Identification of Heparin-Induced Thrombocytopenia in Surgical Critically Ill Patients by Using the HIT Expert Probability Score: An Observational Pilot Study.

Background: Heparin-induced thrombocytopenia (HIT) remains a challenging diagnosis especially in surgical intensive care unit (SICU) patients. The aim of the study was to evaluate for the first time the diagnostic accuracy of the HIT Expert Probability (HEP) score in the early identification of HIT in SICU patients. Methods: The HEP and 4Ts scores were calculated in all patients with suspected HIT during their stay in our SICU.

Egfl7 Represses the Vasculogenic Potential of Human Endothelial Progenitor Cells.

Egfl7 (VE-statin) is a secreted protein mostly specific to the endothelial lineage during development and in the adult and which expression is enhanced during angiogenesis. Egfl7 involvement in human postnatal vasculogenesis remains unresolved yet. Our aim was to assess Egfl7 expression in several angiogenic cell types originating from human bone marrow, peripheral blood, or cord blood.

Underestimation of plasma level of factor V coagulant activity and fibrinogen concentration together with prolonged prothrombin time, activated partial thromboplastin time and thrombin time can result from pre-analytical very low calcium level in citrated sample tube.

Introduction: Pre-analytical phase is a critical step in the haemostasis laboratory cycle. Numerous variations affect tests results, and it is crucial to detect them in order to reject improper specimens before reporting test results. Comparing to prior results or requesting, a repeat sample can help in pre-analytical irregularity assessment.

Thrombin receptor PAR-1 activation on endothelial progenitor cells enhances chemotaxis-associated genes expression and leukocyte recruitment by a COX-2-dependent mechanism.

Background: Endothelial colony forming cells (ECFC) represent a subpopulation of endothelial progenitor cells involved in endothelial repair. The activation of procoagulant mechanisms associated with the vascular wall's inflammatory responses to injury plays a crucial role in the induction and progression of atherosclerosis. However, little is known about ECFC proinflammatory potential.

Targeting VEGFR1 on endothelial progenitors modulates their differentiation potential.

Objectives: We studied whether plasma levels of angiogenic factors VEGF and placental growth factor (PlGF) in coronary artery disease patients or undergoing cardiac surgery are modified, and whether those factors modulate endothelial progenitor's angiogenic potential.

Methods And Results: A total of 143 patients' plasmas from two different studies were analyzed (30 coronary artery disease patients, 30 patients with stable angina, coupled with 30 age and sex-matched controls; 53 patients underwent cardiac surgery). Among factors screened, only PlGF was found significantly increased in these pathological populations.

Forearm ischemia decreases endothelial colony-forming cell angiogenic potential.

Background Aims: Circulating endothelial progenitor cells and especially endothelial colony-forming cells (ECFCs) are promising candidate cells for endothelial regenerative medicine of ischemic diseases, but the conditions for an optimal collection from adult blood must be improved.

Methods: On the basis of a recently reported vascular niche of ECFCs, we hypothesized that a local ischemia could trigger ECFC mobilization from the vascular wall into peripheral blood to optimize their collection for autologous implantation in critical leg ischemia. Because the target population with critical leg ischemia is composed of elderly patients in whom a vascular impairment has been documented, we also analyzed the impact of aging on ECFC mobilization and vascular integrity.

HIF-prolyl hydroxylase 2 inhibition enhances the efficiency of mesenchymal stem cell-based therapies for the treatment of critical limb ischemia.

Upregulation of hypoxia-inducible transcription factor-1α (HIF-1α), through prolyl-hydroxylase domain protein (PHD) inhibition, can be thought of as a master switch that coordinates the expression of a wide repertoire of genes involved in regulating vascular growth and remodeling. We aimed to unravel the effect of specific PHD2 isoform silencing in cell-based strategies designed to promote therapeutic revascularization in patients with critical limb ischemia (CLI). PHD2 mRNA levels were upregulated whereas that of HIF-1α were downregulated in blood cells from patients with CLI.

