Most people don’t go into chemistry for the money. Apparently, though, your own personal chemistry may influence how much money you make. At least if you are a male stockbroker in London.

A new study by researchers at the University of Cambridge showed that British stock traders made more profits on days in which they started with higher levels of testosterone (Proceedings of the National Academy of Sciences, 22 April 2008, vol. 105, pp. 6167–6172; online abstract available). And having a good day financially results in sustained high testosterone levels. On days in which the market is unpredictably volatile, cortisol levels rise.

Who cares? Testosterone and cortisol are closely implicated in regulating emotions around stress and competition, so one’s basic body chemistry may drive risky (or cautious) behavior that in turn influences financial markets.

Two questions spring to mind. Are there similar effects in women? Should Barry Bonds become a stock broker when he retires from baseball?

Many have labored over the past half century (moi aussi) to develop new therapies for cancer treatment. There have been lots of successes, too: lives saved and suffering reduced. In fact we’ve come to expect this from contemporary science.

It is widely appreciated, though, that nobody wants to take these life-saving drugs except when utterly necessary because they are so relentlessly toxic. But what if you could target anticancer drugs just to the tumor and leave normal, healthy tissues unscathed? The holy grail….

A new technology from a research group at Washington University in St. Louis moves us closer to the grail (Winter et al., The FASEB Journal, 24 March 2008). These investigators took advantage of previous work that linked nanoparticles with an antibody that homes in on newly developed blood vessels, allowing for imaging of vessel formation.

In the new work, a potent antivascular agent, fumagillin, was also attached to the nanoparticles, and this concoction delivers a mighty wump to experimental tumors that need a blood supply to flourish. Best of all the fumagillin, normally hideously toxic, is rendered harmless except to the tumor. Voila!

And there may be a freebie as well: drugs that work to inhibit blood-vessel formation will not only starve cancer cells of essential nutrients, but may also inhibit macular degeneration, which is itself a disease of abnormal vascular growth. A twofer!

Fungi are pretty icky. We don’t generally think positively about them, except perhaps when enjoying truffles. And we can be altogether disdainful of this family of living creatures when trying to recover from a nasty fungal infection.

As they did with bacteria and cancer cells, clever scientists have devised means to ward off invading fungi. And, like all forms of chemotherapy, the antifungal drugs approved for use in humans are effective. Unsurprisingly, though, the biota at which we aim our therapeutic arsenal is not content to merely go away; it has the built-in and amazingly effective capacity to develop drug resistance.

Alarmingly often, resistance to one drug means resistance to many drugs, i.e., multidrug resistance (MDR). Bacteria, cancers, and fungi share a propensity for MDR, and they have at least one common mechanism: expression of a protein that pumps the offending drug molecule out of the cell where it can no longer do its medicinal work.

A recent discovery sheds some light on the mechanism of fungal MDR and even offers some prospects for reversing this alarming condition in disease-causing organisms (Thakur et al., Nature, 3 April 2008, pp. 604–609, with related commentary on pp. 541–542). A team of scientists from Harvard, Johns Hopkins, and Iowa showed that antifungals activate MDR by binding to a protein that increases the expression of the pump efflux gene (known to the aficionado as the transcription factor Pdr1p). Besides explaining why resistance arises, the results also suggest that blocking drug binding to the transcription factor would prevent MDR from emerging. No doubt clever chemists are already dreaming up ways to construct molecules that are themselves nontoxic.

One nagging question: the results imply that (1) when the drug goes away drug resistance should also go away; and (2) MDR would not be inherited since it is provoked by an epigenetic mechanism. Do these predictions fit the observed reality of antifungal treatment?

Do you get a headache every time someone trots out the latest statistics showing how poorly U.S. students fare in measures of science literacy? Me, too. The story is so worn and, besides, why aren’t we doing something about it?

At last week’s meeting of the American Chemical Society, interested people gathered to see what could be done about the lowly state of science education. Organized by ACS president Bruce Bursten on a languid Sunday afternoon, the symposium featured four excellent, albeit quite different, speakers.

Truth be told, it’s easy to relate horror stories of how little purportedly educated citizens know about technical matters. Harder to do is to suggest useful solutions, so here is my oversimplified guide to suggestions you missed if you couldn’t trek to New Orleans for the ACS confab:

Bruce Fuchs (National Institutes of Health): Take a close look at Finland, which ranks #1 in a measure of international science literacy (the United States is 29th).

Shirley Malcolm (American Association for the Advancement of Science): Ask a physicist, because talent is not overlooked in the discipline, at least as indicated by the proportion of women and people of color on university faculties matching their percentage in the Ph.D. pool.

Lawrence Krauss (Case Western Reserve University): Use humor to make serious points, or at least put Darwin on your currency as the British do.

Arthur Ellis (University of California, San Diego): Construct a “Map of Science,” which is so wonderfully beguiling that nobody can fail to catch the spirit of excitement.

See, there are good ideas out there for ramping up our science quotient.