You probably don’t need scientists to tell you that your metabolism slows with age. But they’re studying it anyway—and coming up with exciting research to help rev it up again. The average woman gains 1½ pounds a year during her adult life—enough to pack on 40-plus pounds by her 50s, if she doesn’t combat the roller coaster of hormones, muscle loss, and stress that conspire to slow her fat-burning engine. But midlife weight gain isn’t inevitable: We’ve found eating strategies that will tackle these changes.
But first, the basics: To boost over-40 weight loss, make sure your meals are around 400 calories, the amount needed to fuel your body while keeping you satisfied, translating into effortless weight loss. The following metabolism-boosting food rules were developed by Dan Benardot, PhD, RD, an associate professor of nutrition and kinesiology at Georgia State University, and Tammy Lakatos, RD. Here’s how to adjust your eating plan to help your body burn fat.
Mistake: You don’t eat enough
You need to cut calories to lose weight, but it’s important not to overdo it. Going too low delivers a double whammy to your metabolism. When you eat less than you need for basic biological function (about 1,200 calories for most women), your body throws the brakes on your metabolism. It also begins to break down precious, calorie-burning muscle tissue for energy, says Benardot. “Eat just enough so you’re not hungry—a healthy snack midmorning and midafternoon between three meals (about 430 calories each) will keep your metabolism humming.” By eating a meal every 3 to 4 hours, you’ll stay satisfied and keep from overeating later in the day.
Mistake: You avoid caffeine
Caffeine is a central nervous system stimulant, so your daily java jolts can rev your metabolism 5 to 8%—about 98 to 174 calories a day. A cup of brewed tea can raise your metabolism by 12%, according to one Japanese study. Researchers believe the antioxidant catechins in tea provide the boost.
Mistake: Your carbs are white
Boost your fiber intake by switching to whole wheat bread, pasta, and eating more fruits and vegetables. Research shows that some fiber can rev your fat burn by as much as 30%. Studies find that women who eat the most fiber gain the least weight over time. Aim for about 25 g a day—the amount in about three servings each of fruits and vegetables. (Here’s how to sneak more fiber into your diet.)
Mistake: Your water is room temperature
Photo by hdere/Getty Images
German researchers found that drinking 6 cups of cold water a day (that’s 48 ounces) can raise resting metabolism by about 50 calories daily—enough to shed 5 pounds in a year. The increase may come from the work it takes to heat the water to body temperature. (Not a plain water fan? Try these 25 slimming Sassy Water recipes.)
Mistake: Your food is covered with pesticides
Canadian researchers report that dieters with the most organochlorines (pollutants from pesticides, which are stored in fat cells) experience a greater than normal dip in metabolism as they lose weight, perhaps because the toxins interfere with the energy-burning process. Other research hints that pesticides can trigger weight gain. Always choose organic when buying peaches, apples, bell peppers, celery, nectarines, strawberries, cherries, lettuce, imported grapes, and pears; non-organic versions tend to have the highest levels of pesticides. But going organic is just the first step. Here are 23 more ways to eat clean.
Mistake: Your meal lacks protein
Photo by Liv Friis/Getty Images
Make sure protein is a component in every meal. Your body needs it to maintain lean muscle. Add a serving, like 3 ounces of lean meat, 2 tablespoons of nuts, or 8 ounces of low-fat yogurt, to every meal and snack. Research shows protein can up postmeal calorie burn by as much as 35%.
Mistake: Your diet needs to pump iron
Iron-rich foods are essential for carrying the oxygen your muscles need to burn fat, says Lakatos. Until menopause, women lose iron each month through menstruation. Unless you restock your stores, you run the risk of low energy and a sagging metabolism. Shellfish, lean meats, beans, fortified cereals, and spinach are excellent sources or iron.
Mistake: You’re missing vitamin D
Vitamin D is essential for preserving metabolism-revving muscle tissue. Unfortunately, researchers estimate that a measly 4% of Americans over age 50 take in enough through their diet. Get 90% of your recommended daily value (400 IU) in a 3.5-ounce serving of salmon. Other good sources: tuna, shrimp, tofu, fortified milk and cereal, and eggs. (Check out these 8 excellent sources of vitamin D.)
