CU Boulder researchers have developed a new type of malleable, self-healing and fully recyclable “electronic skin” that has applications ranging from robotics and prosthetic development to better biomedical devices.
Electronic skin, known as e-skin, is a thin, translucent material that can mimic the function and mechanical properties of human skin. A number of different types and sizes of wearable e-skins are now being developed in labs around the world as researchers recognize their value in diverse medical, scientific and engineering fields.
The new CU Boulder e-skin has sensors embedded to measure pressure, temperature, humidity and air flow, said Jianliang Xiao, an assistant professor in CU Boulder’s Department of Mechanical Engineering who is leading the research effort with Wei Zhang, an associate professor in CU Boulder’s Department of Chemistry and Biochemistry as well as a faculty member in the Materials Science and Engineering Program.
The technology has several distinctive properties, including a novel type of covalently bonded dynamic network polymer, known as polyimine that has been laced with silver nanoparticles to provide better mechanical strength, chemical stability, and electrical conductivity.
“What is unique here is that the chemical bonding of polyimine we use allows the e-skin to be both self-healing and fully recyclable at room temperature,” said Xiao.
“Given the millions of tons of electronic waste generated worldwide every year, the recyclability of our e-skin makes good economic and environmental sense.”
A paper on the subject was published today in the journal Science Advances. Co-authors on the study include Zhanan Zou and Yan Li of mechanical engineering and Chengpu Zhu and Xingfeng Lei of chemistry and biochemistry. The study was funded in part by the National Science Foundation.
Many people are familiar with the movie The Terminator, in which the skin of film’s main villain is “re-healed” just seconds after being shot, beaten or run over, said Zhang. While the new process is not nearly as dramatic, the healing of a cut or broken e-skin, including the sensors, is done by using a mix of three commercially available compounds in ethanol, he said.
Another benefit of the new CU Boulder e-skin is that it can be easily conformed to curved surfaces like human arms and robotic hands by applying moderate heat and pressure to it without introducing excessive stresses.
“Let’s say you wanted a robot to take care of a baby,” said Zhang.
“In that case, you would integrate e-skin on the robot fingers that can feel the pressure of the baby. The idea is to try and mimic biological skin with e-skin that has desired functions.”
To recycle the skin, the device is soaked into recycling solution, making the polymers degrade into oligomers (polymers with polymerization degree usually below 10) and monomers (small molecules that can be joined together into polymers) that are soluble in ethanol. The silver nanoparticles sink to the bottom of the solution.
“The recycled solution and nanoparticles can then be used to make new, functional e-skin,” said Xiao
Could the Discovery of New Subtypes of Melanoma Influence Treatment?
Melanoma, a relatively rare but deadly skin cancer, has been shown to switch differentiation states — that is, to regress to an earlier stage of development — which can lead it to become resistant to treatment. Now, UCLA researchers have found that melanomas can be divided into four distinct subtypes according to their stages of differentiation. Cell subtypes that de-differentiated — meaning that they reverted back to a less-mature cell — showed sensitivity to a type of self-inflicted cell death called ferroptosis.
The research also showed that certain subtypes of melanoma cells could be successfully treated using multiple cancer therapies in combination with ferroptosis-inducing drugs.
Melanoma arises from melanocytes, cells that produce pigments. Although targeted therapies and a greater understanding of cancer immunology have significantly improved survival, many patients either relapse or do not respond to treatment.
The UCLA team, led by Dr. Thomas Graeber, analyzed the gene expression of melanoma cells and compared them to information in public genetic databases to identify the four different subtypes of melanoma with different drug sensitivities. The team organized the melanoma cells according to characteristic patterns of genes turned on by the cells. Comparing the gene expression patterns to data from stem cells induced to differentiate into melanocytes, they found that melanomas can be categorized into four distinct differentiation states.
“This refined characterization improves our understanding of the progressive changes that occur in melanoma cells during dedifferentiation, which can help develop better strategies to target this form of therapy resistance,” said Jennifer Tsoi, who was a member of the research team as a UCLA graduate student and now is a postdoctoral fellow at UCLA.
The investigators then searched pharmacogenomics databases for compounds that could best be used to treat melanomas characterized by the dedifferentiation expression pattern, either individually or in combination with other drugs.
The study introduces a new area of therapeutic possibilities for melanoma, because it is the first to link ferroptosis to melanoma differentiation states. It also more precisely defines different subtypes of melanoma, based on specific gene expression and metabolic profiles. Those subtypes characterize four steps along a trajectory taken by melanoma cells as they respond to exogenous stresses, such as drug treatments.
The approach for targeting dedifferentiated melanomas could complement existing standard-of-care therapies, since kinase inhibitors and immunotherapies are much more effective against differentiated cells than de-differentiated cells.
“Furthermore, these standard-of-care therapies can induce dedifferentiation, and thus in a co-treatment setting, ferroptosis induction can potentially block melanoma cells attempting to take this escape route,” Graeber said.
