Insights from behavioral economics and other fields suggest strategies that could increase participation in mass screening programs.In October, Dr. Folasade May, an internist and public health researcher at the University of California, Los Angeles, began a new workplace routine. Once a week, she would make the three-minute walk from her office to a campus coronavirus testing site. After having her temperature checked and scanning a bar code on her phone, she would carefully swab the inside of her nose. Within a day or two, an email would arrive with her results.Week after week, her results came back negative. She continued to participate in the testing program even after being vaccinated, and she continued to test negative. And then, two weeks ago, an email landed in her inbox that stunned her: Her sample was positive for the coronavirus.The result — which turned out to be a false positive — briefly threw her life into chaos.“Our whole family was turned upside-down for an afternoon trying to figure out how to separate ourselves in our small house, trying to figure out who’s going to take care of the kids and who else did we expose,” Dr. May said.It is a situation that other families may soon find themselves in as mass coronavirus screening programs ramp up in schools and workplaces. Some of these programs will make testing mandatory, but many others will rely on voluntary participation — or on people regularly self-administering tests in their own homes.The more people who participate, the more effective these programs will be at slowing the spread of the virus, and keeping tabs on it. But there are also clear disincentives to participating, ranging from inconvenience to anxiety over the consequences of a positive result, which can mean missing work, keeping a child home from school or days of quarantine.“There are huge implications of a positive Covid test that a lot of people are very wary of, especially if they’re feeling well,” said Dr. May, who studies health disparities and the barriers to accessing health care. “I don’t know that people are going to come out in droves to get it done.”Although coronavirus screening is new, researchers in several fields — including behavioral economics, implementation science and health psychology — have spent years studying how to encourage people to engage in other kinds of health-related behaviors, including cancer screening, H.I.V. testing and vaccination. Some of these same strategies, they say, could help health officials design coronavirus screening programs, or even vaccination programs, with better participation rates.“The reality is that people are going to have to wake up and decide whether this is something they intend to do on any given day or any given week,” said Harsha Thirumurthy, associate director of the Center for Health Incentives and Behavioral Economics at the University of Pennsylvania. “And we know — from lots of examples of people’s decisions to seek testing for other health conditions, or even people’s decisions to engage in other health-related behaviors — that people are constantly weighing the costs and benefits of engaging in these services.”Here are five ways that health officials say can help shift the calculus.Make it easyHumans have a bias toward the status quo, a tendency to want to keep things as they are rather than shake them up. Many studies have shown that people are more likely to engage in various behaviors, from becoming an organ donor to enrolling in a 401(k) plan, when those behaviors are presented as the default choice.In a randomized clinical trial of nearly 5,000 emergency room patients, researchers found that the share of patients who were willing to take a rapid H.I.V. test climbed to 66 percent from 38 percent when the test was presented as a medical service they had to deliberately decline, rather than one they had to proactively ask for.Similarly, coronavirus screening programs are more likely to see wider participation if they are opt-out rather than opt-in. “The more you ask people to put in their own cognitive efforts and behavioral efforts into this, the less likely they’re going to do it,” said Derek Reed, who directs the applied behavioral economics laboratory at the University of Kansas.And, of course, the actual testing process should be quick and convenient, experts say, with strategically located testing sites and streamlined procedures that allow people to easily incorporate testing into their routines.Ask people to planExperts also suggested asking people to think through the logistics of when and how they plan to get tested. Studies show that people who clearly formulate a plan for how they intend to accomplish something — whether it’s voting in an upcoming election or getting a flu vaccine — are more likely to follow-through.One possibility, Dr. Reed said, would be to text people reminders of their testing appointments, and ask them to reply with, say, a 1 if they plan to walk to the appointment, a 2 if they plan to drive or a 3 if they plan to take the bus. “And then depending on the response, you just automatically ping back Google map directions or a link to campus or community bus system maps or timetables,” he said.These kinds of nudges are likely to be most effective for people who are already motivated to get tested but may have trouble following through. “Often you need to nudge them a little bit by just removing frictions to get rid of these small costs,” said Sebastian Linnemayr, a behavioral economist at the