin-antithrombin III complex was significantly lower in the
APL
-positive group. beta2-Glyoprotein I (beta2-GPI) is the antigen primarily responsible for
APL
.
At the DNA
level
, 4 different types of allelic polymorphisms have been detected in beta2-GPI.
[MeSH-minor]
Adult. Alleles. Antibodies,
Antiphospholipid
/ genetics.
Antiphospholipid
Syndrome / genetics. Female. Genotype. Humans. Leucine / genetics. Male. Middle Aged. Platelet Factor 4. Risk Factors. Valine / genetics. beta-Thromboglobulin
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.
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.
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L-Valine
.
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.
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(PMID = 19069167.001).
[ISSN]
1881-6096
[Journal-full-title]
Brain and nerve = Shinkei kenkyū no shinpo
[ISO-abbreviation]
Brain Nerve
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / beta 2-Glycoprotein I; 0 / beta-Thromboglobulin; 37270-94-3 / Platelet Factor 4; GMW67QNF9C / Leucine; HG18B9YRS7 / Valine
[Number-of-references]
22
80.
Vogrinc Z, Trbojević-Cepe M, Coen D, Vitale K, Stavljenić-Rukavina A:
Apolipoprotein H (apoH)-dependent autoantibodies and apoH protein polymorphism in selected patients showing lupus anticoagulant activity.
Clin Chem Lab Med
; 2005;43(1):17-21
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Apolipoprotein H (apoH) is considered to be a necessary cofactor for the binding of certain
antiphospholipid
antibodies to
anionic phospholipids
.
Some apoH-dependent
antiphospholipid
antibodies also exert lupus anticoagulant (LA) activity, which seems to depend on
antiphospholipid
antibody epitope specificity.
We selected patients with confirmed LA activity and none or low titers of anticardiolipin antibodies that had been sent to the laboratory for routine
antiphospholipid
antibody determination.
Many of them had some
clinical
manifestation of
antiphospholipid
syndrome.
Antibodies to apoH were determined
with a
commercially available anticardiolipin/apoH ELISA kit.
Our results showed that 47/74 (63.5%) of our selected LA-positive patients also had elevated apoH-dependent
antiphospholipid
antibody titers.
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(PMID = 15653437.001).
[ISSN]
1434-6621
[Journal-full-title]
Clinical chemistry and laboratory medicine
[ISO-abbreviation]
Clin. Chem. Lab. Med.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Autoantibodies; 0 / Glycoproteins; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / Protein Isoforms; 0 / beta 2-Glycoprotein I
81.
Membre A, Wahl D, Latger-Cannard V, Max JP, Lacolley P, Lecompte T, Regnault V:
The effect of platelet activation on the hypercoagulability induced by murine monoclonal antiphospholipid antibodies.
Haematologica
; 2008 Apr;93(4):566-73
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[Title]
The effect of platelet activation on the hypercoagulability induced by murine monoclonal
antiphospholipid
antibodies.
BACKGROUND: To identify the mechanisms of the hypercoagulability associated
with antiphospholipid
antibodies, we investigated antibody-mediated platelet activation and interference of antibodies
with phospholipid
-dependent reactions.
Platelet activation was assessed by
phospholipid
-related platelet procoagulant activity.
RESULTS: Both monoclonal antibodies mimicked the effect of IgG in 11 out of a series of 40 patients
with antiphospholipid
antibodies in thrombography.
In the presence of their target, 7F6G and 28F4 at 200 microg/mL exhibited comparatively low and high binding to platelets and elicited low and high
levels
of procoagulant
phospholipids
on platelet surface, respectively.
In platelet-poor
plasma
, these antibodies induced a 1.6 and >
12
-fold increase in IC(50)-APC, respectively, thus providing evidence for a procoagulant effect independent of platelet activation.
In platelet-rich
plasma
, this anticoagulant effect was significantly less (23% decrease in ETP(0)), demonstrating that a high increase in procoagulant surfaces by platelet activation significantly antagonizes the anticoagulant effect of
antiphospholipid
antibodies.
In both types of
plasma
, the inhibition of thrombin generation (reduced ETP(0)) was less than the inhibition of activated protein C activity (increased IC(50)-APC).
