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University of Wyoming researchers have gained further insight into how tardigrades survive extreme conditions and shown that proteins from the microscopic creatures expressed in human cells can slow down molecular processes.

This makes the tardigrade proteins potential candidates in technologies centered on slowing the aging process and in long-term storage of human cells.

The new study, published in the journal Protein Science, examines the mechanisms used by tardigrades to enter and exit from suspended animation when faced by environmental stress. Led by Senior Research Scientist Silvia Sanchez-Martinez in the lab of UW Department of Molecular Biology Assistant Professor Thomas Boothby, the research provides additional evidence that tardigrade proteins eventually could be used to make life-saving treatments available to people where refrigeration is not possible — and enhance storage of cell-based therapies, such as stem cells.

A man who was paralyzed from the neck down after a surfing accident seven years ago is now able to stand and walk on his own, thanks in part to a potentially groundbreaking stem cell treatment.

Chris Barr was the very first patient in a Mayo Clinic study that collected stem cells from his own stomach fat, expanded them in a laboratory to 100 million cells and then injected the cells into Barr’s lumbar spine.

Over five years after undergoing the therapy, Barr said he is continuing to gain more independence and get faster at walking.

A new study in the Journal of Perinatology finds that when it comes to diagnosing early-onset infant sepsis, how blood samples are connected matters more than how many cultures are taken.

A team led by Yale Pediatrics’ Noa Fleiss, MD, finds obtaining more than one bloodculture doesn’t significantly…


Clinicians diagnose neonatal sepsis by taking a blood culture. New research evaluates factors that influence diagnostic utility while taking blood from infants.

Two progressively degenerative diseases, amyotrophic lateral sclerosis (ALS, commonly known as Lou Gehrig’s disease) and frontotemporal dementia (FTD, recently in the news with the diagnoses of actor Bruce Willis and talk show host Wendy Williams), are linked by more than the fact that they both damage nerve cells critical to normal functioning—the former affecting nerves in the brain and spinal cord leading to loss of movement, the latter eroding the brain regions controlling personality, behavior and language.

Research studies have repeatedly shown that in patients with ALS or FTD, the function of TAR DNA-binding protein 43, more commonly called TDP-43, becomes corrupted. When this happens, pieces of the genetic material called ribonucleic acid (RNA) can no longer be properly spliced together to form the coded instructions needed to direct the manufacture of other proteins required for healthy nerve growth and function.

The RNA strands become riddled with erroneous code sequences called “cryptic exons” that instead affect proteins believed to be associated with increased risk for ALS and FTD development.

When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last.

It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City.