Issue Archive
Table of Contents
Inside Blood
Blood Work
Plenary Paper
Perspectives
Review Article
How I Treat
Clinical Trials and Observations
A prognostic model to predict survival in 867 World Health Organization–defined essential thrombocythemia at diagnosis: a study by the International Working Group on Myelofibrosis Research and Treatment
Clinical Trials & Observations
Long-term outcomes of 107 patients with myelofibrosis receiving JAK1/JAK2 inhibitor ruxolitinib: survival advantage in comparison to matched historical controls
Clinical Trials & Observations
Hematopoiesis and Stem Cells
Immunobiology
The folliculin-FNIP1 pathway deleted in human Birt-Hogg-Dubé syndrome is required for murine B-cell development
Lymphoid Neoplasia
A phase 2 trial of standard-dose cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) and rituximab plus bevacizumab for patients with newly diagnosed diffuse large B-cell non-Hodgkin lymphoma: SWOG 0515
ER stress and autophagy: new discoveries in the mechanism of action and drug resistance of the cyclin-dependent kinase inhibitor flavopiridol
Identification of a 3-gene model as a powerful diagnostic tool for the recognition of ALK-negative anaplastic large-cell lymphoma
Myeloid Neoplasia
Overexpression of IL-1 receptor accessory protein in stem and progenitor cells and outcome correlation in AML and MDS
Phagocytes, Granulocytes, and Myelopoiesis
Induced pluripotent stem cells from CINCA syndrome patients as a model for dissecting somatic mosaicism and drug discovery
Platelets and Thrombopoiesis
Polymorphisms of protein tyrosine phosphatase CD148 influence FcγRIIA-dependent platelet activation and the risk of heparin-induced thrombocytopenia
Intracellular cyclophilin A is an important Ca2+ regulator in platelets and critically involved in arterial thrombus formation
Transplantation
Vascular Biology
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Cover Image
Cover Image
The cover shows efflux of 0.45-μm red microspheres from the vascular circulation (labeled in green) toward collagen matrix (in blue) within an inflamed joint of a mouse. These observations document the presence of gaps between endothelial cells in the vasculature during inflammation, consistent with increased tissue edema and likely similar to human inflammatory conditions such as arthritis. Although platelets are conventionally assigned the role of preserving vascular integrity, they are capable of triggering the formation of gaps during inflammation via serotonin release, a process inhibited by serotonin-specific reuptake inhibitor antidepressant drugs. This demonstration that platelets are capable of amplifying and maintaining vascular permeability adds to the rapidly growing list of unexpected functions for platelets. See the article by Cloutier et al on page 1334.
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