CONCLUSIONS: Our findings show that platelet activation reinforces the hypercoagulability induced by competition between
antiphospholipid
antibodies/target complexes and pro- and anticoagulant complexes for
phospholipid
surfaces.
[MeSH-major]
Antibodies,
Antiphospholipid
/ pharmacology. Blood Coagulation / drug effects. Immunoglobulin G / pharmacology. Platelet Activation / drug effects. Thrombophilia / immunology
[MeSH-minor]
Animals. Antibody Specificity. Blood Platelets / immunology. Humans. Lupus Coagulation Inhibitor / physiology. Mice.
Phospholipids
/ physiology. Platelet-Rich
Plasma
. Protein C / physiology. Prothrombin / immunology. Thrombin / biosynthesis. Thrombin Time. beta 2-Glycoprotein I / immunology
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(PMID = 18322249.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Immunoglobulin G; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids; 0 / Protein C; 0 / beta 2-Glycoprotein I; 9001-26-7 / Prothrombin; EC 3.4.21.5 / Thrombin
82.
Dore AI, Santana-Lemos BA, Coser VM, Santos FL, Dalmazzo LF, Lima AS, Jacomo RH, Elias J Jr, Falcão RP, Pereira WV, Rego EM:
The association of ICAM-1 Exon 6 (E469K) but not of ICAM-1 Exon 4 (G241R) and PECAM-1 Exon 3 (L125V) polymorphisms with the development of differentiation syndrome in acute promyelocytic leukemia.
J Leukoc Biol
; 2007 Nov;82(5):1340-3
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[Title]
The association of ICAM-1 Exon 6 (E469K) but not of ICAM-1 Exon 4 (G241R) and PECAM-1 Exon 3 (L125V) polymorphisms with the development of differentiation syndrome in
acute promyelocytic leukemia
.
The use of all trans-retinoic acid (ATRA) is the basis of treatment of
acute promyelocytic leukemia
(
APL
) and represents the paradigm of differentiation therapy.
In general, ATRA is well-tolerated but may be associated
with a
potentially lethal side-effect, referred to as retinoic acid or differentiation syndrome (DS).
As leukocyte extravasation is a key event in DS pathogenesis, we analyzed the association between the polymorphisms at Exon 4 (G241R) and Exon 6 (E469K) of ICAM-1 and Exon 3 (L125V) of PECAM-1 genes with DS development in
APL
patients treated with ATRA and anthracyclines.
DS was diagnosed in 23/127 (18.1%)
APL
patients at an average of 11.5 days after the start of ATRA.
Our results suggest that susceptibility to DS in
APL
patients may be influenced by genetic variation in adhesion molecule loci.
[MeSH-major]
Antigens, CD31 / genetics. Exons / genetics. Intercellular Adhesion Molecule-1 / genetics.
Leukemia
,
Promyelocytic
,
Acute
/ genetics. Polymorphism, Genetic / genetics
[MeSH-minor]
Adult. Antineoplastic Agents / adverse effects. Cell Differentiation.
Diagnosis
, Differential. Female. Humans. Male. Syndrome. Tretinoin / adverse effects
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(PMID = 17704297.001).
[ISSN]
0741-5400
[Journal-full-title]
Journal of leukocyte biology
[ISO-abbreviation]
J. Leukoc. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD31; 0 / Antineoplastic Agents; 126547-89-5 / Intercellular Adhesion Molecule-1; 5688UTC01R / Tretinoin
83.
Han DH, Kim JH:
Difference in growth suppression and apoptosis induction of EGCG and EGC on human promyelocytic leukemia HL-60 cells.
Arch Pharm Res
; 2009 Apr;32(4):543-7
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[Title]
Difference in growth suppression and apoptosis induction of EGCG and EGC on human
promyelocytic leukemia
HL-60 cells.
Growth suppression and apoptosis inducing effect of (-)-epigallocatechin 3-gallate (EGCG) and (-)-epigallocatechin (EGC) were studied against human promyeolcytic
leukemia
, HL-60 cells.
The expression
level
of Bcl-2 was decreased and caspase-3 was activated by EGCG or EGC treatment.
[MeSH-major]
Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Catechin / analogs & derivatives. Cell Proliferation / drug effects.
Leukemia
,
Promyelocytic
,
Acute
/ pathology
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(PMID = 19407972.001).
