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    E&E provides daily coverage of essential energy and environmental news at www.eenews.net.Scientists have created a mystery material that seems to conduct electricity without any resistance at temperatures of up to about 15 °C. That’s a new record for superconductivity, a phenomenon usually associated with very cold temperatures. The material average price of cialis daily itself is poorly understood, but it shows the potential of a class of superconductors discovered in 2015. The superconductor has one serious limitation, however.

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    He adds that it vindicates a line of work that he started in 2015, when his group reported the first high-pressure, high-temperature superconductor—a compound of hydrogen and sulfur that had zero resistance up to −70 °C. In 2018, a high-pressure compound of hydrogen and lanthanum was shown average price of cialis daily to be superconductive at −13 °C. But the latest result marks the first time this kind of superconductivity has been seen in a compound of three elements rather than two—the material is made of carbon, sulfur and hydrogen. Adding a third element greatly broadens the combinations that can be included in future experiments searching for new superconductors, says study co-author Ashkan Salamat, a physicist at the University of Nevada, Las Vegas.

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    €œI think there were very few people outside of the high-pressure community who took him seriously,” Somayazulu says. Mystery material Physicist Ranga Dias at the University of Rochester in New York, along with Salamat and other collaborators, placed a mixture of carbon, hydrogen and sulfur in a microscopic niche they had carved between the tips of two diamonds. They then triggered average price of cialis daily chemical reactions in the sample with laser light, and watched as a crystal formed. As they lowered the experimental temperature, resistance to a current passed through the material dropped to zero, indicating that the sample had become superconductive.

    Then they average price of cialis daily increased the pressure, and found that this transition occurred at higher and higher temperatures. Their best result was a transition temperature of 287.7 kelvin at 267 gigapascals—2.6 million times atmospheric pressure at sea level. The researchers also found some evidence that the crystal expelled its magnetic field at the transition temperature, a crucial test of superconductivity. But much about the material remains average price of cialis daily unknown, researchers warn.

    €œThere are a lot of things to do,” says Eremets. Even the crystal’s exact structure and chemical formula are not yet understood. €œAs you go to higher average price of cialis daily pressures, the sample size gets smaller,” says Salamat. €œThat’s what makes these types of measurements really challenging.” High-pressure superconductors made of hydrogen and one other element are well understood.

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    As flu season cialis website creeps up on the Northern Hemisphere, cold and flu relief medications will inevitably fly off store shelves http://www.amisdepasteur.fr/is-it-safe-to-buy-cialis-online/. A natural remedy that shoppers might reach for is elderberry, a small, blackish-purple fruit that companies turn into syrups, lozenges and gummies. Though therapeutic uses of the berry date back centuries, Michael Macknin, a pediatrician at the cialis website Cleveland Clinic, hadn’t heard of using elderberry to treat the flu until a patient’s mother asked him about it. Some industry-sponsored research claims that the herbal remedy could cut the length of the symptoms by up to four days. For a comparison, Tamiflu, an FDA-approved treatment, only reduces flu duration by about a single day cialis website.

    €œI said, 'Gee, if that’s really true [about elderberry], it would be a huge benefit,'” Macknin says. But the effectiveness and safety of elderberry is still fairly unclear. Unlike the over-the-counter medicines at your local pharmacy, elderberry hasn't been through cialis website rigorous FDA testing and approval. However, Macknin and his team recently published a study in the Journal of General Internal Medicine, which found that elderberry treatments did nothing for flu patients. This prompts a need for further studies into the remedy — work that unfortunately stands a cialis website low chance of happening in the future, Macknin says.

    Looking For ProofElderberries are full of chemicals that could be good for your health. Like similar fruits, the berries contain high levels of antioxidants, compounds cialis website that shut down reactions in our bodies that damage cells. But whether or not elderberry's properties also help immune systems fend off a virus is murky. There are only a handful of studies that have examined if elderberries reduced the severity or duration of the flu. And though some of the work prior to Macknin’s was well-designed and supported this herbal remedy as a helpful flu aid, at least some — and potentially all — of those studies were funded by elderberry treatment manufacturers.Macknin says an elderberry cialis website supplement company provided his team with their products and a placebo version for free, but that the company wasn’t involved in the research beyond that.

    Macknin's study is the largest one conducted on elderberry to date, with 87 influenza patients completing the entire treatment course. Participants in the study were also welcome to take Tamiflu, for ethical reasons, as the team didn’t want to exclude anyone from taking a proven flu therapy cialis website. Additionally, each participant took home either a bottle of elderberry syrup or the placebo with instructions on when and how to take it. The research team called participants every day for a symptom check and to remind them to take their medication.By cialis website chance, it turned out that a higher percentage of the patients given elderberry syrup had gotten their flu shot and also chose to take Tamiflu. Since the vaccination can reduce the severity of infection in recipients who still come down with the flu, the study coincidentally operated in favor of those who took the herbal remedy, Macknin says.

    Those patients could have dealt with a shorter, less-intense illness because of the Tamiflu and vaccination. €œEverything was stacked to have cialis website it turn out better [for the elderberry group],” Macknin says, “and it turned out the same.” The researchers found no difference in illness duration or severity between the elderberry and placebo groups. While analyzing the data, the team also found that those on the herbal treatment might have actually fared worse than those on the placebo. The potential for this intervention to actually harm cialis website instead of help influenza patients explains why Macknin thinks the therapy needs further research.But, don't expect that work to happen any time soon. Researchers are faced with a number of challenges when it comes to studying the efficacy of herbal remedies.

    For starters, cialis website there's little financial incentive to investigate if they actually work. Plant products are challenging to patent, making them less lucrative prospects for pharmaceutical companies or research organizations to investigate. Additionally, investigations that try and prove a proposed therapy as an effective drug — like the one Macknin and his team accomplished — are expensive, Macknin says. Those projects need FDA oversight and cialis website additional paperwork, components that drive up study costs. €œIt’s extraordinarily expensive and there’s no money in it for anybody,” Macknin says.Talk To Your DoctorUltimately, research on elderberry therapies for flu patients is a mixed bag, and deserves more attention from scientists.

    However, if you still want to discuss elderberry treatments for the flu with your doctor, that’s a conversation you should feel comfortable having, says Erica McIntyre, an expert focused on health and environmental psychology in the School of cialis website Public Health at the University of Technology Sydney. Navigating what research says about a particular herbal medicine is challenging for patients and health practitioners alike. The process is made more complex by the range of similar-sounding cialis website products on the market that lack standardized ingredients, McIntyre says. But when doctors judge or shame patients for asking about non-conventional healthcare interventions, the response can distance people and push them closer to potentially unproven treatments. Even worse, those individuals might start to keep their herbal remedies a secret.

    €œIt is that fear about being judged for use of that medication,” McIntyre says, that cialis website drives up to 50 percent of people taking herbal treatments to withhold that information from healthcare practitioners. That’s a dangerous choice, as some herbal and traditional medications can interact and cause health problems.If a physician shames someone for asking about alternative medicines, it’s likely time to find a new doctor, McIntyre says. Look for someone who will listen to your concerns — whether it's that you feel traditional treatments cialis website haven’t worked for you, or that you didn’t like the side effects, the two common reasons people pursue herbal treatments in the first place. €œYou’re not necessarily looking for a doctor that will let you do whatever you want,” McIntyre says, “but that they actually consider you as a patient, your treatment choices and your treatment priorities, and communicate in a way that’s supportive.” And if a doctor suggests that you avoid a treatment you’re interested in, ask why. They generally have a good reason, McIntyre says.For now, know that even if your doctor doesn’t support you taking elderberry, there are other proven preventative measures that are worth your while — like the flu shot.

