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.
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 electric field to disrupt biofilm infection. 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 medical device, 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.
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 ‘single-cell genomics’, 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 tadpole cells when they regenerate their tails.
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 health systems 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 mast cells—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 osteoarthritis typically induced by a classic experimental procedure. The results were supported by findings in human cells 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.
A sensational new study conducted at the University of Copenhagen disproves traditional knowledge of stem cell development. The study reveals that the destiny of intestinal cells is not predetermined, but instead determined by the cells’ surroundings. The new knowledge may make it easier to manipulate stem cells for stem cell therapy. The results have been published in Nature.
All cells in the foetal gut have the potential to develop into stem cells, a new study conducted at the Faculty of Health and Medical Sciences at the University of Copenhagen concludes. The researchers behind the study have discovered that the development of immature intestinal cells—contrary to previous assumptions—is not predetermined, but affected by the cells’ immediate surroundings in the intestines. This discovery may ease the path to effective stem cell therapy, says Associate Professor Kim Jensen from the Biotech Research & Innovation Centre (BRIC) and the Novo Nordisk Foundation Center for Stem Cell Biology (DanStem).
“We used to believe that a cell’s potential for becoming a stem cell was predetermined, but our new results show that all immature cells have the same probability for becoming stem cells in the fully developed organ. In principle, it is simply a matter of being in the right place at the right time. Here signals from the cells’ surroundings determine their fate. If we are able to identify the signals that are necessary for the immature cell to develop into a stem cell, it will be easier for us to manipulate cells in the wanted direction.”
Your mother was right: Broccoli is good for you. Long associated with decreased risk of cancer, broccoli and other cruciferous vegetables—the family of plants that also includes cauliflower, cabbage, collard greens, Brussels sprouts and kale—contain a molecule that inactivates a gene known to play a role in a variety of common human cancers. In a new paper published today in Science, researchers, led by Pier Paolo Pandolfi, MD, Ph.D., Director of the Cancer Center and Cancer Research Institute at Beth Israel Deaconess Medical Center, demonstrate that targeting the gene, known as WWP1, with the ingredient found in broccoli suppressed tumor growth in cancer-prone lab animals.
“We found a new important player that drives a pathway critical to the development of cancer, an enzyme that can be inhibited with a natural compound found in broccoli and other cruciferous vegetables,” said Pandolfi. “This pathway emerges not only as a regulator for tumor growth control, but also as an Achilles’ heel we can target with therapeutic options.”
A well-known and potent tumor suppressive gene, PTEN is one of the most frequently mutated, deleted, down-regulated or silenced tumor suppressor genes in human cancers. Certain inherited PTEN mutations can cause syndromes characterized by cancer susceptibility and developmental defects. But because complete loss of the gene triggers an irreversible and potent failsafe mechanism that halts proliferation of cancer cells, both copies of the gene (humans have two copies of each gene; one from each parent) are rarely affected. Instead, tumor cells exhibit lower levels of PTEN, raising the question whether restoring PTEN activity to normal levels in the cancer setting can unleash the gene’s tumor suppressive activity.
