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Category: biotech/medical – Page 21
IPSC-induced multilineage liver organoids, small intestinal organoids and brain organoids sustain pangenotype hepatitis E virus propagation
Liu et al. present via https://bit.ly/4bV6X0s (Original research, Hepatology section).
A major step forward for translational research, this study shows that human organoid systems can support replication of multiple hepatitis E virus genotypes—offering a powerful new platform for studying infection and testing therapies.
Background Hepatitis E virus (HEV), the leading global cause of acute viral hepatitis, lacks robust in vitro models for virology and pathogenesis research.
Objective We evaluated induced pluripotent stem cell (iPSC)-induced human liver, intestinal and brain organoids (hLOs, hIOs and hBOs) as platforms for HEV infection and replication.
Methods Multilineage organoids were infected with clinical HEV genotypes 1, 3 and 4. Viral tropism, host responses and antiviral efficacy were assessed.
Results All organoids supported the complete life cycle of HEV. hLOs exhibited infection in hepatocytes, cholangiocytes, macrophages and stellate cells, accompanied by elevated interleukin-6 levels, impaired hepatic function (reduced secretion of albumin and Factor IX) and increased levels of alanine aminotransferase and aspartate aminotransferase, indicating hepatocellular injury.
Fluid restriction in patients with heart failure: a systematic review
Background Fluid restriction is a commonly prescribed non-pharmacological intervention in the management of heart failure (HF). However, data on its efficacy and safety are scarce. Recent randomised clinical trial (RCT) data prompt reassessment of the available evidence.
Methods CINAHL, EMBASE, PubMed and the Cochrane Library were searched up to 1 May 2025. RCTs were included if adults with HF were randomised to fluid restriction in comparison to a liberal or unrestricted intake, less strict restriction or usual care. Outcomes of interest were mortality, HF hospitalisation, quality of life (QoL), thirst distress, New York Heart Association (NYHA) class and N-terminal pro-Brain Natriuretic Peptide (CRD42022292319). No meta-analysis was performed due to high heterogeneity of the included trials.
Results In total, four RCTs were included, comprising 682 randomised inpatient, recently discharged and stable outpatient patients (ranging from 46 to 504 patients per trial). Only one study had a low risk of bias. None of the four trials found a significant difference in mortality or HF hospitalisations. For QoL, the results are contradictory, but overall, there is no clear benefit for fluid restriction, but it resulted in more thirst distress. No significant differences in NYHA class or (NT-pro)BNP were observed.
Temporal Dynamics of the No-Reflow Phenomenon on Serial Perfusion MRI After Thrombectomy
Now online! STING signaling modulation by COPII cargo recognition: Lyu et al. identify the STING-ER-exit motif and the mechanism of its recognition by the COPII vesicle cargo-binding protein SEC24C. This study reveals how STING achieves controlled rather than constitutive ER exit and how COPII cargo recognition of STING can be modulated to control STING signaling.
What changes happen in the aging brain?
A new study from the Salk Institute maps how the aging brain changes at the epigenetic level — cell type by cell type.
The researchers created one of the most detailed single-cell atlases yet of the aging mouse brain, spanning 8 brain regions, 36 cell types, and hundreds of thousands of cells. They found major age-related changes in DNA methylation, chromatin structure, and gene activity, with some of the strongest changes appearing in non-neuronal cells.
This kind of work matters because it moves brain aging closer to mechanism — not just describing decline, but identifying the molecular regulatory shifts that may drive vulnerability to neurodegenerative disease.
Highlights Salk researchers create epigenetic atlas of cell type-specific changes in the aging mouse brain The atlas represents eight different brain regions and 36 different cell types, and shows clear epigenetic differences associated with different ages The new resource—available publicly on Amazon Web services—can be used to unravel age-related contributions to neurodegenerative diseases like Alzheimer’s, Parkinson’s, and ALS LA JOLLA—Neurodegenerative diseases affect more than 57 million people globally. The incidence of these diseases, from Alzheimer’s to Parkinson’s to ALS and beyond, is expected to double every 20 years. Though scientists know aging is a major risk factor for neurodegenerative diseases, the full mechanisms behind aging’s impact remain unclear.
From engineered fungal molecules to drug leads, chem-bio hybrid synthesis enables antiparasitic drug discovery
Amebiasis is a parasitic disease caused by the microscopic protozoan Entamoeba histolytica. Infection occurs through the ingestion of cysts from contaminated water or food. Worldwide, approximately 50 million symptomatic cases are estimated annually, mainly in tropical and subtropical regions.
Fumagillin, a fungal natural product, has been studied for decades as a potential antiparasitic drug, but its more potent relative, ovalicin, was never developed. Now, a study published in the Journal of the American Chemical Society reveals why: although ovalicin is highly active against amebiasis, liver enzymes rapidly break it down in the body. Researchers used a chem-bio hybrid approach to turn that insight into metabolically stable drug candidates that worked in animal models of amebiasis, including liver infection with abscess formation.
