A 63-year-old man in Norway appears to be cured of HIV after receiving a stem cell transplant from his brother, who turned out to have a rare mutation that makes immune cells resistant to HIV. "Four years after the transplant, and two years after the man stopped antiretroviral therapy, he still appears to be free of the infection," reports Gizmodo. From the report: According to the report, the man was first diagnosed with myelodysplastic syndrome, a type of cancer that weakens blood cell production from bone marrow, in 2018. Though he seemed to initially respond to treatment, the cancer returned after two years, and doctors decided to perform a stem cell transplant. Because the man also had HIV (diagnosed in 2006), the doctors were hoping to treat both conditions at once, though they knew their chances were low. Most of these cases have involved the use of stem cells taken from people with two copies of a particular mutation in their CCR5 gene, which regulates the CC5R receptor on white blood cells. This mutation, named CCR5-delta 32, makes immune cells naturally resistant to infection from strains of HIV-1 (the most common type of the virus). However, only about 1% of the population carries two copies of the mutation. After initial screening failed to find someone who both possessed the mutation and had compatible bone marrow, the doctors decided to move ahead with the man's brother, who was already known to have compatible bone marrow. But to everyone's surprise, testing on the day of the transplant showed that the brother also had the mutation. Though the man did experience some complications from the procedure, his body successfully started to produce new blood cells with the mutation. The doctors decided to take him off antiretroviral medication two years after the transplant. And in the two years since then, regular follow-up tests have failed to show any signs of the virus in his system. [...] According to AFP, there have only been roughly 10 cases worldwide involving an HIV cure through stem cell transplantation. This is the first to involve a family donor.

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Plants, toads, and mushrooms "can all produce psychedelic substances," writes ScienceAlert. "And now their powers have been combined in one plant." [S]cientists have taken the genes these organisms use to make five natural psychedelics and introduced them into a tobacco plant ( Nicotiana benthamiana), which then produced all five compounds simultaneously. As interest grows in psychedelics as potential treatments for illnesses such as depression, anxiety, and PTSD, the newly developed system could offer scientists a new way to produce these compounds for research purposes... [P]rogress in this field remains limited, in part due to regulatory restrictions, underscoring the need for more research. This creates practical challenges for scientists. "Traditionally, the supply of psychedelics relies on natural producers, mainly plants, fungi, and the Sonoran Desert toad," the researchers write. "Harvesting these organisms for their psychoactive compounds raises ecological and ethical concerns, being increasingly threatened by habitat loss and overexploitation..." [T]he team carefully monitored the plant's production of five psychedelic tryptamines: DMT originally from plants; psilocin and psilocybin from mushrooms; and bufotenin and 5-MeO-DMT from toads. The modified tobacco plants were found to produce all five compounds simultaneously. The article points out that the researchers "also took it a step further." By tweaking the enzymes they were able to "produce modified versions of the compounds that do not naturally occur in plants, and which may also have therapeutic value."

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Longtime Slashdot reader fahrbot-bot writes: CU Boulder researchers are reporting that they have discovered an appetite-suppressing compound in python blood that helps the snakes consume enormous meals and go months without eating yet remain metabolically healthy. The findings were published in the journal Natural Metabolism on March 19, 2026. Pythons can grow as big as a telephone pole, swallow an antelope whole, and go months or even years without eating -- all while maintaining a healthy heart and plenty of muscle mass. In the hours after they eat, research has shown, their heart expands 25% and their metabolism speeds up 4,000-fold to help them digest their meal. The team measured blood samples from ball pythons and Burmese pythons, fed once every 28 days, immediately after they ate a meal. In all, they found 208 metabolites that increased significantly after the pythons ate. One molecule, called para-tyramine-O-sulfate (pTOS) soared 1,000-fold. Further studies, done with Baylor University researchers, showed that when they gave high doses of pTOS to obese or lean mice, it acted on the hypothalamus, the appetite center of the brain, prompting weight loss without causing gastrointestinal problems, muscle loss or declines in energy. The study found that pTOS, which is produced by the snake's gut bacteria, is not present in mice naturally. It is present in human urine at low levels and does increase somewhat after a meal. But because most research is done in mice or rats, pTOS has been overlooked. "We've basically discovered an appetite suppressant that works in mice without some of the side-effects that GLP-1 drugs have," said senior author Leslie Leinwand, a distinguished professor of Molecular, Cellular and Developmental Biology who has been studying pythons in her lab for two decades. Drugs like Ozempic and Wegovy act on the hormone glucagon-like petide-1 (GLP-1).

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