While Europe faces a shortage of vaccines and governments argue about who gets what, one company in north Wales is producing jabs solely for the UK population.Almost all of the UK’s AstraZeneca supply comes through here; it’s where the vaccine’s filled into sterile vials, inspected dozens of times, and sent out for distribution.The Prime Minister Boris Johnson called it a “saviour of humanity” and it’s fair to say the staff inside are feeling immense pressure – and pride – from their role in the vaccination programme.BBC Breakfast was given world-first access to the production line.Camera/Edit: Brijesh PatelProducer: Josh ParryReporter: Jayne McCubbin

Scientists can now sequence an entire genome overnight. This technology has been the key tool in identifying and tracking Covid […]

Scientists have identified new genetic clues in people who’ve had small and often apparently ‘silent’ strokes that are difficult to treat and a major cause of vascular dementia, according to research funded by the British Heart Foundation (BHF) and published in The Lancet Neurology.
Researchers discovered changes to 12 genetic regions in the DNA of people who have had a lacunar stroke — a type of stroke caused by weakening of the small blood vessels deep within the brain. Over time, damage to the blood vessels and subsequent interruption to blood flow can lead to long-term disability, causing difficulty with thinking, memory, walking and ultimately dementia.
There are few proven drugs to prevent or treat lacunar strokes. The blood vessels affected are less than a millimetre wide and a lacunar stroke can strike without the person knowing. It’s not usually until someone has had a number of these strokes and starts to see signs of dementia that they realise something is wrong.
To date, only one genetic fault has been associated with lacunar strokes. However, after over a decade of research, Professor Hugh Markus and his team at the University of Cambridge working with researchers from around the world now believe their genetic breakthrough holds the key to finding much-needed treatments for lacunar stroke and vascular dementia.
Researchers scanned and compared the genetic code of 7,338 patients who had a lacunar stroke with 254,798 people who had not. Participants were recruited from across Europe, United States, South America and Australia after they attended hospital and had an MRI or CT brain scan.
They discovered that many of the 12 genetic regions linked to lacunar strokes were involved in maintaining the neurovascular unit — the part of the brain that separates the blood vessels from the brain and ensures that nerves function normally. These genetic changes are thought to make the small blood vessels ‘leakier’, causing toxic substances to enter the brain, and meaning that messages travelling around the brain slow down or don’t arrive at all.

Heightened activity in the brain, caused by stressful events, is linked to the risk of developing a rare and sometimes fatal heart condition, according to research published today (Friday) in the European Heart Journal.
The study found the greater the activity in nerve cells in the amygdala region of the brain, the sooner the condition known as Takotsubo syndrome (TTS) can develop. The researchers suggest that interventions to lower this stress-related brain activity could help to reduce the risk of developing TTS; these could include drug treatments or techniques for lowering stress.
TTS, also known as “broken heart” syndrome, is characterised by a sudden temporary weakening of the heart muscles that causes the left ventricle of the heart to balloon out at the bottom while the neck remains narrow, creating a shape resembling a Japanese octopus trap, from which it gets its name. Since this relatively rare condition was first described in 1990, evidence has suggested that it is typically triggered by episodes of severe emotional distress, such as grief, anger or fear, or reactions to happy or joyful events. Patients develop chest pains and breathlessness, and it can lead to heart attacks and death. TTS is more common in women with only 10% of cases occurring in men.*
The amygdala is the part of the brain that controls emotions, motivation, learning and memory. It is also involved in the control of the autonomic nervous system and regulating heart function.
“The study suggests that the increased stress-associated neurobiological activity in the amygdala, which is present years before TTS occurs, may play an important role in its development and may predict the timing of the syndrome. It may prime an individual for a heightened acute stress response that culminates in TTS,” said Dr Ahmed Tawakol, co-director of the Cardiovascular Imaging Research Center at Massachusetts General Hospital and Harvard Medical School (Boston, USA), who led the study.
“We also identified a significant relationship between stress-associated brain activity and bone marrow activity in these individuals. Together, the findings provide insights into a potential mechanism that may contribute to the ‘heart-brain connection’.”
In the first study to look at brain scans using F-fluorodeoxyglucose positron emission tomography/computed tomography (PET-CT) to assess brain activity before TTS develops, Dr Tawakol and colleagues analysed data on 104 people with an average age of 68 years, 72% of whom were women.

