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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).
The US should revamp rules on informed consent to ensure that people have all of the information and support they need before deciding to enroll in clinical trials.
The death of a participant in a gene therapy trial has thrown the entire field into question–as it did once before in 1999. Can the field survive this second setback? Virginia Hughes investigates.
In early August, a court in the southern Indian city of Chennai dismissed a lawsuit filed by pharmaceutical giant Novartis. James Love, director of the nonprofit organization Knowledge Ecology International, explains the local lawsuit’s global impact.
Oxidized products of low-density lipoproteins (LDLs) activate platelets through CD36, demonstrating a link between deregulated lipoprotein levels, oxidative stress and thrombosis (pages 1086–1095).
The S6K1 kinase lies downstream of a signaling network crucial for muscle hypertrophy. It now seems that S6K1 also interacts with another kinase—AMPK—to integrate muscle-cell growth with metabolic regulation.
A drug that activates glutamate receptors offers promise for a new class of anti-psychotic therapeutics and sheds light on the pathophysiology of this devastating disease (pages 1102–1107).
In the inherited anemia β-thalassemia, diseased red blood cell precursors release a blood-borne signal that promotes excessive intestinal iron absorption, predisposing affected individuals to multiorgan damage (pages 1096–1101).
The bone-specific protein osteocalcin has now been shown to act as a hormone that profoundly affects glucose and fat metabolism. This discovery completes an endocrine circuit with the skeleton as a ductless gland.
T cells attack Plasmodium-infected hepatocytes when fighting malaria, and it was thought that T cells first encountered Plasmodium antigens in the liver. Instead, immediately after infection, small numbers of parasites drain to skin lymph nodes where they can prime T cells to mount a protective immune response (pages 1035–1041).