[ISSN]
0253-6269
[Journal-full-title]
Archives of pharmacal research
[ISO-abbreviation]
Arch. Pharm. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 1617-55-6 / gallocatechol; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
84.
Podrazilová L, Peterová V, Olejárová M, Seidl Z, Dostál C:
[Antiphospholipid syndrome--the description of two cases].
Vnitr Lek
; 2006 Jan;52(1):89-94
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[Title]
[
Antiphospholipid
syndrome--the description of two cases].
Antiphospholipid
syndrome (APS) often occurs in young people, it is defined by the presence of venous or arterial thromboses, repeated miscarriages, thrombocytopenias and increased
levels
of
antiphospholipid
antibodies.
Clinical
symptoms are different, there is often experienced the phlebothrombosis of lower limbs, miscarriages or neurological symptoms characterized by transient ischemic attacks (TIA).
If APS is associated with other system
disease
, most often with systemic lupus erythematosus (SLE), it is called secondary APS.
At another elder patient there was stated the
diagnosis
of non-differentiated
disease
of bonding agent with secondary APS with cardial, pneumonic and neurological
clinical
symptoms.
[MeSH-major]
Antiphospholipid
Syndrome /
diagnosis
[MeSH-minor]
Adult. Aged. Antibodies,
Antiphospholipid
/ analysis. Female. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic /
diagnosis
. Lupus Erythematosus, Systemic / immunology
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[CommentIn]
Vnitr Lek. 2006 Jan;52(1):17-20
[
16526193.001
]
(PMID = 16526206.001).
[ISSN]
0042-773X
[Journal-full-title]
Vnitr̆ní lékar̆ství
[ISO-abbreviation]
Vnitr Lek
[Language]
cze
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Czech Republic
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid
85.
Guvendag Guven ES, Okur H, Beksac MS:
Placental fas/fas ligand expression in early pregnancy losses.
Am J Reprod Immunol
; 2008 Jul;60(1):1-7
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[Title]
Placental fas/fas
ligand
expression in early pregnancy losses.
PROBLEM: The aim of this study was to compare the expression
levels
of Fas and Fas
ligand
(FasL) in first-trimester placentas obtained from spontaneous abortions in patients
with antiphospholipid
antibody syndrome (APS) or factor V (FV) Leiden mutation, compared with values in placentas from induced abortions in patients negative for these conditions.
[MeSH-major]
Abortion, Spontaneous / metabolism. Antigens, CD95 / biosynthesis. Fas
Ligand
Protein / biosynthesis. Placenta / metabolism
[MeSH-minor]
Antiphospholipid
Syndrome / complications. Factor V / metabolism. Female. Flow Cytometry. Fluorescent Antibody Technique. Humans. Immune Tolerance / physiology. Pregnancy. Pregnancy Trimester, First
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.
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(PMID = 18422813.001).
[ISSN]
1046-7408
[Journal-full-title]
American journal of reproductive immunology (New York, N.Y. : 1989)
[ISO-abbreviation]
Am. J. Reprod. Immunol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / factor V Leiden; 9001-24-5 / Factor V
86.
Bozic B, Cucnik S, Kveder T, Rozman B:
Avidity of anti-beta-2-glycoprotein I antibodies.
Autoimmun Rev
; 2005 Jun;4(5):303-8
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[Title]
Avidity of
anti
-beta-2-glycoprotein I antibodies.
Since affinity refers to monovalent binding of antibodies to a monovalent epitope, the majority of data on the binding of
anti
-beta2-glycoprotein I antibodies (
anti
-beta2-GPI) characterized their avidity rather than affinity.
Anti
-beta2-GPI were generally believed to be of low avidity, but heterogeneous avidity of patients' IgG
anti
-beta2-GPI has been demonstrated.
High avidity
anti
-beta2-GPI monoclonals were reported to possess higher pathogenicity than low avidity
anti
-beta2-GPI.
Polyclonal high avidity
anti
-beta2-GPI were found to be more common in patients
with antiphospholipid
syndrome (APS) and associated with thrombosis.
Some conformational changes of beta2-GPI are required for the binding of polyclonal
anti
-beta2-GPI to the antigen: neither high density of the antigen nor high avidity of the
anti
-beta2-GPI alone is sufficient for the recognition.
