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One of the serious complications that can occur during late pregnancy happens when the amniotic sac (also called the bag of waters) breaks too early, which can allow bacterial infections to cause dangerous tissue inflammation around the placenta.
This condition, called chorioamnionitis, occurs in about 4% of pregnancies that reach full term. But it’s even more common in preterm deliveries, where it happens in 25-40% of preterm deliveries.
Infant deaths from chorioamnionitis are rare, but aggressive use of antibiotics to prevent infections is common in suspected cases. Unfortunately, those antibiotic treatments also can interfere with the formation of tiny vital air sacs called alveoli and disrupt formation of the lungs’ immune defenses. As a result, newborns treated for chorioamnionitis face higher risks of developing bronchopulmonary dysplasia (BPD). As survivors grow, they also face higher risks of developing asthma and struggling with other lung infections later in life.
Now, experts at Cincinnati Children’s may have discovered a way to prevent lung damage linked to chorioamnionitis. The researchers report, based on animal models, that the combined use of two drugs known to block cell signals that trigger inflammation in other conditions also blocked inflammation damage related to chorioamnionitis.
Details were published online March 30, 2022, in Science Translational Medicine. The first author is Andrea Toth, BCE, an MSTP student in the Molecular and Developmental Biology Graduate Program, and the senior author is William Zacharias, MD, PhD.
“Our finding that IL1 and TNF blockade protects the lung from injury…provides proof of principle that anti-inflammatory therapies could be used in the future to treat infants. These data support the idea that future therapies targeting the immune system may hold promise for treatment of multiple kinds of perinatal inflammation,” the co-authors state.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBruce Willis will step away from his acting career after being diagnosed with aphasia, a condition that impedes a person’s ability to speak and write.The actor’s family, including his wife Emma Heming-Willis and ex-wife Demi Moore, announced his condition on Instagram on Wednesday. Aphasia is “impacting his cognitive abilities”, the statement said.Willis, 67, is best known for playing John McClane in the Die Hard films, which made him a star. “With much consideration Bruce is stepping away from the career that has meant so much to him,” his family wrote in a joint statement. “This is a really challenging time for our family and we are so appreciative of your continued love, compassion and support.”Willis has five daughters, three with Ms Moore and two with Ms Heming-Willis. What is aphasia?It’s when a person has difficulty with their language or speechUsually caused by damage to the left side of the brain, like a strokeHampers reading, listening, speaking, typing or writingSpeaking problems are most common and can involve putting words together incorrectlySource: National Health ServiceHis acting career began in the early 1980s but he did not become a household name until later in that decade – first after starring opposite Cybill Shepherd in the ABC TV series Moonlighting and then in his 1988 performance as John McClane in the first Die Hard film. Since then, his films including The Sixth Sense, Armageddon and Pulp Fiction have grossed more than $5bn worldwide, according to Variety. He’s been nominated for five Golden Globes, winning one for Moonlighting, and three Emmys, winning two. Several actors and other stars offered their condolences to Willis and his family following the news.”Grace and guts! Love to you all!” actress Jamie Lee Curtis wrote in response to Demi Moore’s post. “Sending lots of love and healing to you all!” wrote journalist Katie Couric. Image source, Getty ImagesMore on this storyDemi Moore in ‘shock’ at pool deathBruce Willis admits ‘error of judgement’ over mask

Taking these seven steps now can lower your risk and minimize the disruption to your family’s life.The next wave of Covid-19 is coming, and in some parts of the United States, it’s already here. Are you ready?The culprit this time is BA.2, a subvariant of the highly infectious Omicron variant. Nobody knows for sure how much havoc it will cause, but BA.2 has already led to a surge of cases in Europe and is now the dominant version of the coronavirus in the United States and around the world.Researchers are tracking an uptick in cases in the United States, and they’ve detected a rise in the viral particles recovered from nearly 150 wastewater-surveillance sites. Because people can shed the coronavirus even if they never develop symptoms, pieces of the virus collected in wastewater can serve as advance warning several days before official case counts rise, said Bronwyn MacInnis, who directs pathogen genomic surveillance at the Broad Institute in Cambridge, Mass. Over the past two weeks, Dr. MacInnis’s group has seen a rapid increase in levels of the BA.2 subvariant in the Northeast.