thrombocytopenia/phosphatase

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Extreme Elevation of Alkaline Phosphatase in a Pregnancy Complicated by Gestational Diabetes and Infant with Neonatal Alloimmune Thrombocytopenia.

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There have been few case reports of isolated elevation of alkaline phosphatase beyond the normal physiologic amount with subsequent return to baseline after delivery. Here we present a similar case of extreme elevation of alkaline phosphatase in a pregnancy complicated by gestational diabetes and

Polymorphisms of protein tyrosine phosphatase CD148 influence FcγRIIA-dependent platelet activation and the risk of heparin-induced thrombocytopenia.

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Heparin-induced thrombocytopenia (HIT) is due primarily to IgG antibodies specific to platelet factor 4/heparin complexes (PF4/Hs) that activate platelets via FcγRIIA. CD148 is a protein tyrosine phosphatase that regulates Src kinases and collagen-induced platelet activation. Three polymorphisms

Plasma acid phosphatase in idiopathic and secondary thrombocytopenias.

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Interplay between the tyrosine kinases Chk, Csk and phosphatase PTPRJ is critical for regulating platelets in mice.

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The Src family kinases (SFKs) Src, Lyn and Fyn are essential for platelet activation and also involved in megakaryocyte (MK) development and platelet production. Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which phosphorylates a conserved tyrosine in their C-terminal tail, and are

Clinical analysis and TPO levels in three patients with refractory thrombocytopenia.

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Refractory thrombocytopenia (RTC) is a counter-concept to refractory anemia, which is characterized by isolated thrombocytopenia associated with clonal chromosomal abnormality. The diagnosis of RTC is difficult to establish based on morphologic features alone. And steroid therapy for RTC is often

A fatal myeloproliferative syndrome in a family with thrombocytopenia and platelet dysfunction.

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Three siblings with a lifelong history of a bleeding disorder and thrombocytopenia died from a myeloproliferative disease. In 2, the terminal event resembled juvenile chronic myelogenous leukemia, and in the third, the diagnosis was acute monocytic leukemia. A family study revealed that the mother

Three patients with glucose-6 phosphatase catalytic subunit 3 deficiency

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Objectives Severe congenital neutropenia (SCN) is a primary immunodeficiency (PID) characterized by persistent severe neutropenia, recurrent infections, and oral aphthous lesions. Severe congenital neutropenia is caused by various genetic defects such as ELANE, GFI, HAX-1, JAGN1, SRP54, and

[The role of miR-155 in pathogenesis of immune thrombocytopenia].

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OBJECTIVE To explore the role of microRNA-155 (miR-155) in pathogenesis of immune thrombocytopenia (ITP) through investigate the relevance between the expression of miR-155 in CD19(+) B cells in peripheral blood and the function of B lymphocytes in patients with ITP. METHODS A total of 55 ITP

Predictors of Severe Thrombocytopenia Secondary to Peginterferon Alfa-2a Treatment in Subjects With Hepatitis C Virus Infection.

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In this study, we aim to identify patient characteristics that predict severe thrombocytopenia induced by peginterferon alfa-2a in hepatitis C virus-infected patients. Demographic, clinical, and genetic data collected from patients with chronic hepatitis C virus infection (n = 232; age ≥18 years)

Phase I Dose Escalation Study of Sodium Stibogluconate (SSG), a Protein Tyrosine Phosphatase Inhibitor, Combined with Interferon Alpha for Patients with Solid Tumors.

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OBJECTIVE Sodium stibogluconate (SSG), a small molecule inhibitor of protein tyrosine phosphatases, combined with IFN-alpha-2b (IFN-α) inhibited solid tumor cell line growth in vitro. We conducted a phase I clinical trial with SSG plus IFN-α in advanced cancer patients to assess tolerance, maximum

PTPN22 -1123G > C polymorphism is associated with susceptibility to primary immune thrombocytopenia in Chinese population.

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Primary immune thrombocytopenia (ITP) is an acquired autoimmune disorder characterized by autoantibody-mediated platelet destruction. Multiple factors have been implicated in ITP pathogenesis, including T-lymphocyte dysfunctions. The protein tyrosine phosphatase, non-receptor type 22 (PTPN22) gene

[Leucocyte tartrate-resistant acid phosphatase as marker for the transition of monocyte to macrophage].

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The presence of the 5 degrees isoenzyme of leukocyte tratrate-resistant acid phosphatase (FATRE) was investigated in human peripheral blood monocytes in 32 samples: 26 normal, 4 thrombocytopenia, 1 anemia and 1 hairy cell leukemia. The Cobe Spectra Version 4 cell separador was used for 3 samples

The first case of thrombocytopenia, anasarca, fever, renal impairment or reticulin fibrosis, and organomegaly (TAFRO) syndrome with unilateral adrenal necrosis: a case report.

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BACKGROUND TAFRO syndrome, which was first reported in 2010 in Japan, is a relatively rare disease characterized by thrombocytopenia, anasarca, fever, renal impairment, reticulin fibrosis, and organomegaly. Although this disease is considered similar to multicentric Castleman disease, some of the

Reduced PTEN involved in primary immune thrombocytopenia via contributing to B cell hyper-responsiveness.

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Phosphatase and tensin homolog (PTEN) is thought to mediate B cell activation by negatively regulating the phosphoinositide 3-kinase (PI3K) signaling pathway. This pathway is important for activation, growth, and proliferation. Although enhanced B cell receptor (BCR) signaling contributes to

Novel G6B gene variant causes familial autosomal recessive thrombocytopenia and anemia.

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OBJECTIVE To characterize the underlying genetic and molecular defects in a consanguineous family with lifelong blood disorder manifested with thrombocytopenia (low platelets count) and anemia. METHODS Genetic linkage analysis, exome sequencing, and functional genomics were carried out to identify

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