Avidity of
anti
-beta2-GPI should be considered in any attempt of inter-laboratory standardisation and/or evaluation of
anti
-beta2-GPI enzyme-linked immunosorbent assay (ELISA).
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(PMID = 15990078.001).
[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 / Autoantibodies; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I
[Number-of-references]
40
87.
Yamasaki Y, Narain S, Yoshida H, Hernandez L, Barker T, Hahn PC, Sobel ES, Segal MS, Richards HB, Chan EK, Reeves WH, Satoh M:
Autoantibodies to RNA helicase A: a new serologic marker of early lupus.
Arthritis Rheum
; 2007 Feb;56(2):596-604
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OBJECTIVE: To investigate the
clinical
and immunologic significance of autoantibodies to RNA helicase A (RHA) in patients with systemic rheumatic diseases.
RESULTS:
Anti
-RHA was observed in
17
(6.2%) of 276 patients with systemic lupus erythematosus (SLE), 2 patients
with antiphospholipid
antibodies, and 3 other patients, but
anti
-RHA was not observed in any patient with polymyositis/dermatomyositis, systemic sclerosis, rheumatoid arthritis, or Sjögren's syndrome.
Anti
-RHA was present in only 2.9% of African American patients, compared with 6.0% of white patients and
12
-25% of patients of other races; this was in striking contrast to the frequency of
anti
-Sm in African American patients (27.2%).
Among patients with SLE,
anti
-RHA was common in young patients (26% of those whose initial visit was at an age younger than 20 years versus 3-4% of those who were initially seen at ages 20-49 years) and at an early stage of
disease
(23% of those whose first clinic visit was within 1 year of
disease
onset versus 2-8% of those whose first visit was at least 1 year after
disease
onset).
In 9 of 11 patients,
levels
of
anti
-RHA decreased to <10% of the initial value within 9-37 months, while
levels
of coexisting
anti
-Ro or
anti
-Su remained the same.
New specificities developed in 2 patients (
anti
-nuclear RNP and
anti
-Sm, and
anti
-ribosomal P, respectively).
These data suggest that the
level
of
anti
-RHA diminishes over time, and that
anti
-RHA is regulated via a mechanism different from that for other lupus-related autoantibodies.
CONCLUSION:
Anti
-RHA is a new serologic marker for SLE.
It is produced mainly in young non-African Americans at an early stage of their
disease
.
Anti
-RHA has a unique tendency to diminish over time.
The production of
anti
-RHA may depend on a process restricted to early SLE, or it may be highly sensitive to treatment.
[MeSH-major]
Autoantibodies / blood. DEAD-box RNA Helicases / immunology. Lupus Erythematosus, Systemic /
diagnosis
. Lupus Erythematosus, Systemic / immunology. Neoplasm Proteins / immunology
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(PMID = 17265494.001).
[ISSN]
0004-3591
[Journal-full-title]
Arthritis and rheumatism
[ISO-abbreviation]
Arthritis Rheum.
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / AI-39645; United States / NIAID NIH HHS / AI / AI-47859; United States / NIAMS NIH HHS / AR / AR-050661; United States / NIAMS NIH HHS / AR / AR-40391; United States / NCRR NIH HHS / RR / M01-RR-00082
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Autoantibodies; 0 / Autoantigens; 0 / Neoplasm Proteins; 0 / Ribonucleoproteins, Small Nuclear; 0 / snRNP Core Proteins; EC 3.6.1.- / DHX9 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
88.
Surga N, Makdassi R, Choukroun G, Vandwalle J, Petit J, Saint F:
[Adrenal hemorrhage acutised by adrenocorticotropin hormone].
Prog Urol
; 2010 Jun;20(6):425-9
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We associated
a clinical
, endocrine and radiologic staging to treat those patients.
Two patients suffered of the condition of the
antiphospholipid
syndrome.
The
clinical
attitude has thus to be defined clearly.
The patient must be under close
clinical
evaluation.
Antiphospholipid
syndrome must also be excluded.
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.
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[Copyright]
Copyright 2010 Elsevier Masson SAS. All rights reserved.
(PMID = 20538206.001).
[ISSN]
1166-7087
[Journal-full-title]
Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
[ISO-abbreviation]
Prog. Urol.
