Baby with microcephaly (Harold Ruiz, PAHO)
1 September 2016. Takeda Pharmaceutical Company is receiving $19.8 million from a U.S. public health agency for initial steps to develop a vaccine to prevent Zika infections. Work to develop the vaccine could earn Takeda, in Osaka, Japan, as much as $312 million if the Biomedical Advanced Research and Development Authority or BARDA, in the U.S. Department of Health and Human Services, exercises all options with the company including late-stage clinical trials and filing a biologics drug application at the Food and Drug Administration.
The Zika virus is transmitted primarily by aedes aegypti mosquitoes, the same species carrying chikungunya, dengue, and yellow fever pathogens. The virus may also be spread through sexual contacts. Most people contracting the Zika virus report symptoms such as mild fever, conjunctivitis or pink eye, and muscle and joint pain. The current Zika outbreak, however, is resulting in increasing numbers of cases of birth defects, notably microcephaly and Guillain-Barré syndrome.
Microcephaly is a rare neurological condition where the baby’s head is noticeably smaller in size, with the children often experiencing developmental issues. Guillain-Barré syndrome is an autoimmune disorder, where the immune system attacks part of the peripheral nervous system, leading to progressive muscle weakness and eventual paralysis. The paralysis can become life-threatening if it affects breathing and heart muscles.
Centers for Disease Control and Prevention reports as of 31 August 2016, some 2,700 Zika cases in U.S. states and more than 14,000 cases in U.S. territories, with 624 pregnant women showing evidence of Zika infection in U.S. states and another 971 pregnant women with Zika infections in U.S. territories. There are currently no treatments for Zika infections, nor is there a vaccine to prevent infections.
The agreement with BARDA calls for Takeda to develop a vaccine for Zika with an inactivated virus, as well as adjuvants or boosters to increase its potency. The current funding covers initial research and development and preclinical studies leading to a vaccine candidate submitted in an investigational new drug application to FDA. The funding also covers an early-stage clinical trial of the vaccine by 2017. Takeda’s facilities in Hikari, Japan will manufacture the vaccine.
Rajeev Venkayya, president of Takeda’s vaccines division, says in a company statement that “The Zika emergency demands swift action by governments, public health agencies, medical and scientific communities, industry, and others, and partnerships are essential for success.” The company says its work with vaccines goes back 70 years and includes vaccines for dengue, norovirus, and polio.
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Stick-ribbon model of amyloid-beta peptides (public domain/Wikimedia Commons)
1 September 2016. A clinical trial shows older individuals with early or mild cases of Alzheimer’s disease treated for a year with an engineered human antibody have less decline in mental functions associated with Alzheimer’s disease. Results of the trial and a related preclinical study with lab mice were reported yesterday in the journal Nature (paid subscription required).
Alzheimer’s disease is progressive neurodegenerative disease affecting growing numbers of older people worldwide. People with Alzheimer’s disease often have deposits of abnormal substances in spaces between brain cells, known as amyloid-beta peptides, as well as misfolded tangles of proteins inside brain cells known as tau. The Alzheimer’s Association says some 5.4 million individuals in the U.S. have the disorder, of which 5.2 million are age 65 or older. By 2050 that number is expected to increase to 13.8 million.
The Nature paper reports on work at University of Zurich in Switzerland, led by neuroscientist Roger Nitsch, director of the university’s Institute of Regenerative Medicine. Nitsch and colleagues from the biotechnology company Biogen and University of Zurich spin-off enterprise Neurimmune, tested aducanumab, an engineered antibody designed to reduce amyloid-beta peptide plaques in the brain associated with Alzheimer’s disease. Nitsch is a founder of Neurimmune and the company’s president.
Neurimmune, in Zurich, first developed aducanumab using a technology the company calls reverse translational medicine that derives antibodies from B cells, white blood cells in the immune system, donated by healthy older individuals with either no signs or very slow cognitive decline. While engineered and designed to attack specific targets, the antibodies retain many human properties, according to the company, and invoke little if any immune reactions. Biogen, in Cambridge, Massachusetts, licensed aducanumab from Neurimmune, and the two companies are collaborating on further development, including clinical trials.
