I didn’t have a lot for today, but luckily Adam Jones on Twitter got me started with this one:
It sounds like someone’s figured out how to insert a much more powerful carbon fixation pathway into leaves than ordinary photosynthesis can manage:
The artificial leaf is a device that, when exposed to sunlight, mimics a natural leaf by splitting water into hydrogen and oxygen. This led to the development of a bionic leaf that pairs the water-splitting catalyst with the bacteria Ralstonia eutropha, which consumes hydrogen and takes carbon dioxide out of the air to make liquid fuel. Last June, Nocera’s team reported switching the device’s nickel-molybdenum-zinc catalyst, which was poisonous to the microbes, with a bacteria-friendly alloy of cobalt and phosphorus. The new system provided biomass and liquid fuel yields that greatly exceeded that from natural photosynthesis….
Heh. By “liquid fuel,” they may well just mean “sugars like glucose” — in other words, this look like photosynthesis. But they seem to be moving on to do the same with nitrogen, thus potentially giving other plants the advantage now enjoyed mostly be legumes, which use symbiotic bacteria to fix atmospheric nitrogen.
Well, it’s meant to boost outputs in areas like Sub-Saharan Africa. Those are areas that haven’t really yet fully utilized the methods of the first Green Revolution. Looks like they may get in on the ground floor of a second Green Revolution.
Here’s another cool technological item:
The sought-after development could aid the millions of people without ready access to clean drinking water. … The ultimate goal is to create a filtration device that will produce potable water from seawater or wastewater with minimal energy input.
Potentially very important for all kinds of uses, especially for the millions of people without easy access to clean drinking water. That’s a very serious health hazard for a huge number of people, so let’s hope this graphene sieve tests out.
Okay, and here’s something that seems too cool to be true:
In people with type 2 diabetes, the short stimulus triggered by GLP-1 isn’t sufficient to maintain a proper blood sugar balance. As a result, medication that includes a longer lasting form of the hormone is needed to help provide an extended release of insulin. “Our research team has discovered that monotremes – our iconic platypus and echidna – have evolved changes in the hormone GLP-1 that make it resistant to the rapid degradation normally seen in humans,” says co-lead author Professor Frank Grutzner, from the University of Adelaide’s School of Biological Sciences and the Robinson Research Institute. “We’ve found that GLP-1 is degraded in monotremes by a completely different mechanism. Further analysis of the genetics of monotremes reveals that there seems to be a kind of molecular warfare going on between the function of GLP-1, which is produced in the gut but surprisingly also in their venom,” he says. … “We’ve discovered conflicting functions of GLP-1 in the platypus: in the gut as a regulator of blood glucose, and in venom to fend off other platypus males during breeding season. This tug of war between the different functions has resulted in dramatic changes in the GLP-1 system,” says co-lead author Associate Professor Briony Forbes, from Flinders University’s School of Medicine. “The function in venom has most likely triggered the evolution of a stable form of GLP-1 in monotremes. Excitingly, stable GLP-1 molecules are highly desirable as potential type 2 diabetes treatments,” she says.
Platypus venom! Very cool.
Okay, and then there’s this:
I doubt anything of this kind will pan out IN TIME FOR ME PERSONALLY, which is highly disappointing, let me tell you. However:
When the mice turned eight months, the differences between both groups became evident. The mice from the first control group started to rapidly losing their weight and showed other signs of aging like spinal deformation and hair loss. At the same time, the mice that were fed with a SkQ1 containing supplement didn’t show typical signs of aging for at least additional 40-45 days. … All in all, they managed to prolong the lives of the mice by 15%.
Anti-aging developments can’t happen fast enough.
Moving on to something that caught my eye:
The disease is caused by a mutation in certain genes that normally produce a protein called myotubularin, which is essential for proper muscle function in dogs. Symptoms of this naturally occurring disease are usually visible when the dogs are young puppies, and they normally exhibit several of the features that babies with the same defective gene also demonstrate. The disorder, which only affects males, is relatively rare, and is called myotubular myopathy, or MTM. The major result of the disease is that it causes fatal muscle wasting, meaning that both dogs and boys who suffer from the disease will typically succumb in their early life due to severe breathing difficulties. … recent reports have now claimed that four collaborating research groups, in the United States and France, have now found a way to safely replace the gene that causes MTM with a healthy gene, throughout the entire musculature of dogs that are affected by it. The scientific paper reports that the diseased dogs that had been treated with just one single infusion of the corrective therapy were then indistinguishable from normal animals who had never had the disease, within the space of just one year. Dr. Martin K. “Casey” Childers, a UW Medicine researcher and physician, describes the success of the new research by saying, “This regenerative technology allowed dogs that otherwise would have perished to complete restoration of normal health.”
This isn’t an issue in Cavaliers. But I’m sure the dog people involved with breeds where we see this problem would be happy to test out gene therapy on a wide scale, hopefully quickly leading to these therapies getting approved for people.