Nature research paper: A method is presented to harness the paper-folding mechanism of reconfigurable macroscale systems to create reconfigurable DNA origami structures, in anticipation that it will advance the development of complex molecular systems.
Robotic finger. Illustration showing the cutting and healing process of the robotic finger (A), its anchoring structure (B) and fabrication process ©. ©2022 Takeuchi et al.
Researchers from the University of Tokyo pool knowledge of robotics and tissue culturing to create a controllable robotic finger covered with living skin tissue. The robotic digit has living cells and supporting organic material grown on top of it for ideal shaping and strength. As the skin is soft and can even heal itself, the finger could be useful in applications that require a gentle touch but also robustness. The team aims to add other kinds of cells into future iterations, giving devices the ability to sense as we do.
Professor Shoji Takeuchi is a pioneer in the field of biohybrid robots, the intersection of robotics and bioengineering. Together with researchers from around the University of Tokyo, he explores things such as artificial muscles, synthetic odor receptors, lab-grown meat, and more. His most recent creation is both inspired by and aims to aid medical research on skin damage such as deep wounds and burns, as well as help advance manufacturing.
University of British Columbia (UBC) and BC Children’s Hospital scientists discovered that disease-causing bacteria in the gut feed on sialic acid, a sugar found in the intestinal mucus layer.
Michael Levin, a developmental biologist at Tufts University, has a knack for taking an unassuming organism and showing it’s capable of the darnedest things. He and his team once extracted skin cells from a frog embryo and cultivated them on their own. With no other cell types around, they were not “bullied,” as he put it, into forming skin tissue. Instead, they reassembled into a new organism of sorts, a “xenobot,” a coinage based on the Latin name of the frog species, Xenopus laevis. It zipped around like a paramecium in pond water. Sometimes it swept up loose skin cells and piled them until they formed their own xenobot—a type of self-replication. For Levin, it demonstrated how all living things have latent abilities. Having evolved to do one thing, they might do something completely different under the right circumstances.
Slime mold grows differently depending on the music playing.
Not long ago I met Levin at a workshop on science, technology, and Buddhism in Kathmandu. He hates flying but said this event was worth it. Even without the backdrop of the Himalayas, his scientific talk was one of the most captivating I’ve ever heard. Every slide introduced some bizarre new experiment. Butterflies retain memories from when they were caterpillars, even though their brains turned to mush in the chrysalis. Cut off the head and tail of a planarian, or flatworm, and it can grow two new heads; if you amputate again, the worm will regrow both heads. Levin argues the worm stores the new shape in its body as an electrical pattern. In fact, he thinks electrical signaling is pervasive in nature; it is not limited to neurons. Recently, Levin and colleagues found that some diseases might be cured by retraining the gene and protein networks as one might train a neural network.
The Fourth of July holiday celebrates the day America’s Founding Fathers, representing the 13 colonies, officially adopted the Declaration of Indepen | Cancer.
Analysis of data from more than 22,000 people with multiple sclerosis helped researchers identify a genetic variant that is associated with the severity of the disease.
By Grace Wade
Cancer spreads throughout the human body in cunning, almost militaristic, ways. For example, it can manipulate our genetic make-up, take over specific cell-to-cell signaling processes, and mutate key enzymes to promote tumor growth, resist therapies, and hasten its spread from the original site to the bloodstream or other organs.
Enzyme mutations have been of great interest to scientists who study cancer. Scientists in the Liu and Tan labs at UNC’s Lineberger Comprehensive Cancer Center have been studying mutations of enzyme recognition motifs in substrates, which may more faithfully reflect enzyme function with the potential to find new targets or directions for cancer treatment.
“We think understanding the roles of mutations on enzyme substrates, instead of the enzyme as a whole, may help to improve efficacy of targeted therapies, especially for enzymes that have both oncogenic and tumor suppressive function through controlling distinct subsets of substrates,” said Jianfeng Chen, Ph.D., who is first author and a postdoctoral fellow in the Liu lab in the UNC Department of Biochemistry and Biophysics.
An interdisciplinary team of clinicians and scientists has published a consensus paper recommending appropriate quantitative imaging techniques for coronary artery stenosis and atherosclerosis related treatment and procedural planning. The paper has been published in Nature Reviews Cardiology.
Quantitative imaging has become increasingly important for the diagnosis of coronary artery disease (CAD) over the past five years. This is because new quantitative techniques can detect narrowed coronary arteries (coronary artery stenoses) and atherosclerosis, which play a major role in CHD patients.
It is important to correctly diagnose and accurately assess the severity of coronary artery stenosis or the extent of atherosclerotic burden for the selection of appropriate measures of therapy and the related further course of the disease. However, the complexity and variety of different quantitative imaging modalities, such as computed tomography (CT), magnetic resonance imaging (MRI), invasive coronary angiography (ICA), intravascular ultrasound (IVUS), and optical coherence tomography (OCT), necessitated a comprehensive clinical consensus.
Artificial intelligence can predict on-and off-target activity of CRISPR tools that target RNA instead of DNA, according to new research published in Nature Biotechnology.
The study by researchers at New York University, Columbia University, and the New York Genome Center, combines a deep learning model with CRISPR screens to control the expression of human genes in different ways—such as flicking a light switch to shut them off completely or by using a dimmer knob to partially turn down their activity. These precise gene controls could be used to develop new CRISPR-based therapies.
CRISPR is a gene editing technology with many uses in biomedicine and beyond, from treating sickle cell anemia to engineering tastier mustard greens. It often works by targeting DNA using an enzyme called Cas9. In recent years, scientists discovered another type of CRISPR that instead targets RNA using an enzyme called Cas13.
Regular physical exercise, such as resistance training, can prevent Alzheimer’s disease, or at least delay the appearance of symptoms, and serves as a simple and affordable therapy for Alzheimer’s patients. This is the conclusion of an article published in Frontiers in Neuroscience by Brazilian researchers affiliated with the Federal University of São Paulo (UNIFESP) and the University of São Paulo (USP).
Although older people and dementia patients are unlikely to be able to do long daily runs or perform other high-intensity aerobic exercises, these activities are the focus for most scientific studies on Alzheimer’s. The World Health Organization (WHO) recommends resistance exercise as the best option to train balance, improve posture and prevent falls. Resistance exercise entails contraction of specific muscles against an external resistance and is considered an essential strategy to increase muscle mass, strength and bone density, and to improve overall body composition, functional capacity and balance. It also helps prevent or mitigate sarcopenia (muscle atrophy), making everyday tasks easier to perform.
To observe the neuroprotective effects of this practice, researchers in UNIFESP’s Departments of Physiology and Psychobiology, and the Department of Biochemistry at USP’s Institute of Chemistry (IQ-USP), conducted experiments involving transgenic mice with a mutation responsible for a buildup of beta-amyloid plaques in the brain. The protein accumulates in the central nervous system, impairs synaptic connections and damages neurons, all of which are features of Alzheimer’s disease.
