Syndicate content

Archive - Feb 20, 2019


Study Investigates If Nerve Injury Can Trigger ALS (Lou Gehrig’s Disease)

A growing collection of anecdotal stories raises the possibility that nerve injury in an arm or a leg can act as a trigger for the development amyotrophic lateral sclerosis, or ALS--a progressive neurodegenerative disease also known as Lou Gehrig's disease, named after the famous New York Yankee who died of it in 1941. The connection between ALS and athletes runs deeper than a single ballplayer; people who engage in intense physical activities, such as professional athletes and people in the military, are more likely to be affected by ALS. In some, the disease seems to start after an injury -- muscle weakness at the site of the injury slowly spreads to new areas until weakness in the muscles responsible for breathing causes suffocation. Now, researchers at the University of Illinois at Chicago (UIC) are the first to demonstrate that a peripheral nerve injury can trigger the onset and spread of the disease in an animal model of ALS. Their findings, published in the April 2019 issue of Neurobiology of Disease, show that rats genetically engineered to develop ALS-like symptoms have an abnormal inflammatory response in the region of the spinal cord associated with an injured peripheral neuron. As the spinal cord inflammation and other damaging processes spread, they cause progressive muscle weakness throughout the body. The article is titled “Mutant SOD1 Prevents Normal Functional Recovery Through Enhanced Glial Activation and Loss of Motor Neuron Innervation After Peripheral Nerve Injury.” "We know that in some patients with ALS the weakness starts in a hand or leg, and the disease spreads. Coincidentally, the patient will describe a recent or remote injury to that same hand or leg that matches the location of their disease onset.

New Work Suggests Exosomes May Play Key Role in Labor & Delivery

A group of scientists led by Ramkumar Menon, PhD, at The University of Texas Medical Branch at Galveston (UTMB) have gained new insight on a poorly-understood, but possibly key player in the timing of labor and delivery. This new information may bring scientists closer to being able to prevent preterm births. This study was published online on January 24, 2019 in Scientific Reports. The open-access article is titled “Exosomes Cause Preterm Birth in Mice: Evidence for Paracrine Signaling in Pregnancy.” According to the World Health Organization, an estimated 15 million infants are born too early each year. Complications from preterm birth are the leading cause of death among children under five years old, responsible for about one million deaths each year globally. In the U.S., approximately 1 of every 10 infants was born prematurely in 2017. When a woman is at the end of her pregnancy, the normal childbirth process begins when the fetus releases chemicals signaling that his/her organs have matured enough for delivery. This chemical release shifts the mother’s hormone levels, which increases inflammation in the uterus and begins labor and delivery. “There’s another component of the biological clock that contributes to the timing of birth – a type of cell-to-cell communication between the maternal and fetal cells called paracrine signaling,” said senior author Dr. Menon, UTMB Associate Professor in the Department of Obstetrics and Gynecology. “Because little is known about what this type of signaling does during pregnancy, we investigated the role of paracrine signals called (editor’s note: carried by) exosomes in the timing of labor and delivery.” The researchers collected blood plasma samples from pregnant mice and isolated the exosomes.

Great White Shark Genome Decoded; Sequence Reveals Adaptations Related to Faster Wound Healing and to Genome Stability Linked to Cancer Resistance; Study Co-Conceived by Renowned Geneticist Stephen O’Brien

The great white shark is one of the most recognized marine creatures on Earth, generating widespread public fascination and media attention, and spawning one of the most successful movies in Hollywood history (“Jaws”). This shark possesses notable characteristics, including its massive size (up to 20 feet and 7,000 pounds) and diving to nearly 4,000-foot depths. Great whites are also a significant conservation concern given their relatively low numbers in the world's oceans. In a major scientific step to understand the biology of this iconic apex predator and sharks in general, the entire genome of the great white shark has now been decoded in detail. A team led by scientists from (NSU) Nova Southeastern University's Save Our Seas Foundation Shark Research Center (Miami, Florida) and Guy Harvey Research Institute (GHRI) (Miami, Florida), Cornell University College of Veterinary Medicine (Ithaca, New York), and Monterey Bay Aquarium (Monterey, California), completed the white shark genome and compared it to genomes from a variety of other vertebrates, including the giant whale shark and humans. The findings were reported online on February 19, 2019 in PNAS. The PNAS article is titled “White Shark Genome Reveals Ancient Elasmobranch Adaptations Associated with Wound Healing and the Maintenance of Genome Stability.” Decoding the white shark's genome revealed not only its huge size - one-and-a-half times the size of the human genome - but also an abundance of genetic changes that could be behind the evolutionary success of large-bodied and long-lived sharks.