He was a top executive at Memorial Sloan Kettering before resigning over payments from health care companies. He went on to lead cancer research at AstraZeneca.Dr. José Baselga, a renowned cancer researcher and pharmaceutical executive whose work helped transform the treatment of breast cancer patients, died on Sunday. He was 61.His employer, the drug maker AstraZeneca, confirmed the death but did not say where he died. The Washington Post reported that he died at his home in the Cerdanya region of Spain and that he had maintained another home in New York City. His family confirmed that the cause was Creutzfeldt-Jakob disease, a rare neurological disorder, but declined to comment further.Dr. Baselga had worked at AstraZeneca since 2019 as the executive vice president for research and development in oncology. Before that he was chief medical officer at Memorial Sloan Kettering Cancer Center in Manhattan, until he resigned in 2018 following revelations reported jointly by The New York Times and ProPublica that in his published research he had failed to disclose payments from health care companies.“His visionary leadership, deep scientific expertise and strategic insight have delivered so many achievements that we can all be proud of and that will benefit patients’ lives in the years to come,” Pascal Soriot, AstraZeneca’s chief executive, said in a statement.In a decades-long career in the United States and his native Spain, Dr. Baselga was known for his work in developing and testing targeted cancer treatments, including the breast cancer treatment Herceptin, a monoclonal antibody that zeroes in on a particular protein, known as HER2, which is implicated in aggressive and deadly breast cancers.Targeted cancer drugs allow doctors to tailor treatment to specific types of cancer cells. This can lead to fewer side effects and better results than those obtained through blunter instruments like chemotherapy.Dr. Baselga led an early-stage clinical trial of Herceptin, and his research contributed to the recognition that when the drug was combined with chemotherapy, it extended the lives of women with so-called HER2-positive breast cancer, said Dr. Clifford Hudis, the chief executive of the American Society of Clinical Oncology.“It’s the dream that everybody has when you do research,” said Dr. Hudis, who had known Dr. Baselga since the 1980s. “He was dedicated to translational research, and he was unbelievably demanding when it came to execution. He expected everything and everybody to understand his vision and to deliver on it.”Dr. Baselga was also involved in the clinical development of other breast cancer drugs like Perjeta, or pertuzumab, and Afinitor, or everolimus. More recently he studied the development of drugs targeting tumors that have a mutation known as PI3K. His work also focused on drug resistance in some cancers.José Baselga was born in Barcelona on July 3, 1959, and earned his medical and doctoral degrees from the Autonomous University of Barcelona. He caught the attention of cancer researchers after participating in a medical fellowship at Memorial Sloan Kettering, where he worked with Dr. John Mendelsohn in researching the use of monoclonal antibodies in targeting certain proteins associated with aggressive cancers, including lung and breast cancers.Dr. Larry Norton, a senior vice president at Memorial Sloan Kettering and the medical director of the hospital’s Evelyn H. Lauder Breast Center, quickly took an interest in Dr. Baselga and served as an early mentor. “He was an artist,” Dr. Norton recalled, adding that he had “a driving force within him, and he would focus all of his energies on accomplishing what was necessary to fulfill that vision.”Dr. Baselga returned to Spain in 1996 to found the Vall d’Hebron Institute of Oncology at Vall d’Hebron University Hospital in Barcelona. Under his leadership, the center became an international powerhouse in cancer research, testing targeted cancer therapies in early-stage clinical trials. Dr. Baselga became a well-known figure in Spain.“Spain was not known in the world as a cancer research place,” Dr. Antoni Ribas, the president of the American Association for Cancer Research, who did his medical residency at Vall d’Hebron just before Dr. Baselga assumed his role there, said in a phone interview. “He put Vall d’Hebron, Barcelona and Spain on the map of cancer research.”Following a stint from 2010 to 2013 at Massachusetts General Hospital, where he was the chief of the division of hematology and oncology, Dr. Baselga returned to Memorial Sloan Kettering in 2013 to become physician in chief and, later, chief medical officer.He also held several leadership roles in the world of cancer research, including president of the American Association for Cancer Research and editor of Cancer Discovery and other medical journals.Dr. Baselga resigned from Sloan Kettering in September 2018 under pressure after The Times and ProPublica, the nonprofit investigative journalism outfit, reported that he had failed to disclose millions of dollars in payments from drug and health care companies in dozens of research articles in The New England Journal of Medicine and other publications.In resigning, he said he was “extremely proud” of his work at Sloan Kettering and added, “It is my hope that this situation will inspire a doubling down on transparency in our field.”His departure led the cancer center to overhaul its conflict-of-interest policy. Dr. Baselga later stepped down from the boards of Bristol-Myers Squibb and the radiation equipment manufacturer Varian Medical Systems.The Post said his survivors include his wife of 30 years, Silvia Garriga; four children, Marc Baselga, Clara Baselga-Garriga, Pepe Baselga-Garriga and Alex Baselga-Garriga; his mother, Esther Torres; two sisters; and a brother.AstraZeneca announced in January 2019 that it had hired Dr. Baselga to lead its cancer research. In his time with the company, Mr. Soriot, AstraZeneca’s chief executive, said, Dr. Baselga had championed the company’s collaboration with Daiichi Sankyo to develop two cancer treatments and built a “world-class” team of cancer researchers at the company.“I will continue to be inspired by his work and vision,” Mr. Soriot said.