RAND Corporation, a think tank in California.Provide (the right) incentivesHealth officials could also reward people who participate in testing programs. “There probably needs to be some sort of incentive at the patient level,” Dr. May said. “We’ve seen the same thing in cancer screening. We’ve seen health insurers provide incentives to patients to participate in healthy lifestyles, to participate in screening measures.”But the specific incentives matter, and some studies suggest that people are more motivated by an opportunity to win a large reward than the guarantee of a smaller payout.In a November survey of 200 undergraduate students at the University of Kansas, Dr. Reed and his colleagues found that 70 percent of them said they would be willing to get tested if the university gave them a $5 gift card. But if the university instead entered them in a lottery, in which they had a 5 percent chance of winning $100, 88 percent said they would participate, said Dr. Reed, who shared his findings with the university.These kinds of lotteries may be effective because people tend to overestimate their chances of winning them. “The other part of it is that the lottery does introduce an element of fun or engagement in this idea that you’re part of something that other people are also participating in,” Dr. Thirumurthy said.Leverage social tiesPeer pressure can be a powerful public health tool; research has shown, for instance, that college women are more willing to get the human papillomavirus vaccine if they believe that their peers are also doing so.Government, school and workplace leaders can help coronavirus testing become a social norm by making it public how many others are participating. “Then, send out that information over and over again: ‘Don’t be left out, 85 percent already got tested and are making the school a better place,’” Dr. Linnemayr said. He added, “It’s really important that you signal, ‘This is an activity that we, as a community, value and reward.’”Health officials could also consider leveraging social networks more explicitly. In a randomized trial conducted in Kenya, Dr. Thirumurthy found that providing women with two H.I.V. self-testing kits, and encouraging them to give one to their male partners, significantly increased the share of men tested for H.I.V.He is now working with colleagues to evaluate a similar program for the coronavirus, asking people to distribute self-testing kits to others in their social circles.“Who has the strongest ability to persuade you to test?” Dr. Thirumurthy said. “Is it going to be your employer or somebody in the community? Or is it going to be someone who is a close friend or a family member?”Support people who test positiveEven the cleverest nudges, however, will not be enough to convince people to get tested if they think a positive result will have a devastating effect on their lives. A major barrier to H.I.V. testing has been the fear among potential recipients that testing positive would cost them their friends, jobs, housing or health insurance.A positive coronavirus test doesn’t necessarily carry the same stigma, but it can still have serious ripple effects on people’s lives. “If it keeps you out of work and you can’t earn an income to support your family, that’s a non-starter for a lot of people,” said Jennifer Nuzzo, an epidemiologist at Johns Hopkins University.So governments, employers and community organizations should do what they can to reduce the costs associated with testing positive, health experts said. That could mean providing paid leave or allowing employees to work remotely if they must quarantine; offering hotel vouchers so people have a safe place to isolate; or offering financial and food assistance. Such services can “soften the blow” of testing positive, Dr. Thirumurthy said: “There needs to be some type of safety net.”

WEHI researchers have discovered a key differentiation process that provides an essential immune function in helping to control cancer and infectious diseases.
The research, published in Science Immunology, is the first to show a new factor — DC-SCRIPT — is required for the function a particular type of dendritic cell — called cDC1 — that is essential in controlling the immune response to infection.
Led by WEHI Professor Stephen Nutt, Dr Michael Chopin and Mr Shengbo Zhang, it defines the role for a new regulatory protein — DC-SCRIPT — in producing dendritic cells.
At a glance WEHI researchers have uncovered a key step in the formation of a particular type of dendritic cell — called cDC1 — in controlling the immune response to infection. The research highlights the importance of DC-SCRIPT in the production of effective dendritic cells. Through gaining a better understanding of how dendritic cells are produced, researchers hope to be able to determine a way of directing the body to produce large numbers of dendritic cells, to enable it to better fight off cancer and infections.DC-SCRIPT essential in the production of cancer-fighting cells
Dendritic cells are immune cells that activate ‘killer’ T cells, which are vital for clearing viral infections and for triggering a response to cancer tumours.

If you walk with your spouse or partner on a regular basis, you might want to speed up. Or tell them to.
A new study by Purdue University nursing, health and kinesiology, and human development and family studies researchers shows that couples often decreased their speed when walking together. Speed further decreased if they were holding hands.
