The following is surely one of the funnier exchanges in movies of the last few decades:

Arthur:  Hobson, do you know what the worst thing is about being me?

Hobson:  I should imagine your breath, sir.

(Dudley Moore and Sir John Gielguid in Arthur)

But what foul chemistry lies behind bad breath?

The villainous reaction is perpetrated by Gram negative bacteria, which break proteins down to amino acids. The sulfur-containing ones can then form stinky chemicals called volatile sulfide compounds (VSCs to the aficionado).

Recent work from Tel Aviv University adds a new twist. Sterer et al. show that prior to breakdown, oral proteins have to be denuded of their sugars by an enzyme called beta-galactosidase. This activity is produced mainly by Gram positive organisms, so it takes a flourishing microbial ecology to lead to the dreaded halitosis (Journal of Breath Research 3:1 [March 2009] doi: 10.1088/1752-7155/3/1/016006 ).

And based on this work there’s new hope for dragon-breath sufferers. The researchers have applied for a patent for a new device that measures both kinds of bacteria. It’s small, cheap, and turns blue if you’re in danger. Best of all is its name: OkayToKiss.

The mainstream media regularly barrages us with the fact that citizens of developed countries tend to being overweight, even obese. So we diet, we exercise, we pop pills, and sometimes we even resort to surgery to shed the unwanted poundage.

All this obsession on weight loss appears to be high on the futility list. The World Health Organization reports that about 400 million of us are obese, with another 1.2 billion way overweight.

So if behavior modification doesn’t yield good results, could science rescue us from fatness? Possibly, at least according to a new study from UCLA.

Anyone who ever studied biochemistry at least dimly recalls the Krebs cycle, which is involved in the metabolism of sugars and fats. The glyoxylate shunt is a less-remembered feature of the famous cycle, most likely because it is only found in microorganisms and plants, not in humans.

The lure of the shunt pathway is that it enables fat to be made into sugar, not just the reverse. And it’s the biosynthesis of fat from sugar-rich diets that bedevils so many otherwise healthy folks. Accordingly, Dean et al. engineered the two key enzymes from the glyoxylate shunt into mouse livers (Cell Metabolism, [3 June 2009], 525–536).

The results of the experiment are striking: mice with the new enzymes are resistant to diet-induced obesity. For reasons unknown, females appear to benefit even more than their male counterparts in resisting the portly consequences of a high-fat diet.

Don’t start eating lots of dessert just yet though. Effective and safe gene therapy in humans is still in the future, so for now we’ll have to stick to the old-fashioned but virtuous routine of diet and exercise to control our urge toward corpulence.

Most of us give little thought to the countless batteries we encounter every day. They power cell phones, iPods, cameras, computers, watches, and myriad other electronic devices, without which life would be ever so less pleasant.

Chemistry, of course, is the driver of battery technology. From lithium-ion to zinc-carbon to lead-acid, chemical energy is the underlying force that produces electrical energy. But battery technology has not kept pace with other innovations in modern life, and power output, weight, cost, and longevity remain major challenges for those hoping to score big with a battery breakthrough.

So to score big, think small. At least that’s the approach taken by a collaborative project between MIT and the Korea Advanced Institute for Science and Technology (Science 324 [22 May 2009], 1051–1055).

These investigators used a tiny bacterial virus (M13) modified to bind both carbon nanotubes and amorphous iron phosphate, and thus to align charges along a conducting electrode. Doing so allowed creation of a bioengineered Li-ion battery that is small, dense, and high performing.

Alas, it’s not a practical product yet, but does offer new meaning to the much-used term “going viral.”

The standard mindset in treating cancer is to kill as many of the offending cells as possible with whatever artillery you can devise. Traditionally, the weaponry has comprised surgery, radiation, and chemotherapy, or, for the irreverent, “cuts, burns, and poisons.”

The military metaphor is intentional, as it conveys the all-out-assault, no compromise, take-no-prisoners attitude that has marked treatment for the last several decades. And besides, the first broadly effective anticancer drug (nitrogen mustard) was courtesy of gas warfare in WWI.

And now along comes Robert A. Gatenby from Florida’s Moffitt Cancer Center. His counsel? Forget conventional wisdom, don’t try to eliminate the tumor, treat it just enough to keep it from growing any bigger.

Gatenby makes the case in Nature ( [28 May 2009], 508–509). The basic argument is a comparison to controlling the invasion of exotic species in ecosystems. Examples include moths in a farmland or snails in a cityscape. Such pests are rarely eliminated, but they can be controlled in a way that doesn’t interfere with essential functioning.

Applying this lesson to cancer means the disease would not be cured, but neither would you die from it once treatment failed, as it inevitably does with most cancers.

The response of the cancer establishment is predictably skeptical, even hostile. I’m unconvinced myself, because even if drug resistance is skirted, the constant presence of a malignancy increases the equally deadly probability of metastasis to other sites.

But doubt should always be tempered by the wise observation of Arthur C. Clarke: “New ideas pass through three periods:

1. It can’t be done.
2. It probably can be done, but it’s not worth doing.
3. I knew it was a good idea all along!