“Without Delay”: Federally funded research will be free and open

Out of seemingly nowhere, a major announcement from the White House: Data from all publicly funded research will have to be made available to everyone free and immediately, starting Christmas 2025.

No more paywalls. No more $1,000 access fees. No more embargos. It’s a huge boost for research not only in the U.S. but around the world.

For-profit companies like Elsevier and “non profit” organizations like the American Chemical Society have made millions charging through the nose to access the $80 billion worth of taxpayer-funded research they publish — even those very institutions that did the research. (At least in the case of the ACS they try to justify those fees by claiming to ‘add value’ by editing and formatting the work.)

No longer.

There have been workarounds, like requesting copies directly from researchers, or using sites like sci-hub, but that can be clunky and ineffective.

And what of the publishers? It may not be getting through to them. In response to the directive, Springer Nature said “that funding agencies must increase their financial support for the publications in exchange for the research to be free to the public.” (Hint: There is no “in exchange.” Do what you’re told.)

Unexpected diabetes trigger

Another gut bacteria story? Yep. How about this: Mice given the Parabacteroides distasonis bacteria in their guts develop type 1diabetes. And humans? While it’s probably unethical to infect people (even grad students) with P. distasonis to see what happens, Boston College biologists looked at records from a European database and found that people whose guts have P. distasonis (especially as infants) have a greater risk of developing type 1 diabetes later in life. In fact, “100 percent of the infants who were eventually diagnosed with type 1 diabetes had signs of P. distasonis in their gut.”

What’s going on?

This is likely because the microbe produces a peptide similar enough to part of an insulin molecule that it can lead to the production of insulin-targeted antibodies, priming the immune system to launch an attack against insulin and the cells that produce it.

Obviously the development of diabetes is complex, but this could be a pretty big step toward understanding it.

Annnnnnnnd fight!

If you’re head of the company that makes one of the two biggest Covid-19 vaccines, and you and that other vaccine maker are looking forward to profitable booster shots debuting this fall, what might be going through your head?

Perhaps, “This is great! We’re both making billions, lives have been saved, and more importantly our shareholders and CEOs sleep on mattresses made of shredded hundred-dollar bills and pillows filled with down passenger pigeons.”

Ha! No, no. You sue the other guy, of course.

Moderna has filed patent infringement lawsuits in the U.S. and Germany accusing Pfizer and its partner BioNTech of stepping on patents that Moderna says it filed between 2010 and 2016.

A better brain-garbage cleaner

A weird brain protein may lead to a treatment for neurodegenerative diseases. It seems that some forms of a protein called aquaporin 4 are created with a tail, thanks to an error called readthrough.

Weirdness: Unlike “normal” aquaporin 4, that “long form” version appears in brain cells called astrocytes where it helps clear unwanted proteins out of the brain — proteins like the kinds associated with Parkinson’s and Alzheimer’s. So (thought Washington University researchers), is there a way to get the body to produce more of it?

There is. Actually, there are at least two compounds that do the trick — apigenin and sulphaquinoxaline. Great! Next question: Does having more long aquaporin 4 actually clear more waste? Why yes, yes it does. They tested the compoundeds on mice, and found the treated rodents’ brains cleared amyloid beta proteins significantly faster than controls.

Now, while sulphaquinoxaline is toxic for humans, apigenin isn’t. In fact, it’s found in chamomile, parsley, onions and other plants. Although the lead researcher “cautions against consuming large amounts of apigenin in an attempt to stave off Alzheimer’s” this is still good (preliminary) news:

“There’s a lot of data that says reducing amyloid levels by just 20% to 25% stops amyloid buildup, at least in mice, and the effects we saw were in that ballpark. That tells me that this could be a novel approach to treating Alzheimer’s and other neurodegenerative diseases that involve protein aggregation in the brain.”

Unintended consequences

So what’s been the result of prescription drug monitoring databases? Tracking and limiting patients’ use of pharmacies to fill opioid scripts has worked … sort of.

Marketing researchers (!) at the University of Texas examined the national data from 2006 through 2015. Prescription drug monitoring programs, they said, decreased opioid prescriptions by 6.1%. W00t!

But “the policy did not reduce deaths due to prescription opioids.” Huh?

That’s because “prescription opioids” doesn’t necessarily mean “opioids dispensed by a legitimate pharmacist.” Cut off from their pharmacies, people are going to the streets “to seek out dangerous and illegal alternatives.” And that includes, obviously, heroin — and “heroin-related deaths increased 50.1% under PDMP mandates.”

Listening for Parkinson’s

You go to sleep, a small device by your bed. When you wake up, a red light is blinking. Oh no — you have Parkinson’s. How do you know? Apparently MIT researchers have found a way (using artificial intelligence, of course) to determine whether someone has the neurological disease by monitoring their breathing patterns while they sleep.

“A relationship between Parkinson’s and breathing was noted as early as 1817 […] Some medical studies have shown that respiratory symptoms manifest years before motor symptoms, meaning that breathing attributes could be promising for risk assessment prior to Parkinson’s diagnosis.”

Don’t kiss that frog

If you woke up at 3:00 am wondering, “Is rat lungworm disease really only caused by slugs and snails?” researchers from the universities of Hawai’i and London have your answer:

[A]t least 13 species of prawns/shrimp, crabs, flatworms, fish, frogs, toads, lizards, and centipedes have been associated with causing rat lungworm disease in humans.

The good news is that rat lungworm disease is mostly confined to the tropics and subtropics, so as long as nothing changes Georgia’s climate, it shouldn’t be an issue. Sweet dreams.