The study looked at walking times and gait speeds of 141 individuals from 72 couples. The participants ranged from age 25-79 and were in numerous settings, including clear or obstacle-filled pathways, walking together, walking together holding hands and walking individually.
“In our study, we focused on couples because partners in committed relationships often provide essential support to promote one another’s healthy lifestyle behaviors, including exercise,” says Melissa Franks, associate professor of human development and family studies.
Libby Richards, associate professor of nursing, says, “We were hoping that there would not be a reduction in speed where partners walked together. We hoped that slower partners would speed up to match the faster partner, but that was not the case. However, it’s important to note that any physical activity or walking — regardless of speed — is better than none.”
Richards says it is common for people to walk or exercise with a spouse, partner or friend, as it increases one’s likelihood to be active, especially as Americans are encouraged to meet a goal of 150 minutes of moderate activity every week.
“If someone substantially slows down when they are walking with someone else, that could negate some of the health benefits recognized if they walked alone at a faster pace,” Richards says.
Shirley Rietdyk, professor of health and kinesiology who specializes in biomechanics, says there are many reasons to measure gait speed.
“Gait speed is important to measure because it is related to overall health. Typical gait speed is predictive of fall risk, functional ability, disability recovery and mortality,” Rietdyk says.
“Common exercise interventions, including strength, coordination and multimodal training, are all effective in increasing gait speed. These interventions can also delay the onset of slower gait speed and help slow the loss of gait speed. No one type of training is better than the other, so do the activity you are most likely to stick with.”
While walking is one of the easiest activities, people tend to walk slower as they get older and may have to find other fitness routines to stay active.
“Older adults who are more active tend to maintain their gait speed,” Rietdyk says. “In other words, slower gait speed is not an inevitable aspect of aging. Older adults who walk slower tend to have poorer health and lower functional status.”
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Materials provided by Purdue University. Original written by Matthew Oates. Note: Content may be edited for style and length.

Understanding what drives food choices can help high-volume food service operations like universities reduce waste, according to a new study.
Researchers have concluded that food waste in places like university cafeterias is driven by how much people put on their plates, how familiar they are with what’s on the menu and how much they like — or don’t like — what they’re served.
Food waste has been studied often in households, but not so often in institutional settings like university dining commons. What drives food choices in these “all-you-care-to-eat” facilities is different because diners don’t perceive personal financial penalty if they leave food on their plates.
Published in the journal Foods, “Food Choice and Waste in University Dining Commons — A Menus of Change University Research Collaborative Study” was conducted by a team of experts from Rice University; the University of California, Davis; Stanford University; Lebanon Valley College; the University of California, Santa Barbara; and the University of California, Berkeley.
Co-author Eleanor Putnam-Farr, assistant marketing professor at Rice’s Jones Graduate School of Business, is available to discuss the findings and potential impact with news media.
The researchers conducted student surveys during the 2019 spring and fall semesters to study foods types, diner confidence and diner satisfaction. They used photos taken by diners themselves before and after eating to measure how much food was taken and how much of it went to waste. “Diners were intercepted at their dining halls and asked if they wanted to participate in a study about food choices and satisfaction, but the objective of investigating food waste behavior was not disclosed,” the authors wrote.
The study found the amount of food wasted didn’t significantly differ among types of food. Instead, researchers discovered waste was related to the amount of food diners put on their plates, how satisfied they were with their meals and how often they went to the dining commons. If students were satisfied with their food, they tended waste less of it. And diners who visited the commons most often — making them more familiar with the menus and more confident in their choices — tended to waste less.
Mixed dishes, like sandwiches or stir-fry, took up a greater percentage of the surface area on surveyed plates than animal proteins or grains and starches. Those three types of food took up a greater area of the plates than fruits, vegetables or plant proteins. The amount of food wasted, however, did not significantly differ among the various food categories.
The mixed dishes and animal proteins that took up greater portions of the plate tended to be pre-plated by the commons staff or have a suggested serving size. The study’s results showed that greater amounts of food taken by diners correlated with the item being pre-plated or served by others.
The authors recommend future research on the topic uses their multicampus approach — which enabled them to study food choice among a large and diverse group — to better understand what causes food waste and find out if it can be reduced by interventions such as posting signs that encourage healthier choices.
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Materials provided by Rice University. Note: Content may be edited for style and length.

