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JCI table of contents: June 23, 2011

EDITOR'S PICK: What makes a happy meal?

Many people when stressed turn to high calorie "comfort foods". Despite the contribution this behavior makes to the current obesity epidemic, little is known about the molecules and nervous system circuits that control it. Insight into this could provide new targets for the development of therapeutics to curb this potentially detrimental behavior. In this context, a team of researchers, led by Jeffrey Zigman, at The University of Texas Southwestern Medical Center, Dallas, working with a new mouse model of prolonged psychosocial stress that features aspects of major depression and posttraumatic stress disorder, has now found that the hormone ghrelin is required for prolonged psychosocial stress to promote preference for and intake of high-fat food. Further analysis revealed the nervous system circuits that mediate these effects of ghrelin. The team hopes that further studies will provide additional insight into the control of stress-induced food-reward behavior and identify additional therapeutic targets.

TITLE: Ghrelin mediates stress-induced food-reward behavior in mice

Jeffrey M. Zigman
The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214.648.8621; Fax: 214.648.5612; E-mail:

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EDITOR'S PICK: Understanding the antiepileptic benefits of an Atkins-like diet

Some individuals with epilepsy fail to respond to treatment with conventional drugs but benefit from consuming a ketogenic diet a high-fat, low-carbohydrate diet similar to the more commonly known Atkins diet. A team of researchers, led by Detlev Boison, at the Legacy Research Institute, Portland, has now identified in mice the molecular mechanism responsible for the antiepileptic effects of the ketogenic diet.

The team found that a ketogenic diet reduces seizures in mice by decreasing expression of the protein Adk, which is responsible for clearing the natural antiepileptic agent adenosine from the brain. The clinical relevance of these data are highlighted by the team's finding that brain tissue from patients with epilepsy that fails to respond to treatment with conventional drugs shows increased levels of Adk. The team suggests that their data could lead to the development of less-restrictive antiepileptic diets and alternate pharmaceutical approaches to treatment, notions with which Robert Greene, at The University of Texas Southwestern Medical Center, Dallas, concurs in an accompanying commentary.

TITLE: A ketogenic diet suppresses seizures in mice through adenosine A1 receptors

Detlev Boison
Legacy Research Institute, Portland, Oregon, USA.
Phone: 503.232.0589; Fax: 503.232.5465; E-mail:

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TITLE: Adenosine: front and center in linking nutrition and metabolism to neuronal activity

Robert W. Greene
The University of Texas Southwestern Medical Center and Dallas VA Medical Center, Dallas, Texas, USA.
Phone: 214.648.5108; Fax: 214.648.7037; E-mail:

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EDITOR'S PICK: "Good" cholesterol function as important as its levels

High levels of "good" cholesterol (HDL cholesterol) are associated with a decreased risk of coronary artery disease (CAD) a disease of the major arterial blood vessels that is one of the major causes of heart attack and stroke. This suggests that therapeutics that increase HDL levels could be clinically useful. However, such therapies have not yielded clear-cut decreases in disease, indicating that the beneficial effects of HDL are likely not related simply to its abundance. More evidence to support this notion has now been provided by a team of researchers, led by Ulf Landmesser, at the University of Zurich, Switzerland, who found that HDL from patients with (CAD) had different effects on cells lining blood vessels than did HDL from healthy individuals. In particular, the HDL from patients with CAD was found to lack anti-inflammatory effects on blood vessellining cells and could not stimulate repair of the blood vessel lining. As noted by the team and, in an accompanying commentary, Philip Shaul and Chieko Mineo, at The University of Texas Southwestern Medical Center, Dallas, these data indicate that if the protective potential of HDL is to be harnessed, its biological functions as well as its abundance must be considered.

