Defects in cilia function can lead to an inherited form of renal disease. In this issue, Germino and his colleagues (p. 1490) explore how cilia help guide the kidney into the right shape. Image courtesy of Klaus Piontek and Gregory Germino.

On page 1375, William Harnett and his colleagues report that ES-62, a protein of filarial nematodes, inhibits the release of allergy mediators from human mast cells. This observation helps explain why the prevalence of allergy has steeply increased in developed countries, but not in regions in which infection by parasitic worms is common. The cover shows a micrograph of a human mast cell. Credit: CNRI/Photo Researchers, Inc

LINGO-1 is a member of a family of molecules known to inhibit axonal growth. In this issue, Wu and colleagues (p 1228) show that LINGO-1 inhibits myelination in an animal model of multiple sclerosis. The cover shows a cross section of myelinated axons in the central nervous system. Source: Corbis.

Schizophrenia has long been treated with drugs that target dopamine-mediated neurotransmission. In this issue, Patil and his colleagues (p 1102) show that people with the disease can also be treated with an agonist of metabotropic glutamate receptors. Cover image: "Inner voices" (Corbis).

In this issue, Richard Lee and colleagues use a genetic fate-mapping approach to implicate the contribution of stem cells to heart tissue (p 970). Mouse cardiomyoctyes were irreversibly marked with green fluorescence protein (GFP), and then the mice were allowed to age normally or had their hearts injured. After injury—but not after normal aging—the percentage of GFP-positive cardiomyocytes dropped, implying that new cardiomyocytes were derived from stem cells. The cover image shows cardiomyocytes harvested 3 months after injury (GFP, green; β-galactosidase, red; 4',6-diamidino-2-phenylindole (DAPI), blue).

In this issue, Lois Smith and colleagues find that mice fed a diet high in ω–3 polyunsaturated fatty acids have reduced pathological retinal angiogenesis, and the authors propose that such a diet could be used to prevent retinopathy. The cover image shows the retinal vasculature (isolectin B4 labeling, red) interacting with microglia (Csf1r–positive, green) in a 1–day–old mouse.

Two papers in this issue (pp 730 and 736) identify possible new targets for lymphoid malignancies. Credit: Steve Gschmeissner / Photo Researchers, Inc.

Understanding how external stimuli promote muscle growth and maintenance is key to developing therapies for muscular dystrophies. In this issue, Montminy and colleagues identify a molecular mechanism involving CREB by which catecholamines and electrical activity induce myogenesis and muscle repair. The cover image depicts nuclear (dark blue) and cytoplasmic (magenta)staining of HDAC5 in wild-type muscle. Photo courtesy of Rebecca Berdeaux and Marc Montminy.

The germinal matrix of premature infants, densely packed with neural precursor cells and blood vessels, is selectively vulnerable to hemorrhage. In this issue, Ballabh et al. show that antiangiogenic therapy can reduce the incidence and severity of germinal matrix hemorrhage. Germinal matrix of a 24-week-old premature infant was stained to show blood vessels (laminin, white), radial glia (VEGF, red; GFAP, green) and nuclei (blue). Image courtesy of Xiaoning Han and Takahiro Takano.

In this issue, Epstein and colleagues show that histone deacetylase 2 (Hdac2) regulates cardiac hypertrophy by modulating the activity of Gsk3β. The cover shows Hdac2 immunostaining (red) in the heart of an E11.5 mouse embryo.

In this issue (p 204) Cohn et al. show that excess TGF-β signaling is associated with myopathy in mouse models of Marfan syndrome and Duchenne muscular dystrophy. They further demonstrate that treatment with either antibodies to TGF-β or the heart medication losartan leads to normalization of muscle architecture and function in vivo. The cover depicts muscle, stained for nuclear DNA (blue), myosin (red) and laminin-λ 1 (green), displaying regeneration in the Duchenne mouse model treated with losartan. Image courtesy of Ronald Cohn and Harry Dietz.

Breast cancer often metastasizes to bone, yet the mechanisms underlying bone colonization and destruction are unclear. In this issue, Park et al. report that expression of the transcription factor NF-κ B in breast cancer cells results in secretion of a cytokine–GM-CSF–that stimulates osteoclast development and mediates bone metastasis. The cover image depicts a scanning electron micrograph of breast cancer cells (Steve Gschmeissner, Photo Researchers, Inc.).