Glaxo says the heartburn drug doesn’t cause tumors. But the company was warned by its own scientists and independent researchers about the potential danger.
A decades-old drug used to treat urinary tract infections (UTIs) appears to have saved the life of a man infected by the “brain-eating” amoeba — and his case highlights the tremendous potential of a new type of genetic sequencing technology.
The patient: In 2021, a 54-year-old man was admitted to a Northern California hospital following a seizure. After an MRI revealed a mass in his brain, he was transferred to the UCSF Medical Center, where the mass was biopsied.
Continue reading “‘Brain-eating’ amoeba beaten by old European drug” »
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Scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have removed a major roadblock to better understanding of mpox (formerly, monkeypox). They developed a mouse model of the disease and used it to demonstrate clear differences in virulence among the major genetic groups (clades) of mpox virus (MPXV).
The research, appearing in Proceedings of the National Academy of Science, was led by Bernard Moss, M.D., Ph.D., chief of the Genetic Engineering Section of NIAID’s Laboratory of Viral Diseases.
Historically, mpox, a disease resembling smallpox, was only occasionally transmitted from rodents to non-human primates or people, and was observed primarily in several African countries. Mpox rarely spread from person to person. That pattern changed in 2022 with an outbreak in which person-to-person mpox transmission occurred in more than 100 locations worldwide.
Artificial enzymes can fight the COVID-causing virus by selectively snipping apart its RNA genome, a new study suggests. Researchers say the technique may overcome key problems with previous technologies and could help create rapid antiviral treatments as threats emerge.
When the COVID pandemic struck, University of Cambridge chemical biologist Alexander Taylor scrambled to repurpose a gene-cutting technology he and his colleagues had been developing: synthetic enzymes called XNAzymes (xeno nucleic acids) formed from artificial RNA. Working single-handedly during lockdown, Taylor generated five XNAzymes targeting sequences in SARS-CoV-2’s genome in a matter of days.
Enzymes are natural catalysts that facilitate chemical transformations—in this case, by chopping other molecules apart. But previous DNA-and RNA-based enzymes have struggled to cut long, highly structured molecules such as virus genomes. Instead they destroy targets by recruiting existing enzymes inside cells—a less precise process that can lead to “off-target” cuts and increased side effects.
Summary: Tracking hippocampal neurons in mice as they watched a movie revealed novel ways to improve artificial intelligence and track neurological disorders associated with memory and learning deficits.
Source: UCLA
Even the legendary filmmaker Orson Welles couldn’t have imagined such a plot twist.
One question for Brad Ringeisen, a chemist and executive director of the Innovative Genomics Institute. Founded by Nobel Prize-winning biochemist Jennifer Doudna, it aims to bridge revolutionary gene-editing tool development to affordable and accessible solutions in human health and climate.
Will CRISPR cure cancer?
We’re always thinking about: What are those targets in the future? Cancer is one of those things. The biggest impact is going to be what’s called systemic delivery, or in vivo delivery. There’s been one example of this in the community right now—to treat a liver disease. Intellia Therapeutics, a biotech company, has shown that you can actually intravenously apply CRISPR-Cas9 treatment. (CRISPR is the guide RNA, the targeting molecule, and Cas9 is the cutting molecule that edits DNA.) It can go to the liver and target the liver cells, and make edits at a high enough efficacy to treat genetic liver disease. The problem is that the liver is the easiest. It’s like the garbage can of the body. Pretty much anything that you put into the body is ultimately going to find its way to the liver. So that’s absolutely the easiest tissue to deliver to. But trying to deliver to a solid tumor, or to the brain, is much more difficult.
A team of undergraduate and graduate chemistry students in Jennifer Hines’ lab at Ohio University recently uncovered a new class of compounds that can target RNA and disrupt its function. This discovery identified a chemical scaffold that could ultimately be used in the development of RNA-targeted medicines to treat bacterial and viral infections, as well as cancer and metabolic diseases.
RNA is chemically like DNA but also controls the extent to which the DNA’s instructions are carried out within a living cell. It is this essential regulatory role in the function of the cell that makes RNA such an attractive target.
“Trying to target RNA is at the forefront of medicinal chemistry research with enormous potential for treating diseases,” said Hines, professor of chemistry and biochemistry in the College of Arts and Sciences. “However, there are relatively few compounds known to directly modulate RNA activity which makes it challenging to design new RNA-targeted therapeutics.”
A team of neuroscientists at the New York University School of Medicine has found a link between chronic pain and overactive pyramidal neurons during sleep periods. In their study, published in the journal Nature Neuroscience, the group conducted experiments with injured mice experiencing chronic pain.
Prior research has shown that there is often a link between chronic pain and insomnia. After experiencing a neural injury of some sort, many patients are left with some degree of lasting pain. This tends to result in poor sleep and sometimes insomnia. Once that happens, the pain becomes worse, and over time becomes chronic. But why this happens has been a mystery. In this new effort, the team in New York conducted experiments with mice hoping to find the answer.
The work involved inducing chronic pain in mice by damaging two of the three branches that make up a group of sciatic nerves. Doing so led to skin sensitivity in the legs. The researchers scanned the brains of each of the mice before and after the damage. They observed that pyramidal neurons in the part of the cerebral cortex responsible for sensation processing in the skin became more active. And over the course of several weeks, the activity increased, peaking during non-REM sleep.
Approximately 9,000 people are admitted to Norwegian hospitals with stroke each year. About half of these patients feel exhausted afterwards, and many patients sleep more during the day than before the stroke. These after-effects are challenging and significantly affect patients’ everyday life.
However, we still have a limited understanding of which factors lead to increased fatigue and daytime sleep after stroke. Our research group therefore wanted to investigate whether cognitive and emotional complaints are related to increased fatigue and sleep during the day.
Our results were recently published in an article in the journal Frontiers in Neurology.