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Hormones; 16960-16-0 / Cosyntropin; 53468-06-7 / adrenocorticotropin zinc
89.
Binet F, Girard D:
Novel human neutrophil agonistic properties of arsenic trioxide: involvement of p38 mitogen-activated protein kinase and/or c-jun NH2-terminal MAPK but not extracellular signal-regulated kinases-1/2.
J Leukoc Biol
; 2008 Dec;84(6):1613-22
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Arsenic trioxide (ATO) is known for treating
acute promyelocytic leukemia
and for inducing apoptosis and mitogen-activated protein kinases (MAPKs) in promyelocytes and cancer cells.
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ARSENIC TRIOXIDE
.
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CALCIUM, ELEMENTAL
.
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HYDROGEN PEROXIDE
.
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(PMID = 18728151.001).
[ISSN]
0741-5400
[Journal-full-title]
Journal of leukocyte biology
[ISO-abbreviation]
J. Leukoc. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Reactive Oxygen Species; BBX060AN9V / Hydrogen Peroxide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; 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; EC 3.4.24.- / Gelatinases; S7V92P67HO / arsenic trioxide; SY7Q814VUP / Calcium
90.
Gigante A, Gasperini ML, Cianci R, Barbano B, Giannakakis K, Di Donato D, Fuiano G, Amoroso A:
Antiphospholipid antibodies and renal involvement.
Am J Nephrol
; 2009;30(5):405-12
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[Title]
Antiphospholipid
antibodies and renal involvement.
Antiphospholipid
antibodies are a heterogeneous group of autoantibodies associated with the hypercoagulable state affecting all vascular districts with thrombosis named
antiphospholipid
syndrome (APS).
APS is an autoimmune
disease with
multifactorial etiology that includes cellular, molecular, genetic and pathogenic mechanisms.
The APS
clinical
features are a combination of arterial and/or venous thrombosis, hematological events, recurrent fetal losses, neurological disorders and intra-abdominal manifestations.
Clinical
features include hypertension, renal artery stenosis, thrombotic microangiopathy and other histological manifestations of the nephropathy (APSN), venous renal thrombosis, APSN in the course of systemic lupus erythematosus and renal failure.
APSN is an independent risk factor that should be included in the classification criteria for definite APS with characteristic
clinical
and histological features.
[MeSH-major]
Antibodies,
Antiphospholipid
/ blood.
Antiphospholipid
Syndrome / immunology. Kidney / immunology. Kidney Diseases / immunology
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[Copyright]
Copyright 2009 S. Karger AG, Basel.
(PMID = 19713697.001).
[ISSN]
1421-9670
[Journal-full-title]
American journal of nephrology
[ISO-abbreviation]
Am. J. Nephrol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid
[Number-of-references]
40
91.
O'Neil KM:
High-intensity warfarin versus conventional antithrombotic therapy to prevent thrombosis in antiphospholipid syndrome.
Curr Rheumatol Rep
; 2007 Jun;9(3):188-9
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[Title]
High-intensity warfarin versus conventional antithrombotic therapy to prevent thrombosis in
antiphospholipid
syndrome.
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[CommentOn]
Lupus. 2005;14(2):120-8
[
15751816.001
]
(PMID = 17531170.001).
[ISSN]
1523-3774
[Journal-full-title]
Current rheumatology reports
[ISO-abbreviation]
Curr Rheumatol Rep
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
92.
Bhowmik D, Dadhwal V, Dinda AK, Handa R, Dash SC:
Steroid-responsive focal segmental glomerulosclerosis in primary antiphospholipid syndrome with successful pregnancy outcome.
Nephrol Dial Transplant
; 2005 Aug;20(8):1726-8
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[Title]
Steroid-responsive focal segmental glomerulosclerosis in primary
antiphospholipid
syndrome with successful pregnancy outcome.
[MeSH-major]
Antiphospholipid
Syndrome / drug therapy. Glomerulosclerosis, Focal Segmental / drug therapy. Glucocorticoids / therapeutic use. Nephrotic Syndrome / drug therapy. Pregnancy Complications
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.
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.
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.
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PREDNISOLONE
.
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(PMID = 15919690.001).
