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UCLA scientists have developed a new method to engineer more powerful immune cells that can potentially be used for “off-the-shelf” cell therapy to treat challenging cancers.
“Off-the-shelf” cell therapy, also known as allogenic therapy, uses immune cells derived from healthy donors instead of patients. The approach can bring cell therapies, like chimeric antigen receptor (CAR) T cell therapy, to more patients in a timelier manner, which is one of the major barriers in getting these life-saving treatments to patients.
“Time is often of the essence when it comes to treating people with advanced cancers,” said Lili Yang, associate professor of microbiology, immunology and molecular genetics and member of the UCLA Health Jonsson Comprehensive Cancer Center. “Currently, these types of therapies need to be tailored to the individual patient. We have to extract white blood cells from a patient, genetically engineer the cells and then re-infuse them back into the patient. This process can take weeks to months and can cost hundreds of thousands of dollars to treat each patient.”
This new approach, described in Nature Communications, is a crucial step toward developing more effective cell therapies that have a lower cost and wait that can be mass-produced and shipped to hospitals around the world, making CAR-T cell therapy more affordable and accessible to a broader range of patients.
For the study, Yang and her team focused on gamma delta T cells, an immune cell known for its ability to target a wide array of cancers — including solid tumors — without causing graft-versus-host disease, a common complication in allogeneic cell therapies.
While gamma delta T cell-based treatments have been studied before, they have had limited clinical success due to donor variability, short-lived persistence and cancer cells’ ability to escape or avoid the body’s immune response.
However, Yang and her team found that donor gamma delta T cells with high expressions of a CD16 surface marker had a greater ability to kill cancer cells.

Results from a new clinical trial suggest that a group of brain regions known as the “salience network” is activated after a drug is taken intravenously, but not when that same drug is taken orally. When drugs enter the brain quickly, such as through injection or smoking, they are more addictive than when they enter the brain more slowly, such as when they are taken orally. However, the brain circuits underlying these differences are not well understood. This study offers new information that helps explain what may be causing this difference.
The study was published in Nature Communications and led by researchers at the National Institute on Drug Abuse (NIDA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA), parts of the National Institutes of Health, at the NIH Clinical Center.
“We’ve known for a long time that the faster a drug enters the brain, the more addictive it is — but we haven’t known exactly why. Now, using one of the newest and most sophisticated imaging technologies, we have some insight,” said Nora Volkow, MD, NIDA Director, chief of the NIAAA Laboratory of Neuroimaging, and senior author on the study. “Understanding the brain mechanisms that underlie addiction is crucial for informing prevention interventions, developing new therapies for substance use disorders, and addressing the overdose crisis.”
People who smoke or inject drugs — two methods that deliver drugs to the brain quickly — often report doing so to get faster relief from withdrawal or to experience euphoria more quickly. However, drug smoking and injection are associated with developing a substance use disorder more quickly than taking drugs orally or by insufflation (e.g., snorting). In addition, injecting drugs is also associated with higher rates of infectious diseases and overdose. To better understand how route of drug administration impacts the brain’s response to the drug, researchers conducted a double-blind, randomized, counterbalanced clinical trial using simultaneous PET/fMRI imaging.
Twenty healthy adults participated in the trial. Over three separate sessions, participants received either a small dose of a placebo or of the stimulant drug methylphenidate, commonly known as Ritalin, orally or intravenously. Methylphenidate is a safe and effective prescription medication used for the treatment of attention deficit hyperactivity disorder (ADHD). For research purposes, methylphenidate can be a useful model drug to safely study the relationship between how drugs affect the brain and the subjective experience of drug reward.
After participants received the study drug or placebo, researchers then simultaneously looked at differences in dopamine levels (through PET imaging) and brain activity (through fMRI imaging) while people reported their subjective experience of euphoria in response to the drug.
The PET scan gave an estimate of how fast dopamine increased in the brain in response to the different drug administrations. Consistent with previous research, this study showed that when participants received methylphenidate orally, the rate of dopamine increases peaked more than an hour after administration. Comparatively, when participants received an intravenous injection of methylphenidate, the rate of dopamine increases peaked much faster — within 5 to 10 minutes of the administration.

Malaria is caused by a parasite which is spread by the bite of blood-sucking mosquitoes. According to the WHO, there were an estimated 247 million cases of malaria worldwide in 2021 with over 600,000 deaths, mostly in Africa.  Children under 5 accounted for about 80% of all malaria deaths in the region. mosquitoes. According to the WHO, there were an estimated 247 million cases of malaria worldwide in 2021 with over 600,000 deaths, mostly in Africa.  Children under 5 accounted for about 80% of all malaria deaths in the region.
