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In a wide ranging interview about his life after retiring as director of the National Institute of Allergy and Infectious Diseases, Anthony Fauci tells the BBC’s Katty Kay that 96% of the US population has a degree of immunity against the most recent Covid variant but urges people to get a booster shot that will be released in September.”There is enough fundamental community-level protection, it’s not going to be the tsunami of cases that we’ve seen.”

Published3 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Megan McGillin By Aileen MoynaghBBC News NIA medical student who was told at the age of 10 she had the liver of an alcoholic has said rowing has delayed her need for a liver transplant. Megan McGillin, from Northern Ireland, was diagnosed with cirrhosis, or scarring of the liver, 11 years ago which stops her liver working properly.Liver disease in children is rare. A liver specialist said keeping fit and healthy plays a “critical role in maintaining the liver in a stable condition”.Cirrhosis cannot be cured or reversed, and many of the liver disorders that cause cirrhosis in children are not preventable.In Megan’s case, doctors do not know how she got it, but have said the damage could eventually become so extensive that her liver stops functioning, causing it to fail.”[Doctors] told me, initially when I was diagnosed, that at the age of 18 that I would have a transplant, but I kept fit and well,” Megan said.”Then when I was 16 or 17, they told me definitely by 21 that I would need a transplant.”When I turned 21 in November, I didn’t get a transplant for my birthday.”I just kept on powering through, so they have taken away any timelines now.” Image source, Megan McGillinLiver disease such as cirrhosis, can also result in portal hypertension and cause an enlarged spleen.In Megan’s case this meant she had to give up contact sports which she said was a “major thing” for her.She later got into rowing and rowed on the Irish high-performance squad for a couple of years while at school.Megan said this kept her very fit and “as much as I struggled, it was a high intensity sport that I think kept me well all these years because I was constantly training and looking after myself on the inside”.She believes keeping fit has kept her liver functioning for so long.Dr Girish Gupte, a consultant paediatric liver specialist at Birmingham Women’s and Children’s hospital, does outreach clinics in the Royal Belfast Hospital for Sick Children six times a year.”Liver disease is extremely rare in children so that’s why a majority of the population may not have heard about children having chronic liver problems,” he said.”The incidents of liver disease can vary from one in 10,000 within the UK population, to some of the other liver diseases which can be one in a million.”Dr Gupte said there has been an increase in chronic liver disease cases in recent decades, partly due to advances in testing but he also said he feels that environmental factors and lifestyle play a role in the increased incidents of liver disease in children.”Not all children with liver disease need a liver transplant,” he said.”Most of these conditions can be managed with good medical treatments and with a good healthy lifestyle,” he added.”However, in some children there is progression of the liver disease to end-stage liver disease and these children do need liver transplantation, either as children or maybe as adults,” he said. “I think keeping fit and healthy, eating a healthy diet, preventing the accumulation of fat in the liver with a healthy diet, play a critical role in maintaining the liver in a stable condition in the long-run and trying to delay or avoid liver transplantation.” The ‘liver of an alcoholic’People often think of cirrhosis as a disease caused by long-term alcohol abuse.While this is sometimes a factor in adults, cirrhosis in children often stems from a wide variety of liver disorders.Image source, Megan McGillinExplaining the severity of Megan’s condition, doctors told her she “had the liver of an alcoholic”, which at 10 years of age did not make sense.”I’d obviously never drank any alcohol before, and my mum was gobsmacked at the idea that a doctor would tell me that I had the liver of an alcoholic,” she told BBC News NI.”That just shows the correlation between people having liver disease and this assumption that it’s come from alcoholism,” she added.The 21-year-old has never drunk alcohol and does not plan to because of how it affects the liver.’Opportunity to educate some people’Megan said she has had mixed reactions when telling people that she does nott drink alcohol because she has liver disease.The one reaction she does not like is “people saying, ‘oh goodness what have you done? What were you doing in your younger years? How early did you start drinking or did you have a bad event with alcohol or drugs’ that has affected my liver so much?”The medical student said it does give her an “opportunity to educate some people that having liver disease doesn’t necessarily correlate to drinking alcohol or being abusive to alcohol”.’My normal is different’She said getting the diagnosis was “scary”, but she knew she could live with the condition, albeit with limitations, as the condition makes her extremely tired.”On the outside I look normal, I do normal things,” she said.”Now what I call my normal is different from my peers’ normal. I have to have limitations on myself – on certain things I can and can’t do.”It is mostly about managing my energy levels.”Image source, Megan McGillinWhile she is positive about the future she said you “can’t really have a plan” with liver disease.”I could wake up tomorrow and be completely yellow, jaundiced skin and I would know my liver was then beginning to fail,” she said.”That would end up eventually with a transplant.”That could be tomorrow, that could be next week, five years, 10 years, I just don’t know,” she said.Megan said if and when that time comes, she would not hesitate as “to be allowed that opportunity to be given an organ from somebody else is just amazing”.She added: “Organ donation really is life-saving, but it can still be a scary decision to make because you don’t know what’s going to happen.”You don’t know if you’ll be poorly, if your body will accept it or if there are any secondary diseases or infections that you get after having that surgery because it is a major surgery.”My liver as such is working.”It’s not working at full capacity but whatever it’s doing it’s doing something right.”You have to wait until it gets to a certain level of liver function, or your condition has affected your lifestyle in such a way that you’re extremely poorly, but the longer my biological, the liver I was born with, stays in me it’s going to be better.”

