Science Square

  • Issue 115 / January-February 2017



    Blind mice have vision restored

    The Fountain

    Blind mice have vision restored


    Zhu et al. Immunosuppression via loss of IL2r╬│ enhances long-term functional integration of hESC-derived photoreceptors in the mouse retina. Cell Stem Cell, January 2017.


     


    Your ability to read these words relies on your retina, the eye’s nerve center. Light passes through the lens and iris and strikes the retina at the back of the eyeball, which consists of light-sensing rods and cones. This process allows you to see these letters. When things go awry in the retina, people experience partial or complete loss of vision; to date, no efficient treatment has been found to stop or reverse blindness. Researchers have been trying to transplant new photoreceptor cells into the retina for the last decade, but the success has been very limited, and the transplanted cells usually did not survive long enough to restore vision. In a recent study, researchers were able to restore vision in completely blind mice by transplanting photoreceptors derived from human stem cells. They demonstrated that the blind mice were able to perceive light as late as 9-months following the transplantation. The key to their success was simultaneously blocking the immune response that causes transplanted cells to be rejected. The researchers determined that the mice which lack the immunodeficient IL2 receptor gamma (IL2rl), a specific immune cell receptor that rejects transplanted foreign cells, experienced longer-term survival of the transplanted cells. These findings give a lot of hope that the same stem cells used to cure blind mice may also be used to treat humans. It is now possible to identify other small molecules or recombinant proteins to reduce interleukin 2 receptor gamma activity in the body, increasing the possibility the body will accept transplanted stem cells.


    The moon may be formed from a group of smaller moonlets


    Rufu et al. A multiple-impact origin for the moon. Nature Geoscience, January 2017.


    The moon’s formation was a unique event, but it remains poorly understood. However it came to be, our moon ÔÇô like all the moons in the solar system ÔÇô has a stabilizing effect on our planet. Scientists have always been puzzled why Earth only has one moon, while other planets have multiple ÔÇô for instance, Saturn and Jupiter have 62 and 67 moons respectively. A new study suggests that the Earth may have had numerous smaller moons at some point, but they crashed together to form our current moon. Earth was born about 4.5 billion years ago, and scientists think the moon began forming a short time later. The leading explanation for the moon’s origin, known as the giant-impact model, suggests that our moon formed when a large protoplanet, Theia, crashed into Earth 4.4 billion years ago, tearing out a moon-sized cloud of debris. But the new study ran 1000 sophisticated simulations modeling this ancient impact and found that instead of one giant collision, the Earth likely experienced many smaller ones. Each of these smaller impacts would have torn away debris that could have coalesced into a moonlet. The current moon was likely formed by the combination of 20 moonlets over the course of 100 million years. While the new model proposes some compelling ideas, it cannot explain how the Earth got its tilted axis, which was also explained by the giant impact model. Experts say more lunar samples through the Chinese Lunar Exploration Program will help us to differentiate between the two models in the near future.


    Food poisoning bacteria eat cancerous tumors


    Mehta et al. Bacterial Carriers for Glioblastoma Therapy. Molecular Therapy ÔÇô Oncolytics. December 2016.


     


    Who doesn’t hate food poisoning? Salmonella is responsible for more than a million cases of food poisoning every year. But a team of researchers found that Salmonella might be our best ally in fighting the most aggressive form of brain cancer known to man, glioblastomas. Glioblastoma is an extremely aggressive form of tumor. Patients diagnosed with it have a mean lifespan of only 15 months. The cancer is protected from conventional drug and radiation-based therapies due to the blood-brain barrier. Surgery is also an imperfect option, because if even a single cancerous cell is left behind, it can spawn new tumors. In a recent study, scientists genetically engineered the bacterium Salmonella typhimurium so that it does not attack the human gastrointestinal tract, but rather the glioblastoma tumors. Specifically, they made the bacteria deficient in the crucial metabolite purine. Since tumors are packed with purine, genetically engineered bacteria were attracted to the tumors like flies to honey. ┬áScientists also integrated two new genes into Salmonella to produce the compounds Azurian and p53, which both cause cells to self-destruct, specifically in low-oxygen environments such as the interior of a tumor, where bacteria are rapidly multiplying. With this method, both the tumorous cells and bacteria eventually die off over time. A major challenge in treating glioblastomas is that the tumors spread with no clear edge, making them difficult to completely surgically remove. So designing bacteria to actively move and seek out these tumors, and to express their anti-tumor proteins only in hypoxic, purine rich tumor regions, has great therapeutic potential. In rats, the treatment basically doubled the survival rate and lifespan of those suffering from glioblastoma. Although success in rodent-based trials does not guarantee the same for humans, the results are nonetheless impressive and promising.

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