Exoskeletons as Fashion

There’s an interesting article over at the new Discover Magazine blog, the Crux, by Kyle Munkittrick, which you should definitely go read if you’re interested since I’ll just touch on it here. He discusses powered exoskeletons as a coming fashion trend – something I had not at all envisioned. He points out that every fashion is a prosthesis, and most relevantly, glasses and contacts were something first seen only as an aid for a disability, but have now blown up to be very much a part of fashion. Why shouldn’t we adapt to exoskeletons as fashion as well?

Right now powered exoskeletons seem to be mainly considered as aids for the handicapped or for the military, but as they get cheaper and better it’s not hard to imagine them being used in everyday life – there’s plenty of work that requires extra safety or heavy lifting. Hard hats haven’t exactly become sexy, but if it’s something used in a wide variety of circumstances by a variety of demographic groups, and considering there are already a fair amount of companies competing over exoskeletons, it would make sense for companies to try to market their products as fashionably as possible for each niche. 

If you’re wondering about the current state of exoskeletons, below are some examples of modern powered suits in action. Many companies are developing them, but the technology doesn’t seem to be quite developed enough for them to be widespread. Regardless, the exoskeleton seen in the first video (HAL) is being used in over 100 hospitals, according to the Tokyo Times, and the exoskeleton from the second video is being sold for personal use in New Zealand, although it’s currently rather pricey at about $150,000 USD.

Fun fact: the first ever powered exoskeleton was developed by GE and the U.S. military in the 1960’s; it was strong, but too heavy and too difficult to control, so it was never even tested with a person inside. 

And on a side note, the Japanese company that’s working on HAL is called Cyberdyne. They named themselves after the company that created Skynet in the Terminator series, and their exoskeleton has the same name as the homicidal AI from 2001: A Space Odyssey? If they’re trying to tell us something about their future plans, they couldn’t put it any clearer. 

“Lab-Grown Blood Given to Volunteer For the First Time”

From New Scientist:

RED blood cells generated in a lab have been successfully injected into a human volunteer for the first time. This is a vital step towards a future in which all the blood we need for transfusions can be made in the lab, so that blood donors are no longer essential.

Luc Douay at Pierre and Marie Curie University, Paris, and his colleagues extracted what are called hematopoetic stem cells from a volunteer’s bone marrow.

Hematopoietic stem cells are cells that can turn into any kind of blood cell. They’re a step in the path between embryonic stem cells, at the least differentiated extreme, and a specific type of blood cell, at the most differentiated extreme.

These cells were encouraged to grow into cultured red blood cells using a cocktail of growth factors. After labelling the cells so they could be traced, Douay’s team injected 10 billion – the equivalent of 2 millilitres of blood – back into the original donor to see how they survived…

“The results show promise that an unlimited blood reserve is within reach,” says Douay. That blood reserve is needed urgently. Although blood donations are increasing in many developed countries, blood banks struggle to keep up with the demands of ageing populations who need more operations – often involving blood transfusions. And a source of HIV-free blood is essential in countries with high rates of HIV infection…

Douay’s next challenge is to scale up production to a point where the cultured blood cells can be made quickly and cheaply in sufficient quantities for blood transfusions. The 10 billion cells his team made wouldn’t go very far – a transfusion typically requires 200 times that number. With his existing technology, Douay estimates that a single transfusion would require 400 litres of culture fluid, which is clearly impractical. “We are still a long way from the vision of dropping a couple of stem cells into the broth and making endless units of blood,” says John Hess of the University of Maryland in Baltimore.

Douay believes that it may take several years to scale up the technology. Another possibility is to use embryonic stem cells instead, as Lanza did in 2008. “We can generate up to 100 billion red blood cells from a single six-well plate of stem cells,” Lanza says. He also claims to have made red blood cells through yet another technique: generating “induced pluripotent” stem cells from skin samples and coaxing those stem cells into becoming blood cells.