Following its first detection in Djibouti in 2012, the Asian malaria mosquito Anopheles stephensi spread to the Horn of Africa (Ethiopia, Sudan, Somalia, and Eritrea) and beyond (Yemen, Nigeria, Kenya, and Ghana) at a speed unknown before for similar species.
People in households/dormitories with An. stephensi positivity had a 270% higher risk of malaria infection than those in households/dormitories where An. stephensi was not detected.
In addition, two other biological threats for the control of malaria were identified: drug resistance and diagnostic resistance of the parasite.Dr Luigi Sedda from the Lancaster Ecology and Epidemiology Group at Lancaster University Medical School is a joint first author on the paper which is published in Nature Medicine.He said: “‘This is a very important finding. The mosquito that has spread in the Horn of Africa from Asia drove a major urban malaria outbreak in Ethiopia. An. stephensi is posing important public health concerns due to the increase in geographical presence, the capacity to persist throughout the year and to resist current insecticides, and to transmit drug and diagnostic resistant parasites.”The capacity of Anopheles stephensi to use manmade water storage containers which are abundant in rapidly expanding African urban settings, coupled with its unique ecology, behavioural plasticity and resistance to major insecticides, makes it unamenable to conventional mosquito control tools.
This latest evidence can change the prospects of malaria control and elimination in the face of any future intervention that ignores the presence of this invasive species.
Dr Sedda concluded: “The epidemiological characteristics of An. stephensi driven malaria can challenge the expectations for the new malaria vaccines to reduce the burden of malaria disease and deaths in Africa, the continent that was already highly hit by malaria and where successes in malaria reduction are currently stalled.”
The study was led by the Armauer Hansen Research Institute in Ethiopia with the collaboration of Lancaster University (UK), the Adama Science and Technology University (Ethiopia); University of California, San Francisco (USA); The London School of Hygiene and Tropical Medicine (UK); Radboudumc University Medical Center (The Netherlands); U.S. President’s Malaria Initiative (USA) and the Federal Ministry of Health (Ethiopia).

General anesthesia evokes a dual mystery: How does it disrupt consciousness, including sensory perception, and what might that say about the nature of consciousness. A new study led by researchers at The Picower Institute for Learning and Memory at MIT provides evidence in animals that consciousness depends on properly synchronized communication across the brain’s cortex and that the anesthetic drug propofol cancels sensory processing by cutting it off.
In the Journal of Cognitive Neuroscience, researchers report clear evidence that in anesthetized animals, sounds and tactile sensations still produced neural activity in an area of the cortex that receives incoming sensory information. But just as clearly, measurements of neural spiking and broader oscillatory activity showed that those signals failed to propagate to three other cortical regions with higher-level processing and cognitive responsibilities, as seen during normal wakefulness.
“What this study shows is that the cortex isn’t getting on the same page,” said study corresponding author Earl K. Miller, Picower Professor in the Department of Brain and Cognitive Sciences at MIT. “Information is making it to the cortex. It’s being registered in primary sensory areas. It’s just not reaching the rest of the cortex. Because of the anesthesia, it only makes it part of the way through.”
The significance of that, said co-senior author Emery N. Brown, Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience, is that “the study suggests that consciousness requires coordination of activities among cortical regions. Simply activating one or more of these regions is not sufficient.”
Study lead author John Tauber, who recently earned his Ph.D. at MIT in Brown’s lab, said the study could aid efforts to improve anesthesiology care. Brown is an anesthesiologist at Massachusetts General Hospital as well as an MIT professor of Brain and Cognitive Sciences, a member of the Institute for Medical Engineering and Science, and a faculty member of Harvard Medical School.
“We hope our paper further highlights the importance of actively monitoring what is happening in the brain during anesthesia,” Tauber said. “Future studies in this direction will help us develop clear indicators of whether a patient is still processing sensory information. This would allow anesthesiologists to adjust drug dosage and prevent intraoperative awareness from occurring.”
Stymied sensory processing
To conduct the study the team worked with two animal subjects to measure brain activity — both the electrical “spiking” of individual neurons and their collective rhythmic activity — via electrode arrays placed in four areas of the cortex both before and after they underwent propofol general anesthesia. The researchers selected the areas of the cortex to represent its hierarchical continuum of functions from initial sensation (the superior temporal gyrus, or STG) to increasingly high levels of cognition (the posterior parietal cortex, or PPC; Region 8A; and the prefrontal cortex, or PFC).

