ÎçŇą¸ŁŔű1000ĽŻşĎ – latest in science and technology | New Scientist /subject/health/ Science news and science articles from New Scientist Fri, 10 Jul 2026 10:22:02 +0000 en-US hourly 1 https://wordpress.org/?v=7.0.1 242057827 Resuscitated human retinas respond to light 10 hours after death /article/2533673-resuscitated-human-retinas-respond-to-light-10-hours-after-death/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Thu, 09 Jul 2026 15:00:55 +0000 /?post_type=article&p=2533673 2533673 Injection halves risk of chromosome error common in older human eggs /article/2533616-injection-halves-risk-of-chromosome-error-common-in-older-human-eggs/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Thu, 09 Jul 2026 11:00:58 +0000 /?post_type=article&p=2533616 Fluorescence in situ hybridisation (FISH) micrograph of Down's syndrome chromosomes (red) in a foetus' cell nuclei (blue). The FISH technique enables individual chromosomes within the nuclei to be tagged with a fluorescent dye. Here, three copies of chromosome 21 are seen in each nucleus, the cause of Down's syndrome. In a healthy human, each nucleus contains only two copies of chromosome 21. Chromosomes are the parts of a nucleus responsible for carrying the genetic code. Down's syndrome is a genetic disease which causes mental retardation and typically flattened features. It affects around 1 in every 650 babies.
Cells with a signal indicating the presence of too many chromosomes
DEPT. OF CLINICAL CYTOGENETICS, ADDENBROOKES HOSPITAL/SCIENCE PHOTO LIBRARY

Human eggs that contain too many or too few chromosomes can lead to miscarriage, IVF failure and conditions such as Down’s syndrome. Now, researchers have found that giving the eggs a single injection can substantially reduce the problem. The approach could eventually boost the chances of success for older women undergoing IVF.

“It really seems like a big deal,” says at Nilo Frantz Reproductive Medicine in Porto Alegre, Brazil, who wasn’t involved in the new research. “To my knowledge, this is the first [therapy] to show such clinical potential for correcting this major cause of IVF failure.”

During a process called meiosis, egg and sperm cells eject exactly half of their genetic material. This means that when egg and sperm combine during fertilisation, they form an embryo with a complete genome. Sometimes, however, a sperm or egg cell has slightly more or slightly less than the half genome it should contain. This is a condition known as aneuploidy.

Aneuploidy affects about in the early 30s and becomes more common with age. “Already in the late 30s, more than 65 per cent of all eggs are aneuploid,” at Ovo Labs, a biotechnology company in Germany, told the audience at the conference in London on 6 July.

Clinicians sometimes screen IVF embryos for aneuploidy when treating couples at greater risk of miscarriage or IVF failure. , conditions caused by the genetic error – which include Down’s syndrome – are only detected via blood tests and ultrasound scans taken during the first trimester of pregnancy. Until now, there have been no ways to reduce the risk of aneuploidy occurring in the first place, says Zielinska.

Now, Zielinska and her colleagues have found that the level of a protein called shugoshin-1 is substantially lower in older mouse and human eggs than in younger ones. Shugoshin-1 helps with a stage of meiosis in which two copies of each chromosome line up along the middle of an immature egg cell. The protein maintains the molecular glue that holds each pair together.

Upon fertilisation, the two copies of the chromosomes separate and move to opposite sides of the cell. One end ultimately forms the mature egg cell, and the other end is discarded.

But in older eggs, the glue holding the chromosome pairs together degrades, which can cause the two copies of each chromosome to separate before fertilisation. When this happens, the chromosomes spread unevenly throughout the cell – which means the resulting egg may be aneuploid.

To explore whether replenishing shugoshin-1 could prevent aneuploidy by helping to hold chromosome pairs together, the team collected 111 spare, immature eggs from more than 30 women aged between 22 and 43 who were banking eggs or undergoing IVF.

The team injected the genetic code for shugoshin-1, in the form of mRNA, into one or more of each donor’s eggs, and left other eggs from the same donor untreated.