This sounds like great news. Blood donations are always in need; supplementing those with lab-created blood should be a relief for patients in need of transfusions. New Scientist also gave us this handy-dandy timeline of the path to artificial blood, for your learning pleasure:

If you’re wondering what the “Rhesus blood group” it’s referring to above means, it’s a property of different blood types, part of which we’re familiar with by the positive/negative classification of our blood.

Creating a Supermouse

Getting rid of a particular protein in mice by knocking out the gene that codes for it resulted in mice that could run twice as far as regular mice. Wow.

From New Scientist:

Auwerx and his colleagues used a targeted virus to knock out the gene that makes a protein called nuclear receptor corepressor 1 (NCoR1) in the muscle of mice. Without NCoR1, mitochondria, which power cells, keep working at full speed. “Effectively, the mice go further, faster, on the same amount of gas,” says Auwerx.

“The treated mice ran an average of 1600 metres in 2 hours, compared with 800 metres for untreated mice,” he says…

Auwerx warns athletes not to try to grow their muscles and stamina illicitly by somehow targeting the NCoR1 protein, however.

“We only know what happens if it’s knocked out either in fat or muscle, and it could have serious side effects on other organs,” he says. Also, he points out that without NCoR1, all fetuses perish, so it plays a vital but undiscovered role in fetal development.

Maybe I’m just naive, but this seems like a bit of a bombshell to drop without further details. What happened to the health of the mice in the long run? I can’t imagine it would be improved, but it’d be interesting to know exactly what the side effects were. 

The protein they mention, NCoR1, is responsible for down-regulating particular genes, preventing the cell from reading and using them, which is why it’s called a repressor. This raises a mountain of new questions – what do the genes it regulates code for? How are the mitochondria affected, specifically? I must know! 

This sounds like the kind of finding that can lead to the production of dangerous, illegal performance-enhancers in the future – let’s hope it works out for the best. 

Rapid Genetic Testing in a Clinical Setting

For what appears to be the first time, doctors have used rapid genetic testing to immediately inform their treatment of patients. Basically, some people react poorly to a particular drug, and the genetic variant responsible for this is known. Doctors could test whether or not they had this genetic variant and administer the correct drug accordingly. The steps, as outlined in Medical Xpress:

The point-of-care genetic test used in the study is a first in medicine and overcame many of the previous obstacles that had prevented routine clinical genetic testing. The test featured:

— A saliva swab performed by clinical nurses at the bedside with no prior training in genetic laboratory techniques.
— A one-step insertion of the swab into a testing machine.
— Sixty minutes to identify whether individuals carried the at-risk genetic variant.

The Medical Xpress article goes into more detail and background, if you’re interested.

This technology sounds pretty great. How great though depends on how common this kind of situation is – how often medical care depends on genotype. I wouldn’t be surprised if I’d heard of that situation, but nothing comes to mind right now. I guess we’ll find out when we’re getting swabbed. If it is common, well, saving lots of money on healthcare would be pretty fantastic – and, of course, being in better health would be nice.

If you’re curious about DNA sequencing, you should check out this Ars Technica article that I’ve linked to before; it lays out the basics of the science well enough that I won’t try to replicate it here.

Bacteria as Antibiotics

Researchers at the University of Virginia have decoded the genome of a type of bacteria,  Micavibrio aeruginosavorus, that can survive by attaching to another bacterium and “essentially” sucking out its nutrients, killing its prey in the process. If it can be made to target the right pathogenic bacteria in our bodies, this could be used as an antibiotic in the future.

From PhysOrg:

The bacterium, Micavibrio aeruginosavorus, was discovered to inhabit wastewater nearly 30 years ago, but has not been extensively studied because it is difficult to culture and investigate using traditional microbiology techniques…

The bacterium “makes its living” by seeking out prey – certain other bacteria – and then attaching itself to its victim’s cell wall and essentially sucking out nutrients. Unlike most other bacteria, which draw nutrients from their surroundings, M. aeruginosavorus can survive and propagate only by drawing its nutrition from specific prey bacteria. This kills the prey – making it a potentially powerful agent for destroying pathogens.

