Browse Articles

Symmetric Boron-Bridged Carbon Quantum Frameworks for Light-Emitting Diodes with over 20% External Quantum Efficiency

A genetically tractable non-vertebrate system to study complete camera-type eye regeneration

Integrated porosity estimation of partially saturated sand–hematite mixtures using electrical resistivity and elastic wave velocity

Breaking Bonds with Short-Wave Infrared Light: BODIPY Photocages for Two-Photon Activation in the 900–1500 nm NIR-II Window

Sequencing a DNA analog composed of artificial bases

Linking woody plant species richness with selected ecosystem services and dendrometric features in Okalma natural forest reserve

Dipole Characteristics of Polymers with Main-Chain Polar Rings: Impact of Dipole Strength and Orientation on Reactivity and Material Properties

Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice

Abstract Aging increases the risk of developing fibrotic diseases by hampering tissue regeneration after injury. Using longitudinal single-cell RNA-seq and spatial transcriptomics, here we compare the transcriptome of bleomycin (BLM) -induced fibrotic lungs of young and aged male mice, at 3 time points corresponding to the peak of fibrosis, regeneration, and resolution. We find that lung injury shifts the transcriptomic profiles of three pulmonary capillary endothelial cells (PCEC) subpopulations. The associated signatures are linked to pro-angiogenic signaling with strong Lrg1 expression and do not progress similarly throughout the resolution process between young and old animals. Moreover, part of this set of resolution-associated markers is also detected in PCEC from samples of patients with idiopathic pulmonary fibrosis. Finally, we find that aging also alters the transcriptome of PCEC, which displays typical pro-fibrotic and pro-inflammatory features. We propose that age-associated alterations in specific PCEC subpopulations may interfere with the process of lung progenitor differentiation, thus contributing to the persistent fibrotic process typical of human pathology.

Targeting programmed death ligand 1 for anticancer therapy using computational drug repurposing and molecular simulations

Ancient marine reptile was a silent swimmer

Harnessing <i>O</i> -Vinylhydroxylamines for Ring-Annulation: A Scalable Approach to Azaindolines and Azaindoles

Single-faceted IrO2 monolayer enabling high-performing proton exchange membrane water electrolysis beyond 10,000 h stability at 1.5 A cm-2

Network intrusion detection model using wrapper based feature selection and multi head attention transformers

Pushing the Thermodynamic and Kinetic Limits of Near-Infrared Emissive Cr^III Complexes in Photocatalysis

Anti-radar based on metasurface

Assessment of terrestrial radionuclide exposure and contamination rates within the Mbaitoli area, Nigeria

Electronic Textiles Based on Conductive Metal–Organic Frameworks as Scavengers and Sensors of Toxic Oxyanions from Water

IgG autoantibodies in bullous pemphigoid induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes

Sambucus nigra alleviates fenpropathrin-induced hepatorenal toxicity in rats via modulation of NF-κB/TNF-α axis

Abstract This research assessed the effectiveness of Sambucus nigra (SN) in alleviating hepatorenal injury caused by fenpropathrin (FNP) in rodents. Six equal groups were created from the 30 Wistar rats: Group 1 was the negative control, Groups 2 and 3 were the SN control groups, Group 4 was the FNP group, and Groups 5 and 6 were the FNP + SN combination groups. The hepatoprotective and renoprotective effects of SN were assessed by quantifying serum enzyme markers, including ALT, AST, ALP, blood urea nitrogen, and creatinine. Oxidative stress indicators, RT-PCR analysis, histological examination, and immunohistochemistry studies were conducted on the liver and kidneys to confirm the previously indicated parameters. The rats administered FNP injections displayed increased blood marker enzyme levels, altered oxidant-antioxidant equilibrium, and significant pathogenic changes in hepatic and renal tissues. Furthermore, these rats exhibited elevated levels of caspase-3 and iNOS, linked to the triggered expression of TNF-α and NF-κB genes in these tissues. Administering SN enhanced all the aforementioned toxicological parameters. The prospective hepato-renal therapeutic benefits of SN against impairment of the liver and kidneys induced by FNP have been evidenced through its anti-inflammatory, antioxidant, and anti-apoptotic pathways.

Mechanobiology of the blood-brain barrier during development, disease and ageing

Abstract The blood-brain barrier (BBB) preserves brain health through selective permeability, and its disruption is a hallmark of many neurological disorders. Mechanical stimuli such as shear stress and cyclic strain are increasingly recognised to influence BBB integrity and function, while alterations in tissue stiffness and extracellular matrix composition contribute to its breakdown during ageing and disease. Despite its importance, BBB mechanobiology remains underexplored. Here we highlight the central role of mechanics in BBB development, pathology, and ageing, identify key knowledge gaps, and argue that combining innovative BBB model systems with mechanical probing techniques could transform therapeutic strategies targeting brain vascular dysfunction.