Synergistic effect of collagen and CXCL12 in the low doses on human platelet activation.

CXCL12, also known as stromal cell-derived factor-1, is a chemokine classified into CXC families, which exerts its function by binding to specific receptors called CXCR4 and CXCR7. Human platelets express CXCR4 and CXCR7 on the plasma membrane. It has been reported that CXCL12 potentiates to induce platelet aggregation in cooperation with agonists including collagen.

[A Case Report of Surgical Resection of a Supraseller Granuloma in a Patient with Erdheim-Chester Disease].

Erdheim-Chester disease(E-CD)is a rare pathology characterized by systematic granulomatosis that occasionally involves the central nervous system. We report about a 68-year-old woman with E-CD who presented with right-side visual disturbance. Magnetic resonance imaging showed a suprasellar tumor that elevated the right optic nerve and involved the right internal carotid and right anterior choroidal arteries.

Smoking cessation affects human platelet activation induced by collagen.

It is firmly established that smoking is a risk factor of cardiovascular disease, stroke and peripheral vascular disease. Although smoking alters the hemostatic process, the influence of smoking on human platelet activation remains controversial. For patients undergoing surgery, cessation of smoking prior to the procedure is recommended as it increases the risk of postoperative morbidity or mortality.

[A Case of Glioblastoma that Appeared One Year after the Removal of Subcortical Hematoma].

Subcortical bleeding from brain tumors is not rare. In the majority of cases, tumors are revealed within a few months after bleeding. We herein report a relatively rare case of glioblastoma(GBM)that appeared one year after the removal of a subcortical hematoma.

Rac Regulates the TRAP-Induced Release of Phosphorylated-HSP27 from Human Platelets via p38 MAP Kinase but Not JNK.

Background/aims: Thrombin induces the activation of human platelets through protease-activated receptor (PAR) 1 and PAR4, and Rac, a member of the Rho family of small GTPases, is implicated in PAR activation. We previously reported that phosphorylated-heat shock protein 27 (HSP27) is released from the thrombin receptor-activating peptide (TRAP)-stimulated platelets of diabetic patients. In the present study, we investigated the role of Rac in the TRAP-elicited release of phosphorylated-HSP27 from human platelets.

Tailored Strategies in Carotid Artery Stenting to Avoid Periprocedural Complications.

Carotid artery stenting (CAS) has been widely accepted as a valuable therapeutic alternative to carotid endarterectomy (CEA) for high-grade carotid stenosis. Because carotid revascularization including CAS is usually performed in patients with minimal or no neurological deficits, utmost care should be taken to avoid periprocedural complications. The major concerns associated with CAS are embolic stroke, hyperperfusion syndrome (HPS), and perioperative myocardial infarction.

Optimal platelet function test for in-stent tissue protrusion following carotid artery stenting.

Purpose To determine the best platelet function test for in-stent tissue protrusion following carotid artery stenting (CAS). Methods Patients who underwent CAS were recruited prospectively in this observational study. Combination of aspirin 100 mg/day and clopidogrel 75 mg/day was administered for a minimum of 7 days prior to procedure.

Sphingosine 1-phosphate (S1P) suppresses the collagen-induced activation of human platelets via S1P4 receptor.

Sphingosine 1-phosphate (S1P) is as an extracellular factor that acts as a potent lipid mediator by binding to specific receptors, S1P receptors (S1PRs). However, the precise role of S1P in human platelets that express S1PRs has not yet been fully clarified. We previously reported that heat shock protein 27 (HSP27) is released from human platelets accompanied by its phosphorylation stimulated by collagen.

AICAR reduces the collagen-stimulated secretion of PDGF-AB and release of soluble CD40 ligand from human platelets: Suppression of HSP27 phosphorylation via p44/p42 MAP kinase.

We have previously reported that collagen-induced phosphorylation of heat shock protein (HSP) 27 via p44/p42 mitogen-activated protein (MAP) kinase in human platelets is sufficient to induce the secretion of platelet-derived growth factor (PDGF)-AB and the release of soluble cluster of differentiation 40 ligand (sCD40L). Adenosine monophosphate-activated protein kinase (AMPK), which is known to regulate energy homeostasis, has a crucial role as an energy sensor in various eukaryotic cells. The present study investigated the effects of 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranosyl 5'-monophosphate (AICAR), which is an activator of AMPK, on the collagen-induced activation of human platelets.

Diabetes mellitus and carotid artery plaques exhibiting high-intensity signals on MR angiography are related to increased platelet reactivity after carotid artery stenting.

Background: Increased platelet reactivity after carotid artery stenting (CAS) may cause thromboembolic complications.

Objective: This study aimed to investigate the incidence of increased platelet reactivity after CAS and to determine the factors related to it.

Methods: Patients who underwent CAS were recruited prospectively.

Thrombin Receptor-Activating Protein (TRAP)-Activated Akt Is Involved in the Release of Phosphorylated-HSP27 (HSPB1) from Platelets in DM Patients.

It is generally known that heat shock protein 27 (HSP27) is phosphorylated through p38 mitogen-activated protein (MAP) kinase. We have previously reported that HSP27 is released from human platelets associated with collagen-induced phosphorylation. In the present study, we conducted an investigation into the effect of thrombin receptor-activating protein (TRAP) on the release of HSP27 in platelets in type 2 diabetes mellitus (DM) patients.

