Molecularly manipulating pyrazinoquinoxaline derivatives to construct NIR-II AIEgens for multimodal phototheranostics of breast cancer bone metastases.

Multimodal phototheranostics on the basis of single molecular species shows inexhaustible and vigorous vitality, particularly those emit fluorescence in the second near-infrared window (NIR-II), the construction of such exceptional molecules nonetheless retains formidably challenging. In view of the undiversified molecular skeletons and insufficient phototheranostic outputs of previously reported NIR-II fluorophores, herein, electron acceptor engineering based on heteroatom-inserted rigid-planar pyrazinoquinoxaline was manipulated to fabricate aggregation-induced emission (AIE)-featured NIR-II counterparts with donor-acceptor-donor (D-A-D) architecture. Systematical investigations substantiated that one of those synthesized AIE molecules, namely 4TPQ, incorporating a fused thiophene acceptor, synchronously exhibited high molar absorptivity (ε), NIR-II emission, typical AIE tendency, significant reactive oxygen species (ROS) generation, and high photothermal conversion efficiency.

Critical review on emerging photocatalytic membranes for pollutant removal: From preparation to application.

Due to synergistically enhanced separation and degradation performances, photocatalytic membranes offer an environmentally friendly and energy-sustainable method for water purification. However, a comprehensive review on preparation and application of photocatalytic membranes is still lacking. Systematically comparing different photocatalytic membrane fabrication methods and revealing the underlying mechanisms of their respective applications are of particular interest.

Compound heterozygous mutations (p.L68R∗37 and p.T241N) lead to abnormal protein levels and structures in hereditary FVII deficiency.

Background: Congenital factor VII (FVII) deficiency is a genetic disorder characterized by decreased FVII activity, which sometimes leads to fatal bleeding. Numerous variants have been found in FVII deficiency, but mutations vary among patients. Each mutation deserves further exploration for each patient at risk of bleeding.

Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.

The pathogenesis of thoracic aortic aneurysm (TAA) in Marfan syndrome (MFS) is generally attributed to vascular smooth muscle cell (VSMC) pathologies. However, the role of immune cell-mediated inflammation remains elusive. Single-cell RNA sequencing identified a subset of CX3CR1+ macrophages mainly located in the intima in the aortic roots and ascending aortas of Fbn1C1041G/+ mice, further validated in MFS patients.