From Monday 29th March 2021, the rule of six is back as a way of controlling the spread of coronavirus in England.It was first used to prohibit social gatherings of more than six people back in September 2020, but has not been in place during both the second and third lockdowns.But now some tweaks have been made which the government says offers families more flexibility.BBC health reporter Laura Foster explains.Video by Laura Foster and Mel Lou

After a staff member dismissed racism as a problem in medicine on a podcast, a petition signed by thousands demanded a review of editorial processes at the journal.Following controversial comments on racism in medicine made by a deputy editor at JAMA, the editor in chief of the prominent medical journal was placed on administrative leave on Thursday.A committee of the American Medical Association, which oversees the journal, said Dr. Howard Bauchner would be replaced by an interim editor pending results of an independent investigation. The decision was announced on Thursday in an email to employees.JAMA is one of the world’s leading medical journals, publishing research that shapes the scientific agenda and public policy around the globe. The controversy began when Dr. Ed Livingston, a deputy editor, said on a Feb. 24 podcast that structural racism no longer existed in the United States.“Structural racism is an unfortunate term,” said Dr. Livingston, who is white. “Personally, I think taking racism out of the conversation will help. Many people like myself are offended by the implication that we are somehow racist.”The podcast was promoted with a tweet from the journal that said, “No physician is racist, so how can there be structural racism in health care?” The response to both was swift and angry, prompting the journal to take down the podcast and delete the tweet.A week later, Dr. Bauchner addressed the controversy. “Comments made in the podcast were inaccurate, offensive, hurtful, and inconsistent with the standards of JAMA,” Dr. Bauchner said in a statement. “We are instituting changes that will address and prevent such failures from happening again.”Dr. Livingston later resigned. On Thursday night, officials at JAMA did not immediately respond to a request for comment.Many in the medical community said that the journal had not gone far enough and that the events offered an opportunity to make more systemic changes. In an email sent to leaders of the A.M.A., a group of doctors called for “a careful investigation of the JAMA editorial staff and board, up to and including the removal of Dr. Howard Bauchner.”The authors also initiated a petition, now signed by nearly 7,000 people, asking the journal to hold Dr. Bauchner accountable and to review and restructure the editorial process.“It’s not just that this podcast is problematic — it’s that there is a long and documented history of institutional racism at JAMA,” said Dr. Brittani James, a Black physician who practices on the South Side of Chicago and who helped begin the petition.“That podcast should never have happened,” said Dr. Uché Blackstock, an emergency physician in New York. “That tweet should never have happened. The fact that podcast was conceived of, recorded and posted was unconscionable.”“I think it caused an incalculable amount of pain and trauma to Black physicians and patients,” she said. “And I think it’s going to take a long time for the journal to heal that pain.”Recently, other prominent journals have had to reckon with their roles in perpetuating racism in medicine. In January, Alan Weil, editor in chief of Health Affairs, acknowledged that the journal’s “staff and leadership are overwhelmingly white and economically privileged,” and he committed to reviewing its editorial process.In the email to JAMA employees, Dr. James L. Madara, chief executive of the American Medical Association, promised that its investigation would probe “how the podcast and associated tweet were developed, reviewed, and ultimately published,” and said that the A.M.A. had engaged independent investigators to ensure objectivity.He did not offer a date for conclusion of the investigation.