Mistake: You’ve had one drink too many
Skip the second cocktail. When you have an alcoholic drink, you burn less fat, and more slowly than usual, because the alcohol is used as fuel instead. Knocking back the equivalent of about two martinis can reduce your body’s fat-burning ability by up to 73%. (Here’s your body on alcohol in a handy infographic.)
Mistake: You’re not getting enough dairy
“There’s some evidence that calcium deficiency, which is common in many women, may slow metabolism,” says Lakatos. Research shows that consuming calcium through dairy foods such as fat-free milk and low-fat yogurt may also reduce fat absorption from other foods.
Bonus: Here’s a sample calorie-burning day plan:
7 AM: Kick-start your day with yogurt and fruit for breakfast.
10 AM: Your morning java is full of antioxidants.
12 PM: A salad at lunch gives you a healthy dose of fiber.
2 PM: Drink a big glass of water. You need at least 6 to 8 cups a day.
4 PM: Organic grapes make a great snack.
7 PM: Salmon fillets or chicken breasts packs in the protein for dinner.
10 PM: Milk does a body good. Have a glass before bed.
11 PM: Sweet dreams!
After the World Health Organization has reported that these foods can cause cancer, anxiety has increase among many people.
Selecting ingredients requires great caution, which is why we present you a brief guide on how to avoid the dangers that hide in your favorite foods.
These are cases when you should not add bacon, sausages, hot dogs and meat spreads in your shopping cart.
First of all, get a magnifying glass in order to be able to read about what you are buying. Not always, but usually the declarations are written in tiny letters, so even if you do not have vision problems – it will be difficult to read this declaration.
After that, you need to remember these useful advices:
It is mandatory to read the declaration
– If there is a mark “MSM” it means the meat is mechanically separated, ground together with the bones, in which antibiotics, hormones, heavy metals and other toxins that have been in the animal have been deposited.
– The same applies when you find on the declaration emulgator nitrites, which are labeled as E249, E250, E251 and E252.
These emulgators together with the amino acids from meat produce carcinogenic nitrosamine compounds.
– The emulgators Е451, Е252 and Е453 are genotoxic or rather “plastic” and damage the genes.
– You should be extremely careful for the product you purchase not to contain E407, carrageenan mark. This substance sticks to the walls of the intestine, and create wounds which later can turn into colon cancer.
– If the product contains a flavor enhancer, glutamate, it may mean that it has no meat in the product at all.
All the above mentioned information applies to durable and semi-durable meat products.
When it comes to meat, for example, if you are buying pork cutlets, pay attention whether the meat is interspersed with fatty veins. This is proof that the animal has not been fed as bad.
If there is not even one gram of white fat and water is dripping from it, it is proof that besides food the pig received growth hormones and antibiotics.
IT WAS a cryptic email that Juan Maldacena pinged across the US to fellow physicist Leonard Susskind back in 2013. At its heart lay a single equation: “ER = EPR”. The message clicked with its recipient. “I instantly knew what he was getting at,” says Susskind. “We both got quite excited.”
Excited, because that one equation promises to forge a connection between two very different bits of physics first investigated by Albert Einstein almost 80 years ago. Excited, because it could help resolve paradoxes swirling around those most befuddling of cosmic objects, black holes, and perhaps provide a route to a unified theory of physics. Excited, because it might even answer one of the most fundamental questions of all: what is reality made of?
The origins of the story lie precisely a century ago. In November 1915, Einstein presented the final form of his revolutionary theory of gravity .
This quintessential medieval disease, caused by the bacterium Yersinia pestis and transmitted most often by fleabites, still surfaces in a handful of cases each year in the western United States, according to the Centers for Disease Control and Prevention. Its historical record is far more macabre. The plague of Justinian from 541 to 543 decimated nearly half the population in the Mediterranean, while the Black Death of the Middle Ages killed one in every three Europeans.
Now researchers are beginning to reveal a surprising genetic history of the plague. A rash of discoveries show how just a small handful of genetic changes — an altered protein here, a mutated gene there — can transform a relatively innocuous stomach bug into a pandemic capable of killing off a large fraction of a continent.
The most recent of these studies, published in June, found that the acquisition of a single gene named pla gave Y. pestis the ability to cause pneumonia, causing a form of plague so lethal that it kills essentially all of those infected who don’t receive antibiotics. In addition, it is also among the most infectious bacteria known. “Yersinia pestis is a pretty kick-ass pathogen,” said Paul Keim, a microbiologist at Northern Arizona University in Flagstaff. “A single bacterium can cause disease in mice. It’s hard to get much more virulent than that.”