[ISSN]
0931-0509
[Journal-full-title]
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
[ISO-abbreviation]
Nephrol. Dial. Transplant.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Glucocorticoids; 9PHQ9Y1OLM / Prednisolone
93.
Jovanović M, Bozić M, Kovacević T, Radojcić L, Petronijević M, Vićovac L:
Effects of anti-phospholipid antibodies on a human trophoblast cell line (HTR-8/SVneo).
Acta Histochem
; 2010;112(1):34-41
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[Title]
Effects of
anti
-
phospholipid
antibodies on a human trophoblast cell line (HTR-8/SVneo).
Antibodies to
phospholipids
(
aPL
) have been shown to adversely affect trophoblast invasion in vivo and in vitro.
Matrigel invasion assay, cytochemistry and cell-based enzyme-linked immunosorbant assay (ELISA)
with aPL
or normal IgG was used.
Our data show that
aPL
at 100 microg/ml decrease invasiveness of HTR-8/SVneo cells to 60% of control (p<0.01), and this was also shown for primary cytotrophoblast (to
15
.5% of control, p<0.001).
aPL
treatment caused a significant decrease in integrin
alpha
(1),
alpha
(5), and beta(1) proteins (86%, 84%, and 87%, respectively).
We conclude that HTR-8/SVneo cell culture is a suitable model to study mechanisms of action of
aPL
on trophoblast, which in HTR-8/SVneo cells inhibit invasion by decreasing integrins
alpha
(5),
alpha
(1), and beta(1).
[MeSH-major]
Antibodies,
Antiphospholipid
/ pharmacology. Trophoblasts / cytology. Trophoblasts / drug effects
[MeSH-minor]
Antigens, CD29 / metabolism. Cell Line. Cell Survival / drug effects. Female. Humans. Integrin
alpha
Chains / metabolism. Pregnancy. Pregnancy Trimester, First
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[Copyright]
2008 Elsevier GmbH. All rights reserved.
(PMID = 18835012.001).
[ISSN]
1618-0372
[Journal-full-title]
Acta histochemica
[ISO-abbreviation]
Acta Histochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Antigens, CD29; 0 / Integrin alpha Chains
94.
Rangachari V, Reed DK, Moore BD, Rosenberry TL:
Secondary structure and interfacial aggregation of amyloid-beta(1-40) on sodium dodecyl sulfate micelles.
Biochemistry
; 2006 Jul 18;45(28):8639-48
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Alzheimer'
s disease
(AD) is characterized by the presence of large numbers of fibrillar amyloid deposits in the form of senile plaques in the brain.
Here we compared the Abeta(1-40) aggregates produced on sodium dodecyl sulfate (SDS) micelles, which may be a better model of biological membranes
with phospholipids
that have
anionic
headgroups.
At both HFIP and SDS interfaces, changes in
peptide
secondary structure were observed by CD immediately when Abeta(1-40) was introduced.
With HFIP, the change involved an increase in predominant beta-structure content and in fluorescence with thioflavin T, while with SDS, a partial
alpha
-helical conformation was adopted that gave no fluorescence.
[MeSH-major]
Amyloid beta-Peptides / chemistry. Micelles.
Peptide
Fragments / chemistry. Sodium Dodecyl Sulfate / chemistry
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(PMID = 16834338.001).
[ISSN]
0006-2960
[Journal-full-title]
Biochemistry
[ISO-abbreviation]
Biochemistry
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Amyloid beta-Peptides; 0 / Micelles; 0 / Peptide Fragments; 0 / Propanols; 0 / amyloid beta-protein (1-40); 368GB5141J / Sodium Dodecyl Sulfate; 920-66-1 / hexafluoroisopropanol
95.
Duman D, Demirtunc R, Duman D, Sungur F, Agirbasli M, Cakmak M:
Paradoxical mesentery embolism and silent myocardial infarction in primary antiphospholipid syndrome: a case report.
Heart Surg Forum
; 2006;9(2):E592-4
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[Title]
Paradoxical mesentery embolism and silent myocardial infarction in primary
antiphospholipid
syndrome: a case report.
In this case, we describe a 33-year-old man presenting with
acute
mesenteric ischemia.
Coronary angiography revealed complete occlusion of the left
anterior
descending artery.
The
diagnosis
of primary
antiphospholipid
syndrome was confirmed by anticardiolipin antibodies test.