The research team, led by scientists from the Graduate School of Bioagricultural Sciences at Nagoya University, identified the liver cytochrome P450 enzymes responsible for ovalicin breakdown, with CYP 2B1 and CYP 2C6 emerging as the main drivers. Blocking these enzymes with a chemical inhibitor significantly prolonged ovalicin survival, providing strong evidence that rapid liver metabolism limits its effectiveness.
New synthetic origin of replication lets multiple plasmids coexist in one bacterial cell
“If it ain’t broke, don’t fix it,” goes the old adage, which Rice University professor James Chappell completely ignored in a recent Nature Communications publication. In the study, Chappell describes an innovation in plasmids, circular pieces of DNA that have been a workhorse of molecular biology research since the 1970s.
“For decades, we’ve been designing experiments around two major limitations of plasmids: fixed copy numbers and incompatibility,” said Chappell, the corresponding author on the study. “While functional, such workarounds are clunky. We created a synthetic version of a part of the plasmid called the origin of replication that allows us to modify the plasmid instead of modifying the experiment.”
Plasmids are typically put into bacterial cells, where they use the cell’s machinery to build proteins and create copies of themselves. Each plasmid generates tiny pieces of a stop signal, called a negative regulator, which binds to the origin of replication (ORI).
Unlocking scalable entanglement will enable next-generation quantum computing
Quantum computing promises to transform our world in rapid, radical and revolutionary ways: solving in seconds problems that would take classical computers years, accelerating the discovery of new medicines, creating sustainable materials, optimizing complex systems, and strengthening cybersecurity. It does so using qubits, the quantum counterparts of classical bits, which can occupy multiple states simultaneously and enable a fundamentally new kind of computation.
For example, imagine 1,000 trucks need to arrive at 10,000 different locations, each, in different parts of the country. A traditional computation model would examine each of the 10 million possible routes one by one to evaluate their efficacy, but a quantum model would be able to evaluate all those millions of different routes instantaneously.
At the same time, quantum sensing is opening new frontiers in precision measurement, enabling technologies such as ultra-sensitive medical imaging and navigation systems that can detect minute changes in gravity or magnetic fields, capabilities that could allow doctors to identify diseases earlier or help vehicles navigate without GPS. UCF researchers believe the science of light, photonics, may hold the key to unlocking quantum computing’s true potential.
DNA shape explains crucial gene-therapy challenges
CRISPR is a powerful DNA-editing tool that has underpinned huge advancements in human health care in the last decade. It is a precision tool, but is not perfect, and misplaced DNA edits can compromise safety and efficacy, costing billions each year. Researchers at the MRC Laboratory of Medical Sciences (LMS), Imperial College London and the University of Sheffield have published research in Nature showing that the physical twisting of DNA plays an important role in these mistakes. Using a newly developed platform of tiny (nanometer-sized) DNA circles, called DNA minicircles, the team captured never-before-seen interactions between CRISPR and DNA, providing insights that could help eradicate errors altogether.
CRISPR-Cas9 has transformed biology by giving scientists a programmable way to cut and edit DNA. Its ever-growing impact includes groundbreaking therapies for genetic diseases such as sickle cell anemia and an increasing role in personalized cancer treatment and rapid diagnostics. But even carefully designed CRISPR systems can sometimes cut DNA sequences that were not the intended targets.
“It’s a tool that is not perfect and can introduce errors and make edits where it shouldn’t make them,” says Professor David Rueda, head of the Single Molecule Imaging group at the LMS and Chair in Molecular and Cellular Biophysics at Imperial College London. “And it’s an important problem for the industry. It’s been estimated to be $0.3 to $0.9 billions per year in industry costs, in profiling off-targets, redesigning guides and delays.”
Abstract: ADAMTS7 has been repeatedly associated with coronary artery disease
ADAMTS7 has been repeatedly associated with coronary artery disease.
https://doi.org/10.1172/JCI187451 In this Research Article, Robert C. Bauer & team use the largest human atherosclerosis carotid artery scRNA-seq dataset and new mouse models to demonstrate that ADAMTS7 is expressed across multiple vascular cell types and contributes to atherosclerosis by promoting lipid accumulation in smooth muscle cells.
The image shows smooth muscle cells labeled with ZsGreen and counterstained with DAPI (blue) for nuclei—indicating increased foam cells from a diet-induced mouse model of atherosclerosis with Adamts7-overexpressing SMCs were from SMC origin.
1Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University, New York, New York, USA.
2Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Address correspondence to: Robert C. Bauer, Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University, 630 W. 168th Street, PS10-401, New York, New York 10,032, USA. Phone: 1.212.342.0952; Email: [email protected].