The genetic makeover that led to the modern plague is thought to have occurred relatively recently in evolutionary history, anywhere from 1,500 to 20,000 years ago. But last month, a discovery was announced that could extend the history of the plague all the way back to a time before humans. George Poinar Jr., a biologist at Oregon State University in Corvallis, found that a 20-million-year-old flea encased in amberhas a plague-like bacterium on its proboscis that could be an ancestor of Y. pestis. While a definitive identification of the bacterium hasn’t been made — and may not even be possible — an ancient ancestor of the Black Death could help reveal the earliest steps in a tortured evolutionary path, and perhaps help pinpoint at what point the most deadly changes occurred.
A Flea Ride
As long as there has been plague, there have been people trying to figure out where it came from. Plague appears in a boom-and-bust cycle, emerging suddenly to cause huge pandemics and then retreating, sometimes for hundreds of years. The abrupt eruption of death with no apparent cause tended to invite theories involving the supernatural.
The reality is nearly as remarkable. Recent genetic work has traced the plague’s evolutionary precursor back to the relatively harmless gastrointestinal pathogen Y. pseudotuberculosis, which only causes mild diarrhea. “Some people don’t even know they have it,” said Wyndham Lathem, a biologist at Northwestern University who has spent his career studying the plague bacterium. “Yersinia pestis can kill you in three days, and only a few changes were required to make this switch.”
Moreover, these changes did not occur very long ago. In several recent studies, researchers compared plague bacteria samples from two pandemics. The Y. pestisDNA recovered from London’s plague pits and from German graves dating from the plague of Justinian turned out to be largely the same. In addition, bacterial samples from modern plague victims around the world reveal very little variation. The findings indicate that Y. pestis hasn’t yet had time to accumulate lots of mutations. “Yersinia pestis is such a recent species that there’s not very much genetic diversity among plague strains, even the ones from historic graveyards,” said Joe Hinnebusch, a plague researcher at the National Institute of Allergy and Infectious Diseases. The bacteria’s murderous adaptations are only a few thousand years old.
But what are these adaptations? In 2004, an international team of researcherspublished the first full genetic sequence of the plague ancestor Y. pseudotuberculosis.When they compared it to Y. pestis, they found that most of the differences between the two were so-called neutral mutations, changes that did not alter the traits of Y. pestis.
Only a few minor changes stood out. The first was like giving Y. pestis an all-you-can-fly ticket on the bacterium’s favorite ride: the flea. Y. pseudotuberculosis can’t travel on fleas, making it much less infectious than its modern descendant. Hinnebusch showed why it can’t move this way: Y. pseudotuberculosis is deadly to fleas, causing a diarrhea that kills nearly half of them. Y. pestis, on the other hand, gives fleas only a mild illness.
To find out what in the bacteria was causing disease in the fleas, Hinnebusch and Iman Chouikha, a postdoc, chopped up Y. pseudotuberculosis into tiny pieces and fed them to fleas. Only fleas that consumed the bacterium’s protective coat became ill, so the poison had to be located there.
Further detective work published in 2014 in PNAS revealed that the culprit was a protein called urease. This protein is present in Y. pseudotuberculosis, but a genetic mutation stops the Y. pestis bacterium from creating it. When Chouikha and Hinnebusch inserted a functional copy of the urease gene back into Y. pestis and fed these genetically engineered plague microbes to fleas, the tiny arthropods got sick just as they did when they ate pseudotuberculosis. “This shows how very minor changes can have a dramatic effect,” Hinnebusch said.
But fleas are only part of the story of the plague’s development. While Hinnebusch was working on urease, Lathem was examining another small genetic change that allowed the plague to defeat one of the body’s main defense mechanisms: blood clots.
When a flea bites into flesh, the body responds by clotting blood to prevent bleeding and promote healing. If a plague bacterium gets trapped in this clot, it can’t multiply and spread itself through its new host. Lathem showed that Y. pestis has a gene calledpla that its ancestors lack. This gene encodes for a protein that helps to dissolve blood clots. Without a clot, the bacterium is free to spread to the nearest lymph node, where it makes billions of copies of itself.
