The virus is the most contagious in the world, exploiting the human body’s immune system to spread with extreme agility and harming its victims for years.
Category: biotech/medical – Page 2,524
Bioengineers create ultrasmall, light-activated electrode for neural stimulation
Neural stimulation is a developing technology that has beneficial therapeutic effects in neurological disorders, such as Parkinson’s disease. While many advancements have been made, the implanted devices deteriorate over time and cause scarring in neural tissue. In a recently published paper, the University of Pittsburgh’s Takashi D. Y. Kozai detailed a less invasive method of stimulation that would use an untethered ultrasmall electrode activated by light, a technique that may mitigate damage done by current methods.
Searching Tardigrades for Lifesaving Secrets
There are many instances in medicine when it would be helpful to stop, or greatly slow down, time. Doing so could spare a limb from amputation, prevent paralysis after a stroke or save your life following a heart attack.
Across the tree of life, there are many organisms that can essentially cheat time by decelerating their biology. Chief among them is the tardigrade, a creature no bigger than a speck of sand that can survive severe temperatures and pressures, outer space and all sorts of apocalyptic scenarios by entering a dormant state called anhydrobiosis.
A team at Harvard Medical School is studying tardigrades in hopes of finding medical treatments that halt tissue damage. In particular, the scientists are drawing inspiration from special proteins suspected to help tardigrades achieve suspended animation. They aim to synthesize a version of these proteins that can enter human cells and pause processes leading to cell death.
**Suicide system in tuberculosis bacteria might hold key to treatment
Tuberculosis (TB) is one of the top 10 causes of death worldwide. In 2017, 10 million people around the world fell ill with TB and 1.3 million died. The genome of the bacterium that causes TB holds a special toxin-antitoxin system with a surprising function: Once the toxin is activated, all bacterial cells die, stopping the disease. An international research team co-led by the Wilmanns group at EMBL in Hamburg investigated this promising feature for therapeutic targets. They now share the first high-resolution details of the system in Molecular Cell.
Mycobacterium tuberculosis is the bacterium that causes TB in humans. Its genome holds 80 so-called toxin-antitoxin (TA) systems, sets of closely linked genes that encode both a toxic protein and an antitoxin—a toxin-neutralising antidote.
When the bacteria are growing normally, toxin activity is blocked by the antitoxin’s presence. But under stress conditions such as lack of nutrients, dedicated enzymes rapidly degrade the antitoxin molecules. This activates the toxin proteins in the cell and slows down the growth of the bacteria, allowing them to survive the stressful environment.
Great white shark genome decoded
The great white shark is one of the most recognized marine creatures on Earth, generating widespread public fascination and media attention, including spawning one of the most successful movies in Hollywood history. 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 big 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 white shark has now been decoded in detail.
A team led by scientists from Nova Southeastern University’s (NSU) Save Our Seas Foundation Shark Research Center and Guy Harvey Research Institute (GHRI), Cornell University College of Veterinary Medicine, and Monterey Bay Aquarium, completed the white shark genome and compared it to genomes from a variety of other vertebrates, including the giant whale shark and humans.
A new CRISPR/Cas9 therapy can suppress aging
LA JOLLA—(February 18, 2019) Aging is a leading risk factor for a number of debilitating conditions, including heart disease, cancer and Alzheimer’s disease, to name a few. This makes the need for anti-aging therapies all the more urgent. Now, Salk Institute researchers have developed a new gene therapy to help decelerate the aging process.
The findings, published on February 18, 2019 in the journal Nature Medicine, highlight a novel CRISPR/Cas9 genome-editing therapy that can suppress the accelerated aging observed in mice with Hutchinson-Gilford progeria syndrome, a rare genetic disorder that also afflicts humans. This treatment provides important insight into the molecular pathways involved in accelerated aging, as well as how to reduce toxic proteins via gene therapy.
“Aging is a complex process in which cells start to lose their functionality, so it is critical for us to find effective ways to study the molecular drivers of aging,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “Progeria is an ideal aging model because it allows us to devise an intervention, refine it and test it again quickly.”
Fungus provides powerful medicine in fighting honey bee viruses
In field trials, colonies fed mycelium extract from amadou and reishi fungi showed a 79-fold reduction in deformed wing virus and a 45,000-fold reduction in Lake Sinai virus compared to control colonies.
Though it’s in the early stages of development, the researchers see great potential in this research.
“Our greatest hope is that these extracts have such an impact on viruses that they may help varroa mites become an annoyance for bees, rather than causing huge devastation,” said Steve Sheppard, a WSU entomology professor and one of the paper’s authors. “We’re excited to see where this research leads us. Time is running out for bee populations and the safety and security of the world’s food supply hinges on our ability to find means to improve pollinator health.”
Excessive Cell Size Contributes to Senescence
In a new study [1], researchers have identified the reason why cells become defective when they grow too large and why protein creation fails when cells grow larger than their original healthy size, as is typically seen in aged and senescent cells.
They demonstrate that in enlarged yeast and human cells, RNA and protein biosynthesis does not scale in proportion to the additional cell size, which then leads to a dilution of the cytoplasm. This phenomenon is also present in senescent cells, which display similar traits to those of large cells.
The research team concludes that the maintenance of a cell type-specific DNA-to-cytoplasm ratio is essential for the majority of cellular functions, and when cellular growth changes this ratio, it encourages cells to become senescent.
Great white shark genome has been sequenced, revealing clues to longevity and cancer resistance
To many of us, the great white shark is a mysterious and scary creature from the deep – but now it’s a little less mysterious. A team of scientists has sequenced the entire genome of the great white shark, revealing a few clues as to how these animals are so good at healing wounds and resisting cancer.