Bricklaying is a messy story. The mortar consists of clay, sand and horse manure (if available), mixed with water to a fairly loose batter. The best finish is obtained if you work with your hands as the mortar is placed on, and smears with water so that the surface becomes smooth and fine. When then furnace is ready, it is dried through slow heating by wood without blasting, until the moist has been driven out of the mud. At this stage, heating should be quite cautious in order to avoid cracking.

Then, on Friday September 9, we went again with a fully loaded trailer from Dalarna in the direction of Stockholm. More than a few people were probably turning their heads when we passed, because the trailer was dominated by a large bellow — our newly built two chamber bellow with an estimated bladder capacity of up to 800 litres per minute. In addition, we brought fire wood, iron rods, pliers, some stumps and other stuff needed for the furnace operation.
…
We made one run each on Saturday and Sunday. Each time we charged a total of about 10kg ore added in amounts of about 1kg every 20 minute. For each charge, we added about twice the amount of charcoal. Discharging of the loupe was scheduled for two o’clock, and by that time a fairly large crowd had gathered to see the show. This time we managed to get the loupe out of the furnace without too much trouble. Worse was that the process took longer than expected, but the crowd seemed to be patient and people stayed around until the end.

Melander wondered why some populations of scales were becoming able to resist pesticides. Could the sulfur-lime spray trigger a change in their biology, the way manual labor triggers the growth of callouses on our hands? Melander doubted it. After all, ten generations of scales lived and died between sprayings. The resistance must be hereditary, he reasoned. He sometimes would find families of scales still alive amidst a crowd of dead insects.

This was a radical idea at the time. Biologists had only recently rediscovered Mendel’s laws of heredity. They talked about genes being passed down from one generation to the next, yet they didn’t know what genes were made of yet. But they did recognize that genes could spontaneously change–mutate–and in so doing alter traits permanently.
…
In the short term, Melander suggested that farmers switch to fuel oil to fight scales, but he warned that they would eventually become resistant to fuel oil as well. In fact, the best way to keep the scales from becoming entirely resistant to pesticides was, paradoxically, to do a bad job of applying those herbicides. By allowing some susceptible scales to survive, farmers would keep their susceptible genes in the scale population. “Thus we may make the strange assertion that the more faulty the spraying this year the easier it will be to control the scale the next year,” Melander predicted.
…
What’s striking is how many different ways weeds have found to overcome the chemical. Scientists had thought that Roundup was invincible in part because the enzyme it attacks is pretty much the same in all plants. That uniformity suggests that plants can’t tolerate mutations to it; mutations must change its shape so that it doesn’t work and the plant dies. But it turns out that many populations of ryegrass and goosegrass have independently stumbled across one mutation that can change a single amino acid in the enzyme. The plant can still survive with this altered enzyme. And Roundup has a hard time attacking it thanks to its different shape.
…
Another way weeds fight off Roundup is through sheer numbers. Earlier this year an international team of scientists reported their discovery of how Palmer amaranth resists glyphosate. The plants make the ordinary, vulnerable form of the enzyme. But the scientists discovered that they have many extra copies of the gene for the enzyme–up to 160 extra copies, in fact.
…
What makes the evolution of Roundup resistance all the more dangerous is how it doesn’t respect species barriers. Scientists have found evidence that once one species evolves resistance, it can pass on those resistance genes to other species. They just interbreed, producing hybrids that can then breed with the vulnerable parent species.

Disturbing evidence that honeybees are in terminal decline has emerged from the United States where, for the fourth year in a row, more than a third of colonies have failed to survive the winter.

The decline of the country’s estimated 2.4 million beehives began in 2006, when a phenomenon dubbed colony collapse disorder (CCD) led to the disappearance of hundreds of thousands of colonies. Since then more than three million colonies in the US and billions of honeybees worldwide have died and scientists are no nearer to knowing what is causing the catastrophic fall in numbers.
…
It is estimated that a third of everything we eat depends upon honeybee pollination.
…
Potential causes range from parasites, such as the bloodsucking varroa mite, to viral and bacterial infections, pesticides and poor nutrition stemming from intensive farming methods.
…
“We believe that some subtle interactions between nutrition, pesticide exposure and other stressors are converging to kill colonies,” said Jeffery Pettis, of the ARS’s bee research laboratory.
…
“It’s getting worse,” he said. “The AIA survey doesn’t give you the full picture because it is only measuring losses through the winter. In the summer the bees are exposed to lots of pesticides. Farmers mix them together and no one has any idea what the effects might be.” Pettis agreed that losses in some commercial operations are running at 50% or greater.

The 98 pesticides and metabolites detected in mixtures up to 214 ppm in bee pollen alone represents a remarkably high level for toxicants in the brood and adult food of this primary pollinator. This represents over half of the maximum individual pesticide incidences ever reported for apiaries. While exposure to many of these neurotoxicants elicits acute and sublethal reductions in honey bee fitness, the effects of these materials in combinations and their direct association with CCD or declining bee health remains to be determined.

Provocative new research from Boston University’s medical school and department of biomedical engineering now suggests, though, that multi-drug resistance can be acquired in one pass, through a different mutational process triggered by sublethal doses of antibiotics – the same sort of doses that are given to animals on farms.

In earlier work, the authors found that antibiotics attack bacteria not only in the ways they are designed to (the beta-lactams such as methicillin, for instance, interfere with staph’s ability to make new cell walls as the bug reproduces, causing the daughter cells to burst and die), but also in an unexpected way. They stimulate the production of free radicals, oxygen molecules with an extra electron, that bind to and damage the bacteria’s DNA.

That research used lethal doses of antibiotics, and ascertained that the free-radical production killed the bacteria. In the new research, the team uses sublethal doses, and here’s what they find: The same free-radical production doesn’t kill the bacteria, but it acts as a dramatic stimulus to mutation, triggering production of a wide variety of mutations