Fat is a normal and necessary part of the body. Fat cells store and release energy, as well as play significant roles in hormonal regulation and immunity.
In recent decades, a concerning rise in metabolic illnesses — such as cardiovascular disease, high blood pressure and diabetes — has focused scientific attention on the biology and chemistry of fat, resulting in a wealth of information about how fat cells work.
But fat cells and their metabolic activities are only part of the story.
Fat-filled lipid droplets, tiny spheres of fat many times smaller than fat cells, are a growing subject of scientific interest. Found inside many different cell types, these lipid particles have long been little understood. Studies have begun to illuminate these droplets’ participation in metabolic functions and cellular protection, but we still know next to nothing about the physical nature of fat.
Now, researchers at the University of Pennsylvania School of Engineering and Applied Science have looked beyond biochemistry to publish groundbreaking work on the physics of these droplets, revealing them to be a potential threat to a cell’s nucleus. In the August issue of the Journal of Cell Biology, they are the first to discover fat-filled lipid droplets’ surprising capability to indent and puncture the nucleus, the organelle which contains and regulates a cell’s DNA.
The stakes of their findings are high: a ruptured nucleus can lead to elevated DNA damage that is characteristic of many diseases, including cancer.
The study was led by Dennis E. Discher, Robert D. Bent Professor in the Department of Chemical and Biomolecular Engineering, Irena Ivanovska, Ph.D. Research Associate in Penn’s Molecular and Cell Biophysics Lab, and Michael Tobin, Ph.D. Candidate in the Department of Bioengineering.

The mosquito-borne infectious disease malaria resulted in about 241 million clinical episodes and 627,000 deaths in 2020. In young children and pregnant women living in areas where the disease is endemic, a major cause of death is Plasmodium falciparum, the most virulent, prevalent, and deadly human malaria parasite.
Scientists are keen to understand the mechanisms that regulate gene expression through the different stages of P. falciparum’s lifecycle because such knowledge can help in the discovery of novel antimalarial therapies. One focus of their research is “lncRNAs,” which are long noncoding ribonucleic acid molecules found in cells of eukaryotes — organisms whose cells have a nucleus. Many noncoding RNAs have been linked to cancer and neurological disorders. LncRNAs are found also to regulate genome structure and gene expression.
A team led by Karine Le Roch, a professor of molecular, cell and systems biology at the University of California, Riverside, studied the role lncRNAs play in P. falciparum and found that one lncRNA — lncRNA-ch14 — partially regulates sexual differentiation and sex determination in P. falciparum.
“We can now target specific lncRNAs to stop P. falciparum’s life cycle progression, including sexual differentiation,” Le Roch said. “We found evidence that lncRNAs are distributed in distinct cellular compartments in P. falciparum. Depending on their localization, they are found to play important roles in regulating gene expression and the malaria parasite’s life cycle progression.”
Study results appear in Nature Communications.
The research team identified 1,768 lncRNAs in P. falciparum, of which 718 lncRNAs had never before been identified. The team validated that some of these novel lncRNAS are critical for the parasite’s life cycle progression.
“Our findings bring new insight into the role of lncRNAs in P. falciparum’s capacity to cause malaria, gene regulation, and sexual differentiation,” said Le Roch, who directs UCR’s Center for Infectious Disease and Vector Research. “This can open up new avenues for targeted approaches towards therapeutic strategies against P. falciparum that are aimed at stopping the parasite’s life cycle progression and its sexual differentiation and blocking the transmission of the parasite into mosquitoes.”
The research was a collaboration with scientists at the University of Washington, Johns Hopkins Bloomberg School of Public Health, and The Wellcome Sanger Institute.
The research was supported by grants to Le Roch from the National Institutes of Health and UCR.

