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Researchers may have demonstrated a novel way to protect us from some of the world’s deadliest viruses. By genetically engineering immune cells to make more effective antibodies, they have defended mice from a potentially lethal lung virus. The same strategy could work in humans against diseases for which there are no vaccines.

“It’s a huge breakthrough,” says immunologist James Voss of the Scripps Research Institute in San Diego, California, who wasn’t connected to the study.

Vaccines typically contain a disabled microbial invader or shards of its molecules. They stimulate immune cells known as B cells to crank out antibodies that target the pathogen. Not everyone who receives a vaccine gains protection, however. Some patients’ antibodies aren’t up to snuff, for instance. And researchers haven’t been able to develop vaccines against some microbes, such as HIV and the respiratory syncytial virus (RSV), which causes lung infections mainly in children and people with impaired immune systems.

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For the first time, scientists have created life with genetic code that was developed from scratch.

A University of Cambridge team created living, reproducing E. coli bacteria with DNA coded entirely by humans, according to The New York Times. The new bacteria look a little wonky, but they behave more or less the same as natural E. coli. Learning to rebuild genomes from scratch could teach scientists how DNA originally came to be — and how we can manipulate it to create new life.

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Researchers at Indiana University School of Medicine have found a way to charge up the fight against bacterial infections using electricity.

Work conducted in the laboratories of the Indiana Center for Regenerative Medicine and Engineering, Chandan Sen, Ph.D. and Sashwati Roy, Ph.D. has led to the development of a dressing that uses an to disrupt biofilm . Their findings were recently published in the high-impact journal Annals of Surgery.

Bacterial biofilms are thin, slimy films of bacteria that form on some wounds, including burns or post-surgical infections, as well as after a , such as a catheter, is placed in the body. These bacteria generate their own electricity, using their own electric fields to communicate and form the biofilm, which makes them more hostile and difficult to treat. The Centers for Disease Control and Prevention estimates 65 percent of all infections are caused by bacteria with this biofilm phenotype, while the National Institutes of Health estimates that number is closer to 80 percent.

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Researchers at the University of Cambridge have uncovered a specialised population of skin cells that coordinate tail regeneration in frogs. These ‘Regeneration-Organizing Cells’ help to explain one of the great mysteries of nature and may offer clues about how this ability might be achieved in mammalian tissues.

It has long been known that some animals can regrow their tails following amputation—Aristotle observed this in the fourth century B.C. — but the mechanisms that support such regenerative potential remain poorly understood.

Using ‘’, scientists at the Wellcome Trust/ Cancer Research UK Gurdon Institute at the University of Cambridge developed an ingenious strategy to uncover what happens in different cells when they regenerate their tails.

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A groundbreaking project to tackle one of the world’s most pressing and complex health challenges—antimicrobial resistance (AMR)—has secured a $1 million boost. UTS will lead a consortium of 26 researchers from 14 organisations in the development of an AMR ‘knowledge engine’ capable of predicting outbreaks and informing interventions, supported by a grant from the Medical Research Future Fund.

“AMR is not a simple problem confined to health and hospital settings,” explains project Chief Investigator, UTS Professor of Infectious Disease Steven Djordjevic. “Our pets and livestock rely on many of these same medicines, so they find their way into the food chain and into the environment through animal faeces.”

If left unchecked, AMR is forecast to cause 10 million deaths annually by 2050, and add a US$100 trillion burden to worldwide.

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Stanford University School of Medicine scientists have definitively linked mast cells, a class of cells belonging to the immune system, to the development of osteoarthritis, one of the world’s most common causes of pain and immobility.

In a study published online May 14 in eLife, the scientists demonstrated for the first time that banishing —or blocking signals from the most common stimulus activating them in real life, or disabling a cartilage-degrading enzyme they release when activated—all protected mice from developing typically induced by a classic experimental procedure. The results were supported by findings in and tissues.

Osteoarthritis, by far the most frequently occurring variety of arthritis, is characterized by cartilage breakdown and inflammation in joints, which can be further aggravated by excess bone growths called osteophytes.

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