Factor Xa Inhibitor Suppresses the Release of Phosphorylated HSP27 from Collagen-Stimulated Human Platelets: Inhibition of HSP27 Phosphorylation via p44/p42 MAP Kinase.

Selective inhibitors of factor Xa (FXa) are widely recognized as useful therapeutic tools for stroke prevention in non-valvular atrial fibrillation or venous thrombosis. Thrombin, which is rapidly generated from pro-thrombin through the activation of factor X to FXa, acts as a potent activator of human platelets. Thus, the reduction of thrombin generation by FXa inhibitor eventually causes a suppressive effect on platelet aggregation.

Cilostazol ameliorates collagenase-induced cerebral hemorrhage by protecting the blood-brain barrier.

Intracranial hemorrhage remains a devastating disease. Among antiplatelet drugs, cilostazol, a phosphodiesterase 3 inhibitor, was recently reported to prevent secondary hemorrhagic stroke in patients in a clinical trial. The aim of this study was to evaluate whether pre-treatment with cilostazol could decrease the intracranial hemorrhage volume and examine the protective mechanisms of cilostazol.

Delayed Stenosis in the Intracranial Vessels following Endovascular Treatment for Acute Stroke.

Purpose: To evaluate delayed stenosis of the vessels after endovascular thrombectomy using magnetic resonance (MR) angiography.

Materials And Methods: Of 82 consecutive patients who underwent successful endovascular treatment for acute intracranial large vessel occlusion between October 2010 and October 2014 at a single institution, 57 patients for whom 3-month radiologic follow-up examinations using MR angiography were available were included in the analysis. MR angiography images were assessed to detect delayed stenosis, which was defined as a decrease in the diameter of treated vessels > 50% compared with MR angiography images obtained 24 hours after endovascular treatment.

Release of Phosphorylated HSP27 (HSPB1) from Platelets Is Accompanied with the Acceleration of Aggregation in Diabetic Patients.

We investigated the relationship between HSP27 phosphorylation and collagen-stimulated activation of platelets in patients with diabetes mellitus (DM). Platelet-rich plasma was prepared from blood of type 2 DM patients. The platelet aggregation was analyzed in size of aggregates by an aggregometer using a laser scattering method.

αB-crystallin reduces ristocetin‑induced soluble CD40 ligand release in human platelets: suppression of thromboxane A2 generation.

Our group has previously shown that αB-crystallin (HSPB5), a small heat shock protein, inhibits human platelet aggregation by ristocetin, an activator of glycoprotein Ib/IX/V. In addition, it was demonstrated that glycoprotein Ib/IX/V activation induces soluble CD40 (sCD40) ligand release via thromboxane (TX) A2. In the present study, the effect of αB-crystallin on the ristocetin-induced sCD40 ligand release in human platelets was investigated.

Preliminary experience with air transfer of patients for rescue endovascular therapy after failure of intravenous tissue plasminogen activator.

The present report describes our experience with air transfer of patients with acute ischemic stroke in whom intravenous tissue plasminogen activator (IV t-PA) failed for rescue endovascular therapy (EVT). Twenty-three consecutive patients in whom IV t-PA failed were transferred to our hospital for rescue EVT between February 2011 and April 2013. The amount of time required for transfer, distance, clinical outcomes, and complications were compared between patients transferred by ground (TG group; n = 17) and by air (TA group; n = 6).

Rho-kinase regulates human platelet activation induced by thromboxane A2 independently of p38 MAP kinase.

We have previously demonstrated that ristocetin, an activator of GPIb/IX/V, induces the release of soluble CD40 ligand (sCD40L) via thromboxane A2 production in human platelets. It has been shown that thromboxane A2 induces the activation of Rho-kinase, a downstream effector of Rho, in human platelets. In the present study, we investigated the exact roles of Rho-kinase in thromboxane A2-induced platelet activation.

Long-term magnetic resonance angiography follow-up for recanalized vessels after mechanical thrombectomy.

Background: Mechanical thrombectomy is an effective revascularization therapy for acute intracranial large vessel occlusion. We retrospectively evaluated magnetic resonance angiography (MRA) follow-up data to assess the long-term patency of recanalized vessels after mechanical thrombectomy.

Methods: We retrospectively reviewed medical records of consecutive patients who had undergone mechanical thrombectomy for intravenous tissue plasminogen activator-failed/ineligible acute intracranial major vessel occlusion between October 2010 and April 2013 at our institution.

STA-MCA/STA-PCA Bypass Using Short Interposition Vein Graft.

Background And Aims: Superficial temporal artery (STA) is the mainstay of donor vessels for extra-intracranial bypass (EC-IC bypass) in cerebral revascularization. However, the typically used STA frontal or parietal branch is not always adequate in its flow-carrying capacity. In the present study, we provide an update on an alternative strategy: the use of the STA main trunk as a donor vessel, with a short vein interposition graft.

Superficial temporal artery-middle cerebral artery bypass using local anesthesia and a sedative without endotracheal general anesthesia.

Object: Superficial temporal artery (STA)-middle cerebral artery (MCA) bypasses have continually evolved, and new strategies have been advocated for reducing anesthetic or surgical morbidity and mortality. Further simplifying, and decreasing the invasiveness of, STA-MCA bypass by performing this operation without endotracheal general anesthesia was believed to be feasible in certain subsets of patients.

Methods: The authors performed STA-MCA bypass using local anesthesia with a sedative in 10 patients with hemodynamically compromised occlusive cerebrovascular disease, as well as multiple comorbidities, between February 2010 and September 2011.