53 papers
Pharmacology and toxicology explore how substances interact with living systems, ranging from the development of life-saving medicines to understanding the dangers of chemical exposure. This field sits at the critical intersection of chemistry and biology, asking essential questions about how drugs work, how the body processes them, and what happens when things go wrong. It is a dynamic area where researchers constantly strive to improve patient safety while discovering new therapeutic possibilities.
At Gist.Science, we bridge the gap between complex research and public understanding by curating the latest preprints from bioRxiv in this vital category. Our team processes every new submission from bioRxiv as it appears, transforming dense scientific data into both plain-language overviews and detailed technical summaries. This ensures that whether you are a specialist or a curious reader, you can grasp the significance of these emerging findings without getting lost in jargon.
Below are the most recent pharmacology and toxicology papers from bioRxiv, each accompanied by our expert analysis to help you navigate the latest scientific breakthroughs.
This paper introduces a fractional quasi-steady-state approximation (fQSSA) for target-mediated drug disposition models to address memory effects and parameter identifiability challenges, deriving a rigorous validity condition and demonstrating its utility through successful application to recombinant human erythropoietin data.
This study reveals that the vaccine adjuvant lipid A uniquely enhances mitochondrial activity, thereby not only boosting immune responses but also counteracting doxorubicin-induced cardiac dysfunction and preserving antibody production.
The study demonstrates that the nonsteroidal agent DKD99 selectively and allosterically reverses the positive modulatory effects of allopregnanolone on human GABA receptors without altering GABA's action, offering a promising alternative to steroid-based therapies for conditions involving neurosteroid intolerance.
This study reveals that the slow dissociation kinetics of nitazenes from the μ-opioid receptor, driven by specific interactions with receptor subpockets, underlies their high affinity and the increased naloxone doses required to reverse overdoses.
This study demonstrates that inhibiting ERK1/2 and EZH2 increases utrophin expression in human myoblasts, with a unique sustained effect in Duchenne muscular dystrophy (DMD) patient-derived cells that also reverses altered myogenic transcription factor profiles, suggesting a promising therapeutic strategy to compensate for dystrophin loss and restore muscle regeneration.
This study demonstrates that cannabidiol (CBD) promotes recovery from traumatic brain injury in zebra finches by enhancing astrocyte viability and reducing injury-induced glial stress responses across song control nuclei, thereby preserving specialized neural circuits essential for vocal learning.
This study demonstrates that Pinus sp. leaf extracts exhibit potent, non-toxic antileishmanial activity against Leishmania donovani through antioxidant and immunomodulatory effects, with metabolomic and in silico analyses suggesting that flavanone O-glycosides, alkaloids, and diterpenes within the extracts inhibit the parasite via trypanothione reductase.
This study demonstrates that low concentrations of cadmium exposure alter Jamaican fruit bat adaptive immune responses by upregulating B and T cell transcripts and inducing a Th2-dominant profile, without significantly affecting viral replication in kidney cells.
This study demonstrates that chronic nicotine self-administration increases impulsive action in rats, a deficit specifically reduced by the nAChR antagonist mecamylamine but not by agonists or partial agonists, highlighting the utility of the Go/No-Go task for investigating nicotine-induced impulsivity.
This study identifies hydroxysteroid 11-beta dehydrogenase 1 (HSD11B1) as the direct molecular target of magnesium isoglycyrrhizinate (MgIG) and elucidates its therapeutic mechanism in alcohol-associated liver disease through the suppression of the HSD11B1-SREBP2-IDI1 signaling axis, which alleviates hepatic steatosis, inflammation, and apoptosis.