Volume 14 Issue 9, September 2008

A tremendous amount of investment went into the construction of science facilities during the 1950s through the 1970s. And, because huge sums of money went into building up many of these laboratories, which still stand today, they can't just be bulldozed and rebuilt—it would be terribly wasteful. Yet these labs often seem ill suited for modern research. Researchers' complaints range from cluttered countertops to distracting noise to overcrowded work spaces, just to name a few. These problems create stress and drag on productivity. Others say they have simply outgrown their space, or their work has developed beyond their lab's current technical capabilities. What happens when a scientist would like to take her research in a certain direction, but her assigned space doesn't allow it? Remodeling could be the answer. There's a growing industry in rehabilitating and modernizing research facilities. Architectural experts say a few strategic changes can bring much needed relief while boosting productivity. James Hudspeth, director of the F.M. Kirby Center for Sensory Neuroscience at the Rockefeller University in New York, knows firsthand the challenges and rewards of remodeling a lab. As his interdisciplinary research into the biophysical aspects of hearing has expanded over the years, Hudspeth has had to undertake major lab renovations three times during his career. The most recent remodeling of his lab, completed last year, involved revamping a workspace in an entirely different building. Hudspeth's move is a good example of creative problem-solving that employed a team of architects, engineers, his lab manager and an unflappable project manager. On the following pages, leading architects offer suggestions on how you, too, can update your lab space.

Biologist Fotis Kafatos has spent a career balancing his own research endeavors with efforts to create opportunities for other scientists. Born and raised in Crete, Greece, Kafatos moved to the US to study zoology at Cornell University and, later in the 1960s, biology at Harvard University, where he went on to become the university's youngest full professor at age 29. During his three decades at Harvard, Kafatos maintained close ties with Europe, teaching part-time at Greek universities and founding Crete's Institute of Molecular Biology and Biotechnology. In 1993, he returned to Europe to direct the continent's premiere molecular biology center, the Heidelberg-based European Molecular Biology Laboratory (EMBL), where he strived to create an equal-opportunity environment for scientists from all corners of Europe. More recently, in late 2005, Kafatos was elected chairman of the policy-setting body for the European Research Council (ERC). Kafatos now divides his time between studying malaria-causing mosquitoes at Imperial College London and leading an organization charged with doling out some €7.5 billion ($11 billion) to Europe's most promising scientists from 2007 to 2013—an infusion of money intended to revitalize the continent's research community. Kafatos talks about his research and his stewardship of the ERC with Coco Ballantyne.

Epidemiologists at the University of Stellenbosch, near Cape Town, South Africa, have assembled a vast collection of tuberculosis strains. With it, they're revealing how drug-resistant strains evolve and spread through human populations. Charlie Schmidt reports.

Upregulation of a protein involved in lysosomal degradation of proteins helps stave off some of the cellular decline observed with aging. The findings could lead to new approaches to fend off age-related disease or even extend lifespan (pages 959–965).

A relatively obscure immune cell, the eosinophil, has a dramatic way of defending against pathogens. It rapidly ejects mitochondrial DNA, ensnaring bacteria and hastening their demise (pages 949–953).

Investigation of a genetically attenuated malaria parasite—which infects but does not kill its host—provides insight into how to develop a malaria vaccine (pages 954–958).

Extracellular DNA floating around in blood plasma provides an accessible template for detecting mutations associated with tumors. A new technique is able to quantify such mutated DNA and predict relapse in individuals with colorectal cancer. The technique complements other approaches, such as the analysis of tumor cells in the plasma (pages 985–990).

The complexity of factors that regulate bleeding and coagulation has long confounded researchers. Andrew Wei and Shaun Jackson help clear the air by examining clinical findings pointing to a mechanistic basis for a common bleeding disorder, immune thrombocytopenic purpura. Mark Kahn tackles two research studies that could lead to improved therapies for a coagulation syndrome that hits people with severe sepsis.

Currently, there are few options for treating chronic kidney disease. The immunosuppressant cyclosporine A is effective, but the mechanism has been unclear. In this new report, the authors now show that the benefit of cyclosporine A is not through an effect on the immune system but rather through stabilizing the cytoskeleton, and thus the integrity, of a key cell type needed for proper kidney function.

Resistance to drugs is a clinical problem. Downregulating the gene RPN2, which encodes part of an N-oligosaccharyl transferase complex, sensitized breast cancer cells to the cancer drug docetaxel in vivo and in vitro. RPN2 might be a therapeutic target against drug resistance in cancer.

Yousefi et al. reveal a new function of eosinophils and suggest they have an antibacterial role in the gut. The cells fire spurts of mitochondrial DNA and granule proteins in response to infection, entrapping and killing the extracellular bacteria (pages 910–911).

Malaria parasites lacking an enzyme from the purine salvage pathway show attenuated replication in red blood cells and are cleared from mice. The findings suggest a strategy for the development of blood-stage malaria vaccine strains (pages 912–913).

Chaperone-mediated autophagy (CMA), a mechanism for the lysosomal degradation of proteins, declines in aging cells. Using transgenic mice in which such a decline does not occur in the liver, the authors found that preserving CMA leads to reduced accumulation of damaged proteins and improved organ function in aged mice (pages 909–910).

Brain-type creatine kinase (Ckb) has an unexpected role in bone biology. Decreasing its activity suppresses the bone-resorbing activity of osteoclasts, and mice lacking Ckb are protected from osteoporosis-inducing treatments. These findings identify Ckb as a new molecular against bone loss.

Promising results using cell therapy in animal models of muscular dystrophy have recently been reported. However, a limitation of this previous work is that therapeutic effects have been shown only in young animals, whereas many patients who could benefit from such therapy are at advanced stages of disease. As dystrophic muscle ages, it becomes sclerotic and is infiltrated by fat, presenting an obstacle to cell delivery. This paper reports that this obstacle can be overcome by pretreatment of the muscle with tendon fibroblasts that have been genetically modified to express an angiogenic factor and a metalloprotease.

Traykova-Brauch et al. have developed a new approach to modeling renal diseases such as polycystic kidney disease, renal fibrosis and renal cancer in transgenic mice. In contrast to currently available tools, Pax8-rtTA–transgenic mice have high levels of transgene expression in a highly kidney-specific, uniform and tetracycline–dependent manner. The usefulness of the Pax8–rtTA system, which is both inducible and reversible, has been shown in three different settings.