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Three articles this month tackle problems in cardiovascular research. Work by Crone et al.(page 459) suggests that Herceptin therapy-associated cardiomyopathy stems from inhibition of cardiac ErbB2 receptor tyrosine kinase signaling. Miki et al.(page 466) find that Kir6.1, a sulfonylurea-coupled K+ channel, is implicated in Prinzmetal angina and essential to regulating vascular tone. Finally, Hafezi-Moghadam et al.(page 473) show that high doses of corticosteroids induce cardioprotective levels of nitric oxide. The cover presents a stylized image of the human heart.
It is widely anticipated that the sequencing of the human genome, the characterization of the human proteomic map and the underlying advance in technological know-how will give rise to an unprecedented leap in biomedical science over the next half century. It may be that the bottleneck in the equation is the availability of staff trained to understand the scientific data generated and transform it successfully into something with medical value. Such people must have detailed knowledge both of medicine and the practice of scientific investigation. Here, we present three commentaries that endeavor to explain how such hybrid researchers can be recruited, trained and retained.
Transporters for vitamin C keep vitamin concentrations optimal in the body. A new mouse knockout of one transporter reveals previously unknown requirements for the vitamin. (pages 514–517)
Nicotinic receptors are a well known culprit in tobacco addiction. Studies on rats now show that these receptors also enhance the long-term effects of cocaine and amphetamines.
Neurodenerative disorders such as Huntington disease lead to neuronal cell death in discrete regions of brain. A new study implicates the CREB transcription factor family as critical mediators that prevent such neuronal death.
Brain lesions exhibiting inflammation and neuronal damage are an important part of the pathology of multiple sclerosis. Microarray analysis compares gene expression in two forms of these lesions, and points to new therapies for the disease. (pages 500–508)
New findings in mice suggest that corticosteroids mediate nitric oxide production in the endothelium, which in turn protects the heart against damage when deprived of oxygen. The mechanism explains, at least in part, the cardioprotective effects of these anti-inflammatory agents. (pages 473–479)
Do autoimmune diseases develop 'spontaneously' or are they induced by environmental triggers, such as infectious agents? This is a central—and challenging—question in the autoimmunity field. A new study in this issue provides strong evidence for a virus-induced autoimmune process in a human neurological disease. (pages 509–513)