One bacterium it targets is Pseudomonas aeruginosa, which is a chief cause of serious lung infections in cystic fibrosis patients…

Additionally, because M. aeruginosavorus is so selective a feeder, it is harmless to the thousands of beneficial bacteria that dwell in the general environment and in the human body…

Another benefit of the bacterium is its ability to swim through viscous fluids, such as mucus. P. aeruginosa, the bacterium that colonizes the lungs of cystic fibrosis patients, creates a glue-like biofilm, enhancing its resistance to traditional antibiotics. Wu noted that the living cells of M. aeruginosavorus can swim through mucus and biofilm and attack P. aeruginosa.

M. aeruginosavorus also might have industrial uses, such as reducing bacteria that form biofilms in piping, and for medical devices, such as implants that are susceptible to the formation of biofilms.

This is a pretty interesting idea to me. One would hope that we could engineer M. aeruginosavorus to hunt down very specific pathogenic bacteria, but there’s definitely a potential danger of accidentally killing beneficial bacteria in our bodies and producing nasty side effects. They don’t say at all how M. aeruginosavorus works, but another potential issue is that some individual bacteria will be resistant to its attack, and bacteria populations will develop resistance to it just like any other drug. 

In any case, the more potential pathogen-killers the merrier, so I’m interested to see where this research goes in the future.

Edit: PhysOrg accidentally called Pseudomonas aeruginosa “Pseudomonas aeruginosavorus“, seemingly mixing it up with M. aeruginosavorus, so I edited the quote above for accuracy. Many thanks to johan for pointing that out. 

A TED Talk on Prosthetic Arms

Since I’ve mentioned prosthetic limbs a few times, I thought I might as well link to this TED talk discussing the concept behind current and coming prosthetic arms. This researcher, Todd Kuiken, uses a different method than what I’ve discussed before: instead of interacting directly with the brain, his arms interact with the nerves that had previously projected to the hand, but in amputees now end in the chest.

He also touches on the possibility of arms that can transmit sensory information. While my related post today was on a technology for a better sensor that could be used in prosthetic arms, it looks like the technological barrier in the arms Kuiken discusses is how to transmit sensory information to the patient’s sensory nerves with good resolution, which is a separate issue. 

The Science of Cloning

LiveScience has a good FAQ article on the basics of how animals are cloned. Cloning is only going to get more prominent in the future, so it wouldn’t hurt to have an idea of what it is and how it’s done. I won’t summarize it here, since it’s already explained briefly and nicely. The last paragraph mentions the recent successful cloning of a human embryo for harvesting embryonic stem cells, which I discussed a while ago along with some background on stem cells.

As always, feel free to let me know if you’d like any aspect explained in more detail.

Curing Allergies By Presenting the Allergen With Blood Cells

Allergies are a pretty significant and growing health issue. There exist treatments for allergies, but nothing quite like an easy cure. It looks like a team from Northwestern University may have done just this, by attaching peanut proteins to a subject’s blood cells and reintroducing it into them, signaling to the immune system that these proteins are non-harmful.

From Science Daily:

Peanut allergies often cause life-threatening allergic reactions, called anaphylaxis. Each year there are between 15,000 and 30,000 episodes of food-induced anaphylaxis and 100 to 200 related deaths in the United States, according to the National Institutes of Health. There is no safe treatment to protect people from a severe allergic reaction to food.

When an allergic person eats a peanut, the proteins are absorbed through the intestine and can activate a life-threatening, full-body immune response. This includes constriction of the airways, low blood pressure and/or shock and can lead to loss of consciousness and death.

Using a mouse model that mimics a life-threatening peanut allergy (which the Northwestern team developed several years ago), researchers attached peanut proteins onto white blood cells called leukocytes and infused those back into the mice. After two treatments, the mice were fed a peanut extract. They did not have the life-threatening allergic reaction because their immune system now recognized the protein as safe.

“Their immune system saw the peanut protein as perfectly normal because it was already presented on the white blood cells,” Bryce said. “Without the treatment, these animals would have gone into anaphylactic shock.” Bryce thinks more than one protein can be attached to the surface of the cell and, thus, target multiple food allergies at one time.