This is the first reported case presenting with
acute
paradoxical mesentery embolism accompanying an old myocardial infarction in a young patient with primary
antiphospholipid
syndrome.
[MeSH-major]
Antiphospholipid
Syndrome / complications. Embolism, Paradoxical / complications. Embolism, Paradoxical /
diagnosis
. Mesenteric Vascular Occlusion / complications. Mesenteric Vascular Occlusion /
diagnosis
. Myocardial Infarction / complications. Myocardial Infarction /
diagnosis
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(PMID = 16543157.001).
[ISSN]
1522-6662
[Journal-full-title]
The heart surgery forum
[ISO-abbreviation]
Heart Surg Forum
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
96.
Rückert A, Glimm H, Lübbert M, Grüllich C:
Successful treatment of life-threatening Evans syndrome due to antiphospholipid antibody syndrome by rituximab-based regimen: a case with long-term follow-up.
Lupus
; 2008 Aug;17(8):757-60
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[Title]
Successful treatment of life-threatening Evans syndrome due to
antiphospholipid
antibody syndrome by rituximab-based regimen: a case with long-term follow-up.
An association of
antiphospholipid
antibody syndrome with antibodies directed against either
phospholipids
or
plasma
proteins strongly suggest that B-cell dysfunction may be involved in its pathogenesis.
Antiphospholipid
antibody syndrome with autoimmune cytopenias shows a poor response rate to conventional treatment with anticoagulants, glucocorticosteroids, immunosuppressive agents, intravenous immunoglobulin or plasmapheresis.
We report a case of life-threatening
antiphospholipid
antibody syndrome with Evans syndrome receiving successful multimodal treatment including
anti
-CD20 monoclonal antibody rituximab with long-term follow-up.
[MeSH-major]
Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use.
Antiphospholipid
Syndrome / complications. Thrombocytopenia / drug therapy
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.
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(PMID = 18625656.001).
[ISSN]
0961-2033
[Journal-full-title]
Lupus
[ISO-abbreviation]
Lupus
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide
97.
Haferlach T, Kohlmann A, Schnittger S, Dugas M, Hiddemann W, Kern W, Schoch C:
AML M3 and AML M3 variant each have a distinct gene expression signature but also share patterns different from other genetically defined AML subtypes.
Genes Chromosomes Cancer
; 2005 Jun;43(2):113-27
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[Title]
AML M3
and
AML M3
variant each have a distinct gene expression signature but also share patterns different from other genetically defined
AML
subtypes.
Acute promyelocytic leukemia
(
APL
) with t(
15
;
17
) appears in two phenotypes:
AML M3
, with abnormal promyelocytes showing heavy granulation and bundles of Auer rods, and
AML M3
variant (M3v), with non- or hypogranular cytoplasm and a bilobed nucleus.
We investigated the global gene expression profiles of 35
APL
patients (19
AML M3
, 16
AML
M3v) by using high-density DNA-oligonucleotide microarrays.
First, an unsupervised approach clearly separated
APL
samples from other AMLs characterized genetically as t(8;21) (n = 35), inv(16) (n = 35), or t(11q23)/MLL (n = 35) or as having a normal karyotype (n = 50).
Second, we found genes with functional relevance for blood coagulation that were differentially expressed between
APL
and other AMLs.
Furthermore, a supervised pairwise comparison between
M3
and M3v revealed differential expression of genes that encode for biological functions and pathways such as granulation and maturation of hematologic cells, explaining
morphologic
and
clinical
differences.
Discrimination between
M3
and M3v based on gene signatures showed a median classification accuracy of 90% by use of 10-fold CV and support vector machines.
Additional molecular mutations such as FLT3-LM, which were significantly more frequent in M3v than in
M3
(P < 0.0001), may partly contribute to the different phenotypes.
However, linear regression analysis demonstrated that genes differentially expressed between
M3
and M3v did not correlate with FLT3-LM.
[MeSH-major]
Gene Expression Profiling.
Leukemia
,
Promyelocytic
,
Acute
/ genetics
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Blood Coagulation / genetics. Chromosomes, Human, Pair
15
. Chromosomes, Human, Pair
17
. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 15751046.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
98.
Alijotas-Reig J:
[The complement system as a main actor in the pathogenesis of obstetric antiphospholipid syndrome].
