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JCI online early table of contents: Feb. 7, 2011

EDITOR'S PICK: Profiling malaria-causing parasites

The majority of fatal cases of malaria are caused by infection with the parasite Plasmodium falciparum. Most at risk are young children and women who are pregnant. A team of researchers, led by Patrick Duffy, at the National Institutes of Health, Rockville, has now developed an approach to profile P. falciparum parasites in such a way that they are able to identify parasite genes associated with severe infection.

In the study, they identified a distinct subset of genes in parasites infecting pregnant women, including a gene whose protein product is already known to be important for severe disease in these at risk patients and is a well-established pregnancy malaria vaccine candidate. They also identified a subset of genes that distinguished parasites infecting children from those infecting pregnant women. The team hopes that this information will provide new understanding of the nature of severe childhood malaria. Future experiments will attempt to validate the protein products of these genes as biomarkers of disease severity and targets for new intervention strategies.

TITLE: NSR-seq transcriptional profiling enables identification of a gene signature of Plasmodium falciparum parasites infecting children

Patrick E. Duffy
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA.
Phone: 301.443.4605; Fax: 301.480.1959; E-mail:

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CARDIOVASCULAR DISEASE: Teaching the old drug niacin new tricks

A team of researchers, led by Stefan Offermans, at the Max-Planck-Institute for Heart and Lung Research, Germany, has now identified in mice a new mechanism by which the drug nicotinic acid (niacin) mediates its beneficial effects.

Niacin is one of the oldest drugs used to prevent and treat atherosclerosis, a disease of the major arterial blood vessels that is a major cause of heart attack and stroke. The antiatherosclerotic effects of niacin are believed to be a result of its effects on lipid (fat) levels in the blood, in particular, its ability to decrease levels of 'bad' cholesterol (LDL) and increase levels of 'good' cholesterol (HDL). However, Offermans and colleagues have now determined that niacin can have antiatherosclerotic effects in mice that are independent of its effects on lipids. Specifically, it had anti-inflammatory effects on immune cells, in particular macrophages, decreasing their recruitment to atherosclerotic plaques and reducing the progression of atherosclerosis. Thus, the authors conclude that the antiatherosclerotic effects of niacin are mediated via effects on both lipid levels in the blood and immune cells.

TITLE: Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells

Stefan Offermanns
Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Phone: 49.0.6032.705.1201; Fax: 49.0.6032.705.1204; E-mail:

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INFLAMMATION: Ironing out the details of the role of macrophages in chronic inflammation

A critical event in chronic inflammatory diseases such as atherosclerosis (also known as hardening of the arteries, which is a major cause of heart attack and stroke), multiple sclerosis, and chronic venous leg ulcers is the uncontrolled activation of immune/inflammatory cells known as macrophages. A team of researchers, led by Karin Scharffetter-Kochanek, at the University of Ulm, Germany, has now defined a specific macrophage population that exists in an unrestrained proinflammatory state in human subjects with chronic venous leg ulcers and a newly established mouse model of the main aspects of the condition. The team therefore suggests that this macrophage population, which is induced by iron, could be targeted to treat chronic inflammatory diseases such as chronic venous leg ulcers.

TITLE: An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice

Karin Scharffetter-Kochanek
University of Ulm, Ulm, Germany.
Phone: 49.731.500.57501; Fax: 49.731.500.57502; E-mail:

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VIROLOGY: Depletion of immune cells not a correlate of simian AIDS

Progression to AIDS in individuals infected with HIV has classically been associated with loss of immune cells known as CD4+ T cells. However, recent data have indicated that this might not be the best predictor of disease progression. A team of researchers, led by Donald Sodora, at Seattle Biomedical Research Institute, Seattle, has now provided further support for this position by studying SIV (the primate equivalent of HIV) infection of the natural host species sooty mangabeys, which results in high viral replication without clinical signs of simian AIDS. Specifically, they found that acute, SIV-induced CD4+ T cell depletion in sooty mangabeys does not result in immune dysfunction and progression to simian AIDS and that this is because a population of double negative T cells partially compensate for CD4+ T cell function in these animals. The authors therefore suggest that it will be important to assess double negative T cells in HIV-infected patients, particularly to determine whether these cells are preserved and functional in those who do not progress to AIDS.

TITLE: Lack of clinical AIDS in SIV-infected sooty mangabeys with significant CD4+ T cell loss is associated with double-negative T cells

Donald L. Sodora
Seattle Biomedical Research Institute, Seattle, Washington, USA.
Phone: 206.256.7413; Fax: 206.256.7229; E-mail:

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ONCOLOGY: New promoter of tumor development

Recent human data suggest that the protein CSN6 might have a role in regulating tumor development. Now, a team of researchers, led by Mong-Hong Lee, at the University of Texas M.D. Anderson Cancer Center, Houston, has identified a molecular mechanism by which CSN6 promotes tumorigenesis in mice and generated data that indicate that the gene that templates CSN6 is an oncogene.