University of Michigan researchers have discovered that the same cellular mechanism involved in a form of cystic fibrosis is also implicated in a form of a rare disease called cystinosis.
The mechanism cleans up mutated proteins. In cystinosis, a genetic disease, this allows cystine crystals to build up in the cell. This disrupts the cell, and eventually, tissues and ultimately organs, particularly the kidneys and the eyes.
The problem begins when the lysosome, an organelle within the cell, is unable to do its job. Often called the recycling center of the cell, the lysosome takes in cellular garbage, breaks it down into reusable cellular building blocks, then transports those materials back into the cell.
But when the protein that transports one of the recycled amino acids back into the cell mutates and fails, a cellular mechanism cleans up the faulty protein, allowing amino acid, or cystine, to build up in the lysosome.
“If cystinosis not treated at an early age, some of the effects are irreversible and it could include impaired growth, kidney failure and neurological problems,” said Varsha Venkatarangan, graduate student in the U-M Department of Molecular, Cellular and Developmental Biology and lead author of the study. “Typically, the symptoms of the disease are treated rather than the root problem. So we have been wondering what could be the possible cellular mechanism of this disease.”
Venkatarangan worked with fibroblasts, skin tissue cells derived from patients with the disease. Using these cells, she determined that this disease mechanism called endoplasmic-reticulum-associated degradation, or ERAD, degrades a mutated version of the lysosome cystine transporter.
ERAD is the same mechanism behind other diseases such as a major form of cystic fibrosis. And because this mechanism has been identified, the researchers were able to show that previously identified drug molecules were able to help the transporter protein remain stable. Their findings are now published in the Journal of Clinical Investigation.