James McKerrow, MD, PhD, dean of the Skaggs School of Pharmacy and Pharmaceutical Sciences at University of California San Diego, has long studied neglected tropical diseases — chronic and disabling parasitic infections that primarily affect poor and underserved communities in developing nations. They’re called “neglected” because there is little financial incentive for pharmaceutical companies to develop therapies for them.
One of these neglected diseases is Chagas disease, the leading cause of heart failure in Latin America, which is spread by “kissing bugs” carrying the parasite Trypanosoma cruzi. These parasites produce an enzyme called cruzain that helps them replicate and evade the human immune system. McKerrow’s research team looks for inhibitors of cruzain — small molecules that might form the basis for new anti-parasitic medicines. One particularly effective cruzain inhibitor is called K777.
Then, in the spring of 2020, the COVID-19 pandemic began to sweep through the United States. Researchers quickly reported that SARS-CoV-2, the coronavirus that causes COVID-19, can’t dock on and infect human cells unless a human enzyme called cathepsin L cleaves the virus’ spike protein.
And it just so happens that cathepsin L looks and acts a lot like cruzain.
In a study published March 31, 2021 by ACS Chemical Biology, McKerrow and team show that low concentrations of K777 inhibit cathepsin L can reduce SARS-CoV-2’s ability to infect four host cell lines, without harming the cells.
“Since K777 inhibits a human enzyme, not the virus itself, it’s our hope that it’s less likely the virus will evolve resistance against it,” said McKerrow, co-senior author of the study with Thomas Meek, PhD, of Texas A&M University.

The most common questions about vaccination side effects, answered.Every day nearly three million people in the United States are getting the Covid-19 vaccine. And every new jab prompts new questions about what to expect after vaccination.Last week I asked readers to send me their questions about vaccinations. Here are some answers.Q: I’ve heard the Covid vaccine side effects, especially after the second dose, can be really bad. Should I be worried?Short-lived side effects like fatigue, headache, muscle aches and fever are more common after the second dose of both the Pfizer-BioNTech and the Moderna vaccines, which each require two shots. (The Johnson & Johnson vaccine requires only a single shot.) Patients who experience unpleasant side effects after the second dose often describe feeling as if they have a bad flu and use phrases like “it flattened me” or “I was useless for two days.” During vaccine studies, patients were advised to schedule a few days off work after the second dose just in case they needed to spend a day or two in bed.Data collected from v-safe, the app everyone is encouraged to use to track side effects after vaccination, also show an increase in reported side effects after the second dose. For instance, about 29 percent of people reported fatigue after the first Pfizer-BioNTech shot, but that jumped to 50 percent after the second dose. Muscle pain rose from 17 percent after the first shot to 42 percent after the second. While only about 7 percent of people got chills and fever after the first dose, that increased to about 26 percent after the second dose.The New York Times interviewed several dozen of the newly vaccinated in the days afterward. They recounted a wide spectrum of responses, from no reaction at all to symptoms like uncontrolled shivering and “brain fog.” While these experiences aren’t pleasant, they are a sign that your own immune system is mounting a potent response to the vaccine.Q: Is it true that women are more likely to get worse side effects from the vaccine than men?An analysis of safety data from the first 13.7 million Covid-19 vaccine doses given to Americans found that side effects were more common in women. And while severe reactions to the Covid vaccine are rare, nearly all the cases of anaphylaxis, or life-threatening allergic reactions, occurred in women.The finding that women are more likely to report and experience unpleasant side effects to the Covid vaccine is consistent with other vaccines as well. Women and girls can produce up to twice as many antibodies after receiving flu shots and vaccines for measles, mumps and rubella (M.M.R.) and hepatitis A and B. One study found that over nearly three decades, women accounted for 80 percent of all adult anaphylactic reactions to vaccines.While it’s true that women may be more likely to report side effects than men, the higher rate of side effects in women also has a biological explanation. Estrogen can stimulate an immune response, whereas testosterone can blunt it. In addition, many immune-related genes are on the X chromosome, of which women have two copies and men have only one. These robust immune responses help to explain why 80 percent of autoimmune diseases afflict women. You can read more about women and vaccine side effects here.Q: I didn’t have any side effects. Does that mean my immune system didn’t respond and the vaccine isn’t working?Side effects get all the attention, but if you