A few hours later, chromosomes had prematurely separated in 53 per cent of the untreated eggs, whereas this figure was nearly half – 29 per cent – in the treated ones. In eggs from nine donors who were aged over 35, aneuploidy rates were 65 per cent, on average, in untreated eggs. But in treated eggs, the average figure was just 44 per cent. This reduction wasn’t statistically significant, although this is probably because of the study’s small sample size, according to the researchers.

Further experiments showed the approach could prevent aneuploidy in mouse eggs, which were then successfully fertilised to produce healthy offspring.

No side effects were seen in the mouse or human studies. “We’ve achieved live births in mice, so, from that perspective, we’re confident that this approach is not interfering in the mouse model with any steps of embryo development, and it doesn’t interfere with pup health and pregnancy health,” Zielinska told the conference audience.

The researchers are now working towards testing the effects of shugoshin-1 in people. This would involve tweaking standard IVF to use immature eggs rather than mature ones, but this change would be fairly easy to implement, says Zielinska.

She hopes the therapy, which the team calls EmbryoProtect, will provide an affordable way to improve IVF for older women. “We anticipate that the treatment will cost a fraction of the cost of a full IVF cycle,” says Zielinska. “By meaningfully improving IVF success rates, especially for women over 35 where baseline success is low, we hope that fewer attempts will be needed to conceive.”

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Our fertility window could be extended by making ovaries softer /article/2533507-our-fertility-window-could-be-extended-by-making-ovaries-softer/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Wed, 08 Jul 2026 16:00:42 +0000 /?post_type=article&p=2533507 2533507 Lambs born via IVF using highly immature eggs in major breakthrough /article/2533441-lambs-born-via-ivf-using-highly-immature-eggs-in-major-breakthrough/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Wed, 08 Jul 2026 10:28:58 +0000 /?post_type=article&p=2533441 2533441 Ovary identity shift after menopause may contribute to inflammation /article/2533022-ovary-identity-shift-after-menopause-may-contribute-to-inflammation/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Tue, 07 Jul 2026 06:00:21 +0000 /?post_type=article&p=2533022
The ovaries may play a bigger role in post-menopause health than we thought
magicmine/Getty Images
We used to think that once ovaries had passed through the menopausal transition, the scarred, shrunken organs sat inert in the body. But the discovery that the ovaries of aged mice become infiltrated with immune cells suggests the organ may be linked to widespread inflammation after menopause. “We assumed the organ had done its job [post-reproduction],” says at Northwestern University in Illinois. “What we found was super surprising.” In March, Duncan and her colleagues published a , which hasn’t yet been peer reviewed, looking at the protein composition of ovaries in post-menopausal women aged 50 to 75. They expected all the ovaries to be fairly similar, but instead Duncan found their “molecular signatures changed quite dramatically over the decades, which told us: this organ is not stagnant, it’s changing over time”. To better understand what happens, Duncan and her team have now studied the ovaries of mice in more detail. They analysed the tissue and gene expression within the ovaries of young (aged 2 months), reproductively old (18 months) and post-reproductive (24 months) mice. Mice don’t have a menstrual cycle like us – their uterus lining is reabsorbed, not shed as a period. They also don’t go through the menopause like we do, but their egg reserves deplete with age and their cycles become irregular. “What we are referring to when we talk about menopause is the age-related decline in fertility and [hormonal] function, and mice absolutely go through that same thing,” says Duncan. Some of the results were expected: the older ovaries lost their egg-producing follicles, for example, and showed more scarring. What’s more, genes involved in reproduction and the creation of hormones like estradiol, a form of oestrogen, were downregulated. But the team also found that genes linked to inflammation and immune activity became increasingly active, and the number of immune cells in the ovaries, including T cells and macrophages, increased with age.
Further research is required to uncover what this may mean for immune – and overall – health, but Duncan suspects this represents an identity change for the ovaries, rather than them becoming “an immune superpower”. “[The ovaries are] losing sort of the reproductive signature and taking on an immune signature, but I don’t think that’s necessarily a good thing.” Ageing tissues undergo “inflammaging”, a state of chronic, low-grade inflammation. Immune cells are heavily involved in this, which makes Duncan suspect that post-reproduction, ovaries contribute by releasing inflammatory signalling molecules. “It is possible [this post-reproductive change] means nothing, but it’s also possible it’s sending out these signals and communicating with other parts of the body,” she says. Duncan stresses the study was only in mice, but at the University of California, San Francisco, suspects similar immune changes occur in humans, given . “Both organisms cease cycling when their supply of oocytes [immature egg cells] dips below a critical threshold, and other changes including fibrosis and increased innervation [nerve distribution] are shared,” she says. It is unclear why ageing mice may have evolved this change in signature, says Duncan, but if the same change applies to humans, it could have been an advantage to acquire an immune cell reservoir when fewer people lived to old age. But this may lead to inflammation and even autoimmune conditions in modern life. The findings raise questions about the importance of the ovaries post-menopause. If healthy, they are generally left in place because they , which help maintain bone mineral density and libido. But Laird says the study adds to growing evidence that that causes issues like rheumatoid arthritis post-menopause. “The findings are a call to carry out detailed and functional studies on the cellular and molecular components of the post-reproductive ovary,” she says.
Journal reference:

Molecular Human Reproduction

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5 things to know about sunscreen, according to a skin cancer expert /article/2532744-5-things-to-know-about-sunscreen-according-to-a-skin-cancer-expert/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Mon, 06 Jul 2026 13:00:27 +0000 /?post_type=article&p=2532744
Sunscreen protects your skin, but just how much do you need?
Shutterstock

When the sun is out, many of us reach for sunscreen, but myths and misinformation have left some people confused about when and how to use it, and how to ensure we still get enough vitamin D. , a skin cancer expert at QIMR Berghofer Medical Research Institute in Australia, has led clinical trials looking at the link between sun exposure and skin cancer, and sunscreen use and vitamin D. She also recently led the development of a new that considers how to balance the risks and benefits of sun exposure. Here, she lists five things that everyone should know about sunscreen.

Sunscreen should be used as a last line of defence

Many people think it’s OK to lie on the beach all day in a tiny bikini as long as they rub sunscreen all over their exposed skin and reapply it every 2 hours. They think sunscreen makes them bulletproof. But even if you apply the best sunscreen perfectly, it still lets some ultraviolet (UV) radiation through. If you’re out in the sun for hours, that gradually adds up to a dose that is big enough to cause skin damage. At that point, it doesn’t matter if you apply more sunscreen; the damage is already done.

People often assume that if they reapply sunscreen every 2 hours, they’re sort of starting the protection again, but that’s not how it works. You also need to protect yourself with a hat, sunglasses, rash shirt or other protective clothing, and stay in the shade in the middle of the day. Sunscreen should be considered a last line of defence for the parts of your skin that you can’t easily cover while you’re outdoors, like your hands and neck.

There is good evidence that sunscreen protects against skin cancer and wrinkles

The largest, longest-running study of sunscreen was conducted in the Australian town of Nambour. In 1992, 1600 people in the town were randomised to apply daily sunscreen or continue with their normal sunscreen use, which tended to be minimal. It found that those who applied the daily sunscreen were years down the track.

The researchers also created moulds of the backs of the study participants’ hands to look at damage to the surface of the skin. Those in the daily sunscreen group had compared with those who didn’t. When they were followed up on in 2014, they also had .

The sunscreen to choose is the one you like wearing

It’s no good having sunscreen that sits in your cupboard and doesn’t end up on your skin because you don’t like the feel of it. If you’re going on a hike and you’re going to be out all day, it’s better to wear sunscreen with a high sun protection factor (SPF) of 50+. But it’s harder to get a high-SPF sunscreen that feels really nice, so if you’ll be popping out for only short periods throughout the day, you can choose an SPF 15 or 30 sunscreen. Tinted sunscreens can offer the same protection as normal sunscreens, but only if you apply them thickly. But because these often make the skin look overly tinted, people tend to apply them too thinly. One option is to first put on a thick layer of normal sunscreen, then apply the tinted sunscreen on top of it.

