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The White House recently announced its vision for an Advanced Research Projects Agency for Health, or ARPA-H. RAND researchers explain what it might take to ens… See More.


DARPA also maintains an extremely high tolerance for failure. The modest budgets of the NIH, combined with an enormous pool of applicants, force these institutions to bet on low-risk research that guarantees incremental progress. ARPA-H could take a different approach than NIH by accepting a much higher tolerance for failure, so that researchers are not discouraged from dreaming big.

The scientific methods behind the products of ARPA-H might gain public trust if the agency made a point of being transparent and accessible. Consider how the rapid development of the COVID-19 vaccine was met with incredulity and suspicion, slowing progress toward herd immunity. An investment in ARPA-H could accelerate the time it takes to get innovative ideas from “bench to bedside,” but it could benefit from informing the public about incremental advancements in a way that is easy to understand.

The president’s vision for ARPA-H could help get more medical treatments to market sooner. Building on lessons from DARPA and NIH, the proposed health agency has the potential to pursue the kind of high-risk research that can lead to high-reward results.

The world is one step closer to ultimately secure conference calls, thanks to a collaboration between Quantum Communications Hub researchers and their German colleagues, enabling a quantum-secure conversation to take place between four parties simultaneously.

The demonstration, led by Hub researchers based at Heriot-Watt University and published in Science Advances, is a timely advance, given the global reliance on remote collaborative working, including calls, since the start of the C19 pandemic.

There have been reports of significant escalation of cyber-attacks on popular teleconferencing platforms in the last year. This advance in quantum secured communications could lead to conference calls with inherent unhackable security measures, underpinned by the principles of quantum physics.

At Boston University, a team of researchers is working to better understand how language and speech is processed in the brain, and how to best rehabilitate people who have lost their ability to communicate due to brain damage caused by a stroke, trauma, or another type of brain injury. This type of language loss is called aphasia, a long-term neurological disorder caused by damage to the part of the brain responsible for language production and processing that impacts over a million people in the US.

“It’s a huge problem,” says Swathi Kiran, director of BU’s Aphasia Research Lab, and College of Health & Rehabilitation Sciences: Sargent College associate dean for research and James and Cecilia Tse Ying Professor in Neurorehabilitation. “It’s something our lab is working to tackle at multiple levels.”

For the last decade, Kiran and her team have studied the brain to see how it changes as people’s improve with speech . More recently, they’ve developed new methods to predict a person’s ability to improve even before they start therapy. In a new paper published in Scientific Reports, Kiran and collaborators at BU and the University of Texas at Austin report they can predict recovery in Hispanic patients who speak both English and Spanish fluently—a group of aphasia patients particularly at risk of long-term language loss—using sophisticated computer models of the brain. They say the breakthrough could be a game changer for the field of speech therapy and for stroke survivors impacted by aphasia.

Generation of an ARHGAP11B-transgenic mouse line.

To generate a stable transgenic mouse line that expresses an ARHGAP11B protein, we first determined the temporal and spatial expression patterns of human ARHGAP11A and human ARHGAP11B mRNAs by qPCR of foetal human neocortical tissue at various developmental stages (gestational weeks 12–21; Fig EV1A and B) and by analysing previously published RNA-seq data sets of defined isolated NPC and neuron populations (Florio et al, 2015) (Fig EV1C and D), respectively. As the expression patterns of ARHGAP11A and ARHGAP11B mRNAs were found to be similar, we decided to generate the transgenic mouse line by converting one allele of the mouse Arhgap11a gene into a mutant mouse ARHGAP11B gene (mARHGAP11B), using the CRISPR/Cas9 genome editing technology (for details, see Materials and Methods). In m ARHGAP11B, the 55 nucleotides of Arhgap11a that in humans would be deleted from the ARHGAP11B mRNA by splicing using the new splice-donor site are replaced by the 141 nucleotides encoding the human-specific 47-amino acid sequence plus three nucleotides to generate a translational stop codon (Fig EV1E). Unless indicated otherwise, the ARHGAP11B-transgenic mice obtained (referred to as 11B mice hereafter) were used as heterozygous animals, that is, with one mouse Arhgap11a allele being replaced by m ARHGAP11B. The resulting ARHGAP11B protein will be expressed in developing mouse neocortex under the control of the native mouse Arhgap11a promotor.

