A new device could allow computer processors to operate significantly faster, without generating waste heat.
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Alzheimer’s disease is a neurodegenerative disease characterized by a progressive decline in mental functions and memory loss. Along with frontotemporal dementia and some other neurodegenerative disorders, Alzheimer’s disease has been associated with an accumulation inside neurons of abnormal clumps of a protein called “tau.”
The tau protein is important for brain health, stabilizing structures called microtubules inside neurons. In Alzheimer’s disease and other tauopathies (i.e., diseases linked with the abnormal accumulation of tau), tau proteins aggregate into toxic and insoluble clumps that are harmful to brain cells, gradually leading to their death.
Researchers at Zhejiang University, Xiamen University and other institutes in China recently carried out a study aimed at better understanding the processes via which tau aggregation contributes to the death of neurons in patients with Alzheimer’s disease. Their findings, published in Nature Neuroscience, suggest that these tau clumps prompt the reactivation of transposable DNA elements in neurons, which can in turn lead to their death.
Nine years after wowing the audience at the American Society of Clinical Oncology annual meeting with a CAR-T candidate that would become Carvykti—now the world’s most successful cell therapy—Legend Biotech’s scientific founder, Frank Fan, M.D., Ph.D., is returning to the spotlight with an entirely new playbook.
This time, Fan isn’t showcasing an autologous product engineered with each individual patient’s cells. Instead, with his new venture, Wondercel Therapeutics, Fan hopes an off-the-shelf universal CAR-T platform can tackle two bottlenecks of the cell therapy industry: massive production scalability and the pitfalls associated with gene editing.
“If this approach proves successful, the critical thing is that we can achieve linear scalability in CAR-T production capacity that can match traditional biologics,” Fan said in an interview with Fierce.
Nonlinear interactions between light and matter are at the heart of some of the most powerful tools in modern optics, but pushing these processes to their limits has long been hampered by a fundamental constraint: the stronger you make the laser, the more likely it is to destroy whatever it illuminates.
Through new experiments detailed in Nature, Jian Wu and colleagues at East China Normal University in Shanghai have found a way around this problem, by exploiting the quantum nature of light itself.
Through new research published in Nature, Qing Cao and colleagues at the University of Illinois Urbana-Champaign have developed a new approach that sidesteps these problems, bringing high-performance 3D chips a step closer to reality.
Overheated stacks of transistors
Modern computer chips are built on thin wafers of silicon, with transistors (the tiny switches that process information) arranged in a single flat layer. If multiple layers of transistors could instead be stacked on top of each other on the same chip, it would dramatically increase their density without enlarging the chip’s footprint. However, this 3D design would cause the chip to overheat, which could destroy the circuitry already laid down beneath it.
Researchers at the University of Cambridge have provided the first-ever proof that human nerve regeneration after an injury can be reversed and reactivated. Using stem cell-derived brain and spinal cord organoids, scientists discovered a specific genetic network that acts like a “switch,” shutting down axon growth as neurons mature. Remarkably, by blocking key regulators within this network using an already available human drug called lynestrenol, they successfully retriggered the growth of nerve fibers. While lynestrenol itself is not an immediate cure for spinal cord injuries, this monumental discovery proves that the physiological barrier preventing nerve regeneration can be overcome — opening up incredible new possibilities for reversing paralysis and treating severe neurodegenerative diseases in the future!
Cambridge scientists have grown miniature circuits in the lab that mimic how the brain and spinal cord connect up, which underlies our movements. They used this model to show how damage to these connections previously considered ‘irreversible’ could, in fact, be reversible.
Our sophisticated organoid models help bridge the knowledge gap from animal models to what we see in patients.
Beginning with the Andromeda galaxy in the late 1960s, the astronomer Vera Rubin and her colleague Kent Ford measured how fast stars and gas clouds orbit at different distances from a galaxy’s centre. They expected the outer material to move slowly. It did not. In Andromeda, and then in galaxy after galaxy, the orbital speed stayed high all the way to the edge of what they could measure. The visible stars, gas and dust could not supply enough gravity to hold matter moving that fast in place.
Rubin and Ford published their Andromeda result in 1970, in a paper in the Astrophysical Journal. Over the following decade they extended the work, and by 1980 had measured the same pattern across twenty-one spiral galaxies. The consistency was the point. One odd galaxy could be explained away. Twenty-one could not.