Using birth control pills and other hormone-based contraceptives is known to elevate the risk of blood clots about three-fold, but a new study suggests that this risk largely goes away within two to four weeks after one stops using these contraceptives, according to research published today in Blood.
The findings — the first to provide such confirmatory guidance on the best timing to stop contraception — can help patients and doctors weigh the benefits and risks of hormonal contraceptives and guide when to stop using them ahead of events that could further increase the risk of dangerous clots, such as major surgery, prolonged periods of immobility, or when tapering anticoagulant medications after a blood clot (deep vein thrombosis or pulmonary embolism). Based on the findings, researchers say stopping contraceptives two to four weeks ahead of time should be sufficient in most cases.
Combined hormonal contraceptives have long been known to increase the risk of blood clots, affecting roughly 10 in 10,000 individuals on estrogen-containing birth control, according to the Centers for Disease Control and Prevention. What has been less clear is how long this effect lingers once a person stops using contraceptives. Several medical guidelines recommend stopping hormonal contraceptives ahead of certain medical events, such as major surgery, but most do not specify how long someone should be off birth control beforehand.
“Our goal was not to look at the thrombotic risk of contraceptives, but to determine how long that risk takes to normalize after stopping contraceptives,” Marc Blondon, MD, an expert in vascular medicine at the University Hospitals of Geneva, Switzerland, and the study’s corresponding author. “It’s reassuring to know that that possible harm of the pill goes away rapidly when one stops taking it.”
The study focused on birth control methods known as combined hormonal contraceptives, which include birth control pills, vaginal rings, and transcutaneous patches. These methods prevent pregnancy by releasing estrogen and progestin to stop ovulation and are the most common contraceptives in Europe and North America.
For the study, researchers collected blood samples from 66 women on hormone-based birth control at six timepoints before and after the women stopped using their contraceptives. Participants voluntarily stopped using hormonal contraceptives for personal reasons. Dr. Blondon and team then compared the samples with blood from a control group of 28 women who were not using hormone-based birth control.
The researchers measured several biomarkers that are associated with combined hormonal contraceptives and clotting activity. These include global markers of coagulation activation due to hormones and individual coagulation factors (factor VIII and factors that inhibit clotting).

The most effective way to prevent cervical cancer is to give HPV vaccines to both boys and girls, reports a collaborative study involving researchers from Karolinska Institutet published in Cell, Host and Microbe. Beside personal immunity, such use of the vaccine also induces a herd immunity that will help to eradicate the carcinogenic virus types more quickly.
The human papillomavirus (HPV) comprises over 200 virus types. A viral infection usually clears up on its own, but some HPV types can eventually, after many years, give rise to different kinds of cancer, of which cervical cancer is the most common.
The HPV vaccine has been around since 2006. Initially, it was given exclusively to girls around the age of 12, but since August 2020, the HPV vaccine has been offered to both boys and girls in the year-five general vaccination programme.
The researchers behind the present study have looked at how the composition of HPV types changes over time in post-vaccination populations. This they studied in 33 different towns in Finland, which were randomly assigned to vaccinate boys and girls, to vaccinate girls only or to offer no vaccination at all.
The study included children born between 1992 and 1994 who were followed up at the age of 18 ( over 11,000 individuals) and 22 (over 5,500 individuals), representing four and eight years after vaccination. The vaccine used then protected against HPV types 16 and 18, which cause 70 per cent of all HPV-related cervical cancers, but also transpired to provide cross-protection against types 31 and 45. The vaccine coverage rate was up to 50 per cent.
“The fact that the HPV vaccine study randomised the communities to different treatment programmes is what enabled us to study the effects of vaccination,” says the study’s first author Ville Pimenoff, docent of evolutionary medicine at the Department of Clinical Science, Intervention and Technology, Karolinska Institutet.
The results show that eight years after vaccination, the prevalence of HPV types 16 and 18 declined significantly in the 22 towns in which the vaccine was provided. In the eleven towns that only vaccinated girls, there was a decrease in HPV 31, while in the eleven towns that vaccinated girls and boys, there was a clear decline in both HPV 31 and 45.

A new antifungal molecule, devised by tweaking the structure of prominent antifungal drug Amphotericin B, has the potential to harness the drug’s power against fungal infections while doing away with its toxicity, researchers at the University of Illinois Urbana-Champaign and collaborators at the University of Wisconsin-Madison report in the journal Nature.