Chemical sunscreens, meaning those that contain organic ingredients such as octocrylene and avobenzone, work by absorbing UV radiation from the sun and converting it to harmless heat. Inorganic sunscreens, also known as mineral or physical sunscreens, contain zinc oxide or titanium dioxide particles. They are often reported to work by reflecting or scattering UV radiation, but they actually , like chemical sunscreens.

Wearing two layers of sunscreen helps to achieve adequate coverage

You get the SPF listed on the bottle only if you apply 2 milligrams of sunscreen per square centimetre of skin, which is around in an average adult. But it’s really hard to apply this amount of sunscreen in one go. One day, I decided to measure it out exactly, and I couldn’t rub it all on; it was too much. So now, I apply one layer, let it sink in while I brush my teeth and do other things, and then a second layer, so I can apply the full recommended amount.

I was born in Armidale, Australia, in the late 1960s and didn’t wear sunscreen as a child, despite my pale skin. I’ve since had three skin cancers removed, the first of which appeared when I was just 29. So now, I am careful to protect my skin.

If you’re diligent with sunscreen, you might need to take a vitamin D supplement

We recently conducted a trial called the Sun-D Study to see whether applying SPF 50+ sunscreen every day affects people’s vitamin D levels. We randomly assigned 639 people to apply SPF 50+ sunscreen as part of their daily morning routine on days when the UV index was forecast to reach 3 or higher, or to use it at their own discretion. After about a year, a – about 46 per cent compared with 37 per cent in the control group. If you wear sunscreen every day, I would advise taking a vitamin D supplement so that you don’t become deficient, especially in winter. I take one myself – they are cheap, safe and effective.

People with dark-coloured skin are at greater risk of developing a vitamin D deficiency. I recently led the development of a new that looked at how to balance the various risks and benefits of sun exposure. It brought together experts from many Australian universities and medical organisations, and it concluded that people with dark-coloured skin need to put on sunscreen only if they plan to spend more than 2 hours outdoors on days with high UV radiation levels. This is in recognition of the fact that melanoma incidence is 30 times lower in people with dark-coloured skin than in those with light-coloured skin, and that vitamin D deficiency poses a greater risk.