“I don’t think we’re looking at a crazy lockdown scenario in this part of the world with BA.2,” Dr. MacInnis said. “But we can’t be sure that we won’t have another curveball from this virus in the future.”American health officials have said they are hopeful that BA.2 won’t cause another major surge, in part because so many people were infected by the original Omicron wave this winter and most likely have at least some natural or vaccine immunity to protect them against severe illness and hospitalization.But other variables could turn the BA.2 wave into a more damaging surge. One concern is that less than 70 percent of Americans over 65 have had a first booster shot, leaving a large group vulnerable, said Dr. Eric Topol, a professor of molecular medicine at Scripps Research in La Jolla, Calif. And for many people who got their booster shots in the fall, immune protection may be waning. Unvaccinated people who are counting on natural immunity from a previous infection by a different variant should know that BA.2 can easily sidestep those fading immune defenses.And then there’s the question of whether pandemic fatigue will prevent some people from taking reasonable precautions, like wearing masks and social distancing, when Covid numbers start to rise in their area.“We know how to manage it,” said Dr. Robert Wachter, a professor and the chair of the medicine department at the University of California, San Francisco. “But the big caveat will be that there are lots of parts of the country that will not go back into careful mode. It’s wishful thinking to believe we’re going to stay in a situation as good as we are in now.”While the virus is unpredictable, there are clear ways to protect yourself. The plans you make now can lower your risk of exposure, minimize the disruption to the lives of your family and friends and help to assure you have access to treatments if you or someone you know becomes seriously ill.Here’s what you can do to prepare.Pay attention to Covid indicators in your communityDon’t wait for public health officials to issue warnings. Keep an eye on Covid-19 statistics for your county or region. An easy way to do this is to check the color-coded map from the Centers for Disease Control and Prevention that shows community levels of Covid-19 around the country. The map is mostly a welcoming green right now, which means there are very low rates of community transmission. But there is a growing number of yellow spots, showing medium risk, in Texas, the Northeast and other areas, and orange-colored hot spots are cropping up in Montana, the Dakotas and other states, indicating high rates of community spread.As the map shifts to yellow and eventually orange in your area, it’s time to take extra precautions, including donning masks in public spaces and rethinking large indoor gatherings where you don’t know the vaccination status of others.Jamie Kelter Davis for The New York TimesIf you want even earlier warning of Covid trends, you can bookmark the C.D.C.’s wastewater data tracker map.Another useful indicator is your community’s positive test rate. Experts advise taking more precautions as you see positive test rates start to rise above 5 percent. The Johns Hopkins coronavirus resource center shows daily U.S. and state-by-state testing trends.Have high-quality masks on handEven if you’re not wearing a mask now, check your mask supply and make sure you have plenty of high-quality medical-style masks on hand. A limited number of free N95 respirator masks are available at pharmacies and community centers. Enter your ZIP code on the C.D.C.’s mask locator to find a participating distributor near you. If you want to buy additional masks, use our guide to find a reliable supply of N95, KN95 or KF94 masks and avoid counterfeits.Since many communities have lifted mask mandates, when and how often you use a mask is probably going to be up to you.“The mask needs to go on when you start seeing case numbers going back up,” said Linsey Marr, professor of civil and environmental engineering at Virginia Tech and one of the world’s leading experts on viral transmission.Dr. Marr said she knows people are tired of masks, but wearing one is only a minor inconvenience and is a proven way to lower your risk. “I’m not into fear mongering, but there’s still so much we don’t know about long Covid that I don’t want to get Covid, and I don’t want anyone else to, either,” she said. And the more people who wear masks as cases start to rise, the sooner the next wave will be over. Order home Covid tests sooner rather than laterEach U.S. household is eligible for two sets of four home Covid tests free from the government; if you haven’t ordered them yet, get them now before the weather turns warm. The tests can be damaged by heat, and you don’t want yours sitting for hours in a mail truck on a hot day.“Now is better than a month from now, especially for people in hot locations,” said Dr. Michael Mina, chief science officer for eMed, a company that verifies at-home test results. “Just take advantage of the program, get them and put them in your cupboard for when you need them.”People with insurance can also be reimbursed for eight free tests a month. If you develop respiratory symptoms, have a fever or just feel unusually fatigued, use a test on the first day of symptoms. If symptoms persist and you still test negative at home a few days later, you may want to get a lab-based PCR test to be sure.