Plastics — in particular, microplastics — are among the most pervasive pollutants on the planet, finding their way into the air, water systems and food chains around the world. While the prevalence of microplastics in the environment is well known — as are their negative impacts on marine organisms — few studies have examined the potential health impacts on mammals, prompting University of Rhode Island Professor Jaime Ross’ new study.
Ross and her team focused on neurobehavioral effects and inflammatory response to exposure to microplastics, as well as the accumulation of microplastics in tissues, including the brain. They have found that the infiltration of microplastics was as widespread in the body as it is in the environment, leading to behavioral changes, especially in older test subjects.
“Current research suggests that these microplastics are transported throughout the environment and can accumulate in human tissues; however, research on the health effects of microplastics, especially in mammals, is still very limited,” said Ross, an assistant professor of biomedical and pharmaceutical sciences at the Ryan Institute for Neuroscience and the College of Pharmacy. “This has led our group to explore the biological and cognitive consequences of exposure to microplastics.”
Ross’ team — which includes Research Assistant Professor Giuseppe Coppotelli, biomedical and pharmaceutical sciences graduate student Lauren Gaspar, and Interdisciplinary Neuroscience Program graduate student Sydney Bartman — exposed young and old mice to varying levels of microplastics in drinking water over the course of three weeks. They found that microplastic exposure induces both behavioral changes and alterations in immune markers in liver and brain tissues. The study mice began to move and behave peculiarly, exhibiting behaviors akin to dementia in humans. The results were even more profound in older animals.
“To us, this was striking. These were not high doses of microplastics, but in only a short period of time, we saw these changes,” Ross said. “Nobody really understands the life cycle of these microplastics in the body, so part of what we want to address is the question of what happens as you get older. Are you more susceptible to systemic inflammation from these microplastics as you age? Can your body get rid of them as easily? Do your cells respond differently to these toxins?”
To understand the physiological systems that may be contributing to these changes in behavior, Ross’ team investigated how widespread the microplastic exposure was in the body, dissecting several major tissues including the brain, liver, kidney, gastrointestinal tract, heart, spleen and lungs. The researchers found that the particles had begun to bioaccumulate in every organ, including the brain, as well as in bodily waste.
“Given that in this study the microplastics were delivered orally via drinking water, detection in tissues such as the gastrointestinal tract, which is a major part of the digestive system, or in the liver and kidneys was always probable,” Ross said. “The detection of microplastics in tissues such as the heart and lungs, however, suggests that the microplastics are going beyond the digestive system and likely undergoing systemic circulation. The brain blood barrier is supposed to be very difficult to permeate. It is a protective mechanism against viruses and bacteria, yet these particles were able to get in there. It was actually deep in the brain tissue.”
That brain infiltration also may cause a decrease in glial fibrillary acidic protein (called “GFAP”), a protein that supports many cell processes in the brain, results have shown. “A decrease in GFAP has been associated with early stages of some neurodegenerative diseases, including mouse models of Alzheimer’s disease, as well as depression,” Ross said. “We were very surprised to see that the microplastics could induce altered GFAP signaling.”
She intends to investigate this finding further in future work. “We want to understand how plastics may change the ability for the brain to maintain its homeostasis or how exposure may lead to neurological disorders and diseases, such as Alzheimer’s disease,” she said.
The study was published in the International Journal of Molecular Science. It was supported by the Rhode Island Medical Research Foundation, Roddy Foundation, Plastics Initiative, URI College of Pharmacy, George and Anne Ryan Institute for Neuroscience, and the Rhode Island Institutional Development Award (IDeA) Network of Biomedical Research Excellence from the National Institute of General Medical Sciences of the National Institutes of Health.

“Every successful medicine has its origin story. And research like this is the soil from which new drugs are born,” says Cold Spring Harbor Laboratory Professor Christopher Vakoc.
For six years, Vakoc’s lab has been on a mission to transform sarcoma cells into regularly functioning tissue cells. Sarcomas are cancers that form in connective tissues like muscle. Treatment often involves chemotherapy, surgery, and radiation — procedures that are especially tough on kids. If doctors could transform cancer cells into healthy cells, it would offer patients a whole new treatment option — one that could spare them and their families a great deal of pain and suffering.
A devastating and aggressive type of pediatric cancer, rhabdomyosarcoma (RMS) resembles children’s muscle cells. No one knew whether this proposed treatment method, called differentiation therapy, might ever work in RMS. It could still be decades out. But now, thanks to Vackoc’s lab, it seems like a real possibility.
To carry out their mission, Vakoc and his team created a new genetic screening technique. Using genome-editing technology, they hunted down genes that, when disrupted, would force RMS cells to become muscle cells. That’s when a protein called NF-Y emerged. With NF-Y impaired, the scientists witnessed an astonishing transformation.
“The cells literally turn into muscle,” Vakoc says. The tumor loses all cancer attributes. They’re switching from a cell that just wants to make more of itself to cells devoted to contraction. Because all its energy and resources are now devoted to contraction, it can’t go back to this multiplying state.”
This newfound relationship between NF-Y and RMS may set off the chain reaction needed to bring differentiation therapy to patients. And the mission doesn’t stop at RMS. The technology could be applicable to other cancer types. If so, scientists may someday work out how to turn other tumors into healthy cells.
“This technology can allow you to take any cancer and go hunting for how to cause it to differentiate,” Vakoc explains. “This might be a key step toward making differentiation therapy more accessible.”
Previously, Vakoc and his team succeeded in transforming Ewing sarcoma cells into healthy tissue cells. The Ewing sarcoma and RMS discoveries were supported by local families who’d lost loved ones to these cancers. “They came together and funded us to try to find, with some desperation, a new therapeutic strategy,” says Vakoc.
Those families and Vakoc’s lab may now be heroes of a new origin story: a scientific breakthrough that could someday help save children’s lives and revolutionize cancer treatment as we know it.

