A Pill That May Shrink a Gland, Lynx in the Treetops and a Boron Bond Found by Accident

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A pill that might switch off one cause of high blood pressure, a cat that learned to climb for its dinner, and a molecule chemists had more or less given up on.

Start with a pair of small glands that sit on top of your kidneys. The adrenals make a hormone called aldosterone, which tells the body to hang on to salt. Handy when salt was scarce. In a condition called primary aldosteronism, small benign lumps in the adrenal glands make far too much of it, the body holds too much salt and water, and blood pressure climbs. It's thought to lie behind five to ten percent of all high blood pressure, and very few people who have it are ever tested for it.

The usual fixes are surgery to remove the overactive gland, or lifelong pills that block the hormone's effects. Now a team led by Morris Brown at Queen Mary University of London has reported something more intriguing in the New England Journal of Medicine. Fourteen people with the condition, treated at eight centres in the United States, took a newer kind of drug for six months to a year. It blocks the enzyme the adrenal cells use to make aldosterone in the first place.

The surprise came after they stopped. In follow-up lasting up to two years, their main marker of excess aldosterone was still about ninety-nine percent below where it began, and their blood pressure averaged about twenty-five points lower. Almost a quarter of them, so roughly three people, had normal blood pressure without any medication at all.

The idea traces back to a 2005 experiment in mice. When the gene for that enzyme was deleted, the cells that make aldosterone simply disappeared. If a tablet can do something similar, and those overactive cells wither away, a temporary treatment could become something close to a cure.

That's a big if, and fourteen people is a very small number, with no comparison group. Brown says the approach is "unlikely to be the elixir for most patients with hypertension." The next step is a larger trial, called ELIXIR, that will image the adrenal glands directly to see whether those cells really vanish.

Now to Doñana National Park in southern Spain, a mosaic of marsh, scrub and pine. Two hunters share it: the Iberian lynx, a spotted cat that lives almost entirely on rabbits, and the black kite, a raptor that also eats a lot of rabbit. For decades they mostly ignored each other.

Then in 2013 a new strain of rabbit haemorrhagic disease arrived, and local rabbit numbers fell by more than seventy percent. In wet years, both predators coped by switching to other food; the lynx turns to ducks and other waterbirds. But in drought years the marshes dry out, the ducks go too, and the lynx needs something else.

A team led by Fabrizio Sergio of the Doñana Biological Station, writing in Nature, went through thirty years of records on more than sixteen hundred kite nests. Before the rabbit crash, lynx took about one percent of them. After it, in drought years, the cats began climbing pine trees, up to about twelve metres, to take the chicks. In the worst year, close to half of the young kites nearly ready to fly were killed. Nests with rabbit remains beneath them were attacked more often, so the kites competing hardest with the lynx tended to pay the most.

The effects rippled outward. Kites that lost broods raised about twenty-eight percent fewer young over their lives and were four times more likely to abandon their territories. Fewer kites meant good news for little owls, which kites sometimes eat. The authors call it suggestive of a new arms race among predators. Neither disease nor drought alone set this off. It took both together.

In Brazil's Atlantic Forest, frogs crashed at a research station called Boracéia between 1979 and 1982, and nobody could say why. Researchers from the Smithsonian and Penn State, publishing in Molecular Ecology, went back to more than three hundred and seventy preserved specimens collected there before and after the crash, and tested them for chytrid, a fungus that has devastated amphibians worldwide. Nothing collected before 1979 carried it. More than half of the 1980s specimens did.

The twist is which frogs were infected. The species that collapsed most showed no sign of infection in the preserved specimens, while stable species often carried the fungus. The team's explanation is that the most vulnerable frogs died too quickly to end up in a collector's jar, while tolerant species could carry the infection and live. A museum drawer remembers the survivors best.

Finally, a small triumph of chemistry. Atoms can share one, two or three pairs of electrons in a bond. For more than sixty years, chemists tried to make stable molecules with a triple bond between boron and oxygen, called oxoboranes, and could only catch them fleetingly or under extreme conditions. Nearly everyone had given up. At the University of Würzburg, two doctoral students, working separately, mixed a boron compound with ketones, the chemical family that includes acetone, and kept seeing odd orange and yellow solids appear. Those solids were stable oxoboranes, three of them, reported in Nature Chemistry. Holger Braunschweig, who leads the group, says the team was "stunned to see them spontaneously form."

Sixty years of effort, and the answer turned up as an oddly coloured solid that two students didn't ignore. That's us for today. Have a lovely Sunday.