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Category: biotech/medical

Weight Changes With Tirzepatide and Concomitant Weight-Inducing Medications: Post Hoc Analysis of Randomized Clinical Trials

In three RCTs, Tirzepatide was associated with clinically meaningful weight loss among adults with overweight or obesity, even when concomitant weight-inducing medications were initiated during treatment.

Question What is the association between tirzepatide and weight reduction among patients with overweight or obesity who initiated concomitant weight-inducing medications?

Findings In this post hoc analysis of participants in the SURMOUNT-1,-3, and-4 trials receiving at least 1 concomitant weight-inducing medication (17.3%-20.0%), tirzepatide treatment was associated with comparable weight loss to the primary study results.

Triple pre-surgery therapy may boost immunity against soft tissue sarcoma

Early results from preclinical studies and a clinical trial led by researchers at the UCLA Health Jonsson Comprehensive Cancer Center and Stanford Medicine suggest that combining targeted radiation therapy with an experimental immune-boosting drug called BO-112 and anti-PD-1 therapy before surgery may help the immune system fight aggressive soft tissue sarcomas.

The findings, published in Cancer Discovery, show that the approach can reshape the tumor microenvironment to activate the body’s immune cells against cancer.

Soft tissue sarcomas are a rare and often hard-to-treat group of cancers that typically require a combination of surgery, radiation therapy and other systemic treatments. However, these tumors may still be resistant to standard therapies, highlighting the need for new treatment strategies.

Unraveling the secrets of telomerase, an enzyme linked to aging and cancer

A central question in molecular biology is how cells protect their chromosomes from damage during repeated cell division. At the heart of this protective process is an enzyme called telomerase. Now an international research team has mapped the three-dimensional structure of telomerase in the yeast Saccharomyces cerevisiae, a widely used model organism in genetics.

Using cutting-edge technology, the scientists were able to visualize the architecture of this complex enzyme in unprecedented detail, uncovering unexpected features that may explain how it functions.

This major discovery was the result of an international collaboration between Pascal Chartrand, a professor in the Department of Biochemistry and Molecular Medicine at Université de Montréal, and researchers from Université de Sherbrooke and the MRC Laboratory of Molecular Biology in the U.K. Their findings were recently published in Science.

Individual-Level Factors Associated With 10-Year Incidence of Alzheimer Disease and Related Dementias in the VA Million Veteran Program

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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.

Continue reading “IPSC-induced multilineage liver organoids, small intestinal organoids and brain organoids sustain pangenotype hepatitis E virus propagation” | >

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.

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