Imbalance of circulating endothelial cells and progenitors in idiopathic pulmonary fibrosis.

Background: Fibrogenesis during idiopathic pulmonary fibrosis (IPF) is strongly associated with abnormal vascular remodeling. Respective abundance of circulating endothelial cells (CEC) and endothelial progenitor cells (EPC) might reflect the balance between vascular injury and repair and potentially serve as biomarkers of the disease.

Objectives And Methods: We postulated that CEC and EPC subtypes might be differently modulated in IPF.

The profibrotic cytokine transforming growth factor-β1 increases endothelial progenitor cell angiogenic properties.

Background: Transforming growth factor-β1 (TGF-β1) is a profibrotic cytokine that plays a major role in vascular biology, and is known to regulate the phenotype and activity of various vascular cell populations. Because most fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF), are associated with vascular remodeling, and as endothelial progenitor cells (EPCs) may be involved in this process, we investigated the impact of TGF-β1 modulation of EPC angiogenic properties.

Methods: TGF-β1 plasma levels were determined in 64 patients with IPF and compared with those in controls.

Thrombospondin-1 is a plasmatic marker of peripheral arterial disease that modulates endothelial progenitor cell angiogenic properties.

Objective: We examined whether plasma levels of angiogenic factors are altered in plasma of patients with peripheral arterial disease (PAD) and whether these factors affect endothelial progenitor cell-induced angiogenesis.

Methods And Results: Plasma was collected from 184 patients with PAD and 330 age-matched healthy controls. Vascular endothelial growth factor and placental growth factor concentrations did not differ between the groups, whereas we found a linear correlation between PAD disease and thrombospondin (TSP)-1 plasma level.

Treprostinil increases the number and angiogenic potential of endothelial progenitor cells in children with pulmonary hypertension.

Background: Pulmonary vasodilators in general and prostacyclin therapy in particular, have markedly improved the outcome of patients with pulmonary arterial hypertension (PAH). As endothelial dysfunction is a key feature of PAH, and as endothelial progenitor cells (EPC) may contribute to vascular repair in PAH, we suspected that prostacyclin therapy might enhance EPC numbers and functions. In the present study, objectives were to determine whether EPC may contribute to vasodilator treatment efficacy in PAH.

The Wnt antagonist Dickkopf-1 increases endothelial progenitor cell angiogenic potential.

Objective: To determine the role of Wnt antagonist Dickkopf (DKK) 1 in human endothelial colony-forming cells (ECFCs) in view of the emerging importance of Wnt pathways in vascular biology.

Methods And Results: Endothelial progenitor cells have been proposed to be crucial in tumor neovascularization. Recombinant DKK1 has been tested in ECFC angiogenic properties in vitro.

Interleukin 8 is differently expressed and modulated by PAR-1 activation in early and late endothelial progenitor cells.

The proinflammatory chemokine interleukin 8 exerts potent angiogenic effects on endothelial cells by interacting with its receptors CXCR1 and CXCR2. As thrombin is also a potent inflammatory factor, and as endothelial progenitor cells (EPC) express functional PAR-1 thrombin receptor, we examined whether PAR-1 stimulation interferes with the IL-8 pathway in EPC. EPC were obtained from adult blood (AB) and cord blood (CB).

[Validation of a Bruton's disease genetic analysis method].

Bruton's disease is the most frequently primary X-linked immunodeficiency. Patients are more susceptible to early and recurring infections associated with hypo/agammaglobulinemia and a severe B-cell deficiency. Moreover, 400 mutations were found in the XLA gene which codes the Btk tyrosine kinase and were identified as responsible for Bruton's disease.

[Primary immunodeficiencies and Bruton's disease genetic analysis: which prospects offers this genetic diagnosis?].

Bruton's disease is the most frequently primary X-linked immunodeficiency. Bruton's tyrosine kinase (Btk) is encoded by the XLA gene that when mutated causes bruton's disease. This protein acts in multiple intracellular signaling pathways where the BCR (B-cell receptor) pathway is the most elucidated.