Rhino horns made radioactive to foil traffickers in South African project
Under the collaborative project involving the University of the Witwatersrand, nuclear energy officials and conservationists, five rhinos were injected in what the university hopes will be the start of a mass injection of the declining rhino population, which they are calling the Rhisotope Project.
Last year, about 20 rhinos at a sanctuary were injected with isotopes in trials that paved the way for Thursday's launch. The radioactive isotopes even at low levels can be recognised by radiation detectors at airports and borders, leading to the arrest of poachers and traffickers.
Researchers at Witwatersrand's Radiation and Health Physics Unit said tests conducted in the pilot study confirmed that the radioactive material was not harmful to the rhinos.
'We have demonstrated, beyond scientific doubt, that the process is completely safe for the animal and effective in making the horn detectable through international customs nuclear security systems,' said James Larkin, chief scientific officer at the Rhisotope Project.
'Even a single horn with significantly lower levels of radioactivity than what will be used in practice successfully triggered alarms in radiation detectors,' said Larkin.
The tests also found that horns could be detected inside full 40-foot shipping containers, he said.
The International Union for Conservation of Nature estimates that the global rhino population was about 500,000 at the beginning of the 20th century but has now declined to approximately 27,000 because of demand for rhino horns on the hidden market.
South Africa has the largest population of rhinos with an estimated 16,000 but has high levels of poaching and about 500 rhinos are killed for their horns every year.
The university has urged private wildlife park owners and national conservation authorities to have their rhinos injected.
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Telegraph
2 hours ago
- Telegraph
ME is a real illness, genetic study shows
A genetic cause for ME has been found for the first time, proving the illness is real. In a breakthrough that charities said finally provided 'credibility and validity' for sufferers, the University of Edinburgh found eight areas of genetic code that make a diagnosis more likely. The gene activity was seen mainly in the nervous and immune systems, suggesting that people with ME may struggle to clear infections and experience ongoing symptoms of pain, fatigue and illness that other people recover from. Sonya Chowdhury, co-investigator on the study and chief executive of Action for ME, said: 'For years, many people have been maligned and disbelieved, and our findings will change this. 'We know that many people have experienced comments like 'ME's not real'. They've been to doctors and told that it's not a real illness. 'Being able to take this study into the treatment room and to say there are genetic causes that play a part in ME is going to be really significant. It will rebuff that lack of belief and stigma that exists.' ME, or myalgic encephalomyelitis – which is often known as chronic fatigue syndrome – is a long-term illness characterised by extreme fatigue that is not relieved by rest, and may bring malaise after exercise, sleep problems, brain fog and chronic pain. About 1.35 million people in Britain are thought to suffer with some kind of ME-like symptoms, which often occur following an infection such as flu, Covid or Epstein-Barr. But the vagueness of the illness and difficulty finding a trigger has often led patients to be treated with scepticism, even by medical professionals. In the past, the condition was regularly dismissed as 'yuppie flu'. For the new study, researchers analysed the DNA of more than 15,000 people participating in DecodeMe – the world's largest database of people with the disease. They found eight regions of DNA where genetic differences were significantly more common in people with ME/chronic fatigue syndrome than in the general population. As a person's DNA does not change over time, experts say the genetic signals likely reflect the causes of the disease. Prof Chris Ponting, DecodeME investigator from the University of Edinburgh, said: 'What we are looking at is genetic variants which tilt the balance one way or another towards or away from the risk of diagnosis of ME in exactly the same way as (genes) do for diabetes or Parkinson's. 'These genetic signals lie very close to genes which are now well known to be involved in the first response to infection, and so it could very well be for some people that an infection via viruses or bacteria are less well cleared with people with ME. 'People with ME often report an infection before their first onset of symptoms. This occurs with the majority of people with ME, so overall the genetics align with what people have described.' Among the genes involved is RABGAP1L, which limits virus replication and expels bacteria, but is less active in patients with ME. Another is FBXL4, which is crucial for keeping mitochondria – the cell batteries – functioning correctly, but is under-expressed in some people with ME. Researchers say the findings are not yet ready to inform treatment or diagnosis, but offer vital clues to the disease's origins and could guide future drug development. Andy Devereux-Cooke, an ME patient who has worked as a co-investigator on the project, said the findings were important for patients who had felt 'abandoned'. 'This will be huge for the patient population,' he said. 'Even though it does not provide all the answers, it is a welcome drop in the ocean towards turning the tide.' The DecodeME team is now calling on researchers from around the world to use the dataset to develop new studies that could lead to new insights and possible treatments. They were reported in a pre-print on Wednesday and are to be submitted for publication in the coming months.
