Science Odds and Ends

Two leading makers of lighting products are showcasing LED bulbs that are bright enough to replace energy-guzzling 100-watt light bulbs set to disappear from stores in January.

The new bulbs will also be expensive - about $50 each - so the development may not prevent consumers from hoarding traditional bulbs. The big problem with LEDs is that although they don't produce as much heat as incandescent bulbs, the heat they do create shortens the lifespan and reduces the efficiency of the chips. Cramming a dozen chips together in a tight bulb-shaped package that fits in today's lamps and sockets makes the heat problem worse. The brighter the bulb, the bigger the problem is.

Osram Sylvania, a unit of Germany's Siemens AG, said it has overcome the heat problem and will be showing a pear-shaped 100-watt-equivalent LED bulb this week. It doesn't have a firm launch date, but it usually shows products about a year before they hit store shelves.

Before the 100-watters, there will be 75-watters on the shelves this year. Osram Sylvania will be selling them at Lowe's starting in July. Royal Philips Electronics NV, the world's biggest lighting maker, will have them in stores late this year for $40 to $45.

However, 60-watt bulbs are the big prize, since they're the most common. There are 425 million incandescent light bulbs in the 60-watt range in use in the U.S. today, said Zia Eftekhar, the head of Philips' North American lighting division. The energy savings that could be realized by replacing them with 10-watt LED bulbs is staggering. The DoE expects a 60-watt equivalent LED bulb to cost $10 by 2015

Efficiency is a problem with today's solar panels; they only collect about 20 percent of available light. Now, a University of Missouri engineer has developed a flexible solar sheet that captures more than 90 percent of available light, and he plans to make prototypes available to consumers within the next five years.

To understand what makes the new discoveries so novel, it’s necessary to appreciate how our genes can go wrong. The human genetic code can be thought of as an encyclopedia in multiple volumes. Our normal genome contains 46 chromosomes, so that’s 46 volumes. Each chromosome is a long string of the chemical DNA and the information is “written” in the form of a molecular alphabet with just four letters: A, T, C and G.

There are three ways in which something can go wrong here. First, a whole chromosome can be either missing or duplicated. This drastic change is almost always fatal. (The exceptions include Downs Syndrome.)

Second, single-nucleotide polymorphisms (SNPs, or “snips” as everyone calls them) are when a single base-pair is different, corresponding to a misprinted character.

Finally, copy-number variants (CNVs) are when a stretch of DNA is either missing (deleted), or repeated (duplicated), a bit like a page that’s either fallen out or been printed twice. As you can imagine, CNVs tend to be more serious than SNPs, because they affect more of the DNA. This is only a general rule, however. There are plenty of serious SNPs, and plenty of harmless CNVs. It all depends on where they happen, and whether they interfere with important genes.

For a long time, it was widely assumed that SNPs were responsible for psychiatric disorders, in what’s called the “common-variant model” of disease. Yet this just didn’t work out.

Psychiatric interest in CNVs was sparked by a landmark paper http://www.nature.com/nature/journal/v4 ... 07229.html that appeared in Nature in September 2008. It was authored by an international consortium of schizophrenia researchers, led by employees at an Icelandic company, deCODE Genetics. They found a number of CNVs which seemed to be associated with schizophrenia.

Since then, CNV studies have taken off in the same way as GWAS did 5 years before. There’s now good evidence for the involvement of deletions and duplications in autism, attention-deficit hyperactivity disorder (ADHD), schizophrenia, and intellectual disability (aka mental retardation). By contrast, however, studies in bipolar disorder have been negative.

It’s only early days yet, but as this research advances further, and as technology allows ever-smaller CNVs to be picked up, these kinds of genetic findings may present a serious challenge http://www.scientificamerican.com/artic ... c-genetics for existing psychiatric diagnostic systems.

What is the operon, whose 50th anniversary is being celebrated this week? The word heralded the discovery of how genes are turned on and off, and it launched the now-immense field of gene regulation. The idea was born in André Lwoff's laboratory at the Institut Pasteur. At one end of a long corridor in the loft of a building devoted to research on bacteria were Lwoff, Elie Wollman, and myself. At the other end were Jacques Monod and his group. Lwoff studied lysogenic Eschericia coli bacteria capable of producing bacteriophage without infection. Monod was analyzing the properties of the β-galactosidase enzyme in the same bacterium: an enzyme required for the metabolism of lactose that was produced only when the culture medium contained galactosides. To all and sundry the two systems appeared mechanistically miles apart. But their juxtaposition would produce a critical breakthrough for our understanding of life, demonstrating that we cannot presume to know how new ideas will arise and where scientific research will lead.

Our breakthrough was the result of “night science”: a stumbling, wandering exploration of the natural world that relies on intuition as much as it does on the cold, orderly logic of “day science.”** In today's vastly expanded scientific enterprise, obsessed with impact factors and competition, we will need much more night science to unveil the many mysteries that remain about the workings of organisms.

The ancient debate surrounding the existence of free will appears unresolvable, a metaphysical question that generates much heat yet little light. Common sense and volumes of psychological and neuroscientific research reveal, however, that we are less free than we think we are. Our genes, our upbringing and our environment influence our behaviors in ways that often escape conscious control. Understanding this influence, the advertisement industry spent approximately half a trillion dollars worldwide in 2010 to shape the buying decisions of consumers. Yet nothing approaches the perfidy of the one-celled organism Toxoplasma gondii, one of the most widespread of all parasitic protozoa. It takes over the brain of its host and makes it do things, even actions that will cause it to die, in the service of this nasty hitchhiker. It sounds like a cheesy Hollywood horror flick, except that it is for real.

What elevates this vignette about evolution and life in the wild to epic proportions for humanity is that about a tenth of the U.S. population is infected by T. gondii (in some countries, such as France, the infection rate is seven to eight times higher, possibly because of the widespread consumption of uncooked and undercooked meat).