Lathem’s work, which was published in Science, showed that pla is required for pneumonic plague, a form of plague that can be transmitted from person to person and can kill its host in under 24 hours. But Lathem didn’t know whether pla was the only factor necessary. He turned to several ancestral strains of Y. pestis that continue to circulate in rodents in the highlands of China and Central Asia, likely the ancestral home of the bacterium. These strains provided an intermediate version between Y. pseudotuberculosis and modern Y. pestis. More importantly, some of these particular strains lacked pla.
When Lathem and Daniel Zimbler, a postdoc, tested the pla-free ancestral strains, they found that these could not cause pneumonic plague. But when they added plawhile keeping the rest of the DNA the same, the strains readily caused pneumonic plague. And when they removed pla from modern strains of Y. pestis, the bacteria lost their ability to cause pneumonia. Lathem, Zimbler and colleagues published their results this June in Nature Communications.
“We found the very earliest state at which Yersinia pestis could cause respiratory disease. And as soon as it had pla, it could grow rapidly and cause pneumonia,” Lathem said.
Y. pestis didn’t just acquire pla; the bacterium also changed it. A chance mutation altered one amino acid in pla, which greatly increased its virulence by allowing the bacterium to penetrate more deeply into the body. Once there, it could make more copies of itself, making it more likely to be transmitted to another person, whether by coughing or by fleabite.
The findings change how researchers think about pneumonic plague. The ability to cause pneumonia was thought to have been a last-minute addition to the deadly repertoire of Y. pestis. Lathem’s work suggests that Y. pestis acquired pla, and thus the ability to cause pneumonia, very early. The mutation in pla happened later, transforming a bacterium capable of causing localized outbreaks of disease into the mass killer we know today.
“Our work is pointing to this mutation in pla as one of these Big Bang events in plague,” Lathem said. “It was already ready to cause severe pneumonia, and once it could cause invasive disease, everything could amplify.”
Plague continues to spread, although improvements in pest control, hygiene and antibiotics have dramatically decreased the size of outbreaks and the number of people who die from them. Yet the DNA of these bacteria carries the chilling reminder that the next major pandemic may be only a few mutations away.
By age 32, Sheri Finstad’s epileptic seizures had become unbearable. She frequently fell, injured herself, and got concussions. Her doctors tried neurosurgery to better understand her condition, and a special diet and medication to treat it, to no avail. Then she enrolled in an experimental trial at the Mayo Clinic.
A surgical team implanted two stimulators, each about the size of a deck of cards, below Finstad’s clavicles. They threaded wires up her neck, just beneath the skin, to four probes implanted in her brain. Doctors programmed the device to deliver a constant flow of electricity to electrodes on the probes. In deep regions of the brain, such as the thalamus and the hippocampus, this current affects the electric signals that neurons use to communicate.
“It’s kind of like a pacemaker for the brain,” says Zoltan Mari, director of the Deep Brain Stimulation Center at Johns Hopkins, who uses the therapy to treat dystonia and tremors associated with Parkinson’s disease. But Finstad’s device is even more advanced. In addition to stimulating the brain, it records her brain activity so doctors can better understand her epilepsy.
So far, study results suggest the treatment is effective and has fewer side effects than drugs. It’s now in the final stages of FDA approval. Regulators have already signed off on the therapy (with non-recording devices) to treat epilepsy in 30 countries—including Australia, Canada, and a number of countries in the European Union.
Neuroscientists anticipate deep brain stimulation might also soon be used to treat depression, control blood pressure, and regulate metabolism. In a 2013 pilot study, obese patients who failed to lose weight after getting bariatric surgery did lose weight after stimulation of their hypothalamus, the region associated with hunger.
Finstad must visit the doctor to transmit data from her device, but the next-gen stimulator, now in animal trials, will transfer it directly to a patient’s computer. Mari predicts future devices could be even smarter, reading the neurological activity, and automatically adjusting the settings to deliver a more precise current, right when it’s needed.
This article was originally published in the November 2015 issue of Popular Science under the title “Electricity Tamps Down Epilepsy.”
With the world population expected to reach 9 billion by 2050, engineers and scientists are looking for ways to meet the increasing demand for food without also increasing the strain on natural resources, such as water and energy—an initiative known as the food-water-energy nexus.