“If you can afford it, test when you think you have allergies, test when you think you have a cold,” said Kelly Hills, a bioethicist and risk expert and co-founder of the consulting firm Rogue Bioethics. “This is one of those things I think people need to get in the habit of setting aside money for because tests provide important data for making decisions.”Kenny Holston for The New York TimesGet a booster (when you’re eligible)Federal regulators have authorized a second booster shot for everyone 50 and older. The agency also authorized a second booster for people 12 and older with certain immune deficiencies.While scientists are still debating the value of another booster, most say that people 65 and older and the immune compromised are likely to benefit. If you haven’t gotten your first booster shot, experts agree you should get one now. If you’ve recently had Covid, you most likely have as much natural protection as you’d get from a booster shot — at least for a while.The protective antibodies from a vaccine or an infection tend to wane in four or five months. A well-timed booster shot tells the body to bump up its antibody defenses and helps other parts of the immune system — like B cells and T cells — become better at remembering how to fight the virus, said Theodora Hatziioannou, a virologist at Rockefeller University in New York City.Get a pulse oximeterA pulse oximeter is a small device that clips on your finger and measures your blood oxygen levels. When levels drop to 92 or lower, patients should see a doctor. Low oxygen can be a sign of Covid pneumonia and may raise your risk for serious complications from Covid-19. The devices can be less reliable for people with darker skin, so pay attention to downward trends as well as the number.A study from South Africa found that the risk of dying from Covid-19 was about 50 percent lower among patients who had been instructed to monitor their oxygen saturation at home. You can find the devices for about $30 in pharmacies and online. (Researchers say the pulse oximetry reading on your Apple watch probably is less reliable than the fingertip device.)Make a plan for antiviral drug treatmentTwo oral antiviral therapies are available to treat Covid-19 in the United States, though they require a doctor’s prescription and are authorized only for people who may be at high risk of severe disease. One, called Paxlovid, developed by Pfizer, is taken as three pills twice a day for five days. It is available for high-risk patients 12 and older.The second drug, called molnupiravir, was developed by Merck in partnership with Ridgeback Biotherapeutics. It is taken as four pills twice a day for five days, and is available for high-risk adults 18 and older.For the pills to be most effective, you need to start taking them within five days of the start of your symptoms, so it’s important to have a plan for getting a prescription and knowing which pharmacy can fill it, said Kuldip Patel, the senior associate chief pharmacy officer at Duke University Hospital in North Carolina.You can use the Covid-19 therapeutics locator to track local supply of the drugs and check with your doctor to make sure you can receive the medication should you fall ill. (Some doctors are still declining to prescribe the drugs.) You can also look up qualified pharmacy-based clinics near you, as well as community health centers and long-term care facilities that have an authorized medical provider so you can get tested and, if positive, receive antiviral medication on the spot.People who are immune compromised should also talk to their doctor about Evusheld, an antiviral drug from AstraZeneca that can be given by injection to provide an additional layer of protection on top of vaccines.Have backup plans for social events and travelIf you have plans for a graduation party, wedding or other large event, it’s a good idea to have an outdoor backup plan if your community’s case numbers spike. If you’re planning to travel, do a little advance research into clinics and pharmacies at your destination so you know whether you can get antiviral drugs if you catch Covid-19 on your trip. Make sure you have extra funds or plenty of room on your credit card in case you need to extend your trip to recover from Covid. (You still need proof of a negative Covid test for international travel.)Health experts said planning for the next wave of Covid shouldn’t disrupt your life or prompt you to cancel travel plans or time with friends and family. In fact, being prepared for the unexpected will allow you to keep living your life as normally as possible.“A lot of people feel it’s a terrible inconvenience and they are sick of it, and I understand that,” said Dr. Topol, of Scripps Research. “We’ve had a time out, and it’s been good. But people should be ready to gear up if need be.”

Clinician-scientists in the Smidt Heart Institute at Cedars-Sinai developed a clinical algorithm that, for the first time, distinguishes between treatable sudden cardiac arrest and untreatable forms of the condition.
