A dense galaxy is much different than it appears.
A team of researchers at the Carl Gustav Carus Faculty of Medicine, TUD Dresden University of Technology, led by Prof. Frank Buchholz, has achieved a major breakthrough in genome editing technology. They’ve developed a cutting-edge method that combines the power of designer-recombinases with programmable DNA-binding domains to create precise and adaptable genome editing tools.
Traditional genome editing faced limitations in achieving ultimate precision until now. Prof. Buchholz’s team has broken through this barrier by creating what many have sought after: a zinc-finger conditioned recombinase. This innovative approach involves integrating a zinc-finger DNA-binding domain into specially designed recombinases. These enzymes remain inactive until the DNA-binding domain engages with its target site, adjacent to the recombinase binding area.
The significance of this achievement lies in the fusion of two key strengths: the targeting ease of programmable nucleases and the precise DNA editing capabilities of recombinases. This breakthrough overcomes existing limitations in genome editing techniques and holds vast promise for therapeutic gene editing and various biomedical applications.
This condition is called jaundice. Symptoms can also appear in adults. For adults, it can be a sign of a serious health condition. Learn more about the causes of jaundice:
Jaundice is a yellow coloring of the skin or eyes caused by too much bilirubin in the body. Jaundice can happen for many reasons. Learn about it here.
For years, there has been a long-held belief that acute viral infections like Zika or COVID-19 are directly responsible for neurological damage, but researchers from McMaster University have now discovered that it’s the immune system’s response that is behind it.
The research, published on Feb. 5, 2024, in Nature Communications, was led by Elizabeth Balint, a Ph.D. student at McMaster, and Ali Ashkar, a professor with the Department of Medicine and the Canada Research Chair in Natural Immunity and NK Cell Function.
“We were interested in trying to understand why so many viral infections are associated with neurological diseases,” says Balint. “Our evidence suggests that it’s not the virus itself that causes the damage, but a unique population of T cells, which are part of the immune system, that are actually responsible for the damage.”
Acetamiprid-induced oxidative stress can harm DNA and tRNA, leading to health problems. A study conducted by Huixia Zhang at Macau University of Science and Technology in 2023 introduced a comprehensive approach to assessing acetamiprid-induced oxidative damage to tRNA in human cells through oxidized nucleotide and tRNA profiling. Acetamiprid, a modern insecticide, is known for causing oxidative stress and related toxicity. Despite its impact on oxidative stress, the effects of acetamiprid-induced oxidative stress on RNA, especially tRNA, remained unexplored until this study.
Acetamiprid was found to elevate reactive oxygen species (ROS) production in HepG2 and LO2 cells, contributing to mitochondrial damage, free radical generation, and antioxidant status depletion. Oxidative damage to DNA and RNA can harm organisms, with prior research addressing RNA damage in aging, neurodegenerative diseases, and mental illnesses. However, its role in acetamiprid-induced toxicities has not been investigated.
The study employed TMSD labeling-based LC-MS/MS to measure oxidized nucleotide levels in HepG2 and LO2 cells treated with two mM acetamiprid. It also examined the impact of acetamiprid on the 8-oxo-G content of tRNAs and created volcano plots to compare RNase T1 digestion products of tRNAs from untreated and acetamiprid-treated cells.
This brain-teaser has baffled physicists since 1883. Thanks to some innovative engineering, it finally makes sense.
A new cybercriminal group, ResumeLooters, targets job search platforms in APAC, stealing millions of resumes and personal data.
Immune guardians called complement proteins are manufactured by gut cells and help to protect against pathogens.