Even given a set of possible quantum states for our cosmos, it’s impossible for us to determine which one of them is correct
Given that pk1 is located within the HCV coding region, we next investigated a potential role in translation elongation. We inserted pk1 into the ORF of Gaussia luciferase and used the HCV IRES to initiate translation (Figure 3 B, left). To ensure that the highly structured HCV IRES did not affect pk1 folding, we included a 99-nt linker sequence with low structural propensity between the HCV IRES and pk1. As controls, we used the pk1-unzip mutant and a randomized pk1, where the pk1 sequence was shuffled by three nucleotides, thereby maintaining the same amino acid composition as the WT pk1.
The RNA constructs described above were transfected into cells, and luciferase activity was measured at various time points to assess translation activity (Figure 3B, right). We observed that pk1 significantly inhibited translation elongation at all time points tested compared to the pk1-unzip and random controls. Notably, at 4 h post-transfection, there was nearly a 4-fold difference between the activity of pk1 and the pk1-unzip mutant, indicating that the pseudoknot structure itself, rather than just its constituent stems, is crucial for the observed translation inhibition (Figure 3B). To further examine the structural basis of this effect, we introduced a pk1-compensatory mutant that restores the disrupted base pairing in the pk1-unzip mutant using synonymous G-U wobble and A-U base pairs (sequence shown in Figure 3A).
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.
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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.
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Leading artificial intelligence companies have started to use their own systems to accelerate research and development, with each generation of AI systems contributing to building the next generation. This report distills points of consensus and disagreement from our July 2025 expert workshop on how far the automation of AI R&D could go, laying bare crucial underlying assumptions and identifying what new evidence could shed light on the trajectory going forward.
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.