Ramesh Raliya, PhD, a postdoctoral researcher, and Pratim Biswas, PhD, the Lucy & Stanley Lopata Professor and chair of the Department of Energy, Environmental & Chemical Engineering, both at the School of Engineering & Applied Science at Washington University in St. Louis, are addressing this issue by using nanoparticles to boost the nutrient content and growth of tomato plants. Taking a clue from their work with solar cells, the team found that by using zinc oxide and titanium dioxide nanoparticles, the tomato plants better absorbed light and minerals, and the fruit had higher antioxidant content.
“When a plant grows, it signals the soil that it needs nutrients,” Biswas says. “The nutrient it needs is not in a form that the plant can take right away, so it secretes enzymes, which react with the soil and trigger bacterial microbes to turn the nutrients into a form that the plant can use. We’re trying to aid this pathway by adding nanoparticles.”
Zinc is an essential nutrient for plants, helps other enzymes function properly and is an ingredient in conventional fertilizer. Titanium is not an essential nutrient for plants, Raliya says, but boosts light absorption by increasing chlorophyll content in the leaves and promotes photosynthesis, properties Biswas’ lab discovered while creating solar cells.
The team used a very fine spray using novel aerosolization techniques to directly deposit the nanoparticles on the leaves of the plants for maximum uptake.
“We found that our aerosol technique resulted in much greater uptake of nutrients by the plant in comparison to application of the nanoparticles to soil,” Raliya says. “A plant can only uptake about 20 percent of the nutrients applied through soil, with the remainder either forming stable complexes with soil constituents or being washed away with water, causing runoff. In both of the latter cases, the nutrients are unavailable to plants.”
Overall, plants treated with the nanoparticles via aerosol routes produced nearly 82 percent (by weight) more fruit than untreated plants. In addition, the tomatoes from treated plant showed an increase in lycopene, an antioxidant linked to reduced risk of cancer, heart disease and age-related eye disorders, of between 80 percent and 113 percent.
Previous studies by other researchers have shown that increasing the use of nanotechnology in agriculture in densely populated countries such as India and China has made an impact on reducing malnutrition and child mortality. These tomatoes will help address malnutrition, Raliya says, because they allow people to get more nutrients from tomatoes than those conventionally grown.
In the study, published online last month in the journal Metallomics, the team found that the nanoparticles in the plants and the tomatoes were well below the USDA limit and considerably lower than what is used in conventional fertilizer. However, they still have to be cautious and select the best concentration of nanoparticles to use for maximum benefit, Biswas says.
Raliya and the rest of the team are now working to develop a new formulation of nanonutrients that includes all 17 elements required by plants.
“In 100 years, there will be more cities and less farmland, but we will need more food,” Raliya says. “At the same time, water will be limited because of climate change. We need an efficient methodology and a controlled environment in which plants can grow.”
Eggs of the dwarf tapeworm (Hymenolepsi nana).
A tapeworm that infected a Colombian man deposited malignant cells inside his body that spread much like an aggressive cancer, researchers have reported in a bizarre, but not unprecedented, case.
“We have a situation where a foreign organism is developing as a tumour rather than developing as an organism,” says Peter Olson, a developmental parasitologist at the Natural History Museum in London. He is part of a team that describes the case in a 4 November report in the New England Journal of Medicine1.
Under a microscope, those samples revealed small odd-shaped cells that, like a cancer, appeared to be invading nearby healthy tissue, the CDC team found. Yet the cells tested negative for human proteins. That was a conundrum: although the US investigators knew about the man’s tapeworm infection, the invading cells did not look like they should belong to a complex, multicellular organism such as a tapeworm.
Tumours from tapeworms
Olson believes that the tumorous tapeworm cells are rogue larvae that burrowed from the stomach into the lymph nodes of immunocompromised people (a healthy immune system would stop this invasion). The larvae are loaded with regenerative stem cells, so instead of turning into an adult tapeworm, they proliferate. “Those stem cells that would normally give rise to a segmented worm don’t, because they’re in the wrong place and have the wrong environmental cues,” says Olson.
Elizabeth Murchison, a molecular geneticist at the University of Cambridge, UK, says that she finds the case astonishing. Although there is no evidence that the proliferative tapeworm cells might be transmitted between humans, Murchison (who studies tumour cells that spread between animals) wonders whether proliferative cells from other parasites could become infectious.
“This paper is tremendously important as it presents the existence of a new type of disease process, which may have previously been overlooked,” she says.
