Issue Archive

The hematologic complications of pregnancy may impact both the mother and the fetus and are invariably challenging. In this How I Treat series, edited by Editor-in-Chief Nancy Berliner and Associate Editor Catherine Bollard, clinical experts discuss their approach to 4 scenarios where the standard approach to diagnosis and care has to be adapted to optimize outcomes for both the pregnant mother and her fetus.

The hematologic complications of pregnancy may impact both the mother and the fetus and are invariably challenging. In this How I Treat series, edited by Editor-in-Chief Nancy Berliner and Associate Editor Catherine Bollard, clinical experts discuss their approach to 4 scenarios where the standard approach to diagnosis and care has to be adapted to optimize outcomes for both the pregnant mother and her fetus.

The hematologic complications of pregnancy may impact both the mother and the fetus and are invariably challenging. In this How I Treat series, edited by Editor-in-Chief Nancy Berliner and Associate Editor Catherine Bollard, clinical experts discuss their approach to 4 scenarios where the standard approach to diagnosis and care has to be adapted to optimize outcomes for both the pregnant mother and her fetus.

The hematologic complications of pregnancy may impact both the mother and the fetus and are invariably challenging. In this How I Treat series, edited by Editor-in-Chief Nancy Berliner and Associate Editor Catherine Bollard, clinical experts discuss their approach to 4 scenarios where the standard approach to diagnosis and care has to be adapted to optimize outcomes for both the pregnant mother and her fetus.

The hematologic complications of pregnancy may impact both the mother and the fetus and are invariably challenging. In this How I Treat series, edited by Editor-in-Chief Nancy Berliner and Associate Editor Catherine Bollard, clinical experts discuss their approach to 4 scenarios where the standard approach to diagnosis and care has to be adapted to optimize outcomes for both the pregnant mother and her fetus.

The complexity of regulation of hematopoietic stem cell (HSC) proliferation and differentiation has proved to be a barrier to HSC expansion for clinical application. Subramaniam et al reveal the mechanism by which the clinically tested pyrimidoindole derivative UM171 affects HSC expansion, propagation, fate, and engraftment by inducing rapid proteasome-mediated degradation of lysine-specific demethylase 1A (LSD1) and the the LSD1-containing chromatin remodeling complex.

Using a viral infection model, Tsoukas et al investigated how elevated interleukin-18 (IL-18) triggers hyperinflammation. They demonstrate that IL-18 can induce autoinflammatory amplification of CD8 T-cell responses and interferon-γ overproduction and that hyperinflammation can be exacerbated by even minor defects in impaired cytotoxic responses to a virus.

Primary effusion lymphoma is an aggressive, poor-prognosis malignancy driven by infection with Kaposi sarcoma–associated herpesvirus (KSHV). Chen and colleagues identified ceramide analog compounds that effectively inhibit KSHV-associated lymphoma growth and progression in vitro and in vivo, providing a novel path to potential future treatments.

Margraf et al selectively deleted integrin-linked kinase in myeloid cells of mice to show that this integrin-binding protein suppresses chemokine-induced neutrophil extravasation and ischemia-induced reperfusion injury.

Sangkhae and colleagues used murine model systems and hepcidin analogs to investigate the central role of maternal hepcidin in determining fetal iron status, the deleterious consequences of its elevation during pregnancy, and its potential relevance in the setting of inflammation. They demonstrate that suppression of maternal hepcidin during pregnancy is essential for maternal and embryo iron homeostasis and health.

Protease-activated receptor 4 (PAR4) is one of four thrombin receptors mediating sustained thrombin signaling in platelets and enabling formation of a stable thrombus. Han et al demonstrate for the first time the structural underpinnings for PAR4 activation in platelets and the role of PAR4 activation in venous thromboembolism.