Science fiction aficionados may be familiar with a trilogy by Nancy Kress, in which she imagines the emergence of genetically modified humans who don’t require sleep. Naturally, given all the extra time, the sleepless quickly surpass others who need to rest each day and evolve into a superior race. The trilogy tells the story of the resulting class, cultural, and technological conflict and is a fascinating read.

Alas, most of us need our nightly sleep and function miserably when sleep deprived. But what if the performance hit from too little sleep could be ameliorated by tweaking brain chemistry?

New research from a collaboration between scientists at the Universities of Pennsylvania, Glasgow, and Toronto identifies a chemical-signaling pathway involved in the memory and learning deficits that result from suboptimal sleeping. (Nature 461 [22 October 2009], 1122–1125) Five hours of sleep deprivation in mice caused impairment of hippocampus function by increasing the activity of the enzyme that degrades cyclic AMP—phosphodiesterase. Treating the critters with a drug (rolipram) that inhibits phosphodiesterase restored hippocampus function.

In the words of the authors, the results “lay the groundwork for further analysis of the functional biochemistry of sleep deprivation.” This may be good news for those of us moderns who never seem to find enough time for proper rest. Don’t start pulling all-nighters yet, though, as five sleepless hours for mice doesn’t quite mimic the chronic effects of weeks or years of too little shut-eye for people.

If sleep fascinates you, see my previous post on the subject. On the other hand, don’t bother if my writing makes you drowsy….

In one corner, we have Moore’s law. In the other corner, there is Carlson’s curve.

Moore’s law— named after Gordon Moore, co-founder of Intel—famously predicted over 40 years ago that the transistor density of integrated circuits would double about every two years. So far, it’s been right.

Carlson’s curve—named after biologist Rob Carlson—refers to a graph showing the diminishing cost per base of sequencing DNA over time. Like transistor density, DNA sequencing prowess is similarly exponential, and showing no signs of slowing down.

Of course, neither of these is a fundamental law of nature, only empirical observations, and reality will inevitably deviate from the prediction someday.

So one naturally wonders, if it were a contest, which will hold steady the longest?

If one assumes a conventional mathematics of exponential growth, Moore’s law will be repealed first because it started first (approximately 1965 and 1990 for the two cases), and such a curve always levels off.

Deviations from a standard exponential would most likely come from new discoveries or technological innovation. For Moore’s law, the physical constraint of moving electrons in circuits is certainly limiting, as is the near certainty that a transistor can’t be smaller than a single atom. However, quantum computing or DNA computing might overcome these inherent limits of silicon chips.

For DNA sequencing (or DNA synthesis for that matter), the cost of chemical reagents and the ability to physically resolve DNA fragments cheaply are clearly limiting at some point. However, rapid advances in robotics, miniaturization, and “lab-on-a-chip” technologies can be expected to continue for the foreseeable future.

Based on nothing but the intuition that cost is easier to overcome than physics, my bet is that halving the price tag of DNA sequencing will outlast the course of integrated circuit doubling. Doubtless, readers can present counter-arguments, which I of course welcome and encourage.

The universe is a big place. Estimates vary, but there are something like 10¹⁰ galaxies, 10²² stars, and 10⁸⁰ atoms. Such numbers are hard to get your mind around, even in an era when trillions (10¹²) is commonly used when measuring government debt.

But this is just the observable universe. Cosmologists are now pretty convinced that the true reality is a multiverse, or many parallel universes existing at the same time. Naturally, one wonders how many such universes there might be.

Imponderable as this question may seem, a duo of physicists at Stanford University has taken a stab at answering it. The analysis can be found at the open access preprint site for physics and related disciplines. (Aside—how come chemists don’t do this?)

The mathematics of quantum fluctuations required to understand the work will tax most readers, as will the final answer: 10^10^10^7. This is a number that is virtually impossible to comprehend or even to write down. It has over 10^10,000,000 digits!

With all those uniquely different universes, there surely is lots of potential for chemistry beyond even our wildest imaginations. Perhaps a different periodic table, unusual reactions, compounds we can’t imagine in our own universe. Maybe even altogether inconceivable life forms.

Apparently such gigantic numbers as 10^10^10^7 lead one to unchecked speculation. But perhaps a quantity we can better understand is Douglas Adams’s answer to the “ultimate question of life, the universe and everything,” as recounted in the estimable Hitchhikers Guide to the Galaxy—42. I can relate to that one.

One of the reasons cancer therapy is effective is that conventional drugs are somewhat indiscriminate toxins. Thus, they kill lots of tumor cells, even if those cells are not similar in their molecular properties. This is a good thing since most tumor masses are thought to be heterogeneous at the cell and molecular levels.

The bad news is that indiscriminate toxins can also damage normal tissues. Hence, the agony of awful side effects that accompanies cancer treatment.

A new study (with 30 authors from several research centers in Canada and Britain) describes an incredibly detailed look at how a single tumor—metastatic breast cancer—acquires genetic heterogeneity over time (Nature 461 [8 October 2009], 809–813).

Starting from the initial diagnosis, the research team measured genetic changes over nine years that eventually led to spread of the cancer to other body sites.

The result? Significant molecular evolution occurs as a tumor grows and then spreads. This is the source for tumor cell heterogeneity and ultimately is why some cancer cells will be eradicated by therapy and others not.

It is also a real challenge to personalized medicine to create drugs that will target every variant cell type rather than indiscriminately carpet-bombing them all. Luckily, this new work is a starting point for doing just that.