In Ruijs-Aalfs progeria syndrome, patients experience accelerated aging and liver cancer.
Now, scientists showed that mutations in a certain gene prevent cells from repairing DNA damage during mitosis, triggering inflammatory immune responses that may fuel premature aging.
Read more.
Researchers have shown that harmful bonds between protein and DNA fuel immune attack in progeria. Pumping up a protein that cuts these bonds could prevent symptoms.
Support this channel on Patreon to help me make this a full time job: https://www.patreon.com/whatdamath (Unreleased videos, extra footage, DMs, no ads)
Alternatively, PayPal donations can be sent here: http://paypal.me/whatdamath.
Get a Wonderful Person Tee: https://teespring.com/stores/whatdamath.
More cool designs are on Amazon: https://amzn.to/3QFIrFX
Hello and welcome! My name is Anton and in this video, we will talk about a strange bacterial communication technique similar to radio waves.
Links:
https://www.cell.com/current-biology/fulltext/S0960-9822…all%3Dtrue.
Previous videos: https://www.youtube.com/watch?v=4M872c27bSc.
https://www.science.org/doi/10.1126/sciadv.adj1539
#science #radio #bacteria.
0:00 Bacterial communication and social lives.
1:20 Quorum sensing and multilingual bacteria?
4:20 Physical bridge communication.
5:20 New communication involves radio like processing.
8:00 What this is used for.
9:15 Why this is important for the medical fields.
Enjoy and please subscribe.
Bitcoin/Ethereum to spare? Donate them here to help this channel grow!
Studying mice and two clinical cohorts, researchers in Science TranslationalMedicine show that the protein meteorin-like worsens outcomes during invasive candidiasis by suppressing antifungal macrophages, suggesting the protein could offer a marker and potential target.
📄
METRNL is elevated in candidemia in mice and humans and provides a potential therapeutic target for life-threatening candidemia.
Scientists have identified a previously unknown molecular safeguard that protects the heart during pregnancy, shedding new light on the causes of peripartum cardiomyopathy (PPCM), a rare and life-threatening form of pregnancy-related heart failure.
In a study published in Nature Communications, the team reveal that the gene the peptidyl-tRNA hydrolase 2 (PTRH2) plays a critical role in helping the maternal heart adapt to pregnancy-induced stress.
In wild-type female mice hearts, Ptrh2 protein levels significantly increase during pregnancy and decrease postpartum, demonstrating a protective role in response to pregnancy-initiated cardiac stresses.
Using advanced mouse models, the researchers showed that loss of PTRH2 leads to severe postpartum heart failure. “During pregnancy, the heart increases in size to account for increased blood flow—but without PTRH2, the heart doesn’t return to normal,” explained a co-first author. “That kind of enlargement can be extremely dangerous and, in many cases, fatal.”
The authors also demonstrate that infusion of a caspase 3-specific inhibitor attenuated the PPCM phenotype. Thus, Ptrh2 act as a negative regulator of pregnancy-induced cardiac stresses by activating pro-survival signals and blocking apoptotic signals.
The findings point to new therapeutic possibilities and underscore the urgent need for better treatments. ScienceMission sciencenewshighlights.
Blood pressure is one of the most common health problems worldwide, yet it remains difficult to control for many patients even with daily medication. New research from the United Kingdom suggests a different approach could help. Scientists report that a treatment given just twice a year may offer sustained blood pressure reductions for people whose hypertension has proven hard to manage.
The findings come from a large international clinical trial published in JAMA and led by researchers at Queen Mary University of London. The study focused on a long-acting injectable therapy designed to work alongside existing blood pressure medications rather than replace them.
Here, Sarah Gaffen & team report on the noncanonical RNA binding protein Arid5a as an activator of TNF signaling that is elevated in human RA tissues. And in mice… its loss results in resistance to collagen-induced arthritis:
The figure shows TNF stimulation causes Arid5a accumulation in the cytoplasm in a murine stromal fibroblast cell line untreated (left) and treated (right); Arid5a (red); RPL7A (green); nuclei (blue).
1Division of Rheumatology & Clinical Immunology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
2BIOCEV, First Faculty of Medicine, Charles University, Vestec, Czech Republic.
3School of Medicine, Tsinghua Medicine, Tsinghua University, Beijing, China.
Now online! Organ-level localized delivery is a long-standing challenge, especially for gene therapy. This study establishes a universal conformality theory that enables POCKET—a kirigami-structured bioelectronic patch—to integrate seamlessly with organs and realize precise intracellular electro-delivery of therapeutics without off-target effects.