Artificial cerebrospinal fluid restores aspirin-inhibited physiological hemostasis through recovery of platelet aggregation function.

Background: Optimal hemostasis provides safety and reliability during neurosurgery which improves surgical outcomes. Previously, artificial cerebrospinal fluid (aCSF) and its component sodium bicarbonate were found to facilitate physiological hemostasis by amplifying platelet aggregation. This study aimed to verify whether aCSF amplifies platelet-dependent hemostasis in the presence of antiplatelet agents.

[Acquired platelet dysfunction with severe bleeding tendency in triple-negative myelofibrosis].

A 50-year-old man demonstrated markedly increased number of white blood cells, anemia, severe splenomegaly, and bleeding tendency. Bone marrow analysis revealed remarkable hypercellularity; dysplasia in multilineage cells, including megakaryocytes; and fibrosis. He was eventually diagnosed with triple-negative myelofibrosis.

The effect of roller head pump on platelet deterioration during the simulated extracorporeal circulation.

Roller pumping results in hemolysis and adverse effects on coagulation, but there are few reports on the influence of roller heads on platelets. Here, we evaluate the interaction between roller pumping and platelet function using a simulated extracorporeal circuit incorporating a vinyl chloride tube and roller head pump with 30 min recirculation. Platelet aggregation, platelet count, microparticle, P-selectin, Phosphatidylserine (PS) exposure and Ricinus Communis Agglutinin 1 (RCA-1) were measured before, 5, 10, 20, and 30 min after the recirculation using 100 ml of fresh human blood that had obtained from healthy volunteers (n = 9).

Stratifin Inhibits SCF Formation and Blocks Ubiquitination of Oncoproteins during the Course of Lung Adenocarcinogenesis.

Purpose: Aberrant overexpression of SFN (stratifin) plays an oncogenic role in lung adenocarcinoma. We have shown previously that SKP1, an adapter component of E3 ubiquitin ligase forming an SCF complex, is a unique SFN-binding protein in lung adenocarcinoma cells.

Experimental Design: simulation and mutagenesis analysis were performed to identify the SFN-binding domain on SKP1.

Sodium Bicarbonate Facilitates Hemostasis in the Presence of Cerebrospinal Fluid Through Amplification of Platelet Aggregation.

Background: Appropriate hemostasis is essential for clear visualization of the neural structures and cleavage planes. It is also essential for avoiding heat-induced injury, minimizing blood loss, and reducing operative time.

Objective: To determine the role of cerebrospinal fluid (CSF) in platelet-dependent hemostasis during neurosurgery.

C1galt1-deficient mice exhibit thrombocytopenia due to abnormal terminal differentiation of megakaryocytes.

C1galt1 is essential for synthesis of the core 1 structure of mucin-type O-glycans. To clarify the physiological role of O-glycans in adult hematopoiesis, we exploited the interferon-inducible Mx1-Cre transgene to conditionally ablate the C1galt(flox) allele (Mx1-C1). Mx1-C1 mice exhibit severe thrombocytopenia, giant platelets, and prolonged bleeding times.

Human platelets promote liver regeneration with Kupffer cells in SCID mice.

Background: Platelets contain several growth factors, including vascular endothelial growth factor (VEGF) and insulin-like growth factor. We examined the role of human platelets in liver regeneration with a focus on Kupffer cells (KCs).

Materials And Methods: Severe combined immunodeficiency mice were subjected to 70% hepatectomy and phosphate-buffered saline administration (PBS); 70% hepatectomy and human platelet transfusion (hPLT); 70% hepatectomy, KC depletion, and PBS administration (KD + PBS); 70% hepatectomy, KC depletion, and human platelet transfusion (KD + hPLT); or a sham operation and human platelet transfusion (sham).

Procoagulant properties of microparticles released from red blood cells in paroxysmal nocturnal haemoglobinuria.

Thrombosis in paroxysmal nocturnal haemoglobinuria (PNH) has been suggested to be due to several pathophysiological states: a suppressed fibrinolytic system, increased leucocyte-derived tissue factor, complement (C')-mediated damage to platelets and endothelia, or increased platelet- and endothelium-derived microparticles (MPs). Because haemolytic attack is often accompanied by thrombosis in PNH, we studied the role of C'-induced release of MPs in the thrombogenesis of PNH. C' activation induced procoagulant alteration in PNH red blood cells (RBC), when assessed by thrombin generation in the presence of C'-activated PNH RBC, which was abolished by their subsequent treatment with annexin V.