The researchers reported on preclinical tests of aducanumab on genetically altered mice that developed amyloid-beta plaques, with results showing the antibody entering the brain and binding to the plaques. Most of the paper, however, describes an early-stage clinical trial with 165 individuals, age 50 and older, diagnosed in early stages or with mild cases of Alzheimer’s disease. The trial was designed to test the safety of aducanumab in various dosage levels (against a placebo), and also the antibody’s chemical activity in the body, including clearance of amyloid-beta accumulations in the brain.
The results, measured by positron emission tomography, or PET, scans of participants’ brains show after 1 year of intravenous treatments of aducanumab every 4 weeks, participants receiving the antibody cleared at least some amyloid-beta plaques compared to the placebo, with patients receiving higher doses of the antibody clearing more of the plaques than those receiving lower doses.
The team also used the opportunity to test cognitive performance of participants with two standard rating scales of mental decline, Clinical Dementia Rating and Mini-Mental State Examination. Participants were initially screened with those tests to be included in the trial. The results show participants receiving aducanumab had slower decline in cognitive function than their counterparts receiving a placebo. “While patients in the placebo group exhibited significant cognitive decline,” says Nitsch in a university statement, “cognitive ability remained distinctly more stable in patients receiving the antibody.”
The main adverse effects reported were amyloid-related imaging abnormality, or ARIA, associated with micro-hemorrhages and collection of fluid around cells in the brain that show up on MRI scans, as well as temporary mild to moderate headaches in some cases. The researchers say these adverse effects result from the clearance of amyloid-beta plaques.
Biogen is recruiting participants for 2 late-state clinical trials, code-named Emerge and Engage, each testing aducanumab against a placebo with 1,350 participants, on slowing cognitive and functional impairment.
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Kojo Mensa-Wilmot (University of Georgia)
31 August 2016. An experimental drug designed to treat solid tumor cancers was shown in lab tests to rid mice of human African trypanosomiasis, also known as sleeping sickness. The findings of a team from University of Georgia in Athens, Northeastern University in Boston, and the biotechnology company Cleveland BioLabs Inc. appear in the 26 August issue of the journal Scientific Reports.
The researchers, led by Georgia cellular biology professor Kojo Mensa-Wilmot, are seeking more effective and easily administered drugs to treat human African trypanosomiasis, a disease that occurs in 36 sub-Saharan Africa countries and in 2014 affected nearly 3,800 people, according to World Health Organization. The disease is caused by infections from Trypanosoma brucei parasites, single cell organisms transmitted by tsetse flies found largely in rural regions.
Symptoms begin with fever, headaches, joint pains, and itching, but once the infection crosses the blood-brain barrier, can result in confusion, sensory disturbances, poor coordination, and disturbances in sleep cycles. The disease can also be fatal.
The authors report 5 drugs are now available for treating human African trypanosomiasis, or HAT, but all must be given with injections of eflornithine. As a result, treating the disease requires visits to a clinic, often a difficult task in isolated rural areas. In addition, the authors report only two treatments for HAT in drug companies’ pipelines.
“HAT is a disease of poverty,” says Mensa-Wilmot in a university statement, “so there is little motivation for the pharmaceutical industry to be heavily invested. Because the parasite can become drug resistant, it is very important for us to be vigilant in finding new effective, orally administered treatments for the disease.”
To short-cut the sometimes extended drug discovery process, Mensa-Wilmot and colleagues employed a strategy of finding existing compounds that could treat HAT infections with established safety profiles progressing at least to clinical trials. Among the drugs screened were a class of compounds known as curaxins, small-molecule drugs being developed by Cleveland BioLabs in Buffalo, New York as cancer therapies.
Curaxins work by blocking the expression of genes that produce proteins needed for tumors to survive, and can be applied to a number of solid tumor cancers. And because they do not destroy DNA, curaxins may also be safer to use than chemotherapy. In their review, the team found curaxins targeted the chemical structure of genes, similar to that of the parasites causing HAT infections. Chemical screening of 26 curaxin compounds returned 22 with potential potency against the parasites in the blood stream.
Tests of the 3 most potent curaxins in lab mice infected with HAT parasites show the compound, code-named CBL0137 by Cleveland Biolabs rid all of the mice of their infections, preventing the parasite cells from dividing, and thus proliferating in the body. CBL0137 is also being tested in an early-stage clinical trial for safety and to determine recommended doses among individuals with solid tumor cancers.
The authors believe this strategy of repurposing current drug compounds offers a faster and more economical method of drug discovery, which in this case could lead to a new oral drug for HAT and other tropical diseases caused by parasites.
