Under-16s will be banned from buying high-caffeine energy drinks in England, if Labour wins 4 July’s general election.

For Paula Span, a columnist for The Times’s Health section, the subject of aging doesn’t age.For about 15 years, Paula Span has dedicated much of her journalism career to covering one subject: aging, and the challenges that come with it.Ms. Span writes The New Old Age, a twice-monthly column for the Health section at The New York Times about issues affecting older Americans. Among the topics she has recently explored are the costs of growing older, the rise of robotic pets as companions and the hazards of misinformation on social media.Ms. Span took over the column in 2009, when it was just a blog. Before The Times, she wrote for The Washington Post’s Style desk and magazine, where in 2002, she reported an article about residents at an assisted-living facility in Bethesda, Md.“At the time, people didn’t really know much about assisted living,” Ms. Span said. “It got me interested in spending time with older people and writing about these issues.” Four years later, she began writing her first book, “When the Time Comes,” about the struggles of families with aging parents.In a phone interview from her home in Brooklyn, Ms. Span, 74, discussed how the column’s audience has changed over the years and why she reads every reader comment on her articles. These are edited excerpts from the conversation.What makes for a good column of yours?Something that’s a national trend or a development that’s rooted in fact, science and research and affects people. There is no shortage of such topics when you’re talking about a group as large as elder Americans. There’s something like 60 million people over 65 in the United States. It’s a very heterogeneous group. There are many things that this group is concerned about, like living arrangements; Medicare and other insurance and policy issues; health; end-of-life connections. It’s a big canvas, which makes it enjoyable and continually interesting. When I took the column on, I thought I’d run out of material in a few years. Of course, 15 years later, there’s still so much to talk about.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Collecting wild mushrooms, berries and other foods from public forests and parks has become so popular that state and federal agencies are imposing more restrictions.Beneath a row of fir trees River Shannon Aloia walks along a remote dirt road on national forest land, scanning the ground for morels.“Find it,” she commands her dog, Jasper.The search pays off for Ms. Aloia, an avid forager: She spies a solitary honey-colored morel, and plucks it.“Foraging changes your relationship with nature,” she said. “You are out in the woods using all of your senses. And it’s gratifying when you can identify something and take it home and prepare it for your family.”Spring in the northern hemisphere is a favorite time of year for foragers like Ms. Aloia. It is especially popular in the American West because of the millions of acres of publicly owned lands that give foragers the freedom to roam and harvest to their liking.Once the snow melts, a variety of fungi begin popping their heads above ground — oyster mushrooms, king boletes and several types of morels. A profusion of flowers and other edible and medicinal plants, including wild onions and asparagus, fiddleheads, nettles and miner’s lettuce, are also highly sought.Come summer, the berry crop beckons in the Rocky Mountain West: chokecherries, wild strawberries and plump, purple huckleberries. In late summer and fall, other wild crops emerge, such as piñon or pine nuts in the Southwest and mushrooms like chicken of the woods, shaggy manes and the prized matsutake.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Labour have promised to create 100,000 extra dental appointments for children, in a bid to clear backlogs in England.