The findings, published today in the peer-reviewed Journal of the American College of Cardiology: Clinical Electrophysiology, have the potential to enhance prevention of sudden cardiac arrest — unexpected loss of heart function — based on key risk factors identified in this study.
“All sudden cardiac arrest is not the same,” explained Sumeet Chugh, MD, director of the Center for Cardiac Arrest Prevention and lead author of the study. “Until now, no prior research has distinguished between potentially treatable sudden cardiac arrest versus untreatable forms that cause death in almost all instances.”
Out-of-hospital sudden cardiac arrest claims at least 300,000 U.S. lives annually. For those affected, 90% will die within 10 minutes of cardiac arrest.
For this largely fatal condition, prevention would have a profound impact. The biggest challenge, however, lies in distinguishing between those who stand to benefit the most from an implantable cardioverter defibrillator — and those who would not benefit from the electric jolt.
“Defibrillators are expensive and unnecessary for individuals with the type of sudden cardiac arrest that will not respond to an electrical shock,” said Chugh. “However, for patients with treatable, or ‘shockable,’ forms of the disease, a defibrillator is lifesaving.”
Chugh, also a professor and the Pauline and Harold Price Chair in Cardiac Electrophysiology Research, says this new research provides a clinical risk assessment algorithm that can better identify patients at highest risk of treatable sudden cardiac arrest — and thus, a better understanding of those patients who would benefit from a defibrillator.

High fixed costs for retailing fresh fruit and vegetables means that they cost 40% more than would be efficient, unlike unhealthy alternatives, which trade close to marginal cost, a new study demonstrates.
Introducing a subsidy to counteract the price distortion and reduce the cost of fruit and vegetables will change diets in a way that is not only healthier, but also more in line with what consumers like to eat, according to the research.
Published today (30 March) in Science Advances, the studyby economists at the University of Warwickset out to quantify distortions in the price of fruit and vegetables due to market imperfections, and their impact on our diets.
The economists found that fixed costs in the supply chain play a much larger role in the price of fruit and vegetables than in prices of other foods, distorting the relative price by at least 40%. These high prices imply that consumers on average buy 15% less fruit and vegetables than they would have if these sold at marginal cost. This underconsumption is due to a market imperfection: the fixed costs prevent the ‘invisible hand’ of the market from allocating more fruits and vegetables to consumers, which both they and the producers of these product would prefer.
The 15% underconsumption of fruits and vegetables due to retail market imperfections accounts for a third of the gap between the average amounts of fruit and vegetables consumed and the recommended intake.
Professor Thijs van Rens, one of the authors of the article, also leads the Warwick Obesity Network, which develops evidence-based policy and practitioner briefs supporting a national strategy against obesity. He said: “The food retail market is very competitive, so if there weren’t any fixed costs you would expect food to be sold close to marginal cost. And the fact that they are not affects diets.

High blood glucose is responsible for several complications in type 1 and type 2 diabetes. Researchers at Karolinska Institutet in Sweden have identified a new antidiabetic substance that preserves the activity of insulin-producing beta cells and prevents high blood glucose in mice. The study is published in the journal Science Translational Medicine.
Although several families of glucose-lowering agents are currently used in diabetes therapy, none of them can stop or reverse the progression of the disease. Maintenance of adequate beta cell activity is essential to prevent the progression of type 1 and type 2 diabetes.
“In diabetes, beta cells are challenged to produce high amounts of insulin,” says the study’s first author Erwin Ilegems, senior researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet. “Our study shows that this leads to a hypoxic state that increases the levels of HIF-1alpha protein, which in turn reduces beta cell activity. By treating diabetic mice with the HIF-1alpha inhibitor PX-478 we successfully decreased their blood glucose levels.”
Repurposing an anti-cancer drug
HIF-1alpha (hypoxia-inducible factor-1alpha) regulates the response to hypoxia. The discovery of HIF-1alpha was awarded the Nobel Prize in Physiology or Medicine in 2019 and this protein is involved in many different diseases. The HIF-1alpha inhibitor PX-478 has already been tested in phase I clinical trials as an anticancer drug and was well tolerated in these patients.
In collaboration with Professor Jorge Ruas’ research group at the Department of Physiology and Pharmacology at Karolinska Institutet, the authors could demonstrate that the antidiabetic effect of PX-478 was mainly due to improved pancreatic beta cell activity.
