Implant Generates Electricity From Excess Glucose In the Blood

A fuel cell under the skin that converts blood sugar from the body into electrical energy sounds like science fiction. Yet it works perfectly, as an ETH Zurich research team led by Martin Fussenegger, Professor of Biotechnology and Bioengineering, has shown. In type 1 diabetes, the body does not produce insulin. This means that patients have to obtain the hormone externally to regulate their blood sugar levels. Nowadays, this is mostly done via insulin pumps that are attached directly to the body. These devices, as well as other medical applications such as pacemakers, require a reliable energy supply, which at present is met primarily by power from either single-​use or rechargeable batteries.

Now, a team of researchers led by Martin Fussenegger from the Department of Biosystems Science and Engineering at ETH Zurich in Basel (Switzerland) have put a seemingly futuristic idea into practice. They have developed an implantable fuel cell that uses excess blood sugar (glucose) from tissue to generate electrical energy. The researchers have combined the fuel cell with artificial beta cells developed by their group several years ago. These produce insulin at the touch of a button and effectively lower blood glucose levels much like their natural role models in the pancreas.

“Many people, especially in the Western industrialised nations, consume more carbohydrates than they need in everyday life,” Fussenegger explains. This, he adds, leads to obesity, diabetes and cardiovascular disease. “This gave us the idea of using this excess metabolic energy to produce electricity to power biomedical devices,” he says.

At the heart of the fuel cell is an anode (electrode) made of copper-​based nanoparticles, which Fussenegger’s team created specifically for this application. It consists of copper-​based nanoparticles and splits glucose into gluconic acid and a proton to generate electricity, which sets an electric circuit in motion. Wrapped in a nonwoven fabric and coated with alginate, an algae product approved for medical use, the fuel cell resembles a small tea bag that can be implanted under the skin. The alginate soaks up body fluid and allows glucose to pass from the tissue into the fuel cell within.


Marked Donor Bone Marrow Cells Attack Cancer, Not Healthy Tissue

A groundbreaking process developed by researchers from University of Missouri is offering new hope in the fight against blood cancers, such as lymphoma and leukemia.

A pair of researchers at the School of Medicine have developed a process for marking transplanted donor bone marrow cells so that the immune cells only attack cancerous cells but not healthy tissue. One of the reasons bone marrow transplants are often a last resort for patients with blood cancers is graft-versus-host disease (GVHD), a common occurrence where transplanted donor immune cells attack both malignant and healthy cells in the recipient.

Our ability to biologically label these donor immune cells so that they will attack cancerous cells in the host and then stop themselves from attacking healthy tissue offers new hope that bone marrow transplants can be safer and more effective for patients,” said co-lead researcher, Esma S. Yolcu, PhD, professor of Child Health and Molecular Microbiology and Immunology. “The stem cells in bone marrow have tremendous potential to combat autoimmune diseases, such as type-1 diabetes and blood cancers, such as leukemia, lymphoma and multiple myeloma. It is critical to solve the puzzle of GVHD to unlock the full potential of bone marrow cell transplant treatment regimens.”

Yolcu and Haval Shirwan, PhD, also a professor of Child Health and Molecular Microbiology and Immunology, developed the ProtEx™ platform technology to generate recombinant biologics that instruct immune cells to achieve a desired treatment outcome. Engineered donor cells display on their surface instructions for the transplanted immune cells to attack only the cancerous cells and then self-destruct before attacking healthy tissue in the host, thus preventing GVHD.

This approach has significant potential as a treatment on its own or in combination with other clinical regimens to increase the efficacy of stem cell transplants,” said Shirwan. “The process of engineering the donor cells is straightforward and efficient, making it suitable for clinical translation.”

In their research to date, the ProtEx™ engineered immune cells have been effective in overcoming GVHD following transplantation in mice as well as in a humanized mouse model. Transplantation with the engineered cells was effective in preventing acute GVHD without a detectable negative impact on the recipient immune system. The concept is presently being pursued for testing in a large animal model of GVHD as a prelude to clinical translation for the treatment of hematological cancers.

Yolcu and Shirwan’s research was recently published in Blood Advances, entitled “Engineering donor lymphocytes with Fas ligand protein effectively prevents acute graft-versus-host disease. The lead authors disclosed that they have a provisional patent on using SA-FasL-engineered cells as a prophylactic approach for acute GVHD. The researchers also recently received a National Institutes of Health grant for their research at the Roy Blunt NextGen Precision Health Building on a treatment for type-1 diabetes that uses transplanted stem cells derived insulin producing cells to replace the need for regular insulin injections.


Diabetics die 3 times more of Covid-19

From the outset of the pandemic, data coming out of early coronavirus hot spots like China, Italy, and New York City foretold that certain groups of people would be more vulnerable to Covid-19. The disease hit older people and people with underlying medical conditions the hardest. As early as February, diabetes had emerged as one of the conditions associated with the highest risk. In one large study out of China, people with diabetes were more than three times as likely to die of Covid-19 than the overall population.

But that’s not what brought four diabetes experts from Australia and the United Kingdom onto a Zoom call back in April. They were supposed to just be catching up—a virtual tea among friends. But talk soon turned to something strange that they’d been seeing in their own hospitals and hearing about through the grapevine. The weird thing was that people were showing up in Covid-19 wards, after having tested positive for the virus, with lots of sugar in their blood. These were people with no known history of diabetes. But you wouldn’t know it from their lab results.

After that call, the experts reached out to colleagues in other countries to see if they’d seen or heard of similar cases. They had. Acute viral infections of all sorts can stress the body, causing blood sugar levels to rise. So that in itself wasn’t unusual, says Francesco Rubino, a bariatric surgeon and diabetes researcher at King’s College in London, who was on that first Zoom call. “What we were seeing and hearing was a little bit different.”

Doctors around the world had described to him strange situations in which Covid-19 patients were showing symptoms of diabetes that didn’t fit the typical two-flavor manifestation of the disease. In most people with type 1 diabetes, their immune cells suddenly turn traitorous, destroying the cells in the pancreas that produce insulin—the hormone that allows glucose to exit the bloodstream and enter cells. People with type 2 diabetes have a different problem; their body slowly becomes resistant to the insulin it does produce. Rubino and his colleagues were seeing blended features of both types showing up spontaneously in people who’d recently been diagnosed with Covid-19.

That was the first clinical puzzle,” he says. For clues to an explanation, Rubino and his colleagues looked to ACE2, the protein receptor that SARS-CoV-2 uses to invade human cells. It appears in the airways, yes, but also in other organs involved in controlling blood sugar, including the gut. Doctors in China discovered copies of the coronavirus in the poop of their Covid-19 patients. And a meta-analysis found that gastrointestinal symptoms plague one out of 10 Covid-19 sufferers.

In the last few decades, scientists have discovered that the gut is not the passive digestive organ once thought. It actually is a major endocrine player—responsible for producing hormone signals that talk to the pancreas, telling it to make more insulin, and to the brain, ordering it to make its owner stop eating. If the coronavirus is messing with these signals, that could provide a biological basis for why Covid-19 would be associated with different forms of diabetes, including hybrid and previously unknown manifestations of the disease. Rubino is one of a growing number of researchers who think that the relationship between the coronavirus and diabetes is actually a two-way street. Having diabetes doesn’t just tip the odds toward contracting a worse case of Covid-19. In some people, the virus might actually trigger the onset of diabetes, and the potential for a lifetime of having to manage it.