A University of Arizona Health Sciences researcher examined the role of cholesterol in both Alzheimer’s disease and Type 2 diabetes to identify a small molecule that may help regulate cholesterol levels in the brain, making it a potential new therapeutic target for Alzheimer’s disease.
There is no known cure for Alzheimer’s disease, which affects more than 5.5 million people in the United States. In the last decade, scientists have found increasing evidence linking the underlying causes of Type 2 diabetes and Alzheimer’s disease.
Type 2 diabetes occurs when insulin becomes less efficient at removing glucose from the bloodstream, resulting in high blood sugar that can cause abnormal cholesterol levels. A similar situation occurs in Alzheimer’s disease, but rather than affecting the body as a whole, the effects are localized in the brain.
“Alzheimer’s and diabetes share many common causes,” said Gregory Thatcher, PhD, professor of pharmacology and toxicology in the UArizona College of Pharmacy and the newly named R. Ken and Donna Coit Endowed Chair in Drug Discovery. “Our goal was to develop a way of identifying compounds that would counteract many detrimental changes that contribute to both Alzheimer’s and Type 2 diabetes.”
The paper, “Discovery of Nonlipogenic ABCA1 Inducing Compounds with Potential in Alzheimer’s Disease and Type 2 Diabetes,” was published in the journal ACS Pharmacology and Translational Science.
When cholesterol rises, due to insulin resistence or other factors, the body starts a process known as reverse cholestrol transport, during which specific molecules carry excess cholesterol to the liver to be excreted. Apolipoprotein E (APOE) is one of the proteins involved in reverse cholesterol transport.
APOE is also the strongest risk factor gene for Alzheimer’s disease and related dementia, and an independent risk factor for Type 2 diabetes and cardiovascular disease. Similarly, reduced activity of another cholesterol transporter, ATP-binding cassette transporter A1 (ABCA1), correlates with increased risk of cardiovascular disease, Type 2 diabetes and Alzheimer’s disease.
“While most people are aware of so-called ‘good cholesterol,’ and ‘bad cholesterol,’ associated with risk of heart attack and stroke, these broad concepts are also applicable to a healthy brain,” said Dr. Thatcher, who has been working to develop advanced therapeutics for Alzheimer’s for more than 20 years. “Moving cholesterol to where it is needed in the body has positive effects on many physiological processes and can help clear misfolded proteins that accumulate in the brain.”
Increasing the activity of ABCA1 is expected to positively influence insulin signaling and reduce inflammation in the brain, making it a potential therapy for both Type 2 diabetes and Alzheimer’s disease. In this study, Dr. Thatcher and the research team designed a way to identify small molecules that improve the function of ABCA1 in the body while avoiding unwanted effects to the liver.
In a March 20 paper in the journal EBioMedicine, “Metabolomic analysis of a selective ABCA1 inducer in obesogenic challenge provides a rationale for therapeutic development,” Dr. Thatcher’s team honed in on a specific small molecule, CL2-57, due to its ability to stimulate ABCA1 activity with positive effects on liver and plasma triglycerides. The use of this compound showed improved glucose tolerance and insulin sensitivity, as well as reduced weight gain, among other beneficial effects.
Their future research will seek to improve the properties of the small molecules to increase the levels in the brain. Their long-term goal is to understand which patients suffering from the cognitive and neuropsychiatric symptoms of Alzheimer’s and dementia will benefit from the treatment.
“During the Covid-19 pandemic we hear about the mounting deaths in nursing homes and it’s important to remember that Alzheimer’s and related dementia is a major cause of the elderly moving to nursing homes,” Dr. Thatcher said. “It would be good to think of a future in which healthspan was extended, especially a healthy brain; maybe that’s more important than lifespan.”