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U.S. Patent and Trademark Office in Alexandria, Virginia (A. Kotok)
30 August 2016. A company developing small-molecule treatments for biological targets considered difficult to address is receiving a patent for its core drug identification technology. The U.S. Patent and Trademark Office today awarded patent number 9,428,845 to 7 inventors including Gregory Verdine, a founder of Warp Drive Bio Inc., a biotechnology company in Cambridge, Massachusetts, which owns the patent.
Warp Drive Bio discovers small molecule or low molecular weight drugs directed at disease-causing proteins considered difficult to address with other small molecule drugs or protein biologics alone. These protein targets, says the company, are either inside cells making them inaccessible to biologics, or do not have particular hydrophobic, or water-repelling, binding pockets needed by small molecule drugs. Warp Drive Bio’s technology, known as Small Molecule-Assisted Receptor Targeting, or Smart, combines properties of both small molecule drugs and biologics to penetrate and thus operate inside cells, and create binding surfaces suitable for small molecule drugs.
The patent covers methods and processes for screening compounds for these properties and identifying drug candidates meeting specified criteria. Among the criteria are biological activities of presenter and target proteins interacting with a test compound. The interactions include direct contacts between the test compound and the presenter or target proteins, as well as binding sites on the presenter or target proteins.
The patent also covers contingencies for interactions among test compound and presenter and target proteins, such as when one of the entities is missing, as well as situations where a test compound has a greater affinity for a presenter or target protein, or more complex interactions where a test compound has selective activity with the presenter or target protein.
The Smart technology is based on biochemical research by Verdine and colleagues at Harvard University on synthetic biologics that address processes underlying growth and proliferation of human cancer cells, control of gene expression, and preservation of genomic integrity. Verdine’s lab studies epigenetics, external influences on genetic activity, resulting in changes to DNA that repress activities of genes for transcribing their codes into proteins.
Among the projects of Warp Drive Bio, as reported in Science & Enterprise, is treatments targeting the Ras oncogene, a gene that turns normal function cells into a wide range of tumor cells. Mutations in Ras oncogenes produce proteins that send signals encouraging cell proliferation and inhibit normal cell death resulting in the formation and growth of tumors. These mutations are associated with about 30 percent of human cancers including, non-small cell lung, colorectal, pancreatic, bladder, kidney, thyroid, melanoma, and liver tumors, as well as blood-related cancers.
Verdine founded Warp Drive Bio in 2012 with Harvard University geneticist George Church and protein biochemist James Wells at University of California in San Francisco. The company is a joint project of the French pharmaceutical company Sanofi and venture capital firm Third Rock Ventures, with additional start-up funding from Greylock Ventures.
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30 August 2016. An experimental medication was shown in tests with monkeys to relieve pain for more than a day without the addictive properties or adverse physical effects of opioids. A report of the study conducted by researchers at Wake Forest University in Winston-Salem, North Carolina appears in yesterday’s issue of Proceedings of the National Academy of Sciences (paid subscription required).
The team led by physiology and pharmacology professor Mei-Chuan Ko is seeking an effective alternative to opioid pain relievers, which are responsible for an epidemic of abuse and overdoses due to their addictive nature. Centers for Disease Control and Prevention reports that since 1999, the amount of prescription opioids sold in the U.S. quadrupled, while the overall amount of pain reported by Americans has not changed. In 2014 as well, nearly 19,000 deaths involved prescription opioids, about 52 deaths per day, up from about 16,000 in 2013.
Opioids work by reducing the intensity of pain signals to the brain, particularly regions of the brain controlling emotion, which reduces effects of the pain stimulus. Ko and colleagues identified a synthetic compound code-named BU08028 that binds to nociceptin-orphanin FQ peptide, or NOP, and mu opioid peptide, or MOP, receptors in the brain. These are the same receptors targeted by buprenorphine, an opioid prescribed and given by physicians to control morphine or heroin addiction.
In its study, the Wake Forest team aimed to document the chemical and behavioral effects of BU08028 with animals most resembling humans. Earlier studies suggesting BU08028 targets the NOP and MOP receptors, but without the reinforcing effects that feed opioid addiction. In addition, the researchers sought evidence of the drug’s effects on respiratory and cardiovascular functions, two areas in which opioids can cause distress.