    Anyone six cialis website months or older should get it, Macknin says, and stick to the protocols we’re used to following to prevent COVID-19 infections, like social distancing, mask-wearing and hand-washing. Those measures also help prevent flu transmission, too — something, so far, no elderberry supplement package can claim.The yearly influenza season threatens to make the COVID-19 pandemic doubly deadly, but I believe that this isn’t inevitable.There are two commonly given vaccines – the pneumococcal vaccine and the Hib vaccine – that protect against bacterial pneumonias. These bacteria complicate both influenza and cialis website COVID-19, often leading to death. My examination of disease trends and vaccination rates leads me to believe that broader use of the pneumococcal and Hib vaccines could guard against the worst effects of a COVID-19 illness.I am an immunologist and physiologist interested in the effects of combined infections on immunity. I have reached my insight by juxtaposing two cialis website seemingly unrelated puzzles.

    Infants and children get SARS-CoV-2, the virus that causes COVID-19, but very rarely become hospitalized or die. And case numbers and death rates from COVID-19 began varying greatly from nation to nation and city to city even before lockdowns began. I wondered why.One night I cialis website woke up with a possible answer. Vaccination rates. Most children, cialis website beginning at age two months, are vaccinated against numerous diseases.

    Adults less so. And, both infant and adult vaccination rates vary widely cialis website across the world. Could differences in the rates of vaccination against one or more diseases account for differences in COVID-19 risks?. As someone who had previously investigated other pandemics such as the Great Flu Pandemic of 1918-19 and AIDS, and who has worked with vaccines, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower COVID-19 Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib). I correlated them with COVID-19 case rates cialis website and death rates for 24 nations that had experienced their COVID-19 outbreaks at about the same time.

    I controlled for factors such as percentage of the population who were obese, diabetic or elderly.I found that only pneumococcal vaccines afforded statistically significant protection against COVID-19. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest COVID-19 rates per million cialis website have the poorest pneumococcal vaccination rates among both infants and adults. Nations with the lowest rates of COVID-19 – Japan, Korea, Denmark, Australia and New Zealand – have the highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against COVID-19. This is especially true among minority patients who are bearing the brunt of the coronavirus pandemic cialis website. The report also suggests that other vaccines, or combinations of vaccines, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria – varies by state from 74% to 92%.

    Although the CDC recommends that all adults 18-64 in high risk groups for COVID-19 and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S. And a handful of immunologically compromised adults have cialis website been. Pneumococcal and Hib vaccination rates are significantly lower in minority populations in the U.S. And in countries that have been hit harder by COVID-19 than the U.S.Based on these data, I advocate universal pneumococcal and Hib vaccination among children, at-risk adults and all cialis website adults over 65 to prevent serious COVID-19 disease.Left. Combined rates of childhood and adult (over 65) pneumococcal vaccination (out of a possible 200).

    Right. Cases (per million) population of COVID-19 at about 90 days into the pandemic for 24 nations. Nations with high pneumococcal vaccination rates have low COVID-19 case rates. (Credit. CC BY-SA)How Pneumococcal Vaccination Protects Against COVID-19Protection against serious COVID-19 disease by pneumococcal and Hib vaccines makes sense for several reasons.

    First, recent studies reveal that the majority of hospitalized COVID-19 patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria. Pneumococcal and Hib vaccinations should protect coronavirus patients from these infections and thus significantly cut the risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella vaccines may confer specific protection against the SARS-CoV-2 virus that causes COVID-19 by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another. In this case, proteins found in pneumococcal vaccines and, to a lesser degree, ones found in Hib and rubella vaccines as well look like several proteins produced by the SARS-CoV-2 virus.Two of these proteins found in pneumococcal vaccines mimic the spike and membrane proteins that permit the virus to infect cells. This suggests pneumococcal vaccination may prevent SARS-CoV-2 infection. Two other mimics are the nucleoprotein and replicase that control virus replication.

    These proteins are made after viral infection, in which case pneumococcal vaccination may control, but not prevent, SARS-CoV-2 replication.Either way, these vaccines may provide proxy protection against SARS-CoV-2 infection that we can implement right now, even before we have a specific virus vaccine. Such protection may not be complete. People might still suffer a weakened version of COVID-19 but, like most infants and children, be protected against the worst effects of the infection.Fighting Influenza-related Pneumonias During the COVID-19 PandemicWhile the specific protection these other vaccines confer against COVID-19 has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza. The influenza virus rarely causes death directly. Most often, the virus makes the lungs more susceptible to bacterial pneumonias, which are deadly.

    Dozens of studies around the world have demonstrated that increasing rates of pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these vaccines is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths. In the context of COVID-19, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the coronavirus, independent of any effect these vaccines might have on SARS-CoV-2 itself. In my opinion, that is a winning scenario.In short, we need not wait for a SARS-CoV-2 vaccine to slow down COVID-19.I believe that we can and should act now by fighting the coronavirus with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and COVID-19, and perhaps proxy-vaccinating against SARS-CoV-2 itself, helps everyone. Administering these already available and well-tested pneumococcal and Hib vaccines to people will save money by freeing up hospital beds and ICUs. It will also improve public health by reducing the spread of multiple infections and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University.

    This article was originally published on The Conversation under a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today. A vaguely psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since. Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012.

    Since then, Mazmanian and a small but growing cadre of fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism could, in the end, prove the most transformative. Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the brain disorder have remained speculative. Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life was his plan.

    Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled. The teacher recognized his gift for language and encouraged him to pursue a career in literature. Mazmanian enrolled at UCLA in 1990, planning to major in English.Everything changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders. (Credit.

    Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says. €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body. After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph infections.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria. But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?.

    To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship. But what was it?. Gut InvadersMazmanian set out to study the link between gut microbes and the immune system. As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes.

    He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt. But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue). (Credit. Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?.

    € Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways. Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?. €™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice.

    After receiving the fecal transplant, their T-cell counts shot up. Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined. Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis.

    When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic. The T-cell numbers spiked to normal. Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B. Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B.

    Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells. These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases. It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders. What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson.

    Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe infection in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea. Was it possible, he wondered, that there was a microbiome connection?. As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza virus, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism. Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion.

    The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?. When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed. Could it be that the microbiome was the cause of this inflammation?. And could that, in turn, be somehow connected to the behavioral symptoms?.

    Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice. And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut. They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body.

    They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism. And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step. Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests.

    The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms. The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways. Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain. And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper.

    Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward. While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism. Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues. The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected.

    The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced. At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism. Two years after the initial trial, only 17 percent were rated as severely autistic. And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago.

    €œHis ability to communicate is so much different now. He’s just so much more present. He’s so much more aware. He’s no longer in occupational therapy. He’s no longer in speech therapy.

    After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle. The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people. But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit.

    Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery. In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it. The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons.

    A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes. When their pups were born, the researchers continued to feed the young the substances until they reached adulthood. Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety. Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown.

    €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite. It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light. I don’t know the circuit, I don’t know where the wire is,” Mazmanian says. €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?.

    €Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results. Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity. Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed. In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives.

    €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants. €œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian. €œHealthy skepticism is a good thing. I believe the preclinical data, I believe the mouse data.

    But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything. (Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial. But that was not the most dramatic difference.

    Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary. He seemed to live in his own bubble. He had frequent outbursts. For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!.

    €™â€‰â€ she recalls. €œAnd he was just excited and happy and ready to go about his day with this big smile. It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?. What is wrong with me?.

    €™ And as soon as he did that, I caught my breath. I had to compose myself and say, ‘I don’t know. But do you feel better?. Do you feel different?. Why do you think?.

    €™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says. €œPrior to the study, I was very afraid. My biggest fear was ‘how is he going to navigate the world when I’m not here?. €™ And I think I have a lot of hope now that he is going to be OK now on his own.”There’s something strange about the female orgasm, something that scientists have been unable to explain.

    Biological functions are normally discussed in terms of evolutionary pressure, or reproductive advantage. If a biological trait improves your chances of having more offspring, then it’s more likely to stick around in your species. The male orgasm makes perfect sense — ejaculate contains the genetic material that’s necessary for making babies. But the female orgasm has been harder to nail down. Fertilization doesn’t depend on it, and “fun” isn’t exactly in the pantheon of evolutionary explanations.Researchers that study how the female orgasm relates to reproductive success have two main options — either ask people invasive questions about their most personal moments, or to find a way to stick probes in or on them during said moments.

    Neither of these approaches have resulted in the kind of “wet lab” research that’s the gold standard for biological understanding.What we do know, despite widespread cultural discomfort with talking openly about sex and pleasure, is that there appears to be significant sexual dysfunction in American society. Back in 2014, researchers from the Kinsey Institute, the preeminent U.S. Academy for the study of sex and relationships, said as much. In a survey of nearly 3,000 people, they found that men, straight or gay, orgasmed 85 percent of the time during consensual sexual encounters. Lesbian women orgasmed less often, 75 percent of the time, while straight women fared worst with just a 60 percent chance of orgasm.

    Other studies have shown that something like 10-15 percent of women experience lifelong anorgasmia, meaning they’ve never experienced orgasm. A further 40 percent of women report some kind of inability to reach orgasm in the past year.The orgasm gap is hard to explain. Some think that it comes down to straight men’s finesse, or lack thereof, citing the difference between straight and lesbian satisfaction. Indeed, it makes sense that knowing your way around the territory would help. But for many couples this isn’t a helpful revelation, since the emotional maturity necessary to teach sexual dexterity is often out of reach.

    Shortcut to SatisfactionLuckily, we live in an era of Silicon Valley disruption, which has even started lapping at the shores of sex research. Technologist Liz Klinger is at the forefront of this transition. She and her team have built a platform that lets people become citizen scientists of sex —without ever having to get out from between the sheets.About a decade ago, Klinger’s company, Lioness, released what they billed as the first “smart vibrator,” a sex toy that could actually learn about you. The final product was a far cry from the first prototype, which was much more laboratory object than sex toy.The “test device was this whole mess of wires, with a hard connection. We had to physically send it to our beta testers, who used it and sent it back,” recalls Klinger.

    The researchers would download the data collected by the toy’s four sensors — temperature, motion, acceleration and pressure — and compile it into a chart that represented arousal and orgasm, as told through the story of pelvic-floor muscle contractions.It was an immediate success for sex partners who needed ways to talk about pleasure in a more objective way. Klinger recalled that when she got the first beta-test couple on the phone, “the wife was like ‘holy crap, we finally were able to talk about these things that I’ve had a lot of trouble talking about.’ It turned out that she wanted more foreplay, and he didn’t know quite that that meant. He’d spend more time, but it just didn’t match up, you know?. € With the company’s signature offering in hand — a chart of sexual arousal over time — Klinger found that couples could have a conversation “without the subtext of ‘oh, you’re not good enough, or I don’t like you enough,’ on the husband’s part and ‘I’m so tired of talking about this’ on the wife’s part,” she says. The chart “can change people’s perceptions of their own experiences, and how they talk about them with others.”Doing the Deed — For ScienceThis spring, the company has launched a research platform dubbed Lioness 2.0 — a new optional service that, unsurprisingly, their data-obsessed users have greeted with open arms.

    Now, instead of simply using the toy to understand themselves better, Lioness owners can opt in to the kinds of hands-on studies that are necessary for a deeper understanding of sex and pleasure. So far, the company is working with Nigeria’s Society for Family Health to study how pleasure changes with menopause across age, race and orientation, as well as with the U.S.’s Center for Genital Health and Education to explore the role of pelvic floor muscles in orgasm.Pani Farvid, a professor of applied psychology at The New School in New York City, has some reservations about the platform. €œI really like what they’re trying to do, but there could be more added to make it a bit more comprehensive. My concern is that there's a misconception that sex is just about the orgasm, that it’s just physiological and that pleasure just has to do with the genitals.” From where she’s sitting, “that’s a very mechanical view of sexuality.” If the Lioness is helping to equalize the orgasm gap, or helping people understand their bodies better, “I think that's great,” says Farvid. €œBut as a critical sexologist, I'm interested in delving deeper into what these practices mean.” If sex is hyper-focused on orgasm, to exclusion of everything else, she cautions that these norms “have real-life negative impacts on people's sex lives and their sense of themselves.”At this point, knee-deep in an era of data collection that was once the sole purview of white-coat-wearing scientists, it’s old news that we need to be careful with what our technology is doing to us.

    No tool can serve as a cure-all, even if it comes loaded with a neat app and some space-age sensors. What it can offer, though, is the opportunity to start a conversation, and the chance to take a long, honest look at something about yourself — whether it’s the number of steps you take every day, or the way you want to be touched.Wondering how to keep your glasses from fogging up when your mask is on?. Look no further. If we've learned one thing throughout the COVID-19 pandemic, it's the importance of wearing a mask. Countless studies have shown over the past eight months that wearing a protective barrier over your nose and mouth — whether it's a standard-issue surgical mask or an N95 respirator — can significantly decrease the odds of catching and transmitting disease.

    What's more, some research shows that masking up can reduce the severity of an infection if a masked person does contract COVID-19. But while masks are potentially lifesaving, they can be uncomfortable, often changing your breathing patterns and fogging up your glasses when breath escapes through the top of the mask. Among people who choose not to wear a mask to prevent the spread of COVID-19, many cite discomfort as a key reason why.Wesley Wilson, a tumor immunologist in Pennsylvania, knows how annoying it can be when your glasses are fogging up. He says fogging is “definitely a problem” among his hospital colleagues, who need to wear protective goggles and surgical masks while on the job. Fortunately, they've also picked up a few helpful hacks for keeping their vision clear while wearing a mask with glasses.#1.

    Use Tape“If you have to keep your mask on for hours, tape works like a charm,” Wilson says. This especially applies to healthcare professionals in his practice who are required to keep their masks on at all times, except during lunch. €œIf you're putting on your mask and taking it off a lot, tape probably isn't practical — but two small pieces of tape on the cheeks keep the mask fitted closer to your face, and the hot air out of your glasses,” he says.#2. Fit the Mask to Your FaceWhile some air leakage is to be expected, wearing a mask that fits securely to your face will prevent glass fogging and filter the virus more effectively since less air is coming in or out. Find surgical masks or N95s that come with a nose bridge, a small, flexible piece of metal or plastic that allows the mask to more closely fit the contours of your face.

    Nose bridges can be sewn inside masks or affixed to the front.Read More. Why It Feels Like You Can't Breathe Inside Your Face Mask#3. Adjust Your MaskAccording to the American Academy of Ophthalmology, a minor adjustment in how you wear your mask could be enough to prevent fog as well. Simply pull the mask over your nose and rest your glasses on top of your face mask. As long as the mask is fitted close to your face, this should prevent hot air from slipping out.#4.

    Spray Your GlassesA former ice hockey player, Wilson says the protective visor under his helmet would often fog with hot air while he was on the ice during games. Like an ocean diver, he would use de-misting solution or a defogging spray (such as this one) to keep his visor free of fog. The same concept applies to eyeglass fog caused by masking, he says. €œYou can either buy a spray or you can make your own with either shaving cream or soap and water,” says Wilson. €œWiping some shaving cream on your glasses and then wiping it off will coat them with a similar surface-tension altering compound that prevents fog.”.

    As flu season creeps average price of cialis daily up on the Northern Hemisphere, cold and flu relief medications will inevitably fly off store shelves. A natural remedy that shoppers might reach for is elderberry, a small, blackish-purple fruit that companies turn into syrups, lozenges and gummies. Though therapeutic uses of the berry date back centuries, Michael Macknin, a pediatrician at the Cleveland Clinic, hadn’t heard average price of cialis daily of using elderberry to treat the flu until a patient’s mother asked him about it. Some industry-sponsored research claims that the herbal remedy could cut the length of the symptoms by up to four days. For a comparison, Tamiflu, an average price of cialis daily FDA-approved treatment, only reduces flu duration by about a single day.

    €œI said, 'Gee, if that’s really true [about elderberry], it would be a huge benefit,'” Macknin says. But the effectiveness and safety of elderberry is still fairly unclear. Unlike the over-the-counter medicines at your local pharmacy, elderberry average price of cialis daily hasn't been through rigorous FDA testing and approval. However, Macknin and his team recently published a study in the Journal of General Internal Medicine, which found that elderberry treatments did nothing for flu patients. This prompts a need for further studies into the remedy — average price of cialis daily work that unfortunately stands a low chance of happening in the future, Macknin says.

    Looking For ProofElderberries are full of chemicals that could be good for your health. Like similar fruits, the berries contain high levels of antioxidants, compounds that shut average price of cialis daily down reactions in our bodies that damage cells. But whether or not elderberry's properties also help immune systems fend off a virus is murky. There are only a handful of studies that have examined if elderberries reduced the severity or duration of the flu. And though some of the work prior to Macknin’s was well-designed and supported this herbal remedy as a helpful flu aid, at least some — and potentially all — of those studies were funded by elderberry treatment manufacturers.Macknin says an elderberry average price of cialis daily supplement company provided his team with their products and a placebo version for free, but that the company wasn’t involved in the research beyond that.

    Macknin's study is the largest one conducted on elderberry to date, with 87 influenza patients completing the entire treatment course. Participants in the study were also welcome to take Tamiflu, for ethical reasons, as the team didn’t want to exclude anyone average price of cialis daily from taking a proven flu therapy. Additionally, each participant took home either a bottle of elderberry syrup or the placebo with instructions on when and how to take it. The research team called participants every day for a symptom check and to remind them to take their medication.By chance, it turned out that a higher percentage of the patients given elderberry syrup had gotten their flu shot and also chose to average price of cialis daily take Tamiflu. Since the vaccination can reduce the severity of infection in recipients who still come down with the flu, the study coincidentally operated in favor of those who took the herbal remedy, Macknin says.

    Those patients could have dealt with a shorter, less-intense illness because of the Tamiflu and vaccination. €œEverything was stacked to have it turn out better [for the elderberry group],” Macknin says, “and it average price of cialis daily turned out the same.” The researchers found no difference in illness duration or severity between the elderberry and placebo groups. While analyzing the data, the team also found that those on the herbal treatment might have actually fared worse than those on the placebo. The potential for this intervention to actually harm instead of help influenza patients average price of cialis daily explains why Macknin thinks the therapy needs further research.But, don't expect that work to happen any time soon. Researchers are faced with a number of challenges when it comes to studying the efficacy of herbal remedies.

    For starters, there's little financial incentive to investigate if they actually work average price of cialis daily. Plant products are challenging to patent, making them less lucrative prospects for pharmaceutical companies or research organizations to investigate. Additionally, investigations that try and prove a proposed therapy as an effective drug — like the one Macknin and his team accomplished — are expensive, Macknin says. Those projects need FDA oversight and additional paperwork, components that drive up average price of cialis daily study costs. €œIt’s extraordinarily expensive and there’s no money in it for anybody,” Macknin says.Talk To Your DoctorUltimately, research on elderberry therapies for flu patients is a mixed bag, and deserves more attention from scientists.

    However, if average price of cialis daily you still want to discuss elderberry treatments for the flu with your doctor, that’s a conversation you should feel comfortable having, says Erica McIntyre, an expert focused on health and environmental psychology in the School of Public Health at the University of Technology Sydney. Navigating what research says about a particular herbal medicine is challenging for patients and health practitioners alike. The process is made more complex by the range of average price of cialis daily similar-sounding products on the market that lack standardized ingredients, McIntyre says. But when doctors judge or shame patients for asking about non-conventional healthcare interventions, the response can distance people and push them closer to potentially unproven treatments. Even worse, those individuals might start to keep their herbal remedies a secret.

    €œIt is that fear about being judged for use of that medication,” McIntyre says, that drives up to 50 percent of people taking herbal average price of cialis daily treatments to withhold that information from healthcare practitioners. That’s a dangerous choice, as some herbal and traditional medications can interact and cause health problems.If a physician shames someone for asking about alternative medicines, it’s likely time to find a new doctor, McIntyre says. Look for someone who will listen to your concerns average price of cialis daily — whether it's that you feel traditional treatments haven’t worked for you, or that you didn’t like the side effects, the two common reasons people pursue herbal treatments in the first place. €œYou’re not necessarily looking for a doctor that will let you do whatever you want,” McIntyre says, “but that they actually consider you as a patient, your treatment choices and your treatment priorities, and communicate in a way that’s supportive.” And if a doctor suggests that you avoid a treatment you’re interested in, ask why. They generally have a good reason, McIntyre says.For now, know that even if your doctor doesn’t support you taking elderberry, there are other proven preventative measures that are worth your while — like the flu shot.

    Anyone six months or older should get it, Macknin says, and stick to the protocols we’re used to average price of cialis daily following to prevent COVID-19 infections, like social distancing, mask-wearing and hand-washing. Those measures also help prevent flu transmission, too — something, so far, no elderberry supplement package can claim.The yearly influenza season threatens to make the COVID-19 pandemic doubly deadly, but I believe that this isn’t inevitable.There are two commonly given vaccines – the pneumococcal vaccine and the Hib vaccine – that protect against bacterial pneumonias. These bacteria complicate both influenza and COVID-19, average price of cialis daily often leading to death. My examination of disease trends and vaccination rates leads me to believe that broader use of the pneumococcal and Hib vaccines could guard against the worst effects of a COVID-19 illness.I am an immunologist and physiologist interested in the effects of combined infections on immunity. I have reached average price of cialis daily my insight by juxtaposing two seemingly unrelated puzzles.

    Infants and children get SARS-CoV-2, the virus that causes COVID-19, but very rarely become hospitalized or die. And case numbers and death rates from COVID-19 began varying greatly from nation to nation and city to city even before lockdowns began. I wondered average price of cialis daily why.One night I woke up with a possible answer. Vaccination rates. Most children, beginning average price of cialis daily at age two months, are vaccinated against numerous diseases.

    Adults less so. And, both infant and adult vaccination rates vary average price of cialis daily widely across the world. Could differences in the rates of vaccination against one or more diseases account for differences in COVID-19 risks?. As someone who had previously investigated other pandemics such as the Great Flu Pandemic of 1918-19 and AIDS, and who has worked with vaccines, I had a strong background for tracking down the relevant data to test my hypothesis.Pneumococcal Vaccination Rates Correlate With Lower COVID-19 Cases and DeathsI gathered national and some local data on vaccination rates against influenza, polio, measles-mumps-rubella (MMR), diphtheria-tetanus-pertussis (DTP), tuberculosis (BCG), pneumococci and Haemophilus influenzae type B (Hib). I correlated average price of cialis daily them with COVID-19 case rates and death rates for 24 nations that had experienced their COVID-19 outbreaks at about the same time.

    I controlled for factors such as percentage of the population who were obese, diabetic or elderly.I found that only pneumococcal vaccines afforded statistically significant protection against COVID-19. Nations such as Spain, Italy, Belgium, Brazil, Peru and Chile that have the highest COVID-19 rates per million have the poorest pneumococcal vaccination rates among both infants and adults average price of cialis daily. Nations with the lowest rates of COVID-19 – Japan, Korea, Denmark, Australia and New Zealand – have the highest rates of pneumococcal vaccination among both infants and adults.A recent preprint study (not yet peer-reviewed) from researchers at the Mayo Clinic has also reported very strong associations between pneumococcal vaccination and protection against COVID-19. This is especially true among minority patients who are bearing the brunt of the average price of cialis daily coronavirus pandemic. The report also suggests that other vaccines, or combinations of vaccines, such as Hib and MMR may also provide protection.These results are important because in the U.S., childhood vaccination against pneumococci – which protects against Streptococcus pneumoniae bacteria – varies by state from 74% to 92%.

    Although the CDC recommends that all adults 18-64 in high risk groups for COVID-19 and all adults over the age of 65 get a pneumococcal vaccination, only 23% of high-risk adults and 64% of those over the age of 65 do so.Similarly, although the CDC recommends at all infants and some high-risk adults be vaccinated against Haemophilus influenzae type B (Hib), only 80.7% of children in the U.S. And a handful of immunologically compromised adults have average price of cialis daily been. Pneumococcal and Hib vaccination rates are significantly lower in minority populations in the U.S. And in countries that have been hit harder by COVID-19 than the U.S.Based on these data, I average price of cialis daily advocate universal pneumococcal and Hib vaccination among children, at-risk adults and all adults over 65 to prevent serious COVID-19 disease.Left. Combined rates of childhood and adult (over 65) pneumococcal vaccination (out of a possible 200).

    Right. Cases (per million) population of COVID-19 at about 90 days into the pandemic for 24 nations. Nations with high pneumococcal vaccination rates have low COVID-19 case rates. (Credit. CC BY-SA)How Pneumococcal Vaccination Protects Against COVID-19Protection against serious COVID-19 disease by pneumococcal and Hib vaccines makes sense for several reasons.

    First, recent studies reveal that the majority of hospitalized COVID-19 patients, and in some studies nearly all, are infected with streptococci, which causes pneumococcal pneumonias, Hib or other pneumonia-causing bacteria. Pneumococcal and Hib vaccinations should protect coronavirus patients from these infections and thus significantly cut the risk of serious pneumonia.I also found that pneumococcal, Hib and possibly rubella vaccines may confer specific protection against the SARS-CoV-2 virus that causes COVID-19 by means of “molecular mimicry.”Molecular mimicry occurs when the immune system thinks one microbe looks like another. In this case, proteins found in pneumococcal vaccines and, to a lesser degree, ones found in Hib and rubella vaccines as well look like several proteins produced by the SARS-CoV-2 virus.Two of these proteins found in pneumococcal vaccines mimic the spike and membrane proteins that permit the virus to infect cells. This suggests pneumococcal vaccination may prevent SARS-CoV-2 infection. Two other mimics are the nucleoprotein and replicase that control virus replication.

    These proteins are made after viral infection, in which case pneumococcal vaccination may control, but not prevent, SARS-CoV-2 replication.Either way, these vaccines may provide proxy protection against SARS-CoV-2 infection that we can implement right now, even before we have a specific virus vaccine. Such protection may not be complete. People might still suffer a weakened version of COVID-19 but, like most infants and children, be protected against the worst effects of the infection.Fighting Influenza-related Pneumonias During the COVID-19 PandemicWhile the specific protection these other vaccines confer against COVID-19 has not yet been tested in a clinical trial, I advocate broader implementation of pneumococcal and Hib vaccination for one additional, well-validated reason.Pneumococcal and Hib pneumonias – both caused by bacteria – are the major causes of death following viral influenza. The influenza virus rarely causes death directly. Most often, the virus makes the lungs more susceptible to bacterial pneumonias, which are deadly.

    Dozens of studies around the world have demonstrated that increasing rates of pneumococcal and Hib vaccination dramatically lowers influenza-related pneumonias.Similar studies demonstrate that the price of using these vaccines is balanced by savings due to lower rates of influenza-related hospitalizations, intensive care unit admissions and deaths. In the context of COVID-19, lowering rates of influenza-related hospitalizations and ICU admissions would free up resources to fight the coronavirus, independent of any effect these vaccines might have on SARS-CoV-2 itself. In my opinion, that is a winning scenario.In short, we need not wait for a SARS-CoV-2 vaccine to slow down COVID-19.I believe that we can and should act now by fighting the coronavirus with all the tools at our disposal, including influenza, Hib, pneumococcal and perhaps rubella vaccinations.Preventing pneumococcal and Hib complications of influenza and COVID-19, and perhaps proxy-vaccinating against SARS-CoV-2 itself, helps everyone. Administering these already available and well-tested pneumococcal and Hib vaccines to people will save money by freeing up hospital beds and ICUs. It will also improve public health by reducing the spread of multiple infections and boost the economy by nurturing a healthier population.Robert Root-Bernstein is a Professor of Physiology at Michigan State University.

    This article was originally published on The Conversation under a Creative Commons liscense Read the original here.This story appeared in the November 2020 issue as "Bacteria and the Brain." Subscribe to Discover magazine for more stories like this.It’s not always easy to convince people that the human gut is a sublime and wondrous place worthy of special attention. Sarkis Mazmanian discovered that soon after arriving at Caltech for his first faculty job 14 years ago, when he explained to a local artist what he had in mind for the walls outside his new office.The resulting mural greets visitors to the Mazmanian Lab today. A vaguely psychedelic, 40-foot-long, tube-shaped colon that’s pink, purple and red snakes down the hallway. In a panel next to it, fluorescent yellow and green bacteria explode out of a deeply inflamed section of the intestinal tract, like radioactive lava from outer space.The mural is modest compared with what the scientist has been working on since. Over the last decade or so, Mazmanian has been a leading proponent of the idea that the flora of the human digestive tract has a far more powerful effect on the human body and mind than we thought — a scientific effort that earned him a $500,000 MacArthur Fellowship “Genius Grant” in 2012.

    Since then, Mazmanian and a small but growing cadre of fellow microbiologists have amassed a tantalizing body of evidence on the microbiome’s role in all kinds of brain disorders, including schizophrenia, Alzheimer’s disease, Parkinson’s disease and depression.But the results they’ve seen in autism could, in the end, prove the most transformative. Autism affects about 1 in 59 children in the U.S., and involves profound social withdrawal, communication problems, and sometimes anxiety and aggression. The causes of the brain disorder have remained speculative. Now, Mazmanian and other researchers are finding that autism may be inextricably linked to — or even caused by — irregularities in the gut microbiome.A Biology StoryAt 47, Mazmanian — with his shaved head, flannel shirt and skinny jeans — resembles a young, urban hipster on his way to write at the local café. Originally, literary life was his plan.

    Born in Lebanon to two Armenian refugees, neither of whom had more than a first-grade education, Mazmanian landed in the class of an energetic high school English teacher in California’s San Fernando Valley, where his family first settled. The teacher recognized his gift for language and encouraged him to pursue a career in literature. Mazmanian enrolled at UCLA in 1990, planning to major in English.Everything changed when he took his first biology class. Hunched over his new, thick textbook in the library, reading about basic biological concepts like photosynthesis, Mazmanian felt a vast new world opening up to him.Sarkis Mazmanian, shown in front of a mural that celebrates the human gut, is part of a group of microbiologists researching the effects of the digestive tract on a range of disorders. (Credit.

    Caltech)“For the first time in my life, I wanted to turn the page and see where the story was going to go,” he says. €œI think I decided that minute to become a scientist.”Mazmanian was most fascinated by the idea that tiny organisms, invisible to the naked eye, could function as powerful, self-contained machines — powerful enough to take over and destroy the human body. After graduating with a degree in microbiology, Mazmanian joined a UCLA infectious diseases lab and began studying bacteria that cause staph infections.As his dissertation defense approached, Mazmanian read a one-page commentary penned by a prominent microbiologist, highlighting the fact that our intestines are teeming with hundreds, if not thousands, of different species of bacteria. But it was still largely unknown what they are and how they affect the human body.When Mazmanian dug further, he found that no one had yet answered what seemed to him to be the most obvious question. Why would the human immune system, designed to attack and destroy foreign invaders, allow hundreds of species of bacteria to live and thrive in our guts unmolested?.

    To him, the bacteria’s survival implied that we had evolved to coexist with them. And if that were so, he reasoned, there must be some benefit to both the microbes and the human body — a symbiotic relationship. But what was it?. Gut InvadersMazmanian set out to study the link between gut microbes and the immune system. As a postdoctoral researcher, he joined the lab of Harvard University infectious disease specialist Dennis Kasper.To start, Mazmanian examined how the immune systems of germ-free mice — lab mice completely protected, starting at birth, from all microbes — differed from those of mice with either few or normal levels of microbes.

    He expected this initial census would be just a first step in a long and arduous quest for scientific pay dirt. But when he went to examine a printout of his results in the lab, he realized immediately he might already be onto something big. The germ-free mice had a 30 to 40 percent reduction in a specific type of immune cell known as helper T-cells.This colorized close-up of a mouse’s gut reveals the tight relationship between the gut microbe Bacteroides fragilis (red) and the epithelial surface of the colon (blue). (Credit. Caltech)Since helper T-cells play a key role in coordinating attacks against invading pathogens, the finding suggested that the immune systems of the germ-free mice were far less robust than those found in peers with normal levels of microbes.“That was exciting, right?.

    € Mazmanian recalls. €œObviously I repeated it and tested it in a number of different ways. Then I asked the next question. €˜Can I restore the [immune] function in an adult animal?. €™â€‰â€Mazmanian colonized the guts of the immunocompromised, germ-free mice with microbes from standard lab mice.

    After receiving the fecal transplant, their T-cell counts shot up. Within a month, their numbers were identical to mice raised outside the germ-free bubble.Resolving to identify the microorganisms causing this transformation, Mazmanian resorted to trial and error. One by one, he added strains of bacteria found in the guts of mice to the guts of germ-free mice.He got nowhere with the first five or six species he examined. Then, simply because it was convenient, he decided to test one more that was readily available in his lab. Mazmanian’s adviser, Kasper, had been studying a gut microbe called Bacteroides fragilis.

    When Mazmanian implanted one of Kasper’s specimens into the gut of his germ-free mice, the results were dramatic. The T-cell numbers spiked to normal. Eventually, Mazmanian demonstrated he could reproduce this effect simply by adding a single molecule that these bacteria produce, called polysaccharide A, to their guts.“There was no logic in the choice whatsoever,” Mazmanian recalls. €œ[B. Fragilis] was available, it came from the gut.” In other words, he got lucky.Mazmanian dug deeper and discovered that the biggest impact B.

    Fragilis had was on the population of a subtype of helper T-cells called regulatory, or suppressor, T-cells. These cells play a key role in preventing the immune system from attacking its host body, protecting against autoimmune or inflammatory diseases. It was the first time any scientist had demonstrated that a single compound from a single microbe could reverse a specific problem with the immune system.To Mazmanian, the finding, published in 2005 in the journal Cell, alluded to new approaches to treating a wide array of autoimmune, inflammatory and allergic disorders. What if it were possible to help a faulty immune system by tweaking a patient’s microbiome?. It was with this exploration in mind that he arrived in Pasadena in 2006 to set up his lab at Caltech.A Convenient CollaborationA few years later, Mazmanian was having lunch on campus with neuroscientist and colleague Paul Patterson.

    Patterson had been preoccupied with a mystery that had, for years, confounded those studying autism in humans. When pregnant mothers have a severe infection in the second trimester, their babies are much more likely to develop autism.As Mazmanian tells it, Patterson was a man of few words, and at lunch Mazmanian was “going on and on” about his own work.“You know,” Patterson interjected thoughtfully, “I think kids with autism have GI issues.”Patterson recalled reading that something like 60 percent of children with autism had some form of clinical GI problem, such as bloating, constipation, flatulence or diarrhea. Was it possible, he wondered, that there was a microbiome connection?. As they talked, Mazmanian’s excitement grew.A few years earlier, Patterson had discovered that when he exposed pregnant mice to pathogens like the influenza virus, they gave birth to pups that grew up more likely to be startled by loud noises, to shy away from social contact and to groom themselves repetitively — symptoms that resemble those of autism. Patterson was in the process of comparing the brains of these autism-mimicking mice with their neurotypical cousins to see if he could detect any differences that might explain how the maternal immune system was somehow interfering with the pups’ brain development.Mazmanian had a suggestion.

    The next time Patterson sacrificed one of his autistic mice to study their brains, what if he set the intestines aside for his colleague down the hall?. When the guts arrived in Mazmanian’s lab, he found that the intestines of the neurotypical mice looked normal. But the guts of the autism-mimicking offspring were almost uniformly inflamed. Could it be that the microbiome was the cause of this inflammation?. And could that, in turn, be somehow connected to the behavioral symptoms?.

    Throughout the winter and spring of 2012, Mazmanian and Patterson continued their conversation. Mazmanian found distinct differences in the microbiomes of the mice. And, they noticed, the mice with the features of autism had leaky gut syndrome, an increased permeability of the gut lining that can allow pathogens and allergens to leach out. This condition had also been reported in children with autism.So Mazmanian and Patterson turned their attention outside the gut. They took blood samples to see if any gut microbes, or the compounds they produce, were circulating in the rest of the body.

    They homed in on one molecule in particular, called 4-ethylphenyl sulfate, which was roughly 45 times as abundant in the mice that had symptoms of autism. And it looked familiar. Structurally, it was almost identical to a molecule recently found to be significantly elevated in human children with autism.It was enough to take the next step. Every day for three weeks, Mazmanian injected the molecule, harvested from the mice with autism-like symptoms, directly into the bloodstream of 5-week-old normal lab mice (the age at which the autistic mice normally developed leaky gut). Then Mazmanian and his team gave them a series of behavioral tests.

    The mice were far more easily startled and were less comfortable in large empty spaces than their untreated peers, indications of an increase in anxiety-related behaviors commonly seen in the mice with autism-like symptoms. The researchers published their results in Cell in 2013.Though surprising, the data made sense in some ways. Many drug companies rely on small-molecule drugs that can be taken orally, but still manage to cross the blood-brain barrier and affect behavior. It seemed entirely possible that small molecules, created by bacteria in the gut, could enter the bloodstream and reach the brain. And they don’t even have to leak out of the gut to do so.Of Mice and MenPatterson died in 2014, at age 70, just six months after the publication of the duo’s groundbreaking Cell paper.

    Around the same time, a series of parallel experiments in a clinic hundreds of miles away was already paving the way forward. While Patterson and Mazmanian had been working in mice, Rosa Krajmalnik-Brown, a microbiologist at Arizona State University, had teamed up with Jim Adams, who directs the university’s autism and Asperger’s research program, to study humans.The researchers were conducting a detailed analysis of the microbiome of human autism patients and found that the bacteria were far less diverse in the children with autism. Notably, several important species involved in the digestion of carbohydrates were severely depleted.Krajmalnik-Brown and Adams launched a preliminary trial to test the effects of fecal transplants on 18 children between the ages of 7 and 16 with severe autism, who also had severe GI issues. The researchers administered powerful antibiotics to kill off the microbiomes of the children and followed them with a bowel cleanse. They then replaced the microbes with transplanted flora taken from the guts of healthy neurotypical adult volunteers.The results were better than anyone could have expected.

    The procedure resulted in a large reduction in GI symptoms and increased the diversity of bacteria in the children’s guts. But more significantly, their neurological symptoms were reduced. At the onset of the study in 2017, an independent evaluator found 83 percent of participants had severe autism. Two years after the initial trial, only 17 percent were rated as severely autistic. And 44 percent were no longer on the autism scale.“[My child] did a complete 180,” says Dana Woods, whose then-7-year-old son Ethan enrolled in the initial study five years ago.

    €œHis ability to communicate is so much different now. He’s just so much more present. He’s so much more aware. He’s no longer in occupational therapy. He’s no longer in speech therapy.

    After the study, he tested two points away from a neurotypical child.”In their first report on the trial in 2017, the team highlighted a number of distinct changes in the microbiome after the transplants, in particular a surge in the populations of three types of bacteria. Among them was a four-fold increase in Bifidobacterium, a probiotic organism that seems to play a key role in the maintenance of a healthy gut.But figuring out what was happening on a cellular level — to really look inside some guts — would require another vehicle. The ASU team needed Mazmanian’s mice.“At the end of the day, what we care about is healing people and how the microbiome affects people,” explains Krajmalnik-Brown. €œThat’s why we work with people. But with mice you can do things that are more mechanistic.”The Great Mouse Detective(Credit.

    Caltech)Together, Krajmalnik-Brown, Mazmanian and their collaborators would uncover some tantalizing new insights that go a long way to solving the mystery. In May 2019, the team published another high-profile paper in Cell, after they transplanted stool samples from Krajmalnik-Brown’s severely autistic patients into the guts of Mazmanian’s germ-free mice. The offspring of these mice showed the autism-like symptoms, such as repetitive and compulsive behavior.This time, the team dug even deeper into the biochemical processes playing out in the brain, looking not just at behavior but at the chemicals involved in creating it. The mice that developed autism-like behaviors had measurably lower levels of two substances called taurine and 5-aminovaleric acid (5AV). When they dug into the literature, the team learned that these two substances are known to mimic activity of a key signaling agent in the brain called gamma-aminobutyric acid (GABA) — a neurotransmitter that other studies have found is deficient in the brains of children with autism.What’s more, some have speculated that the tendency of children with autism to experience sensory overstimulation may stem from the inability to tamp down overexcited neurons.

    A lack of GABA could lead to just that.The scientists next orally administered high levels of taurine and 5AV to pregnant mice with the autistic children’s microbiomes. When their pups were born, the researchers continued to feed the young the substances until they reached adulthood. Compared with untreated animals, the second-generation mice had significantly fewer behavioral symptoms. Taurine reduced repetitive behavior, as measured by marble burying, increased the level of social interaction, and relieved anxiety. Mice administered 5AV were more active and social.“We healed humans with behavioral problems,” says Krajmalnik-Brown.

    €œ[And we] transferred some of those deficits and behaviors to mice — basically the opposite. It’s huge.”Mazmanian hopes to take the next step in the months ahead.“I can flip a switch, turn on a light, I know that switch turns on that light. I don’t know the circuit, I don’t know where the wire is,” Mazmanian says. €œExactly how that’s happening … we just don’t understand that.”This most recent study, by itself, hardly proves that dysregulated microbiomes cause the brain disorder — a point that plenty of other scientists skeptical of Mazmanian’s work are happy to make.“The paper made a big splash, but trying to model psychiatric-related human conditions in mice, in my view, is a little bit of a stretch,” says Sangram Sisodia, a neurobiologist at the University of Chicago who studies the microbiome. €œA mouse with autism?.

    €Nor was that the only criticism. Several researchers have suggested that the group didn’t give proper attention to one of their tests ­— one whose results conflicted with their thesis ­— while others found flaws in the statistical methods they used to assess their results. Mazmanian downplays these criticisms, but agrees the work is not yet conclusive.Meanwhile, the ASU trial has also engendered skepticism, mainly due to its tiny sample size, the lack of a control group and the methods by which the children were assessed for autism severity. Krajmalnik-Brown and Adams say they stand by their results, but agree more research is needed. In recent months, they have launched two new studies that will address these issues.Adams insists the work is already changing lives.

    €œWe followed up with every one of our 18 participants,” he says, referring to the children who received fecal transplants. €œSure enough, we found that most of the GI benefits had remained. And family after family said their child just slowly, steadily continued making more improvement.” They published the update in Scientific Reports in spring 2019.“I’m not ready to say the case is closed,” says Mazmanian. €œHealthy skepticism is a good thing. I believe the preclinical data, I believe the mouse data.

    But there’s a lot of studies that still need to be done.” A Healthy Gut, A New OutlookEthan Woods had GI issues and symptoms of autism until researchers introduced new microbes to his gut. His mother says the treatment changed everything. (Credit. Dana Woods)Prior to his fecal transplant at age 7, Ethan Woods suffered from chronic and severe diarrhea, constipation and cramping, symptoms so extreme that to his mother, Dana, he sounded like “a bit like a woman in labor when he was trying to have a bowel movement.” “It was just awful watching your child go through this,” she says, explaining that when she enrolled her autistic son in the Arizona State study, her “only goal was to fix his gut.”Remarkably, Ethan’s agony began to disappear just a few weeks into the trial. But that was not the most dramatic difference.

    Before the transplant, Ethan’s speech was drawn out and slow, his language skills rudimentary. He seemed to live in his own bubble. He had frequent outbursts. For as long as Dana could remember, her mornings with Ethan had been marked by arguing, fighting, pushing and anger. But then one morning, something shocking happened.“He woke me up one morning with his face right in my face with this big smile and he said, ‘Morning, Mom!.

    €™â€‰â€ she recalls. €œAnd he was just excited and happy and ready to go about his day with this big smile. It choked me up to the point where I teared up because I had never experienced a happy kid in the morning.”Later, Ethan carried over an iPad and opened an app with a talking cat that repeats back the words children speak aloud. He played back a video recording of himself from just a few weeks earlier.“[He] looks me in the eye and says, ‘Mom, why did I talk like that?. What is wrong with me?.

    €™ And as soon as he did that, I caught my breath. I had to compose myself and say, ‘I don’t know. But do you feel better?. Do you feel different?. Why do you think?.

    €™â€‰â€Ethan’s communication skills had already begun to improve. Within a year of the study, his speech therapist graduated him from speech therapy because he had met all his goals.“He went from one end of the rainbow all the way to the other end of the rainbow,” she says. €œPrior to the study, I was very afraid. My biggest fear was ‘how is he going to navigate the world when I’m not here?. €™ And I think I have a lot of hope now that he is going to be OK now on his own.”There’s something strange about the female orgasm, something that scientists have been unable to explain.

    Biological functions are normally discussed in terms of evolutionary pressure, or reproductive advantage. If a biological trait improves your chances of having more offspring, then it’s more likely to stick around in your species. The male orgasm makes perfect sense — ejaculate contains the genetic material that’s necessary for making babies. But the female orgasm has been harder to nail down. Fertilization doesn’t depend on it, and “fun” isn’t exactly in the pantheon of evolutionary explanations.Researchers that study how the female orgasm relates to reproductive success have two main options — either ask people invasive questions about their most personal moments, or to find a way to stick probes in or on them during said moments.

    Neither of these approaches have resulted in the kind of “wet lab” research that’s the gold standard for biological understanding.What we do know, despite widespread cultural discomfort with talking openly about sex and pleasure, is that there appears to be significant sexual dysfunction in American society. Back in 2014, researchers from the Kinsey Institute, the preeminent U.S. Academy for the study of sex and relationships, said as much. In a survey of nearly 3,000 people, they found that men, straight or gay, orgasmed 85 percent of the time during consensual sexual encounters. Lesbian women orgasmed less often, 75 percent of the time, while straight women fared worst with just a 60 percent chance of orgasm.

    Other studies have shown that something like 10-15 percent of women experience lifelong anorgasmia, meaning they’ve never experienced orgasm. A further 40 percent of women report some kind of inability to reach orgasm in the past year.The orgasm gap is hard to explain. Some think that it comes down to straight men’s finesse, or lack thereof, citing the difference between straight and lesbian satisfaction. Indeed, it makes sense that knowing your way around the territory would help. But for many couples this isn’t a helpful revelation, since the emotional maturity necessary to teach sexual dexterity is often out of reach.

    Shortcut to SatisfactionLuckily, we live in an era of Silicon Valley disruption, which has even started lapping at the shores of sex research. Technologist Liz Klinger is at the forefront of this transition. She and her team have built a platform that lets people become citizen scientists of sex —without ever having to get out from between the sheets.About a decade ago, Klinger’s company, Lioness, released what they billed as the first “smart vibrator,” a sex toy that could actually learn about you. The final product was a far cry from the first prototype, which was much more laboratory object than sex toy.The “test device was this whole mess of wires, with a hard connection. We had to physically send it to our beta testers, who used it and sent it back,” recalls Klinger.

    The researchers would download the data collected by the toy’s four sensors — temperature, motion, acceleration and pressure — and compile it into a chart that represented arousal and orgasm, as told through the story of pelvic-floor muscle contractions.It was an immediate success for sex partners who needed ways to talk about pleasure in a more objective way. Klinger recalled that when she got the first beta-test couple on the phone, “the wife was like ‘holy crap, we finally were able to talk about these things that I’ve had a lot of trouble talking about.’ It turned out that she wanted more foreplay, and he didn’t know quite that that meant. He’d spend more time, but it just didn’t match up, you know?. € With the company’s signature offering in hand — a chart of sexual arousal over time — Klinger found that couples could have a conversation “without the subtext of ‘oh, you’re not good enough, or I don’t like you enough,’ on the husband’s part and ‘I’m so tired of talking about this’ on the wife’s part,” she says. The chart “can change people’s perceptions of their own experiences, and how they talk about them with others.”Doing the Deed — For ScienceThis spring, the company has launched a research platform dubbed Lioness 2.0 — a new optional service that, unsurprisingly, their data-obsessed users have greeted with open arms.

    Now, instead of simply using the toy to understand themselves better, Lioness owners can opt in to the kinds of hands-on studies that are necessary for a deeper understanding of sex and pleasure. So far, the company is working with Nigeria’s Society for Family Health to study how pleasure changes with menopause across age, race and orientation, as well as with the U.S.’s Center for Genital Health and Education to explore the role of pelvic floor muscles in orgasm.Pani Farvid, a professor of applied psychology at The New School in New York City, has some reservations about the platform. €œI really like what they’re trying to do, but there could be more added to make it a bit more comprehensive. My concern is that there's a misconception that sex is just about the orgasm, that it’s just physiological and that pleasure just has to do with the genitals.” From where she’s sitting, “that’s a very mechanical view of sexuality.” If the Lioness is helping to equalize the orgasm gap, or helping people understand their bodies better, “I think that's great,” says Farvid. €œBut as a critical sexologist, I'm interested in delving deeper into what these practices mean.” If sex is hyper-focused on orgasm, to exclusion of everything else, she cautions that these norms “have real-life negative impacts on people's sex lives and their sense of themselves.”At this point, knee-deep in an era of data collection that was once the sole purview of white-coat-wearing scientists, it’s old news that we need to be careful with what our technology is doing to us.

    No tool can serve as a cure-all, even if it comes loaded with a neat app and some space-age sensors. What it can offer, though, is the opportunity to start a conversation, and the chance to take a long, honest look at something about yourself — whether it’s the number of steps you take every day, or the way you want to be touched.Wondering how to keep your glasses from fogging up when your mask is on?. Look no further. If we've learned one thing throughout the COVID-19 pandemic, it's the importance of wearing a mask. Countless studies have shown over the past eight months that wearing a protective barrier over your nose and mouth — whether it's a standard-issue surgical mask or an N95 respirator — can significantly decrease the odds of catching and transmitting disease.

    What's more, some research shows that masking up can reduce the severity of an infection if a masked person does contract COVID-19. But while masks are potentially lifesaving, they can be uncomfortable, often changing your breathing patterns and fogging up your glasses when breath escapes through the top of the mask. Among people who choose not to wear a mask to prevent the spread of COVID-19, many cite discomfort as a key reason why.Wesley Wilson, a tumor immunologist in Pennsylvania, knows how annoying it can be when your glasses are fogging up. He says fogging is “definitely a problem” among his hospital colleagues, who need to wear protective goggles and surgical masks while on the job. Fortunately, they've also picked up a few helpful hacks for keeping their vision clear while wearing a mask with glasses.#1.

    Use Tape“If you have to keep your mask on for hours, tape works like a charm,” Wilson says. This especially applies to healthcare professionals in his practice who are required to keep their masks on at all times, except during lunch. €œIf you're putting on your mask and taking it off a lot, tape probably isn't practical — but two small pieces of tape on the cheeks keep the mask fitted closer to your face, and the hot air out of your glasses,” he says.#2. Fit the Mask to Your FaceWhile some air leakage is to be expected, wearing a mask that fits securely to your face will prevent glass fogging and filter the virus more effectively since less air is coming in or out. Find surgical masks or N95s that come with a nose bridge, a small, flexible piece of metal or plastic that allows the mask to more closely fit the contours of your face.

    Nose bridges can be sewn inside masks or affixed to the front.Read More. Why It Feels Like You Can't Breathe Inside Your Face Mask#3. Adjust Your MaskAccording to the American Academy of Ophthalmology, a minor adjustment in how you wear your mask could be enough to prevent fog as well. Simply pull the mask over your nose and rest your glasses on top of your face mask. As long as the mask is fitted close to your face, this should prevent hot air from slipping out.#4.

    Spray Your GlassesA former ice hockey player, Wilson says the protective visor under his helmet would often fog with hot air while he was on the ice during games. Like an ocean diver, he would use de-misting solution or a defogging spray (such as this one) to keep his visor free of fog. The same concept applies to eyeglass fog caused by masking, he says. €œYou can either buy a spray or you can make your own with either shaving cream or soap and water,” says Wilson. €œWiping some shaving cream on your glasses and then wiping it off will coat them with a similar surface-tension altering compound that prevents fog.”.

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    It is important to note that information and guidance about COVID-19 continually evolve as conditions change. Workers and employers are encouraged to regularly refer to the resources below for updates:In its ongoing efforts average price of cialis daily to create a culture of compliance assistance within the Department of Labor, the Office of Compliance Initiatives organized a human-centered design class at the Office of Personnel Management’s Innovation Lab in February 2020.Two years ago today, the U.S. Department of Labor launched the Office of Compliance Initiatives (OCI) to complement the Department’s enforcement efforts. OCI works average price of cialis daily with other agencies across the Department to help employers understand how to comply with our laws and regulations and help workers understand their rights. The goal is to ultimately reduce violations, which frees the Department up to focus its enforcement resources on the truly bad actors.As we reflect on OCI’s second anniversary, here are five highlights of what we’ve accomplished working with agency partners at the Department.

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    Publisher. Princeton, NJ. Mathematica Aug 27, 2020 Authors Alex Bohl and Michelle Roozeboom-Baker Updates to the sixth edition include information on. Added newly established codes that capture COVID-related treatments delivered in the hospital setting. As COVID-19 disrupts people’s lives and livelihoods and threatens institutions around the world, the need for fast, data-driven solutions to combat the crisis is growing.

    This primer is designed to help researchers, data scientists, and others who analyze health care claims or administrative data (herein referred to as “claims”) quickly join the effort to better understand, track, and contain COVID-19. Readers can use this guidance to help them assess data on health care use and costs linked to COVID-19, create models for risk identification, and pinpoint complications that may follow a COVID-19 diagnosis. Related NewsNew findings published this month in two prominent journals provide insight into the characteristics and performance of health systems using the latest data from the Compendium of U.S. Health Systems, created by Mathematica for the Agency for Healthcare Research and Quality (AHRQ).Mathematica and AHRQ researchers reported in Health Affairs that there was substantial consolidation of physicians and hospitals into vertically integrated health systems from 2016 to 2018. This resulted in more than half of physicians and 72 percent of hospitals being affiliated with one of the 637 health systems in the United States.

    Among systems operating in both 2016 and 2018 years, the median number of physicians increased by 29 percent, from 285 to 369. This has implications for cost, access, and quality of care.Although most research on health systems suggests that consolidation is associated with higher prices, a new article published in Health Services Research suggests that vertically integrated health systems might provide greater value under payment models that provide incentives to improve value. In this study, the authors found lower costs and similar quality scores from system hospitals compared with non-system hospitals that were participating in Medicare’s Comprehensive Care for Joint Replacement, a mandatory episode payment model.These studies were conducted by researchers at Mathematica, which leads AHRQ’s Coordinating Center for Comparative Health System Performance. This initiative seeks to understand the factors that affect health systems’ use of patient-centered outcomes research in delivering care. Learn more about the Comparative Health System Performance Initiative..

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