The Guardian
4 hours ago
- The Guardian
The Origin of Language by Madeleine Beekman review – the surprising history of speech
The story of human evolution has undergone a distinct feminisation in recent decades. Or, rather, an equalisation: a much-needed rebalancing after 150 years during which, we were told, everything was driven by males strutting, brawling and shagging, with females just along for the ride. This reckoning has finally arrived at language. The origins of our species' exceptional communication skills constitutes one of the more nebulous zones of the larger evolutionary narrative, because many of the bits of the human anatomy that allow us to communicate – notably the brain and the vocal tract – are soft and don't fossilise. The linguistic societies of Paris and London even banned talk of evolution around 1870, and the subject only made a timid comeback about a century later. Plenty of theories have been tossed into the evidentiary void since then, mainly by men, but now evolutionary biologist Madeleine Beekman, of the University of Sydney, has turned her female gaze on the problem. Her theory, which she describes as having been hiding in plain sight, is compelling: language evolved in parallel with caring for our 'underbaked' newborns, because looking after a creature as helpless as a human baby on the danger-filled plains of Africa required more than one pair of hands (and feet). It needed a group among whom the tasks of food-gathering, childcare and defence could be divided. A group means social life, which means communication. The evidence to support Beekman's theory isn't entirely lacking, though a lot of it is, necessarily, circumstantial. We know that the compromise that natural selection hit upon to balance the competing anatomical demands of bipedalism and an ever-expanding brain was to have babies come out early – before that brain and its bony casing were fully formed. One of the discoveries of the newly feminised wave of evolutionary science has been that alloparents – individuals other than the biological parents who contribute parenting services – played a critical role in ensuring the survival of those half-cooked human children. Another is that stone age women hunted alongside men. In the past it was assumed that hunting bands were exclusively male, and one theory held that language arose to allow them to cooperate. But childcare was another chore that called for cooperation, probably also between genders, and over years, not just hours or days. Luckily, the reconfiguration of the head and neck required to accommodate the ballooning brain had a side-effect of remoulding the throat, giving our ancestors more precise control over their utterances. With the capacity to generate a large range of sounds came the ability to convey a large range of meanings. To begin with, this was useful for coordinating childcare, but as speech became more sophisticated, alloparents – particularly grandmothers – used it to transmit their accumulated knowledge, thereby nurturing infants who were even better equipped to survive. The result of this positive feedback loop was Homo sapiens, the sole survivor of a once diverse lineage. Alas, Beekman takes a very long time to get to this exciting idea. She spends about half the book laying the groundwork, padding it out with superfluous vignettes as if she is worried the centre won't hold. Once she gets there, she makes some thought-provoking observations. Full-blown language probably emerged about 100,000 years ago, she thinks, but only in our line – not in those of our closest relatives. 'We may have made babies with Neanderthals and Denisovans,' she writes, 'but I don't think we had much to talk about.' And whereas others have argued that language must have predated Homo sapiens, because without it the older species Homo erectus couldn't have crossed the forbidding Wallace Line – the deep-water channel that separates Asia and Australasia – she draws on her deep knowledge of social insects to show that communication as relatively unsophisticated as that of bees or ants could have done the made a persuasive case for the role of alloparents in the evolution of language, Beekman concludes that we did ourselves a disservice when we shrank our basic unit of organisation down from the extended to the nuclear family. Maybe, but historians including Peter Laslett have dated this important shift to the middle ages, long before the Industrial Revolution where she places it, and the damage isn't obvious yet. Language is still being soaked up by young children; it's still a vehicle for intergenerational learning. It may take a village to raise a child, but as Beekman herself hints, a village can be constituted in different ways. Sign up to Inside Saturday The only way to get a look behind the scenes of the Saturday magazine. Sign up to get the inside story from our top writers as well as all the must-read articles and columns, delivered to your inbox every weekend. after newsletter promotion The Origin of Language: How We Learned to Speak and Why by Madeleine Beekman is published by Simon & Schuster (£25). To support the Guardian buy a copy at Delivery charges may apply.