Critical advances in the investigation of brain functions and treatment of brain disorders are hindered by our inability to selectively target neurons in a noninvasive manner in the deep brain.

This study aimed to develop sonothermogenetics for noninvasive, deep-penetrating, and cell-type-specific neuromodulation by combining a thermosensitive ion channel TRPV1 with focused ultrasound (FUS)-induced brief, non-noxious thermal effect.

The sensitivity of TRPV1 to FUS sonication was evaluated in vitro. It was followed by in vivo assessment of sonothermogenetics in the activation of genetically defined neurons in the mouse brain by two-photon calcium imaging. Behavioral response evoked by sonothermogenetic stimulation at a deep brain target was recorded in freely moving mice. Immunohistochemistry staining of ex vivo brain slices was performed to evaluate the safety of FUS sonication.

The idea is simple: decades of research have found certain genes that seem to increase the chance of Alzheimer’s and other dementias. The numbers range over hundreds. Figuring out how each connects or influences another—if at all—takes years of research in individual labs. What if scientists unite, tap into a shared resource, and collectively solve the case of why Alzheimer’s occurs in the first place?

The initiative’s secret weapon is induced pluripotent stem cells, or iPSCs. Similar to most stem cells, they have the ability to transform into anything—a cellular genie, if you will. iPSCs are reborn from regular adult cells, such as skin cells. When transformed into a brain cell, however, they carry the original genes of their donor, meaning that they harbor the original person’s genetic legacy—for example, his or her chance of developing Alzheimer’s in the first place. What if we introduce Alzheimer’s-related genes into these reborn stem cells, and watch how they behave?

By studying these iPSCs, we might be able to follow clues that lead to the genetic causes of Alzheimer’s and other dementias—paving the road for gene therapies to nip them in the bud.

Biobots could help us with new organs! 😃


Computer scientists and biologists have teamed up to create a creature heretofore unseen on Earth: a living robot. Made from the cells of frogs and designed by artificial intelligence, they’re called xenobots, and they may soon revolutionize everything from how we fight pollution to organ transplants.

#Xenobots #Moonshot #BloombergQuicktake.

All cells on Earth are made of phospholipid membranes. Now astronomers have found the component molecules in interstellar space.


One potential explanation is that the Earth was seeded from space with the building blocks for life. The idea is that space is filled with clouds of gas and dust that contain all the organic molecules necessary for life.

Indeed, astronomers have observed these buildings blocks in interstellar gas clouds. They can see amino acids, the precursors of proteins and the machinery of life. They can also see the precursors of ribonucleotides, molecules that can store information in the form of DNA.

But there is another crucial component for life – molecules that can form membranes capable of encapsulating and protecting the molecules of life in compartments called protocells. On Earth, the membranes of all cells are made of molecules called phospholipids. But these have never been observed in space. Until now.

Many of the fundamental features of life don’t necessarily have to be the way they are. Chance plays a major role in evolution, and there are always alternate paths that were never explored, simply because whatever evolved previously happened to be good enough. One instance of this idea is the genetic code, which converts the information carried by our DNA into the specific sequence of amino acids that form proteins. There are scores of potential amino acids, many of which can form spontaneously, but most life uses a genetic code that relies on just 20 of them.

Over the past couple of decades, scientists have shown that it doesn’t have to be that way. If you supply bacteria with the right enzyme and an alternative amino acid, they can use it. But bacteria won’t use the enzyme and amino acid very efficiently, as all the existing genetic code slots are already in use.

In a new work, researchers have managed to edit bacteria’s genetic code to free up a few new slots. They then filled those slots with unnatural amino acids, allowing the bacteria to produce proteins that would never be found in nature. One side effect of the reprogramming? No viruses could replicate in the modified bacteria.