Moon dust found in storage in a California lab

The dust, gathering dust. But the wrong sort of dust.

I've mislaid some stuff I'd rather not have over the years, but never this badly. Karen Nelson, an archivist for the Lawrence Berkeley National Lab in California, discovered 20 vials of moon dust from the Apollo 11 flight stashed away in the lab's warehouse.

The vials had been sent out to the lab shortly after Apollo 11 returned, and bear handwritten labels dated "24 July 1970"; but once the experiments were conducted, they weren't sent back to NASA, as they should have been. Instead, they found themselves vacuum sealed in a glass jar and left to gather dust for the next four decades.

Berkeley Lab's Julie Chao adds:

Nelson contacted the Space Sciences Laboratory. “They were surprised we had the samples,” she said. She then contacted NASA, who asked that the samples be sent back but allowed her to first open the jar to remove the vials.

Berkeley Lab archivist Karen Nelson holds lunar samples used by Melvin Calvin for scientific experiments 43 years ago. (Photo by Roy Kaltschmidt)

Interestingly, NASA knew that the samples were missing; Space.com reports that of the 382Kg brought back from the moon between 1969 and 1972, very little is unaccounted for:

Of the 68-gram batch of lunar material distributed to Calvin and his collaborators in 1970, NASA knew that only 50 grams was returned, said Ryan Zeigler, NASA's Apollo sample curator at the Johnson Space Center in Houston.

Space agency officials assumed that the unaccounted-for 18 grams had been destroyed during testing. Zeigler thinks the rediscovered, roughly 3-gram sample likely ended up in storage as a result of some miscommunication.

The dust had apparently been used for a paper assessing the carbon content of lunar samples as part of NASA's search for extraterrestrial life. As you may already know, they didn't find any. It was a disappointment.

Moon dust found in Berkeley Lab storage. (Photo by Marilee Bailey)

Alex Hern is a technology reporter for the Guardian. He was formerly staff writer at the New Statesman. You should follow Alex on Twitter.

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Autism and gut bacteria – the surprising link between the mind and the stomach

A recent paper has found that autistic-related social patterns can be reversed when one species of gut bacteria is present in the microbiome of mice. 

Autism – a developmental disorder that causes impediments to social interactions and behaviour – is usually linked by scientists to abnormalities in brain structure and function, caused by a mix of genetic and environmental factors. Scientists have almost always attempted to understand the way autistic people process the world around them by looking to the mind.

According to the National Autistic Society, “There is strong evidence to suggest that autism can be caused by a variety of physical factors, all of which affect brain development; it is not due to emotional deprivation or the way a person has been brought up.”

Recently, however, a lesser-known link to autism has gained traction. This time, the link is not found in the brain but in the gut.

Reporting their findings in the journal Cell, researchers from the Baylor College of Medicine, Texas, found that the presence of a single species of gut bacteria in mice could reverse many behavioural characteristics related to autism.

In the digestive tracts of humans and other animals, there exists a complex, symbiotically integrated network of trillions of microorganisms known as the “gut flora” or “microflora”. The idea that all these bacteria and microorganisms have taken up a home in our gut may initially seem startling, but they serve a number of beneficial purposes, such as aiding digestion and offering immunity from infection.

The potential link between gut flora and autism arose as researchers identified the increased risk of neurodevelopmental disorders, such as autism, among children born from mothers who were obese during pregnancy. The microflora of obese people is demonstrably different from those who are not obese, and as a result, connections have been made to the gut issues often reported in autistic people.

The senior author of the study and neuroscientist Mauro Costa-Mattioli said: “Other research groups are trying to use drugs or electrical brain stimulation as a way to reverse some of the behavioural symptoms associated with neurodevelopmental disorders – but here we have, perhaps, a new approach.”

To determine what the differences in gut bacteria were, the researchers fed 60 female mice a high-fat diet, with the aim of replicating the type of gut flora that would be found among people consuming a high-fat diet which would contribute to obesity. A control group of mice was fed a normal diet to serve as comparison. The mice in each group then mated, and their eventual offspring then spent three weeks with their mothers while being observed to see how behaviour and microflora was affected.

It was found that the offspring from the mice laden with high-fat foods exhibited social impairments, including very little engagement with peers. Meanwhile, a test called ribosomal RNA gene sequencing found that the offspring of the mice that were fed a high-fat diet housed a very different bacterial gut environment to the offspring of mice fed a normal diet.

Discussing the result, co-author Shelly Buffington was keen to stress just how significant the findings were: “By looking at the microbiome of an individual mouse we could predict whether its behaviour would be impaired.”

In an effort to understand whether the variation in microbiome was the reason for differences in social behaviour, the researchers paired up control group mice with high-fat diet mice. Peculiarly, mice eat each other’s faeces, which is why researchers kept them together for four weeks. The high-fat diet mice would eat the faeces of the normal mice and gain any microflora they held. Astonishingly, the high-fat diet mice showed improvements in behaviour and changes to the microbiome, hinting that there may be a species of bacteria making all the difference.

After careful examination using a technique called whole-genome shotgun sequencing, it was found that one type of bacteria – Lactobacillus reuteri – was far less prevalent in the offspring of high-fat diet mice than the offspring of normal-diet mice.

Discussing the method and finding, Buffington said: “We culture a strain of Lactobacillus reuteri originally isolated from human breast milk and introduced it into the water of the high-fat diet offspring. We found that treatment with this single bacterial strain was able to rescue their social behaviour.”

What the Lactobacillus reuteri seemed to be doing was increasing production of oxytocin, a hormone which is known by various other names such as the “trust hormone”, or the “love hormone”, because of its role in social interactions.

The results of the experiment showing that Lactobacillus reuteri can influence social behaviour are profound findings. Though the work would need to be transferred from mice studies to full human clinical trials to see if this could be applied to autistic people, the impact of adding Lactobacillus reuteri to the gut flora of mice can’t be underestimated. It seems then, for now, that research will go with the gut.