Initial analysis indicated that levels of the CSN6 protein are upregulated in human breast and thyroid tumors and that expression of CSN6 positively correlated with expression of the protein MDM2, a potent negative regulator of the tumor suppressor p53. Further analysis confirmed this mechanism in mice and demonstrated that mice lacking one Csn6 gene were less susceptible than mice with both Csn6 genes intact to radiation-induced tumor development. The authors therefore suggest that CSN6 should be investigated as a prognostic marker and therapeutic target in cancers that involve dysregulated MDM2/p53 activity.

TITLE: Subunit 6 of the COP9 signalosome promotes tumorigenesis in mice through stabilization of MDM2 and is upregulated in human cancers

Mong-Hong Lee
University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
Phone: 713.794.1323; Fax: 713.792.6059; E-mail:

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STEM CELLS: Stem cells from different sources are not equivalent

Stem cells are considered by many to be promising candidate sources of cells that can be used as therapies to regenerate and repair diseased tissues. There are currently two types of stem cell considered in this context: human embryonic stem cells (hESCs), which are derived from early embryos, and human induced pluripotent stem cells (hiPSCs), which are derived by reprogramming cells of the body such that they have the ability to generate any cell type. Although hESCs and hiPSCs seem to behave in a functionally similar manner, whether they are equivalent at the single cell level has not been determined. To address this issue, a team of researchers, led by Joseph Wu, at Stanford University School of Medicine, Stanford, used single cell analysis to resolve the gene expression profiles of 362 hiPSCs and hESCs. The team found that hiPSCs exhibited substantially more heterogeneity in gene expression than did hESCs, leading them to suggest that hiPSCs have a less stable pluripotent state than hESCs, information that is important to consider when thinking about using these cells for the purpose of regenerative medicine.

TITLE: Single cell transcriptional profiling reveals heterogeneity of human induced pluripotent stem cells

AUTHOR CONTACT: Joseph C. Wu Stanford University School of Medicine, Stanford, California, USA. Phone: 650.736.2246; Fax: 650.736.0234; E-mail:

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INFLAMMATION: Targeting neutrophilic inflammation

Immune cells known as neutrophils are a key early component of the immune response to invading microbes. However, persistent and inappropriate activation of neutrophils is central to a number of inflammatory diseases. Agents that selectively promote neutrophil death during inflammation are therefore potential therapeutics for inflammatory diseases. A new way to promote neutrophil death has now been suggested by the mouse studies of a team of researchers led by Sarah Walmsley, at the University of Sheffield, United Kingdom. Specifically, the data, which include the observation that mice lacking the protein Phd3 exhibit reduced neutrophilic inflammation in a mouse model of acute lung injury and in a mouse model of colitis, indicate that selective inhibition of PHD3 may provide a good strategy for treating human inflammatory conditions associated with persistent and inappropriate neutrophil activation.

TITLE: Prolyl hydroxylase 3 (PHD3) is essential for hypoxic regulation of neutrophilic inflammation in humans and mice

Sarah R. Walmsley
University of Sheffield, Sheffield, United Kingdom.
Phone: 44.114.2712630; Fax: 44.114.2268898; E-mail:

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PHYSIOLOGY: Regulating bodily fluid volume and composition

The volume and ionic composition of our bodily fluids is determined by fluid and bicarbonate (HCO3) secretion from the body. Such secretion occurs in organs such as the kidney and pancreas as well as the gastrointestinal tract. It is regulated by the epithelial cells that line the secretion ducts. Numerous diseases, including cystic fibrosis, involve aberrant epithelial cell regulation of fluid and bicarbonate secretion. A team of researchers, led by Shmuel Muallem, at the National Institutes of Health, Bethesda, has now provided new insight into the molecular mechanisms that control pancreatic ductal secretion of fluid and bicarbonate in mice. Specifically, the team found that WNK proteins act through the protein SPAK to suppress ductal fluid secretion, whereas the proteins IRBIT and PP1 promote ductal fluid secretion and reverse the effect of the WNKs and SPAK. These data have implications for understanding conditions associated with aberrant epithelial cell regulation of fluid and bicarbonate secretion, including cystic fibrosis and high blood pressure.

TITLE: IRBIT governs epithelial secretion in mice by antagonizing the WNK/SPAK kinase pathway

Shmuel Muallem
National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA.
Phone: 301.402.0262; Fax: 301.402.1228; E-mail:

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Contact: Ushma Neill
Journal of Clinical Investigation

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