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On a typical day, Ali Mullen races from her job at the county health department in Helena, Mont., to pick up dinner for her three children, heads home to feed them and then goes back out for a violin lesson or a school play, crisscrossing the small city in her aging S.U.V., with a rainbow bumper sticker that reads “You Are Loved.”A big pack of gummy bears keeps her going, stashed in her handbag next to a different sort of lifesaver: a gun lock that she carries almost everywhere she goes.In a sparsely populated state where many people own firearms, the small metal contraptions, which fit around a trigger and cost less than $10 on Amazon, are one way Montanans are trying to reduce the high rate of people who kill themselves.For the past year, Ali, 46, has been giving gun locks away to anyone who wants one, her piece of trying to solve the puzzle of suicide in Montana.“It’s in the culture,” she said one afternoon in Helena. “If you don’t know someone, you know of someone who has died.”Murder rates and mass shootings make national headlines, defining the discussion over pervasive gun violence. But most gun deaths in America are self-inflicted. There were about 27,000 gun suicides in 2022. That was a record, and far higher than the 19,500 gun homicides documented that year.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Cambridge scientists have grown ‘mini-guts’ in the lab to help understand Crohn’s disease, showing that ‘switches’ that modify DNA in gut cells play an important role in the disease and how it presents in patients.
The researchers say these mini-guts could in future be used to identify the best treatment for an individual patient, allowing for more precise and personalised treatments.
Crohn’s disease is a form of inflammatory bowel disease (IBD). It is a life-long condition characterised by inflammation of the digestive tract that affects around one in 350 people in the UK, with one in four presenting before the age of 18. Even at its mildest, it can cause symptoms that have a major impact on quality of life including stomach pain, diarrhea, weight loss and fatigue, but it can also lead to extensive surgery, inpatient admissions, exposure to toxic drugs and have a major impact on patient and their families.
While there is some evidence that an individual is at greater risk of developing the condition if a first-degree relative has Crohn’s, there has been only limited success in identifying genetic risk factors. As a result, it’s estimated that only 10% of inheritance is due to variations in our DNA.
Matthias Zilbauer, Professor of Paediatric Gastroenterology at the University of Cambridge and Cambridge University Hospitals NHS Foundation Trust (CUH), said: “The number of cases of Crohn’s disease and IBD are rising dramatically worldwide, particularly amongst younger children, but despite decades of research, no one knows what causes it. Part of the problem is that it’s been difficult to model the disease. We’ve had to rely mainly on studies in mice, but these are limited in what they can tell us about the disease in people.”
In research published today in Gut, Professor Zilbauer and colleagues used cells from inflamed guts, donated by 160 patients, mainly patients and adolescents, at CUH to grow more than 300 mini-guts — known as organoids — in the lab to help them better understand the condition. Samples were donated by patients with Crohn’s disease and ulcerative colitis, as well as by patients unaffected by IBD.
“The organoids that we’ve generated are primarily from children and adolescents,” said Professor Zilbauer. “They’ve essentially given us pieces of their bowel to help with our research. Crohn’s can be a severe condition to have to deal with at any age, but without our volunteers’ bravery and support, we would not be able to make such discoveries as this.”
Organoids are 3D cell cultures that mimic key functions of a particular organ, in this case the epithelium — the lining of the gut. The researchers grew them from specific cells, known as stem cells, taken from the gut. Stem cells live forever in the gut, constantly dividing allowing the gut epithelium to regenerate.

Using these organoids, they showed that the epithelia in the guts of Crohn’s disease patients have different ‘epigenetic’ patterns on their DNA compared to those from healthy controls. Epigenetics is where our DNA is modified by ‘switches’ attached to our DNA that turn genes on and off — or turn their activity up or down — leaving the DNA itself intact, but changing the way a cell functions.
Professor Zilbauer, a researcher at the Stem Cell Institute at the University of Cambridge, said: “What we saw was that not only were the epigenetic changes different in Crohn’s disease, but there was a correlation between these changes and the severity of the disease. Every patient’s disease course is different, and these changes help explain why — not every organoid had the same epigenetic changes.”
The researchers say the organoids could be used to develop and test new treatments, to see how effective they are on the lining of the gut in Crohn’s disease. It also opens up the possibility of tailoring treatments to individual patients.
Co-author Dr Robert Heuschkel, Consultant Paediatric Gastroenterologist at CUH and Lead of the Paediatric IBD Service, said: “At the moment, we have no way of knowing which treatment will work best for a patient. Even those treatments we currently have only work in around half of our patients and become less effective over time. It’s a huge problem.
“In future, you could imagine taking cells from a particular patient, growing their organoid, testing different drugs on the organoid, and saying, ‘OK, this is the drug that works for this person’.”
The research highlighted a specific pathway implicated in Crohn’s, known as major histocompatibility complex (MHC)-I. This pathway allows immune cells to recognise antigens — that is, a toxin or other foreign substance that induces an immune response in the body, and which could include molecules in our food, or our gut microbiota. The team showed that the cells forming the inner lining of the gut in Crohn’s disease patients have an increased activity of MHC-I, which can lead to inflammation in specific parts of the gut.

“This is the first time where anyone has been able to show that stable epigenetic changes can explain what is wrong in the gut epithelium in patients with Crohn’s disease,” said Professor Zilbauer.
The epigenetic modifications were found to be very stable, which may explain why even after treatment, when a patient appears to be healed, their inflammation can return after several months — the drugs are treating the symptoms, not the underlying cause.
Epigenetic changes are programmed into our cells very early on during the development of the baby in the womb. They are influenced by environmental factors, which may include exposure to infections or antibiotics — or even lack of exposure to infection, the so-called ‘hygiene hypothesis’ that says we are not exposed to sufficient microbes for our immune systems to properly develop. The researchers say this may offer one possible explanation for how the epigenetic changes that lead to Crohn’s disease occur in the first place.
The research was largely supported by the Medical Research Council. It was also supported through collaboration with the Milner Therapeutics Institute, University of Cambridge.
Cambridge Enterprise is working with Professor Zilbauer and team and has recently filed a patent for this technology. They are seeking commercial partners to help with the development of this opportunity.

