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Small proteins also promise to revise the current understanding of the genome. Many appear to be encoded in stretches of DNA—and RNA—that were not thought to help build proteins of any sort. Some researchers speculate that the short stretches of DNA could be newborn genes, on their way to evolving into larger genes that make full-size proteins. Thanks in part to small proteins, “We need to rethink what genes are,” says microbiologist and molecular biologist Gisela Storz of the National Institute of Child Health and Human Development in Bethesda, Maryland.

Tiny proteins help power muscles and provide the toxic punch to many venoms.

The newly fashionable pills and foods meant to increase the variety of healthy bacteria in our bodies can actually have the opposite effect.

Evening gowns with interwoven LEDs may look extravagant, but the light sources need a constant power supply from devices that are as well wearable, durable, and lightweight. Chinese scientists have manufactured fibrous electrodes for wearable devices that are flexible and excel by their high energy density. Key for the preparation of the electrode material was a microfluidic technology, as shown in the journal Angewandte Chemie.

Dresses emitting sparkling light from hundreds of small LEDs may create eye-catching effects in ballrooms or on fashion shows. But wearable electronics can also mean sensors integrated in functional textiles to monitor, for example, water evaporation or temperature changes. Energy storage systems powering such wearable devices must combine deformability with high capacity and durability. However, deformable electrodes often fail in long-term operation, and their capacity lags behind that of other state-of-the-art energy storage devices.

Electrode materials usually benefit from a fine balance of porosity, conductivity, and electrochemical activity. Material scientists Su Chen, Guan Wu, and their teams from Nanjing Tech University, China, have looked deeper into the material demands for flexible electrodes and developed a porous hybrid material synthesized from two carbon nanomaterials and a metal-organic framework. The nanocarbons provided the large surface area and excellent electrical conductivity, and the metal-organic framework gave the porous structure and the electrochemical activity.

Insulin, a hormone essential for regulating blood sugar and lipids, is normally produced by pancreatic β cells. In many people with diabetes, however, pancreatic cells are not (or no longer) functional, causing a chronic and potentially fatal insulin deficiency that can only be controlled through daily insulin injections. However, this approach has serious adverse effects, including an increased risk of life-threatening hypoglycaemia, and it does not restore metabolic balance. In order to improve therapy, researchers at the University of Geneva (UNIGE), Switzerland, have identified a protein called S100A9 which, under certain conditions, seems to act as a blood sugar and lipid regulator while avoiding the most harmful side effects of insulin. This discovery, that can be read in Nature Communications, paves the way for better treatment of diabetes and could significantly improve the quality of life for tens of millions of people affected by insulin deficiency.

Today, insulin injections are essential for the survival of patients with type 1 diabetes or a severe form of type 2 diabetes. However, this treatment is not without risk: overdose can trigger hypoglycaemia, i.e. a drop in blood glucose levels that can lead to coma or even death. But underdosed, it can lead to equally dangerous hyperglycaemia. In addition, insulin is involved in the control of ketones, elements that are produced when the liver breaks down lipids in the absence of sufficient glucose reserves, which become toxic in too large quantities. In addition, long-term insulin treatments cause excess fat and cholesterol in the blood and therefore increases the risk of cardiovascular disease.

As early as 2010, Roberto Coppari’s team, a professor at the Diabetes Centre of the UNIGE Faculty of Medicine, highlighted the gluco- and lipid-regulatory properties of leptin, a hormone involved in hunger control. “However, leptin has proved difficult to use pharmacologically in human beings due to the development of leptin resistance,” says Roberto Coppari. “In order to overcome this problem, we shifted our focus on the metabolic mechanisms triggered by leptin rather than on the hormone itself.”

Denis Rebrikov also told Nature that he does not plan to implant gene-edited embryos until he gets regulatory approval.

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Although aging is the greatest risk factor for cancer, a recent study demonstrates how aging cells might, paradoxically, hinder cancer progression.

Contrary to popular belief, cartilage in human joints can repair itself through a process similar to that used by creatures such as salamanders and zebrafish to regenerate limbs, researchers at Duke Health found.

Publishing online Oct. 9 in the journal Science Advances, the researchers identified a mechanism for cartilage repair that appears to be more robust in ankle joints and less so in hips. The finding could potentially lead to treatments for osteoarthritis, the most common joint disorder in the world.

“We believe that an understanding of this ‘salamander-like’ regenerative capacity in humans, and the critically missing components of this regulatory circuit, could provide the foundation for new approaches to repair joint tissues and possibly whole human limbs,” said senior author Virginia Byers Kraus, M.D., Ph.D., a professor in the departments of Medicine, Pathology and Orthopedic Surgery at Duke.

We’re continuing to release talks from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Dr. Andrei Gudkov of the Roswell Park Comprehensive Cancer Center gave a highly technical and in-depth presentation about the retrobiome, a specific subset of genetics that vary between mammalian species, as a key driver of aging. According to this model, as DNA damage accumulates, senescent cells are less efficiently disposed of by the immune system, strongly contributing to the familiar diseases of aging. He also discussed related topics, including how LINE1 (RTL1), a protein that is produced as part of the retrobiome, may be effective against cancer proliferation.