look at the data from vaccine clinical trials and the real world, you’ll see that many people don’t experience any side effects beyond a sore arm. In the Pfizer vaccine trials, about one out of four patients reported no side effects. In the Moderna trials, 57 percent of patients (64 or younger) reported side effects after the first dose — that jumped to 82 percent after the second dose, which means almost one in five patients reported no reaction after the second shot.A lack of side effects does not mean the vaccine isn’t working, said Dr. Paul Offit, a professor at the University of Pennsylvania and a member of the Food and Drug Administration’s vaccine advisory panel. Dr. Offit noted that during the vaccine trials, a significant number of people didn’t report side effects, and yet the trials showed that about 95 percent of people were protected. “That proves you don’t have to have side effects in order to be protected,” he said.Nobody really knows why some people have a lot of side effects and others have none. We do know that younger people mount stronger immune responses to vaccines than older people, whose immune systems get weaker with age. Women typically have stronger immune responses than men. But again, these differences don’t mean that you aren’t protected if you don’t feel much after getting the shot.Scientists still aren’t sure how effective the vaccines are in people whose immune systems may be weakened from certain medical conditions, such as cancer treatments or H.I.V. infection or because they are taking immune suppressing drugs. But most experts believe the vaccines still offer these patients some protection against Covid-19.The bottom line is that even though individual immune responses can vary, the data collected so far show that all three vaccines approved in the United States — Pfizer-BioNTech, Moderna and Johnson & Johnson — are effective against severe illness and death from Covid-19.Q: I took Tylenol before I had my Covid vaccine shots and had very little reaction to the shots. Did I make a big mistake?You shouldn’t try to stave off discomfort by taking a pain reliever before getting the shot. The concern is that premedicating with a pain reliever like acetaminophen (Tylenol) or ibuprofen (Advil, Motrin), which can prevent side effects like arm soreness as well as fever or headache, might also blunt your body’s immune response.While it’s possible that taking a pain reliever before your shots might have dampened your body’s immune response, vaccine experts say you shouldn’t worry, and you shouldn’t try to get another shot. Studies of other vaccines suggest that while premedicating can dull the body’s immune response to a vaccine, your immune system can still mount a strong enough defense to fight infection. A review of studies of more than 5,000 children compared antibody levels in children who took pain relievers before and after vaccinations and those who did not. They found that pain relievers did not have a meaningful impact on immune response, and that children in both groups generated adequate levels of antibodies after their shots.The high efficacy of all the Covid vaccines suggests that even if taking Tylenol before the shot did blunt your body’s immune response, there’s some wiggle room, and you are likely still well protected against Covid-19. “You should feel reassured that you’ll have enough of an immune response that you’ll will be protected, especially for vaccines that are this good,” said Dr. Offit.Q: What about taking a pain reliever after the shot?“It’s OK to treat” side effects with a pain reliever, said Dr. Offit, but if you don’t really need one, “don’t take it.”While most experts agree it’s safe to take a pain reliever to relieve discomfort after you get vaccinated, they advise against taking it after the shot as a preventive or if your symptoms are manageable without it. The concern with taking an unnecessary pain reliever is that it could blunt some of the effects of the vaccine. (In terms of the vaccine, there’s no meaningful difference if you choose acetaminophen or ibuprofen.)During the Moderna trial, about 26 percent of people took acetaminophen to relieve side effects, and the overall efficacy of the vaccine still was 94 percent.Q: Are the side effects worse if you’ve already had Covid-19?Research and anecdotal reports suggest that people with a previously diagnosed Covid-19 infection may have a stronger reaction and more side effects after their first dose of vaccine compared to those who were never infected with the virus. A strong reaction to your first dose of vaccine also might be a sign that you were previously infected, even if you weren’t aware of it.If you previously tested positive for Covid-19 or had a positive antibody blood test, be prepared for a stronger reaction to your first dose, and consider scheduling a few days off work just in case. Not only will it be more comfortable to stay home and recover in bed, the vaccine side effects can resemble the symptoms Covid-19, and your co-workers won’t want to be near you anyway.Q: I had Covid-19 already. Does that mean I can just get one dose?Studies suggest that one dose might be adequate