Expectant women are more likely to give birth early if they have high blood levels of a chemical used in flame retardants compared with those who have limited exposure, a new study finds.
These polybrominated diphenyl ethers (PBDEs) are used in the manufacture of furniture, carpeting, and other products to reduce flammability. Previous studies have found that the substances can leach into household dust and build up in the body where they may interfere with the thyroid, an organ that secretes brain-developing hormones. Childhood exposure to PBDEs has been linked to learning disabilities, autistic symptoms, and behavioral issues, among other developmental problems.
In an investigation led by an NYU Long Island School of Medicine researcher, nearly all pregnant women enrolled in the study had detectable levels of PBDEs in their blood. The findings revealed that women with concentrations above 4 nanograms per milliliter of blood were roughly twice as likely to deliver their children early via cesarean section or intentionally induced labor due to safety concerns for the mother or infant. By contrast, there was no elevated risk for preterm birth among women with PBDE levels below that threshold.
“Our findings illustrate that flame retardants may have a tremendous impact on childbirth even if exposure occurred early on in the pregnancy,” says study lead author Morgan Peltier, PhD. “Although PBDE chemicals are used with good intentions, they may pose a serious health concern that may have lasting consequences for children.” Peltier is an associate professor in the departments of Clinical Obstetrics, Gynecology, and Reproductive Medicine at NYU Long Island School of Medicine, part of NYU Langone Health.
According to Peltier, preterm birth is a leading cause of newborn death and occurs annually in about 15 million pregnancies worldwide. Experts have linked the phenomenon to long-term neurological disorders including cerebral palsy, schizophrenia, and learning problems that can extend into adulthood. Earlier research has pointed to PBDE exposure as a possible culprit behind preterm birth. However, these investigations only looked at exposure to the chemicals late in pregnancy and only examined white and African-American mothers.
The new study, published online Dec. 1 in the Journal of Perinatal Medicine, is the first to explore the link between PBDE exposure in the first trimester of pregnancy, says Peltier. He notes that the investigation looked at a wider demographic group as well, adding Asian and Hispanic women to the analysis.

Extending California’s stringent diesel emissions standards to the rest of the U.S. could dramatically improve the nation’s air quality and health, particularly in lower income communities of color, finds a new analysis published today in the journal Science.
Since 1990, California has used its authority under the federal Clean Air Act to enact more aggressive rules on emissions from diesel vehicles and engines compared to the rest of the U.S. These policies, crafted by the California Air Resources Board (CARB), have helped the state reduce diesel emissions by 78% between 1990 and 2014, while diesel emissions in the rest of the U.S. dropped by just 51% during the same time period, the new analysis found.
The study estimates that by 2014, improved air quality cut the annual number of diesel-related cardiopulmonary deaths in the state in half, compared to the number of deaths that would have occurred if California had followed the same trajectory as the rest of the U.S. Adopting similar rules nationwide could produce the same kinds of benefits, particularly for communities that have suffered the worst impacts of air pollution.
“Everybody benefits from cleaner air, but we see time and again that it’s predominantly lower income communities of color that are living and working in close proximity to sources of air pollution, like freight yards, highways and ports. When you target these sources, it’s the highly exposed communities that stand to benefit most,” said study lead author Megan Schwarzman, a physician and environmental health scientist at the University of California, Berkeley’s School of Public Health. “It’s about time, because these communities have suffered a disproportionate burden of harm.”
The study also points out that exposure to fine particulate matter (PM2.5) has been linked to poor outcomes from COVID-19, adding urgency to the need to reduce air pollution, par¬ticularly for communities of color that are disproportionately affected by both.
Diesel exhaust consists of both particles and gases and contributes significantly to PM2.5 air pollution worldwide. PM2.5 exposure from any source can compromise children’s lung development and can trigger airway inflammation and exacerbate asthma and cardiopulmonary diseases. Diesel exhaust has also been designated a human carcinogen by California’s Office of Environmental Health Hazard Assessment (OEHHA).