Eczema: A New Natural Brake On The Allergic Attack
Eczema affects about 17 percent of children in developed countries and is often the gateway to food allergy and asthma, initiating an “atopic march” toward broader allergic sensitization. There are treatments — steroid creams and a recently approved biologic — but they are expensive or have side effects. A new study in Science Immunology suggests a different approach to eczema, one that stimulates a natural brake on the allergic attack.
The skin inflammation of eczema is known to be driven by “type 2” immune responses. These are led by activated T helper 2 (TH2) cells and type 2 innate lymphoid cells (ILC2s), together known as effector cells. Another group of T cells, known as regulatory T cells or Tregs, are known to temper type 2 responses, thereby suppressing the allergic response.
Yet, if you examine an eczema lesion, the numbers of Tregs are unchanged. Interestingly, Tregs comprise only about 5 percent of the body’s T cells, but up to 50 percent of T cells in the skin.
“Our question was, is there something special about the Tregs that reside in the skin?” says Raif Geha, MD, chief of the Division of Immunology at Boston Children’s Hospital and the senior author of the study.
Geha led an investigation using two separate mouse models of eczema, each recreating a separate pathway leading to allergic skin inflammation. The team purified Tregs from the animals’ skin and blood and compared the genes they express.
Several genes were especially likely to be turned on in the skin Tregs. One encodes retinoid-related orphan receptor alpha (RORα), a transcription factor that itself regulates multiple other genes.
“We then used a genetic trick to remove RORα only from Tregs,” says Geha. “Without RORα, allergic inflammation went crazy in both our mouse models.”
The team saw a three-fold increase in the influx of inflammatory cells, and ILC2s and TH2 cells were at the center of the action.
Restraining allergic skin inflammation
Why did the Tregs stop working when RORα was removed? Geha and colleagues discovered that the cells made less of a receptor for a cytokine called TNF ligand-related molecule 1, or TL1A. TL1A is released by skin cells known as keratinocytes, and activates not only Tregs but also ILC2 and TH2 effector cells.
“The two kinds of immune cells are competing for TL1A,” Geha explains. “If Tregs don’t have this receptor, they can’t ‘see’ TL1A. Not only are they not activated, but more TL1A is available to activate the effector cells. So you have a double whammy.”
Testing human samples, the team documented higher expression of RORα in skin Tregs compared with those in blood, similar to mice.
Geha now wants to see if RORα is expressed less in human eczema and whether it’s important in the atopic march. If so, he sees several possible treatment approaches.
One is to boost RORα’s level or activity with compounds that act as RORα agonists, perhaps given in a topical cream. Geha’s lab also plans to look for factors in the skin that drive RORα activity, which could present other targets for intervention. Finally, the study showed that RORα regulates the expression of several genes important for Treg cell migration and function; those pathways could be potential targets too.
Study Shows Some Skin Bacteria May Protect Against Cancer
Science continues to peel away layers of the skin microbiome to reveal its protective properties. In a study published in Science Advances on February 28, University of California San Diego School of Medicine researchers report a potential new role for some bacteria on the skin: protecting against cancer.
“We have identified a strain of Staphylococcus epidermidis, common on healthy human skin, that exerts a selective ability to inhibit the growth of some cancers,” said Richard Gallo, MD, PhD, Distinguished Professor and chair of the Department of Dermatology at UC San Diego School of Medicine.
“This unique strain of skin bacteria produces a chemical that kills several types of cancer cells but does not appear to be toxic to normal cells.”
The team discovered the S. epidermidis strain produces the chemical compound 6-N-hydroxyaminopurine (6-HAP). Mice with S. epidermidis on their skin that did not make 6-HAP had many skin tumors after being exposed to cancer-causing ultraviolet rays (UV), but mice with the S. epidermidis strain producing 6-HAP did not.
6-HAP is a molecule that impairs the creation of DNA, known as DNA synthesis, and prevents the spread of transformed tumor cells as well as the potential to suppress development of UV-induced skin tumors.
Mice that received intravenous injections of 6-HAP every 48 hours over a two-week period experienced no apparent toxic effects, but when transplanted with melanoma cells, their tumor size was suppressed by more than 50 percent compared to controls.
“There is increasing evidence that the skin microbiome is an important element of human health. In fact, we previously reported that some bacteria on our skin produce antimicrobial peptides that defend against pathogenic bacteria such as, Staph aureus,” said Gallo.
In the case of S. epidermidis, it appears to also be adding a layer of protection against some forms of cancer, said Gallo. Further studies are needed to understand how 6-HAP is produced, if it can be used for prevention of cancer or if loss of 6-HAP increases cancer risk, said Gallo.
More than 1 million cases of skin cancer are diagnosed in the United States each year. More than 95 percent of these are non-melanoma skin cancer, which is typically caused by overexposure to the sun’s UV rays. Melanoma is the most serious form of skin cancer that starts in the pigment-producing skin cells, called melanocytes.
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