The authors tested BU08028 with 12 adult rhesus monkeys. The team found monkeys given BU08028 exhibited the same reactions indicating relief from pain stimuli as monkeys given opioids, including buprenorphine. The pain-relieving effects were also found to last at least 30 hours. Monkeys given BU08028 as well did not exhibit signs of respiratory or cardiovascular problems — even at many times the dose needed to relieve pain — as their counterparts given the synthetic opioid fentanyl.
In addition, the animals were trained to self-administer either BU08028, or known addictive opioids or cocaine. Tests with these drugs show monkeys taking BU08028 did not exhibit the reinforcing effects that feed addiction, like those taking opioids or cocaine. Likewise, monkeys receiving BU08028 did not show signs of excessive itching, or develop a physical dependence with repeated doses, as monkeys given opioids that exhibited withdrawal symptoms.
The authors note that further preclinical work with BU08028 is needed to determine long-term effects, including a build-up of tolerance to the drug over time. Nonetheless, in a Wake Forest statement Ko says, “this compound has almost zero abuse potential and provides safe and effective pain relief.” He calls the findings “a breakthrough for opioid medicinal chemistry that we hope in the future will translate into new and safer, non-addictive pain medications.”
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(National Heart, Lung, and Blood Institute, NIH)
29 August 2016. An artificial form of marine bacteria is being created to speed experiments in biotechnology labs on cloning and design of new therapeutic proteins. The science behind the new microbe, named Vmax by its developer Synthetic Genomics Inc. in La Jolla, California, is described in today’s issue of the journal Nature Methods (paid subscription required).
Synthetic Genomics designed Vmax as an alternative to E. coli bacteria, popularly known as a pathogen causing intestinal infections, but most strains are harmless and are used as a model for higher-order organisms. As reported in Science & Enterprise earlier in August, a research group at Harvard Medical School designed a form of E. coli with a simplified DNA for synthesizing substances not easily produced from nature, such as pharmaceuticals and chemicals.
The Synthetic Genomics team, led by company vice-president Daniel Gibson, took a different approach, namely starting with an organism with faster biological processes than E. coli. Their microbe of choice is Vibrio natriegens, a marine bacteria first found in salt marshes on barrier islands off the U.S. state of Georgia. Vibrio natriegens is particularly fast-growing and reproducing microbe that regenerates itself in less than 10 minutes.
“Despite the known drawbacks and shortcomings,” says Synthetic Genomics chief technologist Todd Peterson in a company statement, “scientists have been necessitated to use E. coli as a laboratory host primarily because there have been no suitable alternatives. We deployed our synthetic biology expertise to develop a new host strain that will drastically improve upon the traditional methods and tools.”
The Nature Methods paper describes genome engineering tools developed by Synthetic Genomics for modifying Vibrio natriegens bacteria for production of products based on biotechnology. Typical cloning projects can take several days with E. coli, say the authors. With Vmax, those timelines can be reduced to a single day. “We are in the process of designing and synthesizing new Vmax cells,” adds Gibson, “that operate at even higher efficiencies and productivity as we move toward a next-generation host for protein production.”
Synthetic Genomics formed a separate subsidiary, SGI-DNA, that commercializes the company’s synthetic DNA technologies. The company produces synthetic DNA and supporting materials, as well as develops technologies for producing synthetic genes and reagents. Synthetic Genomics company filed a U.S. patent for the Vmax technology.
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Mio activity trackers (Mio Global)
29 August 2016. An activity tracking device introduced earlier this year uses data from a major population health study to write its algorithms measuring exercise achievement to prevent heart disease. Javaid Nauman at Norwegian University of Science and Technology in Trondheim, described the use of these data in Mio activity trackers on Saturday, 27 August at a meeting of the European Society of Cardiology in Rome.
The Mio activity tracker, introduced in January 2016, calculates an activity score known as Personal Activity Intelligence or PAI, that offers an overall fitness index based on an individual’s heart rate. Many fitness devices compare the wearer’s activity to general recommended exercise guidelines, such as 10,000 steps a day. While these recommended guidelines can help people get started with more exercise, say the authors, each person’s cardiovascular system has unique requirements.
“People may be insufficiently active,” says Nauman in an ESC statement, “because they do not have personalized, meaningful information about how much physical activity they require, and at what intensity.” Nauman is a researcher in the Cardiac Exercise Research Group at Norwegian University of Science and Technology. He cites data showing lack of exercise contributes each year to more than 5 million deaths globally and over €80 billion ($US 89 billion) in health care spending in Europe.