for people who have a previously confirmed case of Covid-19, but so far the medical guidelines haven’t changed. If you’ve received the Pfizer-BioNTech or Moderna vaccines, you should plan to get your second dose even if you’ve had Covid-19. Skipping your second dose could create problems if your employer or an airline ask to see proof of vaccination in the future. If you live in an area where the single-dose Johnson & Johnson vaccine is available, then you can be fully vaccinated after just one dose. You can read more here about the vaccine response in people who’ve had Covid-19.Q: Will the vaccines work against the new variants that have emerged around the world?The vaccines appear to be effective against a new variant that originated in Britain and is quickly becoming dominant in the United States. But some variants of the coronavirus, particularly one first identified in South Africa and one in Brazil, appear to be more adept at dodging antibodies in vaccinated people.While that sounds worrisome, there’s reason to be hopeful. Vaccinated people exposed to a more resistant variant still appear to be protected against serious illness. And scientists have a clear enough understanding of the variants that they already are working on developing booster shots that will target the variants. The variants identified in South Africa and Brazil are not yet widespread in the United States.People who are vaccinated should still wear masks in public and comply with public health guidelines, but you shouldn’t live in fear of variants, said Dr. Peter J. Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston. “If you’re vaccinated, you should feel pretty confident about how protected you are,” said Dr. Hotez. “It’s unlikely you’ll ever go to a hospital or an I.C.U. with Covid-19. In time you’re going to see a recommendation for a booster.”I hope these answers will reassure you about your own vaccine experience. You can find a more complete list of questions and answers in our special vaccine tool “Answers to All Your Questions About Getting Vaccinated Against Covid-19.”

Eczema, or atopic dermatitis (AD), is sometimes called “the itch that rashes.” Often, the itch begins before the rash appears, and, in many cases, the itchiness of the skin condition never really goes away. Approximately 9.6 million children and 16.5 million adults in the U.S. have AD, which can have a serious effect on quality of life for patients. Although much has been learned about the uncomfortable sensation that triggers the desire to scratch, many mysteries remain about chronic itch, making it a challenge to treat. A paper by authors from Brigham and Women’s Hospital and Harvard Medical School published in The Proceedings of the National Academy of Sciences, offers new clues about the underlying mechanisms of itch. Findings suggest a key molecular player known as cysteine leukotriene receptor 2 (CysLT2R) that may be a new target for intractable chronic itch.
“In atopic dermatitis, the itching can be horrific and it can aggravate disease,” said co-corresponding author K. Frank Austen, MD, a senior physician in the Division of Allergy and Clinical Immunology at the Brigham. Austen is also the AstraZeneca Professor of Respiratory and Inflammatory Diseases, Emeritus, at Harvard Medical School. “We began collaborating for two reasons: one is an interest in science — I wandered into the study of what is now the cysteine leukotriene pathway decades ago, and I’ve been pursuing it ever since. The second reason is itch — understanding its cause and connections to neurons.”
Austen and his lab, which focuses on the molecular components that contribute to allergic inflammation, collaborated with Isaac Chiu, PhD, an assistant professor of Immunology at Harvard Medical School. The team also included researchers at the Center for Immunology & Inflammatory Diseases at Massachusetts General Hospital and at the University of Texas at Dallas.
“As a neuro-immunologist, I’m interested in how the nervous system and immune system cross-talk,” said Chiu, co-corresponding author of the study. “Itch arises from a subset of neurons, and acute itch may be a protective response to help us remove something that’s irritating the skin. However, chronic itch is not protective and can be pathological. The underlying mechanism that activates neurons and causes chronic itch is not well understood and new treatment is needed.”
Chiu, Austen and colleagues set out to elucidate the molecular mechanisms that may trigger chronic itch. To do so, they looked for gene activity in dorsal root ganglia (DRG) neurons linked to itch in mice. They found a striking level of CysLT2R, which was uniquely and highly expressed in these specific neurons. They also found expression of this receptor in human DRG neurons. This led the researchers to focus their analysis on the receptor’s role in itch signaling. Additional studies showed that activating this receptor induced itching in a mouse model of AD, but not in other mouse models. Mice that lacked CysLT2R showed decrease itching. Collectively, their findings pointed to the receptor’s key role in causing itch and potentially contributing to AD.