Since it is well established that the production of insulin decreases during the progression of diabetes, therapeutic strategies have so far mostly focused on improving the insulin production of beta cells. However, this approach has not been as successful as initially predicted.
“Current therapies targeting beta cells have only a temporary positive effect on insulin secretion,” says the study’s last author Per-Olof Berggren, professor at the Department of Molecular Medicine and Surgery, Karolinska Institutet. “In the long-term, these drugs lead to beta cell exhaustion.”
Long-term treatment of diabetes
Unlike other treatments, PX-478 ameliorates beta cell activity without amplifying insulin secretion. The researchers therefore believe that it can prevent the exhaustion of beta cells and thus be more efficient in the long-term treatment of diabetes.
“We are now planning to further investigate the translatability of our findings to hopefully pave the way for future clinical trials,” says Teresa Pereira, researcher at the Department of Medical Cell Biology, Uppsala University (formerly employed by Karolinska Institutet), who is co-last author of the study. “We will start by investigating the impact of PX-478 on human pancreatic beta cell activity by using ‘humanised’ diabetic mice.”
This work was supported by funding from Karolinska Institutet, the Swedish Research Council, the Novo Nordisk Foundation, the Swedish Diabetes Association, the Family Knut and Alice Wallenberg Foundation, Diabetes Research and Wellness Foundation, the Jonas & Christina af Jochnick Foundation, the Family Erling-Persson Foundation, Berth von Kantzow’s Foundation, the Skandia Insurance Company, Ltd., the European Research Council, the European Union’s Seventh Framework Programme, and the European Diabetes Research Programme in Cellular Plasticity Underlying the Pathophysiology of Type 2 Diabetes. Teresa Pereira has filed a patent entitled “Treatment of diabetes,” and co-author Burcak Yesildag is an employee at InSphero AG. All other authors report no competing financial interests.
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Materials provided by Karolinska Institutet. Note: Content may be edited for style and length.

While cancer therapies targeting specific genes or disease pathways have extended lives, they can also lead to highly resistant tumors when small reservoirs of cancer cells survive treatment, grow, and spread.
Searching for ways to extend the survival benefit of targeted therapies, a team led by researchers at the Duke Cancer Institute identified a potential new tactic to disrupt the repair mechanism that cancer cells use after treatment, blunting their ability to regenerate. The approach could present a new treatment strategy.
The team’s findings are reported March 30 in the journal Science Translational Medicine.
“There is a significant need to figure out ways to make targeted therapies work better with more long-lasting effect,” said senior author Kris Wood, Ph.D., associate professor in the Department of Pharmacology and Cancer Biology at Duke. “This research provides a potential strategy to do that with drugs that are currently under investigation.”
Wood and colleagues found that targeted therapies induce breaks in DNA strands of the cancer cells that survive treatment. Efficient repair of those DNA breaks is critical for tumor cell survival and dependent on a molecule called the ataxia telangiectasia mutated (ATM) enzyme.
“We were surprised to find that the ATM pathway was frequently activated by these surviving cancer cells,” Wood said. “That finding led to the next question: Could we disrupt the repair process?”
The researchers used ATM inhibitors that are currently under investigation, and the answer was yes. Testing in non-small cell lung cancer in mouse models and laboratory cultures, they found that an ATM kinase inhibitor, in combination with targeted therapies, eradicated residual cancer cells, leading to more durable remission of the cancer.
Further confirmation was evident in real-world cases. Certain lung cancer patients who harbor an ATM mutation that lessens its function have longer progression-free survival with targeted therapies compared to patients who lacked this ATM mutation.
“Together, these findings establish a rationale for the mechanism-based integration of ATM inhibitors alongside existing targeted therapies,” Wood said.
In addition to Wood, study authors include Moiez Ali, Hazel Xiaohui Ang, Ryan S. Soderquist, Min Lu, Christine E. Eyler, Haley M. Hutchinson, Carolyn Glass, Christopher F. Bassil, Omar M. Lopez, D. Lucas Kerr, Christina J. Falcon, Helena A. Yu, Aaron N. Hata, Collin M. Blakely, Caroline E. McCoach, and Trever G. Bivona.