The genetic disease Huntington’s not only affects nerve cells in the brain but also has widespread effects on microscopic blood vessels according to research.
These changes to the vasculature were also observed in the pre-symptomatic stages of the disease, demonstrating the potential for this research for predicting brain health and evaluating the beneficial effects of lifestyle changes or treatments.
Huntington’s disease is an inherited genetic condition leading to dementia, with a progressive decline in a person’s movement, memory, and cognition. There is currently no cure.
The study, published in Brain Communications, is by Juliane Bjerkan, Gemma Lancaster, Peter McClintock and Aneta Stefanovska from Lancaster University, Jan Kobal, Sanja Šešok and Bernard Meglič from the University Medical Centre in Ljubljana, Karol Budohoski from the Cambridge University Hospitals NHS Trust, and Peter Kirkpatrick from Cambridge University.
The team investigated changes in the coordination between neuronal activity and the brain’s oxygenation in Huntington’s disease.
The vasculature and brain work together to ensure that the brain receives sufficient energy. In fact, the brain needs as much as 20% of the body’s energy consumption despite only weighing approximately 2% of the body’s weight.
The “neurovascular unit” consists of vasculature connected via brain cells called astrocytes to neurons and ensures that this cooperation is successful.

To assess the function of these neurovascular units, the researchers combined non-invasive measurement techniques and novel analysis methods developed by Lancaster’s Nonlinear and Biomedical Physics group.
Probes emitting infrared light were placed on the heads of participants in the study. The infrared light penetrated the skull harmlessly and enabled researchers to measure the brain’s blood oxygenation.
Electrodes, which can measure electrical activity from neurons, were also placed on the heads of participants. The researchers then studied the many rhythms related to the functioning of the brain and the cardiovascular system using mathematical techniques. These rhythms included the heart and respiration rates, related to the transport of nutrients and oxygen, as well as slower rhythms associated with local control of blood flow. Brain activity manifests in faster rhythms.
Efficient functioning of the brain depends on how well all these rhythms are orchestrated. To assess the efficiency of the neurovascular unit, both the strength and the coordination of these rhythms were assessed by computing their “power” and “phase coherence.”
Professor Aneta Stefanovska of Lancaster University said: “We are hopeful that the method described could be used to monitor the disease progression and to evaluate the effect of potential treatments or lifestyle changes in Huntington’s disease and other neurodegenerative diseases. We also hope that our study will stimulate new treatments of Huntington’s disease targeting the vasculature and brain metabolism.”

Researchers from Nagoya University Graduate School of Medicine in Japan have successfully treated the skin diseases epidermolytic ichthyosis (EI) and ichthyosis with confetti (IWC) by transplanting genetically healthy skin to inflamed areas. Transplanting healthy skin to inflamed areas has been used as a treatment option for severe burn injuries. They applied this technique from a common disease to rare diseases. Their research could pave the way for a new and effective treatment strategy for these challenging skin disorders. The study was published in the British Journal of Dermatology.
EI and IWC are rare genetic skin disorders caused by mutations in one of the two genes that make keratin in the skin, KRT1 or KRT10. As keratin is important for maintaining skin integrity, these mutations lead to fragile skin that blisters and forms thick, scaly patches.
Some patients suffering from these diseases exhibit large patches of healthy skin in the affected areas. These spots result from revertant somatic recombination, a process where spontaneous genetic changes correct the mutations by altering the genes that cause the skin condition. This causes the affected areas to return to a healthy state.
The group led by Lecturer Kana Tanahashi, Prof. Masashi Akiyama, and Associate Prof. Takuya Takeichi realized that revertant somatic recombination could be used for a pioneering therapy. By making grafts called cultured epidermal autografts (CEAs), which contain genetic mutation corrections that give healthy skin, and grafting these naturally corrected skin cells to affected areas, outbreaks of the disease could be controlled.
They evaluated the feasibility of transplanting CEAs derived using revertant epidermal keratinocytes — those that lack the keratin mutation — back onto patients. CEAs were transplanted to peeling lesions of the patients. Four weeks after transplantation, two of the patients had no ichthyosis recurrence in the entire treated area, while the third did not show recurrence in more than a third (39.52%) of the affected area.
Although it was initially successful, 24 weeks after transplantation, all three patients experienced some recurrence of ichthyosis at the transplant sites. The researchers concluded that the best use of the technique is to alleviate symptoms when the disease is severe and to treat local EI symptoms in specific regions that affect quality of life.
The research marks a significant step forward in the quest to find effective treatments for EI and IWC. By utilizing the natural genetic correction mechanisms of the body, researchers have demonstrated a novel and promising treatment. Their study opens the door to further studies and clinical trials to refine the approach and extend its benefits to more patients, offering hope for those affected by these intractable skin disorders.

15 minutes agoBBC ImagesTV and podcast presenter Michael Mosley was best known for offering tips on simple ways to improve our health and wellbeing, backed up by science – everything from when to exercise and what to eat to how to get more sleep.