Antiplatelet antibody predicts platelet desialylation and apoptosis in immune thrombocytopenia.

Immune thrombocytopenia (ITP) is a bleeding disorder caused by dysregulated B- and T- cell functions, which lead to platelet destruction. A well-recognized mechanism of ITP pathogenesis involves anti-platelet and anti-megakaryocyte antibodies recognizing membrane glycoprotein (GP) complexes, mainly GPIb/IX and GPIIb/IIIa. In addition to the current view of phagocytosis of the opsonised platelets by splenic and hepatic macrophages via their Fc γ receptors, antibodyinduced platelet desialylation and apoptosis have also been reported to contribute to ITP pathogenesis.

Indirect detection of anti-platelet antibodies in immune thrombocytopenia.

Despite recent advances in the understanding and treatment of immune thrombocytopenia (ITP), its diagnosis remains clinical due to the lack of sensitive laboratory tests. The detection of anti-platelet antibodies (APA) in plasma, although highly specific, is notoriously insensitive. Specialised clinical platelet laboratories routinely perform a screening test of only one dilution for indirect APA testing by flow cytometry.

Acquired Glanzmann thrombasthenia associated with platelet desialylation.

Background: The notable discrepancy between platelet count and bleeding manifestations in immune thrombocytopenia (ITP) patients with acquired Glanzmann thrombasthenia (GT) has been described.

Objectives: We aimed to examine the mechanisms responsible for thrombocytopenia and the bleeding phenotype in a patient with acquired GT.

Patient, Methods, And Results: A patient with primary ITP underwent splenectomy due to steroid intolerance.

Panaxdiol Saponins Component Promotes Hematopoiesis and Modulates T Lymphocyte Dysregulation in Aplastic Anemia Model Mice.

Objective: To investigate the potential efficacy of panaxadiol saponins component (PDS-C) in the treatment of aplastic anemia (AA) model mice.

Methods: Totally 70 mice were divided into 7 groups as follows: normal, model, low-, medium-, high-dose PDS-C (20, 40, 80 mg/kg, namely L-, M-, H-PDS-C), cyclosporine (40 mg/kg), and andriol (25 mg/kg) groups, respectively. An immune-mediated AA mouse model was established in BALB/c mice by exposing to 5.

Ginseng-Derived Panaxadiol Saponins Promote Hematopoiesis Recovery in Cyclophosphamide-Induced Myelosuppressive Mice: Potential Novel Treatment of Chemotherapy-Induced Cytopenias.

Objective: To investigate the potential efficacy of panaxadiol saponins component (PDS-C), a biologically active fraction isolated from total ginsenosides, to reverse chemotherapy-induced myelosuppression and pancytopenia caused by cyclophamide (CTX).

Methods: Mice with myelosuppression induced by CTX were treated with PDS-C at a low- (20 mg/kg), moderate- (40 mg/kg), or high-dose (80 mg/kg) for 7 consecutive days. The level of peripheral white blood cell (WBC), neutrophil (NEU) and platelet (PLT) were measured, the histopathology and colony formation were observed, the protein kinase and transcription factors in hematopoietic cells were determined by immunohistochemical staining and Western blot.

Pharmacodynamics, pharmacokinetics and clinical efficacy of apixaban in the treatment of thrombosis.

Introduction: Venous thromboembolism (VTE) is a common disorder. Heparin and vitamin K antagonists have been the standard treatment for VTE for over 50 years. The development of apixaban and other direct oral anticoagulants has greatly increased the range of anticoagulants available for the treatment of VTE.

The effects of panaxadiol saponins on megakaryocytic maturation and immune function in a mouse model of immune thrombocytopenia.

We have identified a biologically active component, panaxadiol saponins component (PDS-C), from Chinese ginseng herb extract. Panaxadiol saponins component contains five ginsenoside monomers with total purity of 92.44%.

Low prevalence of heparin-induced thrombocytopenia after cardiac surgery in Thai patients.

Introduction: Heparin induced-thrombocytopenia (HIT) has been well recognized in Western countries. However, there are no data in the Thai population. We therefore investigated the prevalence of anti-platelet factor 4 (PF4)/heparin antibodies, HIT, and its thrombotic complications in Thai patients undergoing cardiac surgery using unfractionated heparin.

Research and development of the effective components of panaxdiol saponin as new Chinese patent medicine for treating hemocytopenia.

Pancytopenia (hemocytopenia) such as pr imary immune primary thrombocytopenia (ITP), aplastic anemia and chronic neutropenia (agnogenic leukocytopenia) were of ten t reated by glucocor t icoids, androgen and often treated glucocorticoids, immunosuppressive agents at present, but the response to these treatments has not been always satisfactory, and may cause serious adverse events. Our research has identified a biological active component in ginseng extract and the active component, panaxadiol saponins component (PDS-C), was isolated from total saponins of ginsenosides, and formulated into capsules named as Painengda. We successfully obtained approval from State Food and Drug Administration (SFDA) of China in 2010 to conduct clinical trials of PDS-C as class-five new Chinese patent medicine.

Serum thromboxane B2 compared to five other platelet function tests for the evaluation of aspirin effect in stable cardiovascular disease.

Background: To assess the role of serum thromboxane B(2) (TXB(2)) measurements and the correlation between platelet function studies, in patients with stable cardiovascular disease on aspirin or clopidogrel.

Methods: 76 patients (47 on aspirin, 16 clopidogrel, 13 both) underwent assessment of TXB(2), whole blood aggregometry (WBA) after stimulation with (i) arachidonic acid (0.5mM), (ii) ADP (5 microM), (iii) collagen (1 and 5 microg/ml), PFA-100, and Cone and Plate Analyzer.

Effects of notoginosides on proliferation and upregulation of GR nuclear transcription factor in hematopoietic cells.

Aim: To investigate the effects of panax notoginosides (PNS) on the proliferation of human hematopoietic stem/progenitor cells, and to explore the signaling pathway of the nuclear transcription factor of the glucocorticoid receptor (GR-NTF) initiated by PNS related with the proliferation.

Methods: The human CD34+ cells and bone marrow nuclear cells were exposed to PNS at a concentration of 0, 10, 25, 50, and 100 mg/L, respectively, in semi-solid culture system to observe colony forming unite of all lineages, granulocyte, erythrocyte, and megakaryocyte (CFUGEMM, CFU-GM, CFU-E, and CFU-MK). Three lineages of human hematopoietic cell lines, including granulocytic HL-60, erythrocytic K562, megakaryocytic CHRF- 288, and Meg-01 cells were incubated with PNS at 20 mg/L for 14 d.