The study received funding from the Duke Cancer Institute, the National Institutes of Health (R01CA207083, F30CA220847, F32CA206234), the Duke Medical Scientist Training Program (T32 GM007171), and the Agency for Science, Technology and Research, Singapore.
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Materials provided by Duke University Medical Center. Note: Content may be edited for style and length.

New computational simulations of the behavior of SARS-CoV-1 and SARS-CoV-2 spike proteins prior to fusion with human cell receptors show that SARS-CoV-2, the virus that causes COVID-19, is more stable and slower changing than the earlier version that caused the SARS epidemic in 2003.
Severe acute respiratory syndrome coronaviruses 1 and 2 (SARS-CoV-1 and SARS-CoV-2) have striking similarities, and researchers do not fully understand why the latter has been more infectious.
The spike proteins of each, which bind to host cell angiotensin converting enzyme 2, otherwise known as the human cell receptor, have been targeted as the potential source of the different transmissibility. Understanding the mechanistic details of the spike proteins prior to binding could lead to the development of better vaccines and medications.
The new finding does not necessarily mean that SARS-CoV-2 is more likely to bind to cell receptors, but it does mean that its spike protein has a better chance of effective binding.
“Once it finds the cell receptor and binds to it, the SARS-CoV-2 spike is more likely to stay bound until the rest of the necessary steps are completed for full attachment to the cell and initiation of cell entry,” said Mahmoud Moradi, associate professor of chemistry and biochemistry in the Fulbright College of Arts and Sciences.
To determine differences in conformational behavior between the two versions of the virus, Moradi’s research team performed an extensive set of equilibrium and nonequilibrium simulations of the molecular dynamics of SARS-CoV-1 and SARS-CoV-2 spike proteins, leading up to binding with cell angiotensin converting enzyme 2. The 3D simulations were done on a microsecond-level, using computational resources provided by the COVID-19 High Performance Computing Consortium.
Equilibrium simulations allow the models to evolve spontaneously on their own time, while nonequilibrium simulations use external manipulation to induce the desired changes in a system. The former is less biased, but the latter is faster and allows for many more simulations to run. Both methodological approaches provided a consistent picture, independently demonstrating the same conclusion that the SARS-CoV-2 spike proteins were more stable.
The models revealed other important findings, namely that the energy barrier associated with activation of SARS-CoV-2 was higher, meaning the binding process happened slowly. Slow activation allows the spike protein to evade human immune response more efficiently, because remaining in an inactive state longer means the virus cannot be attacked by antibodies that target the receptor binding domain.
Researchers understand the importance of the so-called receptor-binding domain, or RBD, which is the critical part of a virus that allows it to dock to human cell receptors and thus gain entry into cells and cause infection. Models produced by Moradi’s team confirm the importance of the receptor-binding domain but also suggest that other domains, such as the N-terminal domain, could play a crucial role in the different binding behavior of SARS-CoV-1 and -2 spike proteins.
N-terminal domain of a protein is a domain located at the N-terminus or simply the start of the polypeptide chain, as opposed to the C-terminus, which is the end of the chain. Though it is near the receptor-binding domain and is known to be targeted by some antibodies, function of the N-terminal domain in SARS-CoV-1 and -2 spike proteins is not completely understood. Moradi’s team is the first to find evidence for potential interaction of the N-terminal domain and the receptor binding domain.
“Our study sheds light on the conformational dynamics of the SARS-CoV-1 and SARS-CoV-2 spike proteins,” Moradi said. “Differences in the dynamic behavior of these spike proteins almost certainly contribute to differences in transmissibility and infectivity.”
The researchers’ study, “Prefusion Spike Protein Conformational Changes Are Slower in SARS-CoV-2 than SARS-Cov-1,” was published in Journal of Biological Chemistry.
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Materials provided by University of Arkansas. Original written by Matt McGowan. Note: Content may be edited for style and length.

