In 2001, Charles Vest, then President of the Massachusetts Institute of Technology, announced that MIT would make most of its course material freely available online. Browsing the Web site of MIT's Open Courseware (OCW) project (http://ocw.mit.edu), you feel the stirring of a "my God, it's full of stars" transformation: you can borrow material for your courses, study other teachers' teaching methods, maybe even retake college courses you regret having slept through! Remarkably, OCW is just one highly visible part of an "open education movement." The essays collected in Opening Up Education, edited by Toru Iiyoshi and M.S. Vijay Kumar, describe ways in which individuals and institutions intend to exploit digital communications technology, develop innovative and freely redistributable educational methods and resources, and improve education at all levels throughout the world.
But what does "open education" really mean? What is "closed" about education? Should education be free as in no cost, or is there something about education that needs to be freed as in freedom? This sort of ground is already well-trampled by debates about two better-known "open" predecessors, open-source software and open-access publication, and it is instructive to make the comparison.
After a long day in the microbiology lab, Vibrio harveyi may just want to relax, but if enough of its neighbors are game for a group project, it just can't say no. V. harveyi is a bioluminescent marine bacterium that uses a chemical peer-pressure process called quorum sensing to determine whether to emit light and carry out other collective activities. Quorum sensing, which occurs in other bacteria as well, is both fascinating in itself and instructive for an array of disciplines from entomology to robotics. It goes like this: Quorum-sensing bacteria release small molecules called autoinducers. These molecules convey the presence of the cells to neighboring bacteria. When enough autoinducer molecules float around in the extracellular medium, the bacteria, sensing a critical mass, produce a synchronized response--in V. harveyi's case, this response is a group glow.
Quorum sensing in bacteria that respond to a single autoinducer is understood fairly well to cause changes in gene expression that are induced by the accumulated autoinducer. V. harveyi, however, uses three autoinducers to get its herd mentality message across. The three autoinducers, called AI-1, CAI-1, and AI-2, are detected by the transmembrane receptors LuxN, CqsS, and LuxPQ, respectively, which then inhibit the transcription of genes whose products, in turn, block the production of another protein, LuxR. When the autoinducer concentration "tipping point" is reached, gene transcription is inhibited sufficiently and thus LuxR is produced, causing the bacteria to glow.
Malaria is one of the most common infectious diseases in the world and one of the greatest global public health problems. The Plasmodium falciparum parasite causes approximately 500 million cases each year and over one million deaths in sub-Saharan Africa. More than 40% of the world's population is at risk of malaria. The parasite is transmitted to people through the bites of infected mosquitoes. These insects inject a life stage of the parasite called sporozoites, which invade human liver cells where they reproduce briefly. The liver cells then release merozoites (another life stage of the parasite), which invade red blood cells. Here, they multiply again before bursting out and infecting more red blood cells, causing fever and damaging vital organs. The infected red blood cells also release gametocytes, which infect mosquitoes when they take a blood meal. In the mosquito, the gametocytes multiply and develop into sporozoites, thus completing the parasite's life cycle. Malaria can be prevented by controlling the mosquitoes that spread the parasite and by avoiding mosquito bites by sleeping under insecticide-treated bed nets. Effective treatment with antimalarial drugs also helps to decrease malaria transmission.
Approximately 36% of East Asians (Japanese, Chinese, and Koreans) show a characteristic physiological response to drinking alcohol that includes facial flushing (see Figure 1), nausea, and tachycardia  . This so-called alcohol flushing response (also known as "Asian flush" or "Asian glow") is predominantly due to an inherited deficiency in the enzyme aldehyde dehydrogenase 2 (ALDH2) . Although clinicians and the East Asian public generally know about the alcohol flushing response (e.g., http://www.echeng.com/asianblush/), few are aware of the accumulating evidence that ALDH2-deficient individuals are at much higher risk of esophageal cancer (specifically squamous cell carcinoma) from alcohol consumption than individuals with fully active ALDH2. This is particularly unfortunate as esophageal cancer is one of the deadliest cancers worldwide , with five-year survival rates of 15.6% in the United States, 12.3% in Europe, and 31.6% in Japan .
There has been relatively little apparent interest in the quality of medicines used to treat common life-threatening diseases despite the logical implication that poor-quality medicines will reduce the effectiveness of therapy and encourage drug resistance. Evidence suggests that a significant proportion of drugs consumed in the developing world are of poor quality [1-25]. Translating evidence on drug treatment outcomes into treatment policy is futile if the medicines actually used have substantially inferior efficacy compared with the medicines originally evaluated . Poor-quality medicines are conventionally classified into three main categories: counterfeit, substandard, and degraded (Box 1).