Amphotericin B, a naturally occurring small molecule produced by bacteria, is a drug used as a last resort to treat fungal infections. While AmB excels at killing fungi, it is reserved as a last line of defense because it also is toxic to the human patient — particularly the kidneys.
“Fungal infections are a public health crisis that is only getting worse. And they have the potential, unfortunately, of breaking out and having an exponential impact, kind of like COVID-19 did. So let’s take one of the powerful tools that nature developed to combat fungi and turn it into a powerful ally,” said research leader Dr. Martin D. Burke, an Illinois professor of chemistry, a professor in the Carle Illinois College of Medicine and also a medical doctor.
“This work is a demonstration that, by going deep into the fundamental science, you can take a billion-year head start from nature and turn it into something that hopefully is going to have a big impact on human health,” Burke said.
Burke’s group has spent years exploring AmB in hopes of making a derivative that can kill fungi without harm to humans. In previous studies, they developed and leveraged a building block-based approach to molecular synthesis and teamed up with a group specializing in molecular imaging tools called solid-state nuclear magnetic resonance, led by professor Chad Rienstra at the University of Wisconsin-Madison. Together, the teams uncovered the mechanism of the drug: AmB kills fungi by acting like a sponge to extract ergosterol from fungal cells.
In the new work, Burke’s group worked again with Rienstra’s group to find that AmB similarly kills human kidney cells by extracting cholesterol, the most common sterol in people. The researchers also resolved the atomic-level structure of AmB sponges when bound to both ergosterol and to cholesterol.
“The atomic resolution models were really the key to zoom in and identify these very subtle differences in binding interactions between AmB and each of these sterols,” said Illinois graduate student Corinne Soutar, a co-first author of the paper.

If a delivery person leaves a package on your front step without pinging you, you likely won’t know it’s there. A hungry cell awaiting refuel is in a similar position. It has to be alerted to the presence of nutrients outside of the cell wall by a sensing mechanism so that a transporter protein can bring the nourishment inside.
The handful of these nutrient-sensing mechanisms thus far identified have had a profound impact on human health. One prime example is the discovery of the nutrient sensing mechanism for cholesterol, which led to the development of life-saving statin drugs (and the Nobel Prize).
These discoveries have focused on how an entire cell detects nutrients. But within every human cell are self-contained, membrane-bound organelles, all of which are equally in need of fuel to carry out important functions. Might they, then, have nutrient sensors of their own?
As described in a new paper published in Science, Kıvanç Birsoy and his colleagues in Rockefeller’s Laboratory of Metabolic Regulation and Genetics have discovered the first such sensor for an organelle — specifically mitochondria, the cell’s power center. The sensor is part of a protein that does triple duty: it senses, regulates, and delivers the antioxidant glutathione into the mitochondrial interior, where it plays critical roles in tamping down oxidizing reactions and maintaining appropriate iron levels.
“I believe this is going to be a very fruitful find,” says Birsoy. “Every time people have studied nutrient sensing, we’ve learned a lot about biology, and many drugs have been developed as a result.”
Antioxidant power
Glutathione is an antioxidant produced throughout the body that plays many important roles, including neutralizing unstable oxygen molecules called free radicals, which cause damage to DNA and cells if left unchecked. It also helps repair cellular damage and regulates cell proliferation, and its loss is associated with aging, neurodegeneration, and cancer. As a result, glutathione supplements have become increasingly popular as an over-the-counter approach to wellness.