Daily Mail
5 hours ago
- Daily Mail
Virus spread through oral sex linked to soaring skin cancer rates for first time in major study
One of the UK's most common sexually transmitted infections (STI) which can spread via oral sex has been linked to skin cancer for the first time. Human papillomavirus (HPV) is the second most common STI in the UK, after chlamydia, with around four in five people estimated to have HPV at some point in their lives. The virus is already known to raise the risk of six types of cancer, including anal, head and neck, throat and a number of gynaecological cancers such as cervical. But now, US researchers at the National Institutes of Health (NIH) say the virus could also cause a deadly form of skin cancer, known as squamous cell carcinoma. More than 25,000 people in the UK are diagnosed with the disease every year, making it the second most common form of skin cancer. While it is highly survivable in the early stages, when caught late it can spread to other areas of the body where it becomes far more difficult to treat. The scientists discovered the link after a 34-year-old woman was referred to the clinic, presenting with recurrent skin cancer despite multiple surgeries and a round of immunotherapy. Her local GP initially dismissed her symptoms as an inherited condition, believing she was more sensitive to radiation and struggled to repair cells damaged by UV radiation. But analysis at the NIH revealed HPV had incorporated itself into the genes of her cancer cells, which researchers suspected had led them to become more aggressive. Further tests showed that her skin cells could still repair sun damage, suggesting ultraviolet (UV) exposure was not the main driver of her skin cancer. Dr Andrea Lisco, a virologist who led the study, said: 'This discovery could completely change how we think about the development, and consequently the treatment, of [skin cancer] in people who have a health condition that compromises immune function. 'It suggests that there may be more people out there with aggressive forms of [skin cancer] who have underlying immune defect and could benefit from treatments targeting the immune system.' The findings, published in the New England Journal of Medicine last week, are still preliminary and only suggest a potential link between HPV and skin cancer. More research is needed to confirm the findings, and it is not clear at this time what proportion of skin cancer cases may be caused by the virus. The patient was immunocompromised and unable to produce enough healthy T cells, a key part of the immune system, to fight off the virus. Doctors treated her with a stem cell transplant to restore her immune system. Three years later, her skin cancer has not returned, and other HPV-related complications, such as growths on her tongue and skin, have also disappeared. Researchers said she was infected with beta-HPV, a type of HPV that is present on the skin and can be spread through sexual contact. The variant differs from alpha-HPV, which is linked to cancer in the throat, anus and cervix. Researchers found that the virus had embedded itself in the cancer cells' DNA and was driving them to produce viral proteins, triggering mutations that likely fueled the tumors growth. In persistent HPV infections, studies suggest that mutations occur in cells that lead to the development of cancer. The immune system normally clears the infection by itself, with many patients unaware they ever had HPV. But in some cases the infection can cause symptoms, like warts, with doctors treating these using surgery or prescription creams to destroy the growths. Experts have repeatedly urged people to get the HPV vaccine to reduce their risk of HPV cancers. Yet, according to the World Health Organisation (WHO), the UK's HPV vaccine uptake lags shockingly behind other countries — just 56 per cent among girls and 50 per cent for boys. Denmark, by comparison, records a rate of around 80 per cent. Cases of squamous cell carcinoma, however, have spiked in recent years and risen by 200 percent in the last three decades, estimates suggest. This has primarily been linked to more exposure to UV rays from the sun and tanning beds. Warning signs of the cancer include a firm, raised bump or nodule on the skin, or a scaly, red or pink patch or sore that does not heal. Those with long-term sun exposure, fair skin, or who are over 65 years old are most likely to be diagnosed with the disease. Men are also twice as likely to be diagnosed as women. Doctors normally treat the cancer using surgery or chemotherapy, and it has a good survival rate. More than four in five cases are caught in the early stages, where patients have a five-year survival rate of 99 percent. But if the cancer spreads in the body, this drops to 20 percent.
