Structural investigations into colour-tuneable fluorescent InZnP-based quantum dots from zinc carboxylate and aminophosphine precursors.

Fluorescent InP-based quantum dots have emerged as valuable nanomaterials for display technologies, biological imaging, and optoelectronic applications. The inclusion of zinc can enhance both their emissive and structural properties and reduce interfacial defects with ZnS or CdS shells. However, the sub-particle distribution of zinc and the role this element plays often remains unclear, and it has previously proved challenging to synthesise Zn-alloyed InP-based nanoparticles using aminophosphine precursors.

Biocompatible Magnetic Conjugated Polymer Nanoparticles for Optical and Lifetime Imaging Applications in the First Biological Window.

Conjugated polymers are organic semiconductors that can be used for fluorescence microscopy of living specimens. Here, we report the encapsulation of the bright-red-emitting conjugated polymer, poly[{9,9-dihexyl-2,7-bis(1-cyanovinylene)fluorenylene}-alt-co-{2,5-bis(,'-diphenylamino)-1,4-phenylene}] (CN-FO-DPD), and superparamagnetic iron oxide nanoparticles (SPIONs) within poly(styrene--maleic anhydride) (PSMA) micelles. The resulting particles exhibited an emission peak at 657 nm, a fluorescence quantum yield of 21%, an average diameter of 65 nm, and a ζ potential of -30 mV.

Author Correction: Therapeutic potential of KLF2-induced exosomal microRNAs in pulmonary hypertension.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Therapeutic potential of KLF2-induced exosomal microRNAs in pulmonary hypertension.

Pulmonary arterial hypertension (PAH) is a severe disorder of lung vasculature that causes right heart failure. Homoeostatic effects of flow-activated transcription factor Krüppel-like factor 2 (KLF2) are compromised in PAH. Here, we show that KLF2-induced exosomal microRNAs, miR-181a-5p and miR-324-5p act together to attenuate pulmonary vascular remodelling and that their actions are mediated by Notch4 and ETS1 and other key regulators of vascular homoeostasis.