His ex-wife, Demi Moore, announced on Instagram that the actor has recently received the news.On Wednesday, Demi Moore announced on Instagram that her ex-husband Bruce Willis, the prolific action-movie star, had recently been diagnosed with aphasia — a disorder that affects the brain’s language center, and a person’s ability to understand or express speech — and that he would be stepping away from acting.“To Bruce’s amazing supporters, as a family we wanted to share that our beloved Bruce has been experiencing some health issues and has recently been diagnosed with aphasia, which is impacting his cognitive abilities,” Moore’s post reads. “As a result of this and with much consideration Bruce is stepping away from the career that has meant so much to him.”“We are moving through this as a strong family unit, and wanted to bring his fans in because we know how much he means to you, as you do to him,” it continued. “As Bruce always says, ‘Live it up,’ and together we plan to do just that.”The post is signed “Emma, Demi, Rumer, Scout, Tallulah, Mabel & Evelyn” — referring to Emma Heming Willis, Willis’s wife; and his children. Moore is the mother of Rumer, Scout and Tallulah; and Heming Willis is mother to Mabel and Evelyn.The post was accompanied with a comical photo of a younger, smirking Willis wearing a bathrobe, sunglasses, a gold chain with a cross and a towel around his head.Representatives for Willis did not immediately respond to a request for comment.Willis, who turned 67 this month, is most famous for his role as the rough-around-the-edges, yet clever, New York City cop John McClane in the highly successful “Die Hard” movie series, made up of five films from 1988 to 2013.He has also starred in critically acclaimed films like “Pulp Fiction” (1994) and “Moonrise Kingdom” (2012).While thought of primarily as a movie star, he has received more accolades for his work on television: For his role as the private detective David Addison (played opposite Cybill Shepherd) in “Moonlighting” — an ABC comedy-drama-romance that ran from 1985 to 1989 — he earned three Golden Globe nominations, winning one; and two lead actor Emmy nominations, winning one. He also won a guest actor in a comedy Emmy in 2000 for his role as Paul Stevens, the father of Ross Geller’s much-younger girlfriend, on the NBC series “Friends.”Since 2015, his filmography has mostly been an onslaught of B-movie action productions, including “Breach,” in 2020, and “Fortress,” in 2021. According to his IMDb page, Willis currently has nearly 10 movies in post-production.

A rare type of brain blood vessel malformation known as a cavernous angioma affects more than one million Americans and carries a lifetime risk of stroke and seizures. Only around one-third of cases can be connected to inherited familial genetic mutations. The majority of cavernous angiomas are sporadic and — until now — their cause was unknown.
A new study by researchers at the University of Chicago Medicine, Duke University and the University of Pennsylvania has identified a set of sporadic genetic mutations that make it more likely a person will develop these lesions, along with additional mutations in the same area that fuel the lesion’s growth. Understanding the underlying causes of these brain malformations will be the key to identifying which patients are at risk for their development and finding effective treatments against the condition. The research was published March 14 in Nature Cardiovascular Research.
“We’ve known for more than two decades that there is a familial form of cavernous angiomas that is inherited via genes passed on from generation to generation,” said Issam Awad, MD, the John Harper Seeley Professor of Neurological Surgery and Director of Neurovascular Surgery at UChicago Medicine. “But in the majority of people with this type of brain bleeding, the lesion is not inherited. And until now, we’ve never known why some people randomly end up with this lesion.”
The new research has identified a unique combination of mutations that occurs during the development of the brain that results in a cavernous angioma. First, a mutation in the gene PIK3CA leads to an abnormal pattern of vessels in the brain, known as a developmental venous anomaly, or DVA. The DVA alone is generally innocuous. But when a second mutation in one of several genes, such as MAP3K3, KRIT1, CCM2, or PDCD10, occurs in the area of the abnormal vein, a cavernous angioma develops.
“We’d previously observed that often these lesions grow near a preexisting abnormal vein,” said Awad. “But these DVAs are actually very common — about 6% to 10% of people have one, and the vast majority of them never have any problems. Rarely, those veins grow a cavernous angioma and we’ve never known why. In this study, we were finally able to use mutation analysis on the vein itself, to see why the vein seems predisposed to these angiomas.”
The researchers were able to examine the genetics of both the angioma and its connected DVA, thanks to the delicate surgical method used to repair bleeding lesions. It requires removing small portions of the veins to detangle them from the cavernous angioma lesion. This led to the discovery of the mutation in PIK3CA in the vein, and the realization that the same mutation co-occurs with a second mutation within the angioma.