PAI scores are calculated with algorithms derived from an individual’s heart rate when exercising in any form, adjusted for personal variables including age, gender, and resting and maximum heart rate. Wearers of Mio devices aim for PAI scores of at least 100 over a 7-day period to help prevent premature death from heart disease.
Researchers at the Cardiac Exercise Research Group developed PAI based on data from the Nord-Trøndelag Health Study that uses the Norwegian acronym HUNT, a collection of personal and family medical histories, surveys, and blood samples beginning in 1984. PAI algorithms are based on a subset of HUNT data dealing with fitness from 4,637 individuals, including questions on frequency, duration. and intensity of exercise. Responses to these questions correlated with intensity of heart rate reserve, the difference between resting and maximum heart rate.
The team validated PAI algorithms with data from more than 39,000 men and women in Norway taking part in the HUNT project. Of those individuals, about 10,000 deaths occurred after a median follow-up of nearly 29 years, with nearly 3,900 deaths attributed to cardiovascular disorders. Women with PAI scores of 100 or more were 23 percent less likely to die of cardiovascular disease than completely inactive women, while men with PAI scores of 100 or more were 17 percent less likely to die of cardiovascular disease. Deaths from any cause were also 17 and 13 percent lower for women and men respectively with PAI scores of 100 or more, compared to completely inactive individuals.
“The more elevated your heart rate is during exercise,” notes Nauman, “the more quickly you accumulate PAI points, but you can also work out at lower intensities for longer durations to earn PAI. Our research shows that keeping your PAI score at 100 or above could prevent premature death.”
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NASA Television image of SpaceX’s Dragon spacecraft departing the International Space Station at 6:10 am ET on 26 August 2016 (NASA)
26 August 2016. A SpaceX Dragon spacecraft returned today with samples from several biomedical research studies conducted by astronauts on the International Space Station. NASA says Dragon splashed down in the Pacific Ocean, southwest of Baja, California, today at 11:47 am ET.
The International Space Station provides a lab for astronauts to perform experiments that study effects of microgravity on biological processes. Among the 3,000 pounds of returned cargo were samples from a study of cardiomyocytes, or heart cells, derived from stem cells. The heart cell experiments studied effects of microgravity on growth of heart muscle tissue, as well as muscle contractions and changes in gene expression. The findings are expected to help understand health issues faced by astronauts who travel in space for extended periods of time.
Also returned are mice who experienced long periods in space to study effects of microgravity on molecular and physical changes in the musculoskeletal system. Space flight can cause loss of bone and muscle mass, particularly in the legs and spine, similar to muscle-wasting diseases. This experiment is sponsored by drug maker Eli Lilly and Co. and the Center for the Advancement of Science in Space.
Returned as well are a set of mice in an experiment sponsored by the Japan Aerospace Exploration Agency, which investigates changes in gene expression patterns in organs of male mice traveling in space for a month. The study is also looking into changes in the DNA from offspring of the mice. Still another study by the Japanese space agency, also returning samples, tests human microbial-metabolic cross-talk in microgravity. These experiments analyze the composition of microbes in the human digestive system and changes in metabolites related to astronauts’ immune functions.
The Dragon spacecraft is SpaceX’s cargo vehicle designed to launch 6,000 kilograms (13,228 pounds) and return 3,000 kilograms (6,614 pounds) from space. SpaceX has an agreement with NASA to upgrade the Dragon to fly human crew, which the company expects to take place in 2 to 3 years.
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James Chou, foreground, and Sherine Chan (SherineChan.com)
26 August 2016. A federal grant is funding a project by a start-up enterprise in South Carolina to develop a new class of drugs to treat epilepsy. National Institute of Neurological Disorders and Stroke, part of National Institutes of Health, made the $225,000 award to Neuroene Therapeutics, a spin-off company from Medical University of South Carolina, in Charleston.
Epilepsy is a neurological disorder where nerve cell activity in the brain is disturbed, causing seizures with symptoms ranging from blank stares to tingling sensations to loss of consciousness. World Health Organization estimates some 50 million people worldwide have epilepsy, where in many cultures people with the condition face stigma and discrimination. While epilepsy can be treated in most cases, WHO says as many as 30 percent of episodes do not respond to treatment.
This large percentage of non-responders to current epilepsy treatments is driving research by MUSC faculty members Sherine Chan and James Chou. Chan studies defects in mitochondrial or energy functions of cells, including research with zebrafish models that share many genetic characteristics with humans. Chou investigates drug targets based on histone deacetylases, a class of enzymes associated with cancer and other disorders.