They also tried this with a different allergen model (an egg protein), and it worked then too. Wiping out (food) allergies would be quite an achievement; let’s hope this idea works. The idea itself seems somewhat intuitive, but I assume it’s only coming to light now because there are less obvious hurdles to overcome. 

If it seems like extracting and modifying each person’s blood to use this technique is a little inconvenient, it may not be the final form of the technique:

For autoimmune diseases and allergic airway diseases, Miller also is working with microparticles rather than white cells to induce tolerance, because the microparticles are more easily standardized for manufacturing.

Mass-produced immunity! Doesn’t get better than that. Which reminds me, go get vaccinated this flu season. 

Paralyzed Patients Thought-Control a Robotic Arm

A few days ago I wrote about thought-controlled prosthetic limbs, and how a new experiment showed for the first time that monkeys could both control a virtual limb and receive sensory feedback from it. The Associated Press, via Medical Xpress, brings us news of a new robotic arm made by DARPA capable of relatively complex movement as well as of sensing touch through sensors on its fingertips.

The article tells a story of a paralyzed patient using this arm – through chips implanted into his brain – that won’t quite be the same in summary, so you should check it out yourself if you can. The summary is basically that some paralyzed people are part of a project known as BrainGate, among other presumably similar projects, where they’re learning to use electrodes implanted into their brains to control robotic third arms. They haven’t yet tried transmitting the arm’s sensory information back to the user, but that’s coming up soon, and it will be awesome. 

This all also means I have to take back what I assumed in the monkey post; I didn’t think implanting electrodes into people’s brains (as opposed to recording electrical activity from their scalps) would be a desirable course of action, but it looks like it’s feasible after all. I’m not sure if the electrodes/chips they used in this case had wires coming out or transmitted data wirelessly; I would hope the latter, but even if not, that’s probably not a major hurdle to overcome in the future compared to the rest of it. I also didn’t realize that a touch-sensitive robotic arm was already being used, although it looks like it only has sensors in its fingertips.

This is fantastic stuff, but it’s also going to raise its own issues in the future, especially if prosthetic limbs eventually function better than regular limbs and become desirable. That’s not a major concern compared to ending paralysis and helping amputees though, so again, this will be awesome.

Alzheimer’s as a Contagious Prion Disease

Via ScienceDaily: New research shows that Alzheimer’s disease may in fact be able to spread between individuals in the same fashion as a prion disease.

You may have heard about prions in the news during the recent outbreak of mad cow disease (bovine spongiform encephalopathy). Prions are infectious proteins – a very counterintuitive idea, since we’re used to infectious agents being fungi, bacteria or viruses, as opposed to a single molecule.

Proteins fold into specific configurations that determine their function. A prion is the misfolded form of a certain type of protein, called PrP, that’s very widespread throughout the bodies of humans and other animals. When it comes into contact with the normal form of PrP, it somehow induces misfolding. In this way prions spread, and they end up aggregating into plaques that disrupt the nervous system. (Since it’s Nobel week, I should mention that the discovery of prions led to a Nobel prize in 1997.)

Alzheimer’s disease is also (possibly, not certainly) caused by the formation of plaques by proteins – called amyloid beta – in the nervous system. Now, research from the University of Texas Health Science Center at Houston shows that when brain tissue from human sufferers of Alzheimer’s disease is injected into healthy mice, the mice start developing their own plaques and Alzheimer’s-like symptoms, indicating that these plaques may in fact spread like prions. 

Of course, whether or not this has any impact on human health is still unclear. No one is accidentally inheriting diseased brain tissue from one another, to the best of my knowledge. Still, it’s always possible that misfolded amyloid beta is somehow being transmitted between individuals. If that’s true, it’d be a huge, huge discovery for the study of Alzheimer’s, a disease that affects a very large proportion of the elderly.    

(Edit: Interestingly enough, another article from today discusses how another protein that abnormally aggregates in relation to a neurological disease – alpha synuclein, in Parkinson’s and other diseases – may similarly recruit proteins in other cells to aggregate and spread the disease. This was seen within one organism, though, not spreading between organisms like a prion disease.)