Published19 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, PA MediaThe government has made possession of nitrous oxide, or laughing gas, a criminal offence in England and Wales. Its use soared during the pandemic, becoming one of the most-abused substances, especially by 16 to 24-year-olds.The ban was designed to tackle anti-social behaviour. What is nitrous oxide and what is it used for?Nitrous oxide is a colourless gas that is inhaled and is commonly used as a painkiller in medicine and dentistry. When mixed with oxygen, it is known as “gas and air”, which can help reduce pain during childbirth.It is also used in catering, for example, in the production of whipped cream. Many recreational users bought the gas in small metal canisters, released it into a balloon and then inhaled the contents.What does nitrous oxide do to the body?The gas can make people feel relaxed, light-headed or dizzy.It can also cause headaches and make some users anxious; too much can cause fainting.Heavy use can lead to a vitamin B12 deficiency which can damage nerves in the spinal cord, according to a government report.The most common early symptoms of neurological damage are a tingling sensation and numbness in the hands or feet.Other symptoms highlighted in the report include stiff muscles, weak limbs, bladder or bowel complaints and sexual dysfunction. How dangerous is nitrous oxide?In its 2023 review, the Advisory Council on the Misuse of Drugs concluded the overall harms of the gas were insufficient to merit control.Between 2001 and 2020, there were 56 deaths in England and Wales where nitrous oxide was mentioned on the death certificate. However, that figure includes deaths in medical settings, so not all were due to misuse. Deaths typically occur due to secondary effects of using the gas, most commonly suffocation when the gas was used in confined spaces, for example in a car, or with a plastic bag over the head.”Evidence suggests there is around one death per year in the UK from around one million nitrous oxide users,” said Prof David Nutt, from Imperial College London. “[In comparison] around 28,000 deaths happen per year in around 40 million users of alcohol,” he added.What punishments will recreational users face after the ban?Nitrous oxide was previously controlled under the Psychoactive Substances Act 2016 – which meant production, sale or importation was illegal if the intent was to use it for its psychoactive effects.A retailer found to have recklessly sold nitrous oxide faced six months in prison or an unlimited fine. There were 152 convictions in 2017, 107 in 2018 and 52 in 2019.But no regulations covered individual possession.Nitrous oxide is now a Class C drug under the Misuse of Drugs Act 1971, making possession and sale for recreational purposes a criminal offence. That is the same classification as anabolic steroids and some tranquilisers.Those caught with nitrous oxide for unlawful use face a caution, community service or an unlimited fine. Repeat offenders could serve up to two years in prison. The maximum sentence for production or supply of the drug for unlawful purposes is 14 years.Some health experts warn that criminalising the substance may stop users seeking medical help. Laughing gas ban will not stop use, experts warnDoes the ban mean nitrous oxide will no longer be available?Medical use is unaffected, and you will still be able to buy nitrous oxide as a propellant gas for whipped cream and other industrial purposes. However, individual users will need to demonstrate they are lawfully in possession of the substance, and do not intend to use it for psychoactive effects.The government says “reckless” producers and suppliers who do not thoroughly check the purpose of any sale will be breaking the law: “Turning a blind eye will be committing an offence.”What is the legal position in Scotland and Northern Ireland?Drugs policy is a so-called “reserved matter”, so the ban will extend to Scotland and Northern Ireland. However, policing is devolved. When MPs in Westminster voted through the new legislation in September 2023, SNP MPs voted against the ban, describing drug use as “a public health issue” rather than a criminal matter. The Home Office says it is up to Scottish police to decide how to enforce the ban.Is nitrous oxide harmful to the environment?Nitrous oxide is emitted by natural sources such as oceans and soils. This is roughly balanced by natural processes that remove it from the atmosphere.However, human activities – mainly agriculture but also processes such as burning fossil fuels – have disturbed this balance. The excess nitrous oxide in the atmosphere contributes to rising global temperatures because it is a greenhouse gas, like carbon dioxide and methane. Nitrous oxide also damages the the ozone layer, which helps protect life on Earth from harmful radiation from the sun.Globally, levels of nitrous oxide have risen by nearly a quarter since 1750, but the emissions from medical, industrial and recreational use account for a tiny part of this. As a result, the ban on recreational use is likely to make little or no difference.A really simple guide to climate change What does net zero mean?