Med Clin (Barc)
; 2010 Jan 23;134(1):30-4
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[Title]
[The complement system as a main actor in the pathogenesis of obstetric
antiphospholipid
syndrome].
Pregnancy losses are the main obstetrical complications of the obstetric
antiphospholipid
syndrome (obstetric-APS).
Some cases have low
plasma
C4/C3
levels
.
The beta2-glycoprotein-I/
anti
-beta2-glycoprotein-I complexes activate both, classical and alternative complement pathways.
In the end, the role played in this binomial by certain pro-inflammatory cytokines, mainly TNF-
alpha
, remains to clarify.
[MeSH-major]
Antiphospholipid
Syndrome / immunology. Complement System Proteins / physiology. Pregnancy Complications / immunology
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[Copyright]
Copyright 2009 Elsevier España, S.L. All rights reserved.
(PMID = 19656533.001).
[ISSN]
0025-7753
[Journal-full-title]
Medicina clínica
[ISO-abbreviation]
Med Clin (Barc)
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Spain
[Chemical-registry-number]
9007-36-7 / Complement System Proteins
[Number-of-references]
38
99.
Sanmarco M, Bardin N, Camoin L, Beziane A, Dignat-George F, Gamerre M, Porcu G:
Antigenic profile, prevalence, and clinical significance of antiphospholipid antibodies in women referred for in vitro fertilization.
Ann N Y Acad Sci
; 2007 Jun;1108:457-65
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[Title]
Antigenic profile, prevalence, and
clinical
significance of
antiphospholipid
antibodies in women referred for in vitro fertilization.
The aim of this prospective study was to assess the prevalence of
antiphospholipid
antibodies (
aPL
) in women who had undergone in vitro fertilization (IVF) and the relationship between
aPL
and IVF outcome.
Out of the 101 infertile women, 40 were persistently positive for
aPL
, showing a prevalence significantly higher than in controls (39.6% versus 5%, P < 0.0001).
Among
aPL
, aPE were found
with a
significantly higher prevalence compared with LA, aCL, and aP2GPI (67.5% versus 0%,
15
%, and 40%, respectively).
Interestingly, aPE were found in 70% of the cases in the absence of the other
aPL
.
The predominant isotype of
aPL
was IgA, in particular for abeta2GPI.
Finally, no significant association was found between the presence of
aPL
and IVF outcome.
This prospective study shows aPE as the most prevalent
aPL
in infertile women and IgA as more common than IgG and IgM.
However, our results do not support an association between
aPL
and IVF outcome.
[MeSH-major]
Antibodies,
Antiphospholipid
/ blood. Autoantibodies / blood. Fertilization in Vitro. Infertility / blood
MedlinePlus Health Information.
consumer health - Infertility
.
Immune Epitope Database and Analysis Resource.
gene/protein/disease-specific - Related Immune Epitope Information
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17894010.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Cardiolipins; 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / Phosphatidylethanolamines; 0 / beta 2-Glycoprotein I; 39382-08-6 / phosphatidylethanolamine
100.
Ellis R, Boggild M:
Therapy-related acute leukaemia with Mitoxantrone: what is the risk and can we minimise it?
Mult Scler
; 2009 Apr;15(4):505-8
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Therapy-related
acute
leukaemia with
Mitoxantrone: what is the risk and can we minimise it?
BACKGROUND: Therapy-related
acute
leukaemia
(TRAL) is a concern for neurologists and patients when considering treatment with Mitoxantrone for multiple sclerosis (MS).
RESULTS: Case-series including 5472 patients were identified; mean dose of Mitoxantrone was 74.2 mg/m(2) (range:
12
-120 mg/m(2)).
Acute
Myelocytic
Leukaemia
and
Acute Promyelocytic
Leukaemia
represented 46.4% each of the
leukaemia
subtypes.
Over 80% of cases occurred in patients exposed to >60 mg/m(2),
with a
relative risk of 1.44 (CI95%:1.18-1.70) when comparing total dose >60 mg/m(2) against <60 mg/m(2) strongly suggesting a relationship between risk of TRAL and total dose.
[MeSH-major]
Antineoplastic Agents / adverse effects.
Leukemia
,
Myeloid
,
Ac