TITLE: Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease

Ulf Landmesser
University of Zurich, Zurich, Switzerland.
Phone: 0041.44.255.9595; Fax: 0041.44.255.4251; E-mail:

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TITLE: PON-dering differences in HDL function in coronary artery disease

Philip W. Shaul
The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214.648.2015; Fax: 214.648.2096; Email:

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PULMONARY: New cell population repairs the damaged lung

A team of researchers, led by Harold Chapman and Thiennu Vu, at the University of California San Francisco, San Francisco, has identified a previously unrecognized population of cells in the lungs of mice (alveolar epithelial cells expressing alpha-6-beta-4) and determined that these cells serve as multipotent progenitors during repair of the severely injured lung. The importance of these data for the development of regenerative therapies for the treatment of lung disease is touched upon by the authors and discussed in more detail in an accompanying commentary by Jeffrey Whitsett and Vladimir V. Kalinichenko, at Cincinnati Children's Hospital Medical Center, Cincinnati.

TITLE: Integrin alpha-6-beta-4 identifies an adult distal lung epithelial population with regenerative potential in mice

Harold A. Chapman
University of California San Francisco, San Francisco, California, USA.
Phone: 415.514.0896; Fax: 415.502.4995; E-mail:

Thiennu H. Vu
University of California San Francisco, San Francisco, California, USA.
Phone: 415.514.4266; Fax: 415.514.4365; E-mail:

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TITLE: Integrin alpha-6-beta-4 defines a novel lung epithelial progenitor cell: a step forward for cell-based therapies for pulmonary disease

Jeffrey A. Whitsett
Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Phone: 513.803.2790; Fax: 513.636.7868; E-mail:

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NEPHROLOGY: Long live dopamine production by the kidneys

Dopamine is a natural chemical in the body well known for its role in nerve cell communication; loss of dopamine-producing nerves in a specific region of the brain causes Parkinson disease. However, dopamine also exerts effects on other organs of the body, including the kidneys, where it modulates water transport. The dopamine that acts on the kidneys comes both from the circulation and from the kidneys themselves, which have the capacity to make the chemical, but the roles of these distinct sources of dopamine have not been determined. Raymond Harris, Ming-Zhi Zhang, and colleagues, at Vanderbilt University, Nashville, have now investigated this issue in mice and found that dopamine made within the kidneys is critical for maintaining normal blood pressure. As mice unable to make dopamine within their kidneys developed high blood pressure and lived for a much shorter length of time than normal mice, Harris and colleagues suggest that a functional dopaminergic system in the kidney is important for long-term health and survival.

TITLE: Intrarenal dopamine deficiency leads to hypertension and decreased longevity in mice

Raymond C. Harris
Vanderbilt University School of Medicine and Nashville Veterans Affairs Hospital, Nashville, Tennessee, USA.
Phone: 615.322.2150; Fax: 615.343.2675; E-mail:

Ming-Zhi Zhang
Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Phone: 615.343.1548; Fax: 615.343.2675; E-mail:

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ONCOLOGY: Inflammation can initiate, not just promote, tumor development

Colorectal cancer is one of the most common forms of cancer worldwide. One of the factors that promotes the development of colorectal cancer is chronic inflammation of the gut. Now, a team of researchers, led by Manolis Pasparakis, at the University of Cologne, Germany, has determined that the NF-kappa-B signaling pathway, the predominant signaling pathway regulating the inflammatory response, not only promotes tumor development but can also initiate tumor formation in mice. While Pasparakis and colleagues did not perform any human studies, they suggest that their observations have relevance to human disease because a recent study has determined that genes that template components of the NF-kappa-B signaling pathway are frequently amplified in different types of cancer.

In an accompanying commentary, Thomas Wirth and Yoshiaki Sunami, at the University of Ulm, Germany, discuss the significance of the data generated by Pasparakis and colleagues and suggest that if the same is true in humans, it will provide a series of new therapeutic targets.

TITLE: Constitutive IKK2 activation in intestinal epithelial cells induces intestinal tumors in mice

Manolis Pasparakis
University of Cologne, Cologne, Germany.
Phone: 49.221.470.1526; Fax: 49.221.470.5163; E-mail:

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TITLE: Intestinal carcinogenesis: IKK can go all the way

Thomas Wirth
Institute of Physiological Chemistry, University of Ulm, Ulm, Germany.
Phone: 49.731.500.23270; Fax: 49.731.500.22892; E-mail:

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Contact: Karen Honey
Journal of Clinical Investigation

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