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Beetroot juice is trending – its benefits go beyond the hype /article/2532642-beetroot-juice-is-trending-its-benefits-go-beyond-the-hype/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Mon, 06 Jul 2026 08:00:36 +0000 /?post_type=article&p=2532642 2532642 New Scientist recommends an unsettling deep dive into forensic science /article/2532334-new-scientist-recommends-an-unsettling-deep-dive-into-forensic-science/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Wed, 01 Jul 2026 18:00:00 +0000 http://mg27136023.700 2532334 A type of fibre that stimulates GLP-1 release approved for use in food /article/2532336-a-type-of-fibre-that-stimulates-glp-1-release-approved-for-use-in-food/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Wed, 01 Jul 2026 13:00:56 +0000 /?post_type=article&p=2532336 2532336 I’m the first person whose life was saved by CRISPR base editing /article/2532296-im-the-first-person-whose-life-was-saved-by-crispr-base-editing/?utm_campaign=RSS|NSNS&utm_content=health&utm_medium=RSS&utm_source=NSNS Tue, 30 Jun 2026 12:00:06 +0000 /?post_type=article&p=2532296
Alyssa Tapley received life-saving CRISPR treatment
Alyssa Tapley
When the bone marrow transplant failed to treat my leukaemia, it was like: this is it, there’s nothing else now. The doctors were telling my parents it was a matter of weeks. Not years, not months, but weeks. I’d just turned 13, and I was thinking: “Oh my gosh, this is my last birthday. I’m never gonna grow up and have a family and do all the things that normal people are completely used to, like those normal, everyday things.” But then we heard about the trial and went down to Great Ormond Street Hospital in London. It was like sci-fi. They were like: “Oh, we’re gonna put some CAR Ts in, and they’re gonna multiply and multiply some more, and go around and fight and kill your all your cancer cells.” It all started after Easter in 2021. When I went back to school after the coronavirus lockdown ended, I was really tired. I found it hard to walk home from school; I was falling asleep during breaks and lunches. Eventually, I was too sick to go to school. Really early one morning, my dad noticed my breathing didn’t sound good, and we ended up in A&E. When they put the monitor on me, they started shouting for help. I was in intensive care with double pneumonia for days, and when I woke up, I found out I’d already been put on chemotherapy for leukaemia – that’s when the immune cells in your blood turn cancerous. Mum and Dad say it took the doctors a few days to work out what was wrong. That might be because I had T-cell leukaemia, which is less common than B-cell leukaemia.
Then it all moved really quickly. I had a month of chemo at Leicester Royal Infirmary. It wasn’t working, so I was put on more intense chemo, but that didn’t work either. So at the end of October, I went to Sheffield Children’s Hospital for a bone marrow transplant. The idea is, you kill off the blood stem cells, including the cancerous ones, and then you replace them with the transplant. I was there for five and a half weeks, and I was like, I’m not spending Christmas in hospital, no. And I did get home for Christmas, but afterwards I got a fever and had to go back to Sheffield. That’s when we found out that the transplant hadn’t worked. There was nothing else the doctors could do. For me, I don’t think it really sunk in at the time. But for Mum and Dad, it was hard. Mum says nothing was harder than not having hope. She and Dad started looking everywhere, trying to find out if there was anything at all that could work, if we could go to other countries. They were looking at remortgaging the house and things. And they kept on hearing about CAR Ts – that’s when you change T-cells so they kill cancerous cells – and how they can work when bone marrow transplants fail. But they soon realised it only works for B-cell leukaemia, because if you make T-cells attack T-cells, they just kill each other. Then my consultant from Sheffield heard about a trial Professor was organising. He was using CRISPR base editing to change the CAR T-cells so they don’t look like T cells anymore and so don’t kill each other. And my consultant was like, my patient might be a really good fit. That’s when we went down to Great Ormond Street to meet Professor Waseem and Doctor , who ran the trial. Mum and Dad weren’t sure about me doing the trial. They were worried it wouldn’t work and I’d spent my last weeks in hospital in pain, when we could do stuff like going to Disneyland instead. But they let me make the decision. I was like, I’m doing it. If it’s not gonna help me, it’s gonna help someone else. I was 13 then, I hadn’t really had a chance to do anything, I wasn’t leaving behind anything, I’d had no impact. So it was a way for me to take control of something that I hadn’t been in control of for such a long time, and to try to make a difference for someone else, even if it didn’t work for me. I had two weeks of conditioning in hospital before I had the CAR T-cells. We had some camera crews film it; it was really amazing. A week later, Dr Chiesa told us they’d multiplied. It was the first sign it was working. Everybody at Great Ormond Street was so great. I made a friend even though we didn’t meet each other for two months, we just texted, and got the nurses and the play specialists to put stuff on each other’s windows. And I had another friend who was next door to me, but unfortunately she wasn’t able to have a bone marrow transplant, so she passed away. After four weeks, they tested my bone marrow, and there was nothing there. There were no blood cells to detect. Two weeks later, there was still nothing there, so we went ahead and did my second bone marrow transplant, to replace the blood stem cells. The hardest part was going home. In the hospital, there was almost always someone around that you could talk to. But then when I went home, I wasn’t allowed out of the house in case I caught something, and I wasn’t allowed to see any of my friends. Mum started going back to work, so it was just me and my dog Holly for almost a year. I’m still in remission, but not everything is resolved. My thyroid is underactive, but that’s because of all the chemo, not because of the CAR Ts. This is why it’s so important to keep pushing it, so maybe someday people won’t have to have this intensive chemo and can go straight on to have CAR Ts. I turned 17 in January. I’m doing my A-levels and learning to drive now, which is a bit scary. I want to get a degree apprenticeship in biomedical science. If I can do half as much for someone as the treatment did for me, it would be amazing. I also get to go to conferences to talk about my experience. At one of them, we met Professor David Liu, who developed base editing. I actually cried when I met him. The video’s quite embarrassing. I’m so pleased and privileged to have the opportunity to go and do these things, and talk about why science is so important, and why research is so important. Without it, I wouldn’t be here. As told to Michael Le Page ]]>
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