Published1 day agoShareclose panelShare pageCopy linkAbout sharingBy Ruth GreenBBC NewsLack of access to dentists is costing lives because mouth cancers are not being spotted or treated early enough, a health charity has told BBC News.The disease killed more than 3,000 people in 2021 – up 46%, from 2,075 a decade ago, latest figures obtained by the Oral Health Foundation show.And last year, a BBC News investigation revealed 90% of UK NHS dental practices were not accepting new adult patients. The government has announced plans to increase dental-training places by 40%.It also said the NHS was treating more people for cancer at an earlier stage than ever before. Aggressive tumourRay Glendenning, 64, thought a very painful swelling in his jaw was being caused by one of his teeth – but he did not have an NHS dentist.When he began to find it difficult to open his mouth, he tried to find one and book an emergency appointment.”I must have tried for a week, phoning two or three dentists a day,” he says.”There was an NHS dentist taking on NHS patients – but there were 800 people on the waiting list, so basically waiting for people to die to take new patients on.”When Ray, from County Durham, finally paid £50 to see a private dentist, he was diagnosed with an aggressive tumour. He is convinced the decision saved his life.”The options were surgery or six months of palliative care,” he says. “The options aren’t options really – I didn’t want to die.” Six months ago, just weeks after being diagnosed, Ray had 16 hours of surgery to remove the tumour and a new jaw was formed out of bone and muscle from his leg.He spent six weeks recovering in hospital before starting weekly radiotherapy sessions. He remains limited to a liquid diet and needs a walking stick.”It’s the system that’s broken – not the individual dentists,” Ray says. “We’re lucky we could afford to pay. People that don’t have £50 could be dead.”Oral Health Foundation chief executive Nigel Carter says dental check-ups “are a key place for identifying the early stage of mouth cancer”. “With access to NHS dentistry in tatters, we fear that many people with mouth cancer will not receive a timely diagnosis,” he adds.There were 9,860 cases of mouth cancer in the UK in 2020/21 – up 12% on the previous comparable year, according to the Oral Health Foundation.The independent charity used a Freedom of Information request to obtain the data from:the Office for National StatisticsPublic Health WalesPublic Health Scotlandthe Northern Ireland Cancer RegistryImage source, Ray GlendenningEarly detection results in a roughly 90% survival rate, compared with 50% following delayed diagnosis.”Every dental check-up doubles as an oral-cancer screening,” Eddie Crouch, who chairs the British Dental Association, says. And the crisis millions of people face accessing dentists “will inevitably cost lives”.”This condition causes more deaths than car accidents [cause],” he adds.Head and neck cancers are the eighth most common cancer in the UK.In England, more than two-thirds of mouth cancers are in men.Most cases are linked to smoking – but alcohol misuse and human papillomavirus (HPV) infection through oral sex have been linked to the rise.About a third are on the tongue – but they can also be on the lips, gums and parts of the throat. Symptoms can include:a mouth ulcer lasting more than three weeksa red or white patch inside the moutha lump in the mouth, lips, neck or throat pain inside the mouth difficulty swallowing or speaking or a hoarse or croaky voice Sinead Marland was 39 when she noticed a lump on her tongue that was a bit uncomfortable.Her GP said it was an ulcer, gave her some cream and told her not to worry – but two months later, she had a very different reaction from her NHS dentist, who gave her an urgent referral for a biopsy, which revealed she had tongue cancer.”I had never heard of mouth cancer, so it was quite upsetting and just a bit of a shock,” Sinead says. She had smoked 15 cigarettes a day for about 20 years.During 10 hours of surgery, half of Sinead’s tongue was replaced with part of her forearm and its blood vessels. A second emergency operation removed even more of her tongue.The neck scarring from the operation is the worst, she says.”It’s very visual. It really knocked my confidence,” Sinead says.”If I went out, I would cover up my neck with a scarf and wear long sleeves to hide the skin grafts.”Over the following months, Sinead had to relearn how to speak and eat – but she feels lucky she had a dentist who spotted the early signs of cancer.”If he hadn’t spotted it, I never would have gone back,” Sinead says.”I wouldn’t have been diagnosed. I wouldn’t be here.” How to lower the risk of mouth cancerEat a healthy diet, including five portions of fruit and vegetables a dayExercise regularlyAvoid drinking more than 14 units of alcohol a weekQuit smoking and chewing tobacco, betel nut or paanGet a vaccine to protect against HPVSource: NHS.UK websiteThe Department of Health and Social Care said progress was being made to boost NHS dental services.It said 1.7 million more adults received NHS dental care between June 2021 and June 2023 compared to between June 2020 and June 2022. “The NHS is also treating more people for cancer at an earlier stage than ever before and we have opened 127 community diagnostic centres to speed up checks, including for cancer,” an official said. Additional reporting by Lucy Gilder.​​Have you been affected by the issues raised in this story? Share your experiences by emailing haveyoursay@bbc.co.uk.Please include a contact number if you are willing to speak to a BBC journalist. You can also get in touch in the following ways:WhatsApp: +44 7756 165803Tweet: @BBC_HaveYourSayUpload pictures or videoPlease read our terms & conditions and privacy policy

If you are reading this page and can’t see the form you will need to visit the mobile version of the BBC website to submit your question or comment or you can email us at HaveYourSay@bbc.co.uk. Please include your name, age and location with any submission. More on this storyDriving hundreds of miles for dentist ‘unacceptable’Published14 JulyFull extent of NHS dentistry shortage revealedPublished8 August 2022’I pulled out 11 teeth as no dentist was available’Published4 October 2021’I nearly quit dentistry because of NHS work’Published30 May