A team at IBM recently developed what they call a High Concentration Photo Voltaic Thermal (HCPVT) system that is capable of concentrating the power of 2,000 suns, they are even claiming to be able to concentrate energy safely up to 5,000X, that’s huge.
The process of trapping the sunlight produces water that can be used to produce filtered drinkable water, or used for other things like air conditioning etc. Scientists envision that the HCPVT system could provide sustainable energy and fresh water to communities all around the world.
“Each 1cmX1cm chip can convert 200-250 watts, on average, over a typical eight-hour day in a sunny region. In the HCPVT system, instead of heating a building, the 90 degree Celsius water will pass through a porous membrane distillation system where it is then vaporized and desalinated. Such a system could provide 30-40 liters of drinkable water per square meter of receiver area per day, while still generating electricity with a more than 25 percent yield or two kilowatts hours per day. A large installation would provide enough water for a small town.” (2)
The heat is absorbed into hundreds of tiny solar cells called photovoltaic chips. These gather the energy and are then cooled by microchannled water, which is why they are safely able to concentrate such large amounts of solar energy.
According to Greenpeace, this technology can establish itself as the third largest player in the sustainable power generation industry. A study published in 2009 predicted that solar power could supply all the world’s energy needs, with minimal space. (1) Greenpeace estimates that it would take only two percent of the Sahara Desert’s land area to supply the entire planet’s electricity needs.(1)
A common problem with modern-day solar collectors is that they can only take in a minimal amount of energy. This means that useful heat is wasted, cannot be harnessed and is thrown away. This technology eliminates that problem. Solar panels taking in too much energy run the risk of melting themselves due to mass amounts of heat. This is changing, as we continue to explore more efficient ways of energy generation, it’s becoming clear that it’s time to do away with the old, and usher in the new, clean, green technologies.
This project is being funded by the Swiss Commission for Technology and Innovation. They are supplying a three-year $2.4 million grant to develop the technology. Prototypes have been developed and are being tested.
This is another great technology that could provide power to the entire planet for free! Good reasons as to why we cannot implement this technology are non existent. At the end of the day, it seems that big oil corporations will do whatever they can to prevent change from happening, but the power of the people is greater. All we have to do is come together, create, and cooperate.
This is awesome.
Cleanliness is hugely important in any hospital, but keeping these sprawling sites free from germs and bacteria is no easy task — and that’s why any ways in which the buildings can keep themselves hygienic are a massive help to staff and patients. Enter a new brand of paint from Sherwin-Williams, which can automatically kill off bacteria, according to reports.
Called Paint Shield, the microbicidal paint can kill infection-causing bacteria after just two hours of exposure, Sherwin-Williams says. 99.9 percent of bugs — including those responsible for MRSA and E. coli — can be eradicated from the surfaces before the cleaning team even gets to work. Existing infectious bacteria are killed off and the future growth of common microbes is inhibited as well, and the paint can be effective for up to four years.
“Paint Shield is one of the most significant technological breakthroughs in our nearly 150 year history of innovation,” said Chris Connor, the chairman and chief executive of Sherwin-Williams, in a statement released to the press. “By killing infectious pathogens on painted surfaces, Paint Shield is a game-changing advancement in coatings technology.”
It’s arrived not a moment too soon: according to data from the US Centres for Disease Control and Prevention (CDC), four percent of patients in the United States contract at least one infection during the course of their hospital care. Sherin-Williams says it has been busy working with scientists and expert microbiologists in order to produce the paint, which is going to be available from next year.
If you’re thinking of redecorating a hospital of your own, Paint Shield comes in 590 colours for you to choose from. It can potentially be applied on hard interior non-porous ceilings, walls, doors and trim, not only in hospitals but also in healthcare facilities, athletics venues, day care centres, homes for the elderly and cruise ships.
“Continued progress in combating HAIs [hospital-acquired infections] will require a broad array of measures, including passive methods that are less dependent on human intervention,” commented Steve Revnew of Sherwin-Williams. “By continuing to kill MRSA and other bacteria, even after repeated contamination, Paint Shield offers hospitals and other facilities an important new tool to help in the fight against the spread of HAIs.”
The Paint Shield product still needs to be tested in real-world settings and must meet various health and safety guidelines before it can be used on a large scale, however. If it gets the all-clear for hospital use, it could help in significantly reducing the number of patients who pick up infections while trying to get better.