A new drug offers a breakthrough world first treatment for Lipoprotein(a), a largely genetic form of cholesterol that increases the risk of heart attack and stroke, announced today by study lead Professor Stephen Nicholls, Director of the Monash University’s Victorian Heart Institute and Victorian Heart Hospital.
High levels of Lipoprotein(a), known as Lp(a) or spoken as ‘LP little a’, impact one in five people globally with no approved treatment currently on the market.
The trial demonstrated the success of Muvalaplin — the first oral drug ever developed to target Lp(a) — effectively lowering levels by up to 65%. It works by disrupting the ability for Lp(a) to form in the body.
Professor Stephen Nicholls, cardiologist and Director of Monash University’s Victorian Heart Institute and the Victorian Heart Hospital at Monash Health, led the landmark research and trial, presented at the European Society of Cardiology Congress in Amsterdam today and published in JAMA.
Lp(a) is similar to LDL cholesterol, sometimes called ‘bad cholesterol’, but is more sticky, increasing risk of blockages and blood clots in arteries.
Common LDL lowering drugs such as statins don’t have the same lowering effect on Lp(a). Being largely genetic, Lp(a) is also difficult to control through diet, exercise and other lifestyle changes.
Although Lp(a) was discovered nearly 60 years ago there still aren’t any widely accessible treatments available to lower levels and reduce cardiovascular risk.

Investigators from the Smidt Heart Institute at Cedars-Sinai are one step closer to helping individuals catch a sudden cardiac arrest before it happens, thanks to a study published today in the peer-reviewed journal Lancet Digital Health.
The study, led by sudden cardiac arrest expert Sumeet Chugh, MD, found that 50% of individuals who experienced a sudden cardiac arrest also experienced a telling symptom 24 hours before their loss of heart function.
Smidt Heart Institute investigators also learned that this warning symptom was different for women than it was for men. For women, the most prominent symptom of an impending sudden cardiac arrest was shortness of breath, whereas men experienced chest pain.
Smaller subgroups of both genders experienced palpitations, seizure-like activity and flu-like symptoms.
Out-of-hospital sudden cardiac arrest claims the lives of 90% of people who experience it, marking an urgent need to better predict — and prevent — the condition.
“Harnessing warning symptoms to perform effective triage for those who need to make a 911 call could lead to early intervention and prevention of imminent death,” said Chugh, director of the Center for Cardiac Arrest Prevention in the Smidt Heart Institute and senior author of the study. “Our findings could lead to a new paradigm for prevention of sudden cardiac death.”
For this study, investigators used two established and ongoing community-based studies, each developed by Chugh: the ongoing Prediction of Sudden Death in Multi-Ethnic Communities (PRESTO) Study in Ventura County, California, and the Oregon Sudden Unexpected Death Study (SUDS), based in Portland, Oregon.

Researchers at the University of East Anglia have developed a new way of identifying patients at risk of an irregular heartbeat, known as ‘atrial fibrillation’.
While not life threatening, the condition increases people’s risk of having a transient ischaemic attack (TIA) or stroke by up to five times.
A new study, published today, reveals four specific factors that can predict which patients will have atrial fibrillation.
These include older age, higher diastolic blood pressure and problems with both the coordination and function of the upper left chamber of the heart.
The team went on to create an easy tool for doctors to use in practice to identify those at high risk.
And they hope that this will help diagnose and treat more patients, reducing their risk of future strokes.
Lead researcher Prof Vassilios Vassiliou, from UEA’s Norwich Medical School and Honorary Consultant Cardiologist at the Norfolk and Norwich University Hospital, said: “Identifying who is at high risk and more likely to develop atrial fibrillation is very important.