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Discovering new, powerful electrolytes is one of the major bottlenecks in designing next-generation batteries for electric vehicles, phones, laptops and grid-scale energy storage.

The most stable electrolytes are not always the most conductive. The most efficient batteries are not always the most stable. And so on.

“The electrodes have to satisfy very different properties at the same time. They always conflict with each other,” said Ritesh Kumar, an Eric and Wendy Schimdt AI in Science Postdoctoral Fellow working in the Amanchukwu Lab at the University of Chicago Pritzker School of Molecular Engineering (UChicago PME).

Individuals with retinal degenerative diseases struggle to restore vision due to the inability to regenerate retinal cells. Unlike cold-blooded vertebrates, mammals lack Müller glia (MG)-mediated retinal regeneration, indicating the limited regenerative capacity of mammalian MG. Here, we identify prospero-related homeobox 1 (Prox1) as a key factor restricting this process. Prox1 accumulates in MG of degenerating human and mouse retinas but not in regenerating zebrafish. In mice, Prox1 in MG originates from neighboring retinal neurons via intercellular transfer. Blocking this transfer enables MG reprogramming into retinal progenitor cells in injured mouse retinas. Moreover, adeno-associated viral delivery of an anti-Prox1 antibody, which sequesters extracellular Prox1, promotes retinal neuron regeneration and delays vision loss in a retinitis pigmentosa model. These findings establish Prox1 as a barrier to MG-mediated regeneration and highlight anti-Prox1 therapy as a promising strategy for restoring retinal regeneration in mammals.


Recovery for mammalian retinal degeneration is limited by a lack of Müller glia (MG)-mediated regeneration. Here authors show blocking Prox1 accumulation and intercellular transfer from retinal neurons enables MG reprogramming of retinal progenitor cells, promotes retinal neuron regeneration, and delays vision loss.

Abundant, low-cost, clean energy—the envisioned result if scientists and engineers can successfully produce a reliable method of generating and sustaining fusion energy—has taken one step closer to reality, as a team of researchers from the University of Texas at Austin, Los Alamos National Laboratory and Type One Energy Group has solved a longstanding problem in the field.

One of the big challenges holding back has been the ability to contain inside fusion reactors. When high-energy alpha particles leak from a reactor, that prevents the plasma from getting hot and dense enough to sustain the fusion reaction. To prevent them from leaking, engineers design elaborate magnetic confinement systems, but there are often holes in the , and a tremendous amount of computational time is required to predict their locations and eliminate them.

In their paper published in Physical Review Letters, the research team describes having discovered a shortcut that can help engineers design leak-proof magnetic confinement systems 10 times as fast as the gold standard method, without sacrificing accuracy. While several other big challenges remain for all magnetic fusion designs, this advance addresses the biggest challenge that’s specific to a type of fusion reactor first proposed in the 1950s, called a stellarator.

Urban rats spread a deadly bacteria as they migrate within cities that can be the source of a potentially life-threatening disease in humans, according to a six-year study by Tufts University researchers and their collaborators that also discovered a novel technique for testing rat kidneys.

Leptospirosis is a disease caused by a type of bacteria often found in rats. It’s spread through their urine into soil, water, or elsewhere in the environment, where it becomes a source of infection and contamination for humans, dogs, and other species. While it’s prevalent worldwide, it’s more common in tropical regions, though a changing climate means it could become more common in colder regions as they warm.

In Boston, leptospirosis persists in local rat populations, and different strains of the bacteria move around the city as groups of rats migrate, according to a new study by Marieke Rosenbaum, M.P.H., D.V.M., assistant professor in the Department of Infectious Disease and Global Health at Cummings School of Veterinary Medicine at Tufts University, along with co-authors at Northern Arizona University (NAU), the United States Department of Agriculture (USDA), and the Centers for Disease Control and Prevention (CDC). In addition, their of a 2018 human leptospirosis case in Boston strongly suggests a link to rats as the source.