In a 2014 paper, Chan, Chou, and colleagues screened potential compounds against histone deacetylase targets associated with epilepsy using zebrafish as model organisms. They discovered some synthetic forms of vitamin K, a natural vitamin associated with blood clotting, reduced seizure-like activity in zebrafish. Tests with mice found a particular synthetic form of vitamin K reduced epilepsy-like seizures by improving mitochondrial functions in brain cells.
Chan and Chou founded Neuroene Therapeutics in May 2015 to commercialize their discovery. The company identified a lead compound it calls Alkyne-VK, a vitamin K analog, which they tested with zebrafish and mice. They report Alkyne-VK not only reduces seizures in mice, it penetrates mouse brains in about 15 minutes, is non-toxic, and even provides protection to nerve cells. Its drawback, however, is a short half-life in blood serum, of about 1 hour.
In the project funded by NIH, the Neuroene-MUSC team plans to synthesize 30 to 50 variations of Alkyne-VK that continue to show efficacy with epilepsy in lab cultures and animal models, as well as convey protection for nerve cells. In addition, the researchers will identify an optimal candidate that can retain its anti-seizure activity for at least 6 hours. If this first stage is successful, the company and MUSC will apply for second-stage funding to carry out preclinical and toxicology tests in preparation for an investigational new drug application with FDA.
“This class of compounds has a new molecular mechanism that makes it different from any of the current anti-seizure drugs available to patients with epilepsy,” says Chan in a university statement. ” We intend to provide a new generation of anti-seizure drugs that is clearly needed.”
The award is made under NIH’s Small Business Technology Transfer program that supports commercialization of biomedical technologies undertaken by collaborations between research institutions and small businesses.
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Hydrogen fuel cell being tested at the port of Honolulu, Hawaii (Sandia National Lab)
25 August 2016. An engineering team in Switzerland designed a system for producing hydrogen from solar power with abundant available materials, providing an inexpensive and feasible energy storage method. Researchers from Ecole polytechnique fédérale de Lausanne or EPFL and Swiss Center for Electronics and Microtechnology, or CSEM, in Neuchâtel described their system in the 13 August issue of the Journal of the Electrochemical Society (paid subscription required).
The authors, from the Photovoltaics and Thin Film Electronics Laboratory, a joint EPFL-CSEM facility led by engineering professor Christophe Ballif, are seeking to solve a long-standing need for inexpensive storage of intermittent renewable power sources, such as solar and wind energy. Producing hydrogen with electrolysis from solar energy offers a way to store the power for use in hydrogen fuel cells. Current electrolysis methods, however, require catalysts made from rare earth materials, making them too expensive for widespread use.
The solution devised by Ballif and colleagues proposes increasing the output of solar power produced, as well as redesigning a method for electrolysis that removed the need for expensive catalysts. In both cases, the researchers aimed at using available solutions and materials, emphasizing practicality and affordability.
To generate power, the team combine crystalline-silicon solar cells in alternating layers with amorphous silicon. Crystalline silicon is the most common solar cell in commercial use with high efficiency and long lifetime. Amorphous silicon is the material used in thin-film solar cells, which are inexpensive to produce, but have lower efficiency, and are used to power devices like watches and calculators. The alternating layers of two different materials produce a heterojunction design that combine the advantages of both materials to boost energy output.
The higher-power configuration enables the engineers to use only three solar cells to produce enough power for the electrolysis unit. The electrolysis unit splits water into its hydrogen and oxygen elements, but these devices usually require intensive inputs of energy from existing power grids. In this case, power from the three solar cells produces sufficient energy, which the team estimates would have needed four conventional crystalline-silicon solar cells.
Another drawback of electrolysis units is the high cost of conventional rare earth catalysts that raise the cost of this process, making it infeasible for many applications. For their device, the EPFL-CSEM team uses microstructured nickel catalysts in their proton exchange membrane electrolysis unit.
Tests show the system can convert solar energy to hydrogen at 14.2 percent efficiency, which the authors call unprecedented, and ran for 100 hours, surpassing previous efforts for stability, performance, lifespan, and cost efficiency. In an EPFL statement, Ballif says the system “would allow the generation and storage of enough hydrogen to power a fuel cell car over 10,000 km every year.”
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