Lead author Tiphaine Voisin, PhD, carried out many of the preclinical experiments in mouse models of AD during her time in the Chiu lab at HMS.
“The last ten years or so of research in the field of chronic itch have shown the importance and the complexity of the interactions between the immune system and the nervous system,” said Voisin. “It was very exciting to explore the contribution of cysteine leukotrienes in these neuro-immune cross-talks leading to itch, including in a mouse model of AD.”
Leukotrienes are a class of lipid molecules that originate from white blood cells, such as mast cells, which are involved in allergy and inflammation. Today, the leukotriene inhibitor montelukast, which targets CysLT1R, is used to treat asthma but does not provide relief from itch. No clinically approved inhibitors of CysLT2R currently exist and, while the researchers have seen evidence of the receptors in humans, until an inhibitor is developed and trialed in humans, it will remain an open question as to whether the new target can lead to a therapy for patients.
While Chiu and Austen are eager to see their findings prompt treatment improvements, Austen, who has been pursuing leukotrienes since the 1970s, also notes the importance of making new discoveries and unexpected connections through research.
“I do believe that science is bottom up, not top down,” said Austen. “The joy of research is doing it for the pleasure of finding out something you didn’t know. The immune system is far more complex than we give it credit for. Understanding the involvement of nerves is an immense step forward — it’s been a missing piece in the study of inflammation. In my view, this is immensely important to connect neuroscience with those of us committed to studying inflammation.”

Telehealth has become a critical way for doctors to still provide health care while minimizing in-person contact during COVID-19. But with phone or Zoom appointments, it’s harder for doctors to get important vital signs from a patient, such as their pulse or respiration rate, in real time.
A University of Washington-led team has developed a method that uses the camera on a person’s smartphone or computer to take their pulse and respiration signal from a real-time video of their face. The researchers presented this state-of-the-art system in December at the Neural Information Processing Systems conference.
Now the team is proposing a better system to measure these physiological signals. This system is less likely to be tripped up by different cameras, lighting conditions or facial features, such as skin color. The researchers will present these findings April 8 at the ACM Conference on Health, Interference, and Learning.
“Machine learning is pretty good at classifying images. If you give it a series of photos of cats and then tell it to find cats in other images, it can do it. But for machine learning to be helpful in remote health sensing, we need a system that can identify the region of interest in a video that holds the strongest source of physiological information — pulse, for example — and then measure that over time,” said lead author Xin Liu, a UW doctoral student in the Paul G. Allen School of Computer Science & Engineering.
“Every person is different,” Liu said. “So this system needs to be able to quickly adapt to each person’s unique physiological signature, and separate this from other variations, such as what they look like and what environment they are in.”
The team’s system is privacy preserving — it runs on the device instead of in the cloud — and uses machine learning to capture subtle changes in how light reflects off a person’s face, which is correlated with changing blood flow. Then it converts these changes into both pulse and respiration rate.

In the first study to use whole genome sequencing (WGS) to discover rare genomic variants associated with Alzheimer’s disease (AD), researchers have identified 13 such variants (or mutations). In another novel finding, this study establishes new genetic links between AD and the function of synapses, which are the junctions that transmit information between neurons, and neuroplasticity, or the ability of neurons to reorganize the brain’s neural network. These discoveries could help guide development of new therapies for this devastating neurological condition. Researchers at Massachusetts General Hospital (MGH), the Harvard T. H. Chan School of Public Health, and Beth Israel Deaconess Medical Center report these findings in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
Over the last four decades, MGH has pioneered research on the genetic origins of AD, led by Rudolph Tanzi, PhD, vice chair of Neurology and director of the hospital’s Genetics and Aging Research Unit. Notably, Tanzi and colleagues co-discovered genes that cause early onset (prior to age 60) familial AD (that is, a form that runs in families), including the amyloid protein (A4) precursor (APP), and the presenilin genes (PSEN1 and PSEN2). Mutations in these genes lead to accumulation of amyloid plaques in the brain, a hallmark of AD.
The next 30 AD gene variants that were discovered are primarily linked to chronic inflammation in the brain (or neuroinflammation), which also increases the risk for this cognitive disease. However, loss of synapses is the neurological change that is most closely correlated with the severity of dementia in Alzheimer’s disease, yet no clear genetic links between the disease and these vital connections had previously been identified. “It was always kind of surprising that whole-genome screens had not identified Alzheimer’s genes that are directly involved with synapses and neuroplasticity,” says Tanzi.
Prior to this paper, the genome-wide association study (GWAS) was the primary tool used for identifying AD genes. In a GWAS, the genomes of many individuals are scanned in search of common gene variants that occur more frequently in people who have a given disease, such as AD. But to date, common Alzheimer’s-associated gene variants have accounted for less than half of the heritability of AD. A standard GWAS misses the rare gene variants (those occurring in less than 1% of the population), a problem solved by the WGS, which scans every bit of DNA in a genome.
“This paper brings us to the next stage of disease-gene discovery by allowing us to look at the entire sequence of the human genome and assess the rare genomic variants, which we couldn’t do before,” says Dmitry Prokopenko, PhD, of MGH’s McCance Center for Brain Health, who is lead author of the study.
Identifying less-common gene mutations that increase the risk for AD is important because they may hold critical information about the biology of the disease, says Tanzi. “Rare gene variants are the dark matter of the human genome,” he says, and there are lots of them: Of the three billion pairs of nucleotide bases that form a complete set of DNA, each person has 50 to 60 million gene variants — and 77% are rare.
In their quest to find rare AD gene variants, Tanzi, Prokopenko and their colleagues performed WGS analyses on the genomes of 2,247 individuals from 605 families that include multiple members who have been diagnosed with AD. They also analyzed WGS datasets on 1,669 unrelated individuals. The study identified 13 previously unknown rare gene variants associated with AD. Strikingly, these gene variants were associated with functioning of synapses, development of neurons, and neuroplasticity.
“With this study, we believe we have created a new template for going beyond standard GWAS and association of disease with common genome variants, in which you miss much of the genetic landscape of the disease,” says Tanzi, who sees potential for their methods to be used to study the genetics of many other conditions. Moreover, he plans to use “Alzheimer’s in a dish” — three-dimensional cell culture models and brain organoids he and his colleagues have developed over the past decade — to explore what happens when the rare mutations this paper identified are inserted in neurons. “That could help guide us in novel drug discovery,” says Tanzi.
This study was supported by the Cure Alzheimer’s Fund and grants from the National Institutes of Health.
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Kidney development is a balancing act between the self-renewal of stem and progenitor cells to maintain and expand their numbers, and the differentiation of these cells into more specialized cell types. In a new study in the journal eLife from Andy McMahon’s laboratory in the Department of Stem Cell Biology and Regenerative Medicine at the Keck School of Medicine of USC, former graduate student Alex Quiyu Guo and a team of scientists demonstrate the importance of a molecule called β-catenin in striking this balance.
β-catenin is a key driver at the end of a complex signaling cascade known as the Wnt pathway. Wnt signaling plays critical roles in the embryonic development of multiple organs including the kidneys. By partnering with other Wnt pathway molecules, β-catenin controls the activity of hundreds to thousands of genes within the cell.
The new study builds on the McMahon Lab’s previous discovery that Wnt/β-catenin can initiate progenitor cells to execute a lengthy and highly orchestrated program of forming structures in the kidney called nephrons. A healthy human kidney contains a million nephrons that balance body fluids and remove soluble waste products. Too few nephrons results in kidney disease.
Previous studies from the UT Southwestern Medical Center laboratory of Thomas Carroll, a former postdoctoral trainee in the McMahon Lab, suggested that Wnt/β-catenin signaling plays opposing roles in ensuring the proper number of nephrons: promoting progenitor maintenance and self-renewal, and stimulating progenitor cell differentiation.
“It sounded like Wnt/β-catenin is doing two things — both maintenance and differentiation — that seem to be opposite operations,” said Guo. “Therefore, the hypothesis was that different levels of Wnt/β-catenin can dictate different fates of the nephron progenitors: when it’s low, it works on maintenance; when it’s high, it directs differentiation.”
In 2015, it became more possible to test this hypothesis when Leif Oxburgh, a scientist at the Rogosin Institute in New York and a co-author of the eLife study